PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
2604739-4	1989	Thioridazine was a potent linear mixed-type inhibitor of P-450b-dependent 7-pentoxyresorufin O-depentylase activity in phenobarbital-induced rat liver.	Phenobarbital	119-132	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	57-63
2574176-2	1989	The phenobarbital-inducible P-450 forms IIB1 and IIB2 are identical in sequence except for 14 amino acid differences within the carboxyl-terminal half of the molecule.	Phenobarbital	4-17	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	40-44
2807620-4	1989	Long-term treatment of phenobarbital increased the plasma concentrations of HDL2-cholesterol, HDL3-cholesterol and HDL3-phospholipid, and decreased the plasma concentrations of low density lipoprotein + very low density lipoprotein-cholesterol.	Phenobarbital	23-36	junctophilin 3	Homo sapiens	76-80
2480807-1	1989	The expression of phenobarbital-, pregnenolone 16 alpha-carbonitrile- and polycyclic aromatic hydrocarbon-inducible cytochromes P-450 and of phenobarbital-inducible UDP-glucuronosyltransferase was examined in developing rat liver.	Phenobarbital	141-154	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	165-192
2480807-5	1989	Our contribution definitively demonstrates that the ability of phenobarbital to enhance P-450 and UDPGT RNAs is strictly restricted to hepatocytes and remains roughly unchanged throughout ontogenesis.	Phenobarbital	63-76	UDP glucuronosyltransferase family 2 member B15	Rattus norvegicus	98-103
2628419-0	1989	Role of growth hormone in modulating the constitutive and phenobarbital-induced levels of two P-450(6)beta (testosterone 6 beta-hydroxylase) mRNAs in rat livers.	Phenobarbital	58-71	gonadotropin releasing hormone receptor	Rattus norvegicus	8-22
2628419-0	1989	Role of growth hormone in modulating the constitutive and phenobarbital-induced levels of two P-450(6)beta (testosterone 6 beta-hydroxylase) mRNAs in rat livers.	Phenobarbital	58-71	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	94-139
2576915-1	1989	The effect of low concentration of hepatic glutathione on the induction of GGT by phenobarbitone was investigated.	Phenobarbital	82-96	gamma-glutamyltransferase 1	Rattus norvegicus	75-78
2600817-10	1989	When the rats received D5W and an injection of vasopressin, 25 I.U./kg, or vasopressin only, the infused dose and the serum and CSF concentrations of phenobarbital at LRR were significantly lower than in controls despite the 2.5-hr interval between the respective pretreatments and the phenobarbital infusion.	Phenobarbital	150-163	arginine vasopressin	Rattus norvegicus	47-58
2600817-10	1989	When the rats received D5W and an injection of vasopressin, 25 I.U./kg, or vasopressin only, the infused dose and the serum and CSF concentrations of phenobarbital at LRR were significantly lower than in controls despite the 2.5-hr interval between the respective pretreatments and the phenobarbital infusion.	Phenobarbital	286-299	arginine vasopressin	Rattus norvegicus	47-58
2635735-0	1989	Induction of glutathione S-transferase by phenobarbital in rat hepatocyte culture.	Phenobarbital	42-55	hematopoietic prostaglandin D synthase	Rattus norvegicus	13-38
2635735-1	1989	The in vitro effect of phenobarbital on glutathione S-transferase (GST) activity toward 1-chloro-2,4-dinitrobenzene (CDNB) in rat hepatocyte culture was investigated.	Phenobarbital	23-36	hematopoietic prostaglandin D synthase	Rattus norvegicus	40-65
2635735-1	1989	The in vitro effect of phenobarbital on glutathione S-transferase (GST) activity toward 1-chloro-2,4-dinitrobenzene (CDNB) in rat hepatocyte culture was investigated.	Phenobarbital	23-36	hematopoietic prostaglandin D synthase	Rattus norvegicus	67-70
2635735-2	1989	Treatment of hepatocytes with a medium containing 6 or 8 mM phenobarbital for 20 h increased the specific activity of GST approx.	Phenobarbital	60-73	hematopoietic prostaglandin D synthase	Rattus norvegicus	118-121
2635735-4	1989	When induction of GST by phenobarbital treatment was observed, the cellular level of phenobarbital determined by HPLC was approx.	Phenobarbital	25-38	hematopoietic prostaglandin D synthase	Rattus norvegicus	18-21
2635735-4	1989	When induction of GST by phenobarbital treatment was observed, the cellular level of phenobarbital determined by HPLC was approx.	Phenobarbital	85-98	hematopoietic prostaglandin D synthase	Rattus norvegicus	18-21
2635735-6	1989	Thus, an inductive effect of phenobarbital on GST was observed in vitro as well as in rat liver.	Phenobarbital	29-42	hematopoietic prostaglandin D synthase	Rattus norvegicus	46-49
2584196-3	1989	Animal treatment with phenobarbital results in a 3.7-fold increase in microsomal cytochrome P-450 concentration and a concomitant, regioselective 6.8- and 3.4-fold increase in the liver concentration of 8,9- and 14,15-epoxyeicosatrienoic acids, respectively.	Phenobarbital	22-35	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	81-97
2591538-5	1989	After exposure to phenobarbital an increase in GST 3 and 4 mRNA levels was demonstrated in both culture systems.	Phenobarbital	18-31	glutathione S-transferase pi 1	Rattus norvegicus	47-58
2819695-9	1989	In all 4 types of mice after 4 and 28 days of treatment, PB increased the concentration of cytochrome P-450, the activity of aminopyrine-N-demethylase (AmDm) and 7-ethoxyresorufin-O-deethylase (ErDe) and the oxidation of testosterone (T).	Phenobarbital	57-59	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	91-107
2700066-6	1989	Phenobarbital also increased the activities of glucose-6-phosphate dehydrogenase and malic enzyme in lean animals indicating an increased NADPH generation.	Phenobarbital	0-13	glucose-6-phosphate dehydrogenase	Rattus norvegicus	47-80
2512928-6	1989	However, monoclonal antibodies specific for the phenobarbital-induced cytochrome P-450 enzymes PB-4 and PB-5, while inhibiting O-demethylation of p-nitroanisole and aflatoxin B1 mutagenicity, had not effect on FC mutagenicity.	Phenobarbital	48-61	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	70-86
2559756-2	1989	In the present work we have been able to demonstrate the existence of some interrelationship between intracellular level of cAMP content and phenobarbital induction of delta-aminolevulinic acid synthase, ferrochelatase, and cytochrome P-450 biosynthesis in isolated rat hepatocytes.	Phenobarbital	141-154	ferrochelatase	Rattus norvegicus	204-218
2559756-2	1989	In the present work we have been able to demonstrate the existence of some interrelationship between intracellular level of cAMP content and phenobarbital induction of delta-aminolevulinic acid synthase, ferrochelatase, and cytochrome P-450 biosynthesis in isolated rat hepatocytes.	Phenobarbital	141-154	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	224-240
2597126-8	1989	An increase in glutathione reductase and thioltransferase activities was observed after BHA, PB or CAF treatment; glyoxalase I and Se-dependent glutathione peroxidase were depressed in comparison with the control group in all cases studied.	Phenobarbital	93-95	glutathione reductase	Mus musculus	15-36
2597126-8	1989	An increase in glutathione reductase and thioltransferase activities was observed after BHA, PB or CAF treatment; glyoxalase I and Se-dependent glutathione peroxidase were depressed in comparison with the control group in all cases studied.	Phenobarbital	93-95	glyoxalase 1	Mus musculus	114-126
2597175-0	1989	Absence of an isotope effect in induction of cytochrome P-450 and xenobiotic metabolizing enzyme activities by stable isotope-labelled phenobarbital isotopomers.	Phenobarbital	135-148	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	45-61
2688648-1	1989	The induction by phenobarbital of liver microsomal cytochrome P-450 has been demonstrated to be impaired in rats fed a selenium-deficient diet.	Phenobarbital	17-30	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	51-67
2688648-2	1989	Cytochrome P-450 isozyme specific immunologic and molecular techniques were used in the present study to better define the role of selenium in the induction of cytochrome P-450 by phenobarbital.	Phenobarbital	180-193	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
2688648-2	1989	Cytochrome P-450 isozyme specific immunologic and molecular techniques were used in the present study to better define the role of selenium in the induction of cytochrome P-450 by phenobarbital.	Phenobarbital	180-193	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	160-176
2688648-3	1989	Phenobarbital treatment of the selenium-deficient rats resulted in an increase in the level of total cytochrome P-450 50% of that observed with control rats and in a 10-fold increase in microsomal heme oxygenase.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	101-117
2688648-4	1989	Quantitative immunoblot analyses demonstrated that the levels of cytochromes P-450b + e and P-450p in the phenobarbital-treated selenium-deficient rats were approximately 50% of those found in the phenobarbital-treated control rats.	Phenobarbital	106-119	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	77-83
2688648-4	1989	Quantitative immunoblot analyses demonstrated that the levels of cytochromes P-450b + e and P-450p in the phenobarbital-treated selenium-deficient rats were approximately 50% of those found in the phenobarbital-treated control rats.	Phenobarbital	197-210	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	77-83
2519734-9	1989	The inhibition patterns observed when an antibody inhibitory to cytochrome P-450j was added to microsomes derived from control and ethanol- and phenobarbital-pretreated rats conclusively demonstrate that NDMA and NDEA are preferentially metabolized by distinct isozymes of cytochrome P-450.	Phenobarbital	144-157	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	64-81
2519734-9	1989	The inhibition patterns observed when an antibody inhibitory to cytochrome P-450j was added to microsomes derived from control and ethanol- and phenobarbital-pretreated rats conclusively demonstrate that NDMA and NDEA are preferentially metabolized by distinct isozymes of cytochrome P-450.	Phenobarbital	144-157	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	64-80
2612064-11	1989	These data indicate a differential induction of glutathione S-transferase isoenzymes and suggest that clotrimazole is a phenobarbital-type inducer of enzyme activity.	Phenobarbital	120-133	hematopoietic prostaglandin D synthase	Rattus norvegicus	48-73
2790804-0	1989	Independent mechanisms for tumor promoters phenobarbital and 12-O-tetradecanoylphorbol-13-acetate in reduction of epidermal growth factor binding by rat hepatocytes.	Phenobarbital	43-56	epidermal growth factor like 1	Rattus norvegicus	114-137
2790804-1	1989	Primary cultures of hepatocytes derived from adult Fischer 344 rats were used to test for effects of the liver tumor promoter phenobarbital on several components of the epidermal growth factor (EGF) receptor signal transduction pathway.	Phenobarbital	126-139	epidermal growth factor receptor	Rattus norvegicus	169-207
2790804-7	1989	These results demonstrate that phenobarbital, like TPA and other tumor promoters, can modulate the EGF receptor system but suggest that it does so without directly competing with EGF for binding to its receptor or by activating protein kinase C.	Phenobarbital	31-44	epidermal growth factor receptor	Rattus norvegicus	99-111
2575507-0	1989	Dose-related effects of phenobarbital on hepatic glutathione-S-transferase activity and ligandin levels in the rat.	Phenobarbital	24-37	hematopoietic prostaglandin D synthase	Rattus norvegicus	49-74
2575507-4	1989	Ligandin concentration increased in a dose-dependent fashion, achieving a maximal observed value of 278% of control at the highest administered phenobarbital dose.	Phenobarbital	144-157	glutathione S-transferase alpha 2	Rattus norvegicus	0-8
2575507-9	1989	These studies indicate that phenobarbital is capable of inducing immunoreactive ligandin concentrations and related enzymatic activities at doses as small as 5% of those commonly employed to demonstrate this effect.	Phenobarbital	28-41	glutathione S-transferase alpha 2	Rattus norvegicus	80-88
2514240-6	1989	A group of ovariectomized rats was pretreated with steroid-free bovine follicular fluid (bFF) to suppress LHRH-independent FSH release, and phenobarbital to suppress LHRH-dependent FSH release respectively, 7 and 1 h before administration of LHRH.	Phenobarbital	140-153	gonadotropin releasing hormone 1	Rattus norvegicus	166-170
2514240-6	1989	A group of ovariectomized rats was pretreated with steroid-free bovine follicular fluid (bFF) to suppress LHRH-independent FSH release, and phenobarbital to suppress LHRH-dependent FSH release respectively, 7 and 1 h before administration of LHRH.	Phenobarbital	140-153	gonadotropin releasing hormone 1	Rattus norvegicus	166-170
2514240-10	1989	Rats pretreated with bFF and phenobarbital showed an acute FSH response related to the dose of injected LHRH.	Phenobarbital	29-42	gonadotropin releasing hormone 1	Rattus norvegicus	104-108
2514165-1	1989	Strain differences in the expression of cytochrome P-450 isoenzymes (P-450s) during enhancement of hepatocarcinogenesis by 2-acetylaminofluorene (2-AAF) and phenobarbital (PB) were investigated immunohistochemically using monoclonal antibodies against phenobarbital (PB) (APF3) or 3-methylcholanthrene (3-MC) (APH8) inducible P-450s.	Phenobarbital	157-170	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	40-56
2514165-1	1989	Strain differences in the expression of cytochrome P-450 isoenzymes (P-450s) during enhancement of hepatocarcinogenesis by 2-acetylaminofluorene (2-AAF) and phenobarbital (PB) were investigated immunohistochemically using monoclonal antibodies against phenobarbital (PB) (APF3) or 3-methylcholanthrene (3-MC) (APH8) inducible P-450s.	Phenobarbital	172-174	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	40-56
2514165-1	1989	Strain differences in the expression of cytochrome P-450 isoenzymes (P-450s) during enhancement of hepatocarcinogenesis by 2-acetylaminofluorene (2-AAF) and phenobarbital (PB) were investigated immunohistochemically using monoclonal antibodies against phenobarbital (PB) (APF3) or 3-methylcholanthrene (3-MC) (APH8) inducible P-450s.	Phenobarbital	252-265	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	40-56
2514165-1	1989	Strain differences in the expression of cytochrome P-450 isoenzymes (P-450s) during enhancement of hepatocarcinogenesis by 2-acetylaminofluorene (2-AAF) and phenobarbital (PB) were investigated immunohistochemically using monoclonal antibodies against phenobarbital (PB) (APF3) or 3-methylcholanthrene (3-MC) (APH8) inducible P-450s.	Phenobarbital	267-269	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	40-56
2575452-4	1989	The diastereomers of the phenobarbital and mephobarbital derivatives were resolved by use of C-18 reverse-phase h.p.l.c.	Phenobarbital	25-38	Bardet-Biedl syndrome 9	Homo sapiens	93-97
2818628-3	1989	In Western blotting, both antibodies recognised a single band of Mr 52,000 in liver microsomes from rats pre-treated with phenobarbitone, acetone and isosafrole, which co-migrated with a purified preparation of cytochrome P450b.	Phenobarbital	122-136	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	211-227
2818628-7	1989	Phenobarbitone treatment resulted in a strong, specific immunostain of all hepatic centrilobular cells, antibody titration indicating that induction of cytochrome P450b/e had occurred.	Phenobarbital	0-14	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	152-168
2571427-3	1989	p-Bromophenacyl bromide, an inhibitor of phospholipase A2, significantly inhibited the promotion activity of PB at dose levels of 0.75% and 1.5%, reaching plateau at 0.75%.	Phenobarbital	109-111	phospholipase A2 group IB	Rattus norvegicus	41-57
2571427-7	1989	These results are strongly suggestive of an involvement of phospholipase A2, lipoxygenase and cyclooxygenase arachidonic acid metabolic pathways in the mechanisms underlying PB enhancement of hepatocarcinogenesis.	Phenobarbital	174-176	phospholipase A2 group IB	Rattus norvegicus	59-75
2791210-4	1989	with the cytochrome P-450 inducer phenobarbital (PB; 60 mg/kg) in saline.	Phenobarbital	34-47	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	9-25
2791210-8	1989	PB administration increased relative weight, cytochrome P-450 content and ethoxycoumarin-0-deethylase activity of livers as compared to control rats.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	45-61
2791210-9	1989	In addition, cytochrome P-450-mediated oxidative demethylation of BHA into tert-butyl-hydroquinone (TBHQ), monitored as urinary TBHQ excretion, was significantly increased in PB-induced rats as compared to non-induced rats (0.59 +/- 0.19 versus 0.37 +/- 0.09%; P less than 0.05).	Phenobarbital	175-177	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
2583091-0	1989	Phosphorylation of hepatic phenobarbital-inducible cytochrome P-450.	Phenobarbital	27-40	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	51-67
2583091-1	1989	The major phenobarbital-inducible cytochrome P-450 purified from rat liver, a member of family II of the cytochrome P-450 gene superfamily, is rapidly phosphorylated by cAMP-dependent protein kinase.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	34-50
2583091-1	1989	The major phenobarbital-inducible cytochrome P-450 purified from rat liver, a member of family II of the cytochrome P-450 gene superfamily, is rapidly phosphorylated by cAMP-dependent protein kinase.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	105-121
2583091-8	1989	Peptide mapping and immunoprecipitation with monospecific antibodies identified this protein as the major phenobarbital-inducible cytochrome P-450.	Phenobarbital	106-119	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	130-146
2815822-2	1989	Both phenobarbital and clofibrate pretreatment cause a qualitative change in cytochrome P-450 content in housefly (Musca domestica).	Phenobarbital	5-18	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	77-93
2481574-0	1989	Con A affinity of rat alpha 1-acid glycoprotein (rAGP): changes during inflammation, dexamethasone or phenobarbital treatment as detected by crossed affino immunoelectrophoresis (CAIE) are not only a reflection of biantennary glycan content.	Phenobarbital	102-115	orosomucoid 1	Rattus norvegicus	49-53
2481574-1	1989	Using crossed affino immunoelectrophoresis (CAIE), the secretion of the Con A most reactive form (CAIE-3) of rat alpha 1-acid glycoprotein (rAGP) has been shown to be increased in sera of Wistar and Sprague Dawley rats during inflammation and treatment with dexamethasone or phenobarbital.	Phenobarbital	275-288	orosomucoid 1	Rattus norvegicus	140-144
2514788-1	1989	We have previously shown that phenobarbital (PB) increases hepatic mitochondrial cytochrome P-450 (P-450) content and also the ability to metabolize hepatocarcinogen, aflatoxin B1 [Niranjan, B. G., Wilson, N. M., Jefcoate, C. R., & Avadhani, N. G. (1984) J. Biol.	Phenobarbital	30-43	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	81-97
2514788-1	1989	We have previously shown that phenobarbital (PB) increases hepatic mitochondrial cytochrome P-450 (P-450) content and also the ability to metabolize hepatocarcinogen, aflatoxin B1 [Niranjan, B. G., Wilson, N. M., Jefcoate, C. R., & Avadhani, N. G. (1984) J. Biol.	Phenobarbital	45-47	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	81-97
2804643-3	1989	Immunocytochemical studies on human medulla with antibodies raised to phenobarbital-inducible rat liver cytochrome P-450 indicate that the enzyme is primarily localized in the neuronal cell bodies and to a lesser extent in the axons.	Phenobarbital	70-83	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	104-120
2766463-6	1989	These results indicate that (i) cytochromes P-450b,e and P-450j contribute to benzene metabolism in rat liver; (ii) the former has a low affinity to benzene and is induced by PB; and (iii) P-450j has a high affinity to benzene and is induced by 1-day fasting, pyrazole and ethanol, but decreased by PB treatment.	Phenobarbital	175-177	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	44-50
2766463-6	1989	These results indicate that (i) cytochromes P-450b,e and P-450j contribute to benzene metabolism in rat liver; (ii) the former has a low affinity to benzene and is induced by PB; and (iii) P-450j has a high affinity to benzene and is induced by 1-day fasting, pyrazole and ethanol, but decreased by PB treatment.	Phenobarbital	175-177	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	57-63
2766463-6	1989	These results indicate that (i) cytochromes P-450b,e and P-450j contribute to benzene metabolism in rat liver; (ii) the former has a low affinity to benzene and is induced by PB; and (iii) P-450j has a high affinity to benzene and is induced by 1-day fasting, pyrazole and ethanol, but decreased by PB treatment.	Phenobarbital	175-177	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	189-195
2766463-6	1989	These results indicate that (i) cytochromes P-450b,e and P-450j contribute to benzene metabolism in rat liver; (ii) the former has a low affinity to benzene and is induced by PB; and (iii) P-450j has a high affinity to benzene and is induced by 1-day fasting, pyrazole and ethanol, but decreased by PB treatment.	Phenobarbital	299-301	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	44-50
2766463-6	1989	These results indicate that (i) cytochromes P-450b,e and P-450j contribute to benzene metabolism in rat liver; (ii) the former has a low affinity to benzene and is induced by PB; and (iii) P-450j has a high affinity to benzene and is induced by 1-day fasting, pyrazole and ethanol, but decreased by PB treatment.	Phenobarbital	299-301	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	57-63
2766463-6	1989	These results indicate that (i) cytochromes P-450b,e and P-450j contribute to benzene metabolism in rat liver; (ii) the former has a low affinity to benzene and is induced by PB; and (iii) P-450j has a high affinity to benzene and is induced by 1-day fasting, pyrazole and ethanol, but decreased by PB treatment.	Phenobarbital	299-301	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	189-195
2807620-4	1989	Long-term treatment of phenobarbital increased the plasma concentrations of HDL2-cholesterol, HDL3-cholesterol and HDL3-phospholipid, and decreased the plasma concentrations of low density lipoprotein + very low density lipoprotein-cholesterol.	Phenobarbital	23-36	HDL3	Homo sapiens	94-98
2807620-4	1989	Long-term treatment of phenobarbital increased the plasma concentrations of HDL2-cholesterol, HDL3-cholesterol and HDL3-phospholipid, and decreased the plasma concentrations of low density lipoprotein + very low density lipoprotein-cholesterol.	Phenobarbital	23-36	HDL3	Homo sapiens	115-119
2807620-6	1989	In addition, phenobarbital increased the plasma concentration of apolipoprotein A-I, decreased the plasma concentration of apolipoprotein B, but did not affect the plasma concentration of apolipoprotein A-II.	Phenobarbital	13-26	apolipoprotein A1	Homo sapiens	65-83
2807620-6	1989	In addition, phenobarbital increased the plasma concentration of apolipoprotein A-I, decreased the plasma concentration of apolipoprotein B, but did not affect the plasma concentration of apolipoprotein A-II.	Phenobarbital	13-26	apolipoprotein B	Homo sapiens	123-139
2779523-3	1989	In addition, the CBD-induced cytochrome P-450 was immunoreactive with an antibody raised against the major rat hepatic PB-inducible cytochrome P-450 and exhibited an NH2-terminal amino acid sequence greater than 90% homologous with that of the PB-inducible rat liver isozyme.	Phenobarbital	119-121	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	29-45
2779523-3	1989	In addition, the CBD-induced cytochrome P-450 was immunoreactive with an antibody raised against the major rat hepatic PB-inducible cytochrome P-450 and exhibited an NH2-terminal amino acid sequence greater than 90% homologous with that of the PB-inducible rat liver isozyme.	Phenobarbital	119-121	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	132-148
2779523-3	1989	In addition, the CBD-induced cytochrome P-450 was immunoreactive with an antibody raised against the major rat hepatic PB-inducible cytochrome P-450 and exhibited an NH2-terminal amino acid sequence greater than 90% homologous with that of the PB-inducible rat liver isozyme.	Phenobarbital	244-246	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	29-45
2779523-4	1989	Because of the many similarities between the CBD-induced isozyme and certain other isozymes previously purified from PB-pretreated animals, a cytochrome P-450 isozyme was purified from PB-pretreated mice by a chromatographic procedure similar to that employed for purification of the CBD-induced isozyme.	Phenobarbital	185-187	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	142-158
2818560-5	1989	Immunocytochemical studies demonstrated that the inducible isoenzymes of cytochrome P-450 are not distributed evenly throughout the hepatocyte population, and increasing concentrations of phenobarbitone or beta-naphthoflavone in the medium results in an increasing proportion of "induced" cells.	Phenobarbital	188-202	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	73-89
2753900-2	1989	In the rat, a cytosolic isozyme of aldehyde dehydrogenase, designated ALDH-PB, can be induced in the liver by administration of phenobarbital (PB).	Phenobarbital	128-141	aldehyde dehydrogenase family 1, subfamily A7	Rattus norvegicus	70-77
2804321-4	1989	Phenobarbital and perfluorodecalin induce several cytochrome P-450 isozymes and cause the appearance of a new isozyme with mass 56 kD absent in microsomes of intact CBA mice.	Phenobarbital	0-13	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	50-66
2573050-2	1989	SKF-525A, an inhibitor of phenobarbital-inducible monooxygenase activities has a much weaker effect on COH than the other three drugs, even though COH is a phenobarbital-inducible enzyme.	Phenobarbital	156-169	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	147-150
2803241-6	1989	Antiserum raised to the phenobarbital-inducible form of rat liver cytochrome P-450 [P-450(b+e)] inhibited mouse brain aminopyrine N-demethylase activity by around 80+ mouse brain microsomal protein exhibited cross-reactivity against this antiserum when examined by Ouchterlony double diffusion and immunoblotting.	Phenobarbital	24-37	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	66-82
2803241-7	1989	The present results indicate the presence of a phenobarbital-inducible form of cytochrome P-450 (or a form of cytochrome P-450 that is similar immunologically) in mouse brain microsomes, which is associated with a sex-related difference.	Phenobarbital	47-60	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	79-95
2803241-7	1989	The present results indicate the presence of a phenobarbital-inducible form of cytochrome P-450 (or a form of cytochrome P-450 that is similar immunologically) in mouse brain microsomes, which is associated with a sex-related difference.	Phenobarbital	47-60	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	110-126
2815832-4	1989	Analysis by Western blot showed that PATC induces cytochrome P-450 b, P-450 c and P-450 d, which are the major forms of cytochrome P-450 in liver microsomes of rats when pretreated with phenobarbital and 3-methylcholanthrene.	Phenobarbital	186-199	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	50-68
2587838-2	1989	In both treatment groups, phenobarbital produced a marked and persistent induction of cytochrome P-450 and aminopyrine N-demethylase; the response was greater in the tolerant group than that in the dependent group at the early time periods.	Phenobarbital	26-39	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	86-132
2587838-4	1989	Likewise, the induction of cytochrome P-450b+e content, one of the major phenobarbital inducible species, was maintained at 40% of the total cytochrome P-450 content.	Phenobarbital	73-86	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	27-44
2587838-4	1989	Likewise, the induction of cytochrome P-450b+e content, one of the major phenobarbital inducible species, was maintained at 40% of the total cytochrome P-450 content.	Phenobarbital	73-86	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	27-43
2587838-5	1989	Phenobarbital treatment resulted in increase of delta-aminolevulinate synthetase (ALAS) activity and a decrease in heme oxygenase (HO) activity.	Phenobarbital	0-13	5'-aminolevulinate synthase 1	Rattus norvegicus	48-80
2587838-5	1989	Phenobarbital treatment resulted in increase of delta-aminolevulinate synthetase (ALAS) activity and a decrease in heme oxygenase (HO) activity.	Phenobarbital	0-13	5'-aminolevulinate synthase 1	Rattus norvegicus	82-86
2815832-4	1989	Analysis by Western blot showed that PATC induces cytochrome P-450 b, P-450 c and P-450 d, which are the major forms of cytochrome P-450 in liver microsomes of rats when pretreated with phenobarbital and 3-methylcholanthrene.	Phenobarbital	186-199	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	70-89
2815832-4	1989	Analysis by Western blot showed that PATC induces cytochrome P-450 b, P-450 c and P-450 d, which are the major forms of cytochrome P-450 in liver microsomes of rats when pretreated with phenobarbital and 3-methylcholanthrene.	Phenobarbital	186-199	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	50-66
2804167-0	1989	[The effect of phenobarbital and amidopyrine on the rate of decomposition of isoforms of cytochrome P-450 in mouse liver microsomes].	Phenobarbital	15-28	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	89-105
2753164-0	1989	Effect of phenobarbital on the expression of glutathione S-transferase isoenzymes in cultured rat hepatocytes.	Phenobarbital	10-23	hematopoietic prostaglandin D synthase	Rattus norvegicus	45-70
2753164-1	1989	Cultured adult rat hepatocytes were treated daily with 3.2 mM phenobarbital (PB) in order to study its effect on the expression of cytosolic glutathione S-transferase isoenzymes.	Phenobarbital	62-75	hematopoietic prostaglandin D synthase	Rattus norvegicus	141-166
2753164-1	1989	Cultured adult rat hepatocytes were treated daily with 3.2 mM phenobarbital (PB) in order to study its effect on the expression of cytosolic glutathione S-transferase isoenzymes.	Phenobarbital	77-79	hematopoietic prostaglandin D synthase	Rattus norvegicus	141-166
2753164-2	1989	Glutathione S-transferase (GST) activities, using 1-chloro-2,4-dinitrobenzene and 1,2-dichloro-4-nitrobenzene as substrates, were increased when PB was present in the culture medium.	Phenobarbital	145-147	hematopoietic prostaglandin D synthase	Rattus norvegicus	0-25
2753164-2	1989	Glutathione S-transferase (GST) activities, using 1-chloro-2,4-dinitrobenzene and 1,2-dichloro-4-nitrobenzene as substrates, were increased when PB was present in the culture medium.	Phenobarbital	145-147	hematopoietic prostaglandin D synthase	Rattus norvegicus	27-30
2753164-3	1989	After purification and separation of GST on glutathione Sepharose 6 B and reversed-phase HPLC, respectively, it was observed in vitro that PB caused an increase in the relative amounts of subunits 1, 3 and 7 compared to subunits 2 and 4.	Phenobarbital	139-141	hematopoietic prostaglandin D synthase	Rattus norvegicus	37-40
2787638-0	1989	Dependence of the induction of cytochrome P-450 by phenobarbital in primary cultures of adult rat hepatocytes on the composition of the culture medium.	Phenobarbital	51-64	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	31-47
2787638-4	1989	These studies indicated that the metabolic activity and the response to phenobarbital of the major isozyme of the phenobarbital-inducible family of cytochrome P-450 were maintained in hepatocytes in T1 medium.	Phenobarbital	72-85	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	148-164
2787638-4	1989	These studies indicated that the metabolic activity and the response to phenobarbital of the major isozyme of the phenobarbital-inducible family of cytochrome P-450 were maintained in hepatocytes in T1 medium.	Phenobarbital	114-127	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	148-164
2787638-5	1989	However, there was anomalous expression and induction by phenobarbital of the major 3-methylcholanthrene-inducible isozyme, cytochrome P-450c, in cultured hepatocytes in each of the three media tested, but this response was more pronounced in T1 medium.	Phenobarbital	57-70	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	124-141
2804167-3	1989	Phenobarbital treatment causes both the appearance of a new cytochrome P-450 isozyme with a molecular mass of 56 kDa and the increase in the content of three isozymes with molecular masses of 54, 52.5 and 50 kDa.	Phenobarbital	0-13	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	60-76
2804167-4	1989	The half-life time of cytochrome P-450 isozymes in the livers of intact and phenobarbital-induced mice differs from 15 to 42 hours.	Phenobarbital	76-89	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	22-38
2804167-6	1989	Aminopyrine injections to phenobarbital-pretreated mice result in the breakdown acceleration of the cytochrome P-450 isozyme with a molecular mass of 56 kDa.	Phenobarbital	26-39	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	100-116
2470762-1	1989	P-450IIB genes (P-450b and P-450e in rat) are induced following treatment with phenobarbital predominantly in hepatocytes located in zones 2 and 3 of the liver acinus.	Phenobarbital	79-92	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	16-22
2544042-0	1989	Phenobarbital-induced cytosolic cytoprotective mechanisms that offset increases in NADPH cytochrome P450 reductase activity in menadione-mediated cytotoxicity.	Phenobarbital	0-13	cytochrome p450 oxidoreductase	Rattus norvegicus	83-114
2544042-6	1989	Hepatic microsomes prepared from PB-pretreated rats exhibited a threefold increase in NADPH cytochrome P450 reductase activity over those of controls.	Phenobarbital	33-35	cytochrome p450 oxidoreductase	Rattus norvegicus	86-117
2544042-11	1989	In support of this, we observed PB-induced increases in glutathione levels, glutathione reductase, and DT-diaphorase activities.	Phenobarbital	32-34	glutathione-disulfide reductase	Rattus norvegicus	76-97
2544042-11	1989	In support of this, we observed PB-induced increases in glutathione levels, glutathione reductase, and DT-diaphorase activities.	Phenobarbital	32-34	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	103-116
2786372-0	1989	Characterization of a phenobarbital-inducible dog liver cytochrome P450 structurally related to rat and human enzymes of the P450IIIA (steroid-inducible) gene subfamily.	Phenobarbital	22-35	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	125-133
2786372-1	1989	A cytochrome P450 called PBD-1 isolated from liver microsomes of an adult male Beagle dog treated with phenobarbital (PB) is structurally and functionally similar to members of the P450IIIA gene subfamily in rat and human liver microsomes.	Phenobarbital	103-116	cytochrome P450 3A12	Canis lupus familiaris	181-189
2786372-1	1989	A cytochrome P450 called PBD-1 isolated from liver microsomes of an adult male Beagle dog treated with phenobarbital (PB) is structurally and functionally similar to members of the P450IIIA gene subfamily in rat and human liver microsomes.	Phenobarbital	25-27	cytochrome P450 3A12	Canis lupus familiaris	181-189
2786372-5	1989	P450IIIA-form marker steroid 6 beta-hydroxylase activities increase 2.5-fold upon PB-treatment of dogs and are selectively inhibited by anti-PBD-1 IgG.	Phenobarbital	82-84	cytochrome P450 3A12	Canis lupus familiaris	0-8
2786372-6	1989	NADPH-dependent triacetyloleandomycin (TAO) complex formation and erythromycin demethylase, also marker activities for P450IIIA forms from rats and humans, increase 4- and 5-fold in dog liver microsomes upon PB treatment, whereas immunochemically reactive PBD-1 is induced 3-fold.	Phenobarbital	208-210	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	119-127
2786372-8	1989	TAO complex formation is not inhibited by chloramphenicol, a selective inhibitor of the major PB-inducible dog liver cytochrome P450, PBD-2.	Phenobarbital	94-96	cytochrome P450 2B11	Canis lupus familiaris	117-139
2697484-4	1989	Therapy with PB, but not placebo, reduced fasting IRI and BG in subjects with glucose intolerance and improved the glucose tolerance, insulin response to glucose and antipyrine metabolism.	Phenobarbital	13-15	insulin	Homo sapiens	134-141
2697484-5	1989	The effects of PB on patients with NIDDM were dependent on the insulin availability and duration of the disease.	Phenobarbital	15-17	insulin	Homo sapiens	63-70
2576673-1	1989	The effect of hepatic glutathione concentration on the induction of gamma-glutamyltransferase (GGT) activity by phenobarbitone was investigated.	Phenobarbital	112-126	gamma-glutamyltransferase 1	Rattus norvegicus	95-98
2576673-2	1989	A single dose of phenobarbitone 100 mg/kg weight was given to rats, and the concentration of hepatic glutathione and GGT activity were measured.	Phenobarbital	17-31	gamma-glutamyltransferase 1	Rattus norvegicus	117-120
2815336-1	1989	By means of immunohistochemical methods a study of the liver intralobular localization of cytochromes P-450b(+e) and P-450c(+d) has been carried out after separate and consecutive treatment of rats with phenobarbital (PB) and 3-methylcholanthrene (MC).	Phenobarbital	203-216	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	102-108
2815336-1	1989	By means of immunohistochemical methods a study of the liver intralobular localization of cytochromes P-450b(+e) and P-450c(+d) has been carried out after separate and consecutive treatment of rats with phenobarbital (PB) and 3-methylcholanthrene (MC).	Phenobarbital	203-216	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	117-123
2815336-2	1989	PB-treatment leads to localization of P-450b in the centrilobular region, whereas homogeneous distribution of P-450c in the lobule is observed after MC-treatment.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	38-44
2815336-3	1989	The consecutive treatment with PB and MC is accompanied by the localization of P-450c only in cells of the periportal region of the lobule.	Phenobarbital	31-33	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	79-85
2815336-4	1989	PB-treatment of rats after preliminary MC-injection also results in the periportal localization of P-450c, and a small quantity of P-450b is localized in hepatocytes of the centrilobular region.	Phenobarbital	0-2	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	99-105
2815336-4	1989	PB-treatment of rats after preliminary MC-injection also results in the periportal localization of P-450c, and a small quantity of P-450b is localized in hepatocytes of the centrilobular region.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	131-137
2729997-7	1989	Northern blot analyses with fragments of the rabbit cDNA demonstrate that mEH messenger RNA (mRNA) is expressed constitutively in the liver and induced following exposure to phenobarbital or polychlorinated biphenyls.	Phenobarbital	174-187	epoxide hydrolase 1, microsomal	Mus musculus	74-77
2788542-2	1989	The expression of the phenobarbital-inducible cytochrome P-450 mRNA species (P-450 IIB1 and IIB2) were investigated in different tissues of rats following treatment with 2-allyl-2-isopropylacetamide.	Phenobarbital	22-35	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	46-62
2570834-2	1989	In-vitro metabolism of nefopam in phenobarbitone-induced microsomes leads to the production of a reactive metabolite which complexes with cytochrome P-450.	Phenobarbital	34-48	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	138-154
2768220-3	1989	P450 PB-1 and PB-2 were present in moderate amounts in hepatic microsomes of untreated male rats and were induced 2- to 3-fold with phenobarbital.	Phenobarbital	132-145	cytochrome P450, family 2, subfamily c, polypeptide 12	Rattus norvegicus	0-9
2726759-0	1989	Regulation of cytochrome P-450b/e gene expression by a heme- and phenobarbitone-modulated transcription factor.	Phenobarbital	65-79	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	14-31
2712571-6	1989	The inducibility of coumarin 7-hydroxylase by phenobarbital (PB) and its genetic regulation have been previously studied by A. W. Wood and colleagues ((1974) Science 185, 612-614; (1979); J. Biol.	Phenobarbital	46-59	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	20-42
2712571-6	1989	The inducibility of coumarin 7-hydroxylase by phenobarbital (PB) and its genetic regulation have been previously studied by A. W. Wood and colleagues ((1974) Science 185, 612-614; (1979); J. Biol.	Phenobarbital	61-63	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	20-42
2712571-12	1989	Immunoinhibition of microsomal coumarin 7-hydroxylase is practically 100% for control animals and after pretreatment with pyrazole or PB.	Phenobarbital	134-136	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	31-53
2541521-8	1989	It appears that a PB induced cytochrome P-450 catalysed reactive metabolite(s) may be responsible for the hepatotoxicity caused by pulegone.	Phenobarbital	18-20	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	29-45
2789039-6	1989	Although the P-450 PB-4-specific content of the SD1 microsomes was 15% of that present in phenobarbital-induced rat liver microsomes, the P-450 PB-4-dependent androstenedione 16 beta-hydroxylase activity of the SD1 membrane fraction was only 2-3% of that present in the liver microsomes.	Phenobarbital	90-103	CUP2Q35	Homo sapiens	48-51
2541728-3	1989	Both 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and sodium phenobarbital induced AHH activity.	Phenobarbital	52-72	aryl-hydrocarbon receptor	Mus musculus	81-84
2541728-8	1989	The cytosolic receptor for TCDD (Ah receptor) was characterized to see if phenobarbital induced cytochrome P450IA1 mRNA and the hydroxylase enzyme through the same mechanism as TCDD.	Phenobarbital	74-87	aryl-hydrocarbon receptor	Mus musculus	33-44
2566684-1	1989	The potentiation of the expression of polycyclic aromatic hydrocarbon-inducible cytochromes P450IA1 and P450IA2, and phenobarbital-inducible cytochrome P450IIB1 and NADPH-cytochrome P-450 reductase by dexamethasone in vivo was investigated using adrenalectomized and sham-operated rats.	Phenobarbital	117-130	cytochrome p450 oxidoreductase	Rattus norvegicus	165-197
2504523-8	1989	Analysis of liver mRNA levels using radiolabelled DNA probes demonstrated that one isozyme, UDPGTr-2, is elevated by phenobarbital whereas a second isozyme, 4-nitrophenol GT is elevated by 3-methylcholanthrene.	Phenobarbital	117-130	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	92-100
2708353-2	1989	The rat cytochrome P-450IIB gene family consists of at least 10 members, 2 of which, P-450b and P-450e, have been well characterized and are activated transcriptionally by phenobarbital (PB) in the liver.	Phenobarbital	172-185	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	85-91
2708353-2	1989	The rat cytochrome P-450IIB gene family consists of at least 10 members, 2 of which, P-450b and P-450e, have been well characterized and are activated transcriptionally by phenobarbital (PB) in the liver.	Phenobarbital	187-189	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	85-91
2719684-0	1989	Thyroid hormone suppression of hepatic levels of phenobarbital-inducible P-450b and P-450e and other neonatal P-450s in hypophysectomized rats.	Phenobarbital	49-62	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	73-79
2495802-3	1989	In contrast, the racemic octachlorobiphenyl (III) and its individual enantiomers were only weak phenobarbital-type inducers of cytochrome P-450, and the enantiomers of III were equally (weakly) potent.	Phenobarbital	96-109	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	127-143
2719684-2	1989	The contents of phenobarbital (PB)-inducible P-450b and P-450e, expressed constitutively in livers, were higher in neonate than in adult rats.	Phenobarbital	16-29	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	45-51
2719684-2	1989	The contents of phenobarbital (PB)-inducible P-450b and P-450e, expressed constitutively in livers, were higher in neonate than in adult rats.	Phenobarbital	31-33	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	45-51
2540752-1	1989	The phosphorylation of the two major phenobarbital-inducible cytochrome P450 isoenzymes IIB1 and IIB2 was increased in hepatocytes by the action of the membrane permeating cAMP derivatives N6-dibutyryl-cAMP and 8-thiomethyl-cAMP.	Phenobarbital	37-50	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	88-92
2705461-10	1989	When TRH (500 ng/kg body weight, IV) was given, the increment in serum TSH at 10 minutes was significantly lower in the PB group (PB, 53 +/- 26 microU/ml vs. control, 131 +/- 18 microU/ml, p less than .05).	Phenobarbital	120-122	thyrotropin releasing hormone	Rattus norvegicus	5-8
2705461-10	1989	When TRH (500 ng/kg body weight, IV) was given, the increment in serum TSH at 10 minutes was significantly lower in the PB group (PB, 53 +/- 26 microU/ml vs. control, 131 +/- 18 microU/ml, p less than .05).	Phenobarbital	130-132	thyrotropin releasing hormone	Rattus norvegicus	5-8
2494942-6	1989	A 30-fold induction of hepatic P450b by phenobarbital (PB) was also completely ineffective in increasing P450b-dependent DMBA metabolism.	Phenobarbital	40-53	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	31-36
2494942-6	1989	A 30-fold induction of hepatic P450b by phenobarbital (PB) was also completely ineffective in increasing P450b-dependent DMBA metabolism.	Phenobarbital	55-57	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	31-36
2494942-8	1989	In contrast, PB treatment of F344 rats considerably increased P450b/e-dependent metabolism by liver, lung, and adrenal microsomes.	Phenobarbital	13-15	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	62-67
2574109-10	1989	In both the oxidase activity as well as the MI complex formation phenobarbital induced cytochrome P-450 is involved.	Phenobarbital	65-78	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	87-103
2731660-3	1989	The hepatic inducers employed were phenobarbital (PB), beta-naphthoflavone (BNF), and butylated hydroxyanisole (BHA) which are known to induce cytochrome P-450, cytochrome P-448, and cGST, respectively.	Phenobarbital	35-48	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	143-159
2731660-3	1989	The hepatic inducers employed were phenobarbital (PB), beta-naphthoflavone (BNF), and butylated hydroxyanisole (BHA) which are known to induce cytochrome P-450, cytochrome P-448, and cGST, respectively.	Phenobarbital	35-48	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	161-177
2731660-6	1989	PB, BNF, and BHA produced the expected effects on mEH, cEH, and cGST in rat and mouse livers, whereas the testes were generally nonresponsive to the inducers.	Phenobarbital	0-2	epoxide hydrolase 1, microsomal	Mus musculus	50-53
2731660-6	1989	PB, BNF, and BHA produced the expected effects on mEH, cEH, and cGST in rat and mouse livers, whereas the testes were generally nonresponsive to the inducers.	Phenobarbital	0-2	epoxide hydrolase 2	Rattus norvegicus	55-58
2501941-6	1989	Treatment of rats with phenobarbital (PB) increased 2- to 3-fold the capacities of hepatic microsomes of both sexes (normal and gonadectomized) for 9-hydroxylation of 2-FAA.	Phenobarbital	23-36	fumarylacetoacetate hydrolase	Rattus norvegicus	169-172
2501941-6	1989	Treatment of rats with phenobarbital (PB) increased 2- to 3-fold the capacities of hepatic microsomes of both sexes (normal and gonadectomized) for 9-hydroxylation of 2-FAA.	Phenobarbital	38-40	fumarylacetoacetate hydrolase	Rattus norvegicus	169-172
2920173-1	1989	Expression of the phenobarbitone-inducible cytochrome P-450 mRNA species (cytochrome P450IIB1/IIB2) has been investigated in tissues of rats following administration of 2-allyl-2-isopropylacetamide or phenobarbitone.	Phenobarbital	18-32	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	43-59
2752066-0	1989	[Identification of molecular forms of cytochrome P-450 isolated from liver microsomes of rats induced with phenobarbital and 3-methylcholanthrene].	Phenobarbital	107-120	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	38-54
2920173-1	1989	Expression of the phenobarbitone-inducible cytochrome P-450 mRNA species (cytochrome P450IIB1/IIB2) has been investigated in tissues of rats following administration of 2-allyl-2-isopropylacetamide or phenobarbitone.	Phenobarbital	201-215	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	43-59
2752066-1	1989	Eight electrophoretically homogeneous forms of cytochrome P-450 were isolated from liver microsomes of phenobarbital (PB)- and 3-methylcholanthrene (MC)-induced male Wistar rats, using chromatography on 1.8-diaminooctyl-Sepharose, SEAE-Sephacel and hydroxylapatite.	Phenobarbital	103-116	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	47-63
2752066-1	1989	Eight electrophoretically homogeneous forms of cytochrome P-450 were isolated from liver microsomes of phenobarbital (PB)- and 3-methylcholanthrene (MC)-induced male Wistar rats, using chromatography on 1.8-diaminooctyl-Sepharose, SEAE-Sephacel and hydroxylapatite.	Phenobarbital	118-120	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	47-63
2920173-8	1989	This represents the first report of a phenobarbitone-inducible cytochrome P-450 mRNA in rat kidney.	Phenobarbital	38-52	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	63-79
2743210-5	1989	This results accords with the previous demonstration of a TCBP- and PB-induced decrease in UROG-D activity in this system.	Phenobarbital	68-70	uroporphyrinogen decarboxylase	Gallus gallus	91-97
2645046-0	1989	Infrequent activation of K-ras, H-ras, and other oncogenes in hepatocellular neoplasms initiated by methyl(acetoxymethyl)nitrosamine, a methylating agent, and promoted by phenobarbital in F344 rats.	Phenobarbital	171-184	KRAS proto-oncogene, GTPase	Rattus norvegicus	25-30
2645046-0	1989	Infrequent activation of K-ras, H-ras, and other oncogenes in hepatocellular neoplasms initiated by methyl(acetoxymethyl)nitrosamine, a methylating agent, and promoted by phenobarbital in F344 rats.	Phenobarbital	171-184	HRas proto-oncogene, GTPase	Rattus norvegicus	32-37
2744145-2	1989	The use of GABA under induction of cytochrome P-450 of the liver by phenobarbital or rifampicin was not followed by immunodepression.	Phenobarbital	68-81	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	35-51
2647284-0	1989	Over expression of proto-oncogenes: ki-ras, fos and myc in rat liver cells treated in vitro by two liver tumor promoters: phenobarbital and biliverdin.	Phenobarbital	122-135	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	52-55
2503016-7	1989	Phenobarbital suppressed proliferative response to rIL-2 and CTL activity, but did not suppress NK activity nor LAK activity.	Phenobarbital	0-13	interleukin 2	Rattus norvegicus	51-56
2784534-3	1989	The phenobarbital-responsive cytochromes P-450b/e were also induced strongly by clotrimazole and miconazole, but not by ketoconazole.	Phenobarbital	4-17	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	41-47
2917006-7	1989	Various isozymes of cytochrome P-450 induced by phenobarbital, beta-napthaflavone and clofibrate were also depressed by this interferon.	Phenobarbital	48-61	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	20-36
2917016-8	1989	Collectively, these studies indicate that neonatal exposure to testosterone and PB alters the developmental pattern of EH activities, including final adult levels.	Phenobarbital	80-82	epoxide hydrolase 1, microsomal	Mus musculus	119-121
2917017-5	1989	In phenobarbital- and 3-methylcholanthrene-induced microsomes, 73% and 64%, respectively, of cytochrome P-450 are converted to P-420 in presence of 200 microM ebselen.	Phenobarbital	3-16	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	93-109
2521554-3	1989	In contrast, a main phenobarbital-inducible form, P450b, was enhanced 25- to 30-fold in these diabetic rats.	Phenobarbital	20-33	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	50-55
2536534-1	1989	Antibody-inhibition experiments established that the induction of cytochrome P450c is largely responsible for the marked increase in liver microsomal 7-ethoxyresorufin O-dealkylation in rats treated with 3-methylcholanthrene, whereas the induction of cytochrome P450b and/or P450e is largely responsible for the marked increase in 7-pentoxy- and 7-benzyloxyresorufin O-dealkylation in rats treated with phenobarbital.	Phenobarbital	403-416	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	66-82
2499727-7	1989	Spectral studies revealed a Type II binding of Br to cytochrome P-450 from microsomes of saline and PB pretreated rats.	Phenobarbital	100-102	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	53-69
2542235-3	1989	Experiments with various microsomal preparations induced by phenobarbital (PB), polychlorinated biphenyls (PCB), or 3-methylcholanthrene (3-MC) revealed that the reduction rate was correlated to the concentration of cytochrome P-450 but not to that of NADPH reductase.	Phenobarbital	60-73	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	216-232
2542235-3	1989	Experiments with various microsomal preparations induced by phenobarbital (PB), polychlorinated biphenyls (PCB), or 3-methylcholanthrene (3-MC) revealed that the reduction rate was correlated to the concentration of cytochrome P-450 but not to that of NADPH reductase.	Phenobarbital	75-77	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	216-232
2498247-2	1989	The results of enzyme-linked immunosorbent assay using monoclonal antibodies against rat P-450 isozymes revealed that the amount of cytochrome P-450d induced by 3-MeO-AAB or MC declined rapidly during culture and fell to 10 to 15% of the initial value after 24 h. A similar tendency was observed with PB-induced cytochrome P-450b/e.	Phenobarbital	301-303	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	132-149
2919406-0	1989	Purification and properties of cytochrome P-450 from liver microsomes of phenobarbital-treated marmoset monkeys (Callithrix jacchus).	Phenobarbital	73-86	cytochrome P450 2E1	Callithrix jacchus	31-47
2919406-1	1989	One form of cytochrome P-450 from phenobarbital-induced marmoset liver was purified to apparent electrophoretic homogeneity and compared with the major inducible form isolated from rat liver.	Phenobarbital	34-47	cytochrome P450 2E1	Callithrix jacchus	12-28
2912728-3	1989	While 2-allyl-2-isopropylacetamide, phenobarbitone, dexamethasone, beta-naphthoflavone and clofibrate induced specific cytochrome-P450-mRNA species in rat liver, the levels of these induced mRNAs were not affected by succinylacetone administration.	Phenobarbital	36-50	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	119-134
2774648-7	1989	Further characterization of the cytochrome P-450 isozymes induced in liver by clotrimazole treatment was based on monoclonal antibodies (MAbs) raised against purified rat liver cytochrome P-450 isozymes induced by phenobarbital (MAb 2-66-3) and ethanol (MAb 1-98-1).	Phenobarbital	214-227	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	32-48
2774648-7	1989	Further characterization of the cytochrome P-450 isozymes induced in liver by clotrimazole treatment was based on monoclonal antibodies (MAbs) raised against purified rat liver cytochrome P-450 isozymes induced by phenobarbital (MAb 2-66-3) and ethanol (MAb 1-98-1).	Phenobarbital	214-227	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	177-193
2742497-5	1989	After administration of phenobarbital the content of cytochrome P-450 was approximately two-fold greater in the cells present in fractions 3-5, when compared to the same subpopulations isolated from untreated rats; the activity of benzphetamine N-demethylase was enhanced to a similar extent in all five fractions.	Phenobarbital	24-37	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	53-69
2764709-1	1989	A hepatic soluble aldehyde dehydrogenase (ALDH), inducible by polycyclic aromatic hydrocarbons, was studied in Wistar rats in connection with substances known to affect drug metabolism or aldehyde dehydrogenase activity, such as phenobarbital (PB), disulfiram (DS), beta-diethylaminoethyl diphenylpropylacetate (SKF 525A) and calcium cyanamide (CC).	Phenobarbital	229-242	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	18-40
2764709-1	1989	A hepatic soluble aldehyde dehydrogenase (ALDH), inducible by polycyclic aromatic hydrocarbons, was studied in Wistar rats in connection with substances known to affect drug metabolism or aldehyde dehydrogenase activity, such as phenobarbital (PB), disulfiram (DS), beta-diethylaminoethyl diphenylpropylacetate (SKF 525A) and calcium cyanamide (CC).	Phenobarbital	229-242	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	42-46
2764709-1	1989	A hepatic soluble aldehyde dehydrogenase (ALDH), inducible by polycyclic aromatic hydrocarbons, was studied in Wistar rats in connection with substances known to affect drug metabolism or aldehyde dehydrogenase activity, such as phenobarbital (PB), disulfiram (DS), beta-diethylaminoethyl diphenylpropylacetate (SKF 525A) and calcium cyanamide (CC).	Phenobarbital	244-246	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	18-40
2764709-1	1989	A hepatic soluble aldehyde dehydrogenase (ALDH), inducible by polycyclic aromatic hydrocarbons, was studied in Wistar rats in connection with substances known to affect drug metabolism or aldehyde dehydrogenase activity, such as phenobarbital (PB), disulfiram (DS), beta-diethylaminoethyl diphenylpropylacetate (SKF 525A) and calcium cyanamide (CC).	Phenobarbital	244-246	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	42-46
2541801-3	1989	It was shown that RIII and RIV bind as type I substrates to cytochrome P-450 from rat microsomes induced with phenobarbital or 3-methylcholanthrene as well as to those from control rats.	Phenobarbital	110-123	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	60-76
2535970-0	1989	Phosphorylation of carcinogen metabolizing enzymes: regulation of the phosphorylation status of the major phenobarbital inducible cytochromes P-450 in hepatocytes.	Phenobarbital	106-119	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	142-147
2535970-1	1989	We present data showing that the major phenobarbital inducible cytochromes P-450 (cytochrome P-450IIB1 and cytochrome P-450IIB2) were phosphorylated in intact hepatocytes.	Phenobarbital	39-52	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	75-80
2535970-1	1989	We present data showing that the major phenobarbital inducible cytochromes P-450 (cytochrome P-450IIB1 and cytochrome P-450IIB2) were phosphorylated in intact hepatocytes.	Phenobarbital	39-52	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	82-102
2691105-5	1989	Antibodies to phenobarbital-induced cytochrome P-450 and NADPH-cytochrome P-450 reductase inhibited covalent binding to an extent of 72% and 47%, respectively.	Phenobarbital	14-27	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	36-52
2691105-5	1989	Antibodies to phenobarbital-induced cytochrome P-450 and NADPH-cytochrome P-450 reductase inhibited covalent binding to an extent of 72% and 47%, respectively.	Phenobarbital	14-27	cytochrome p450 oxidoreductase	Rattus norvegicus	57-89
2736674-6	1989	In addition PFDA abolished the inducibility of GST mRNAs by phenobarbital.	Phenobarbital	60-73	glutathione S-transferase kappa 1	Homo sapiens	47-50
2510947-4	1989	Using specific antibodies against cytochromes P-450b and P-450c (which are the main isoenzymes of cytochrome P-450 in the PB- and MC-microsomes respectively), an immunological identity of the cytochrome P-450 isoforms during PFD and PB induction has been found.	Phenobarbital	122-124	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	46-52
2510947-4	1989	Using specific antibodies against cytochromes P-450b and P-450c (which are the main isoenzymes of cytochrome P-450 in the PB- and MC-microsomes respectively), an immunological identity of the cytochrome P-450 isoforms during PFD and PB induction has been found.	Phenobarbital	122-124	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	57-63
2510947-4	1989	Using specific antibodies against cytochromes P-450b and P-450c (which are the main isoenzymes of cytochrome P-450 in the PB- and MC-microsomes respectively), an immunological identity of the cytochrome P-450 isoforms during PFD and PB induction has been found.	Phenobarbital	122-124	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	98-114
2510947-4	1989	Using specific antibodies against cytochromes P-450b and P-450c (which are the main isoenzymes of cytochrome P-450 in the PB- and MC-microsomes respectively), an immunological identity of the cytochrome P-450 isoforms during PFD and PB induction has been found.	Phenobarbital	233-235	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	46-52
2510947-4	1989	Using specific antibodies against cytochromes P-450b and P-450c (which are the main isoenzymes of cytochrome P-450 in the PB- and MC-microsomes respectively), an immunological identity of the cytochrome P-450 isoforms during PFD and PB induction has been found.	Phenobarbital	233-235	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	57-63
2510947-4	1989	Using specific antibodies against cytochromes P-450b and P-450c (which are the main isoenzymes of cytochrome P-450 in the PB- and MC-microsomes respectively), an immunological identity of the cytochrome P-450 isoforms during PFD and PB induction has been found.	Phenobarbital	233-235	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	192-208
2510947-7	1989	A comparison of these forms with cytochromes P-450b and P-450e obtained from the PB-induced rat liver microsomes revealed their similarity in a number of properties, e.g., chromotographic behavior on DEAE-Sephacel column, molecular weight determined by sodium dodecyl sulphate (SDS) electrophoresis in polyacrylamide gel, immunoreactivity, peptide mapping, catalytic activity.	Phenobarbital	81-83	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	45-51
2510947-9	1989	These findings suggest that PFD and PB, which differ in their chemical structure, induce in the rat liver microsomes identical forms of cytochrome P-450.	Phenobarbital	36-38	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	136-152
2576792-11	1989	Pretreatment of rats and plant tissues with biphenyl, Aroclor 1248 and the sodium salt of phenobarbital increased significantly the microsomal protein concentrations, and enzyme activities linked to cytochrome P-450.	Phenobarbital	90-103	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	199-215
2806079-0	1989	Induction of cytochromes P-450b/e by phenobarbital in primary culture of adult rat hepatocytes: test of differentiated liver gene expression.	Phenobarbital	37-50	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	25-31
2566467-8	1989	These findings suggest that 3-methylindole is metabolized to alkylating, electrophilic intermediates preferentially by the homologues of "phenobarbital-inducible" isozymes (presumably forms 2 and 5 in analogy to rabbit lung isozymes) to cytochrome P-450 in pulmonary microsomes, rather than by the polycyclic aromatic hydrocarbon-inducible isozymes.	Phenobarbital	138-151	cytochrome P-450	Oryctolagus cuniculus	237-253
2707121-3	1989	Discriminatory 18-mer oligodeoxynucleotides directed to the phenobarbital (PB) inducible P450s, P450IIB1 (P450b) and P450IIB2 (P450e), were employed as probes for in situ hybridization experiments.	Phenobarbital	60-73	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	106-111
2707121-3	1989	Discriminatory 18-mer oligodeoxynucleotides directed to the phenobarbital (PB) inducible P450s, P450IIB1 (P450b) and P450IIB2 (P450e), were employed as probes for in situ hybridization experiments.	Phenobarbital	75-77	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	106-111
2550216-3	1989	Phenobarbital (PB) and the benzodiazepines (BZDs), diazepam (DZP), clonazepam (CZP), and lorazepam (LZP), also reduced SRF, but only at supratherapeutic free serum concentrations achieved in treatment of generalized tonic-clonic status epilepticus.	Phenobarbital	0-13	serum response factor	Mus musculus	119-122
2550216-3	1989	Phenobarbital (PB) and the benzodiazepines (BZDs), diazepam (DZP), clonazepam (CZP), and lorazepam (LZP), also reduced SRF, but only at supratherapeutic free serum concentrations achieved in treatment of generalized tonic-clonic status epilepticus.	Phenobarbital	15-17	serum response factor	Mus musculus	119-122
2535699-6	1989	Treatment with CCl4 and phenobarbital significantly reduced the number of surface binding sites for asialoorosomucoid (p less than 0.05) and epidermal growth factor (p less than 0.02), although this treatment had no effect on either the binding affinity or the number of binding sites for insulin.	Phenobarbital	24-37	epidermal growth factor like 1	Rattus norvegicus	141-164
2502445-7	1989	Pretreatment with phenobarbitone and 3-methylcholanthrene stimulated both the glutathione S-transferase and organic nitrate reductase activities.	Phenobarbital	18-32	glutathione S-transferase kappa 1	Homo sapiens	78-103
2591634-12	1989	The protocol led to a drop in the PB-inducible ALA synthase RNA concentration and to an increase in that of cytochrome P-450 RNA, measured 6 hr after drug administration.	Phenobarbital	34-36	5'-aminolevulinate synthase 1	Gallus gallus	47-59
2807635-0	1989	Effect of endotoxin to differentially affect cytochrome P-450 monooxygenase activities of untreated rats and animals induced with phenobarbital or 3-methylcholanthrene.	Phenobarbital	130-143	cytochrome P450, family 2, subfamily j, polypeptide 3	Rattus norvegicus	45-75
2807635-1	1989	The effect of endotoxin in decreasing the cytochrome P-450-dependent metabolism of aniline, aminopyrine and ethoxycoumarin was examined in untreated rats, and in rats pretreated with either phenobarbital or 3-methylcholanthrene.	Phenobarbital	190-203	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	42-58
2634093-4	1989	This prediction is achieved by comparing the molecular conformation of these drugs with lanosterol, the substrate of the fungal cytochrome P-450, and with phenobarbitone, an inducing agent of a family of mammalian cytochrome P-450, toward which the antifungal agents show highest inhibitory activity.	Phenobarbital	155-169	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	214-230
2566924-6	1989	Anticonvulsant therapy with phenobarbital (20 mg/kg, i.p., twice daily for three weeks) partially suppressed the rise in NPY levels.	Phenobarbital	28-41	neuropeptide Y	Rattus norvegicus	121-124
2913483-1	1989	Administration of the allylbarbiturate secobarbital (SB) to phenobarbital-pretreated rats is known to result in structural and functional loss of hepatic cytochrome P-450 and generation of N-alkylated prosthetic heme derivatives.	Phenobarbital	60-73	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	154-170
2755909-0	1989	Tissue distribution of inducible aldehyde dehydrogenase activity in the rat after treatment with phenobarbital or methylcholanthrene.	Phenobarbital	97-110	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	33-55
2755909-2	1989	The RR substrain is responsive to phenobarbital (PB), as far as the induction of the hepatic ALDH activity is concerned, whereas the rr substrain is deprived of this biochemical property.	Phenobarbital	49-51	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	93-97
2755909-5	1989	The effect of PB (1 g/l in drinking water, for 12 days) on the inducibility of ALDH in extrahepatic tissues was examined in the RR substrain.	Phenobarbital	14-16	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	79-83
2755909-7	1989	The activity of ALDH was found to be induced by PB in the liver and the intestinal mucosa, when measured with NAD and propionaldehyde (P/NAD) or phenylacetaldehyde (Ph/NAD).	Phenobarbital	48-50	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	16-20
2755909-11	1989	It is concluded, that PB and MC not only induce different types of ALDH activity, but they also reveal differences in the tissue distribution of the inducibility of ALDH.	Phenobarbital	22-24	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	67-71
2755909-11	1989	It is concluded, that PB and MC not only induce different types of ALDH activity, but they also reveal differences in the tissue distribution of the inducibility of ALDH.	Phenobarbital	22-24	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	165-169
2749135-1	1989	The possible effects of a synthetic progesterone, medroxyprogesterone acetate (MPA), on carbon tetrachloride/phenobarbital (CCl4/PB)-induced rat liver injury were studied by morphological methods.	Phenobarbital	109-122	C-C motif chemokine ligand 4	Rattus norvegicus	124-131
2903743-0	1988	Mouse hepatic cytochrome P-450 isozyme induction by 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene, pyrazole, and phenobarbital.	Phenobarbital	110-123	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	14-30
2903743-10	1988	In immunoblot experiments with anti-P-450Coh antibody, the amount of P-450Coh was considerably higher in DBA/2N mice treated with phenobarbital, TCPOBOP, or pyrazole in comparison with the AKR/J mice, indicating a strain specificity in the inducibility of coumarin 7-hydroxylase by pyrazole.	Phenobarbital	130-143	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	256-278
3049217-3	1988	Levels of the 50-kilodalton rat microsomal polypeptide were suppressed in vivo by several drugs known to modulate expression of individual forms (enzymes) of hepatic cytochrome P-450, with the largest decrease effected by phenobarbital.	Phenobarbital	222-235	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	166-182
3148707-6	1988	These findings concerning the effects of 2,4-, 3,5- and 3,4-DCPSO2Mes on the activities of NADPH-cytochrome c reductase and UDPGT support our hypothesis that the methylsulfonyl metabolites derived from m- and o-DCBs are phenobarbital-type inducers of the hepatic microsomal drug-metabolizing enzymes.	Phenobarbital	220-233	UDP glucuronosyltransferase family 2 member B15	Rattus norvegicus	124-129
2541728-10	1989	These data indicate that phenobarbital can be a weak ligand for the Ah receptor and thus induce cytochrome P450IA1 and AHH activity.	Phenobarbital	25-38	aryl-hydrocarbon receptor	Mus musculus	68-79
2541728-10	1989	These data indicate that phenobarbital can be a weak ligand for the Ah receptor and thus induce cytochrome P450IA1 and AHH activity.	Phenobarbital	25-38	aryl-hydrocarbon receptor	Mus musculus	119-122
2563599-3	1989	Promotion by phenobarbital caused an increased expression of both of these genes in altered hepatic focal lesions, although this was somewhat more variable in the case of the GGT gene.	Phenobarbital	13-26	gamma-glutamyltransferase 1	Rattus norvegicus	175-178
2563599-9	1989	The mRNA levels of GST-P were uniformly elevated dramatically in reversible nodules and neoplasms of rat liver that had been induced by diethylnitrosamine and phenobarbital promotion.	Phenobarbital	159-172	glutathione S-transferase pi 1	Rattus norvegicus	19-24
20702289-3	1989	Two different antibodies directed against cytochrome P-450 revealed the ontogenic profile of the phenobarbitone-inducible b and e forms, which appeared at an earlier stage of development, day 1 of culture (equivalent to day 14 of gestation), than did the 3-methylcholanthrene-inducible c form, which appeared on day 3 of culture (equivalent to day 16 of gestation).	Phenobarbital	97-111	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	42-58
20702290-2	1989	The b and e forms of cytochrome P-450 were found to be non-inducible by either in vitro co-incubation for 5 days or by transplacental maternal induction with phenobarbitone (PB), 3-methylcholanthrene (3MC) or beta-naphthoflavone (betaNF) in either cell type.	Phenobarbital	174-176	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	21-37
3145631-5	1988	When the para" substituent was a halogen (F, Cl, Br or I), the derivative induced both cytochromes P-450b and P-450e, and cytochromes P-450c and P-450d, which are the major phenobarbital- and 3-methylcholanthrene-inducible isozymes, respectively.	Phenobarbital	173-186	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	99-105
3145631-5	1988	When the para" substituent was a halogen (F, Cl, Br or I), the derivative induced both cytochromes P-450b and P-450e, and cytochromes P-450c and P-450d, which are the major phenobarbital- and 3-methylcholanthrene-inducible isozymes, respectively.	Phenobarbital	173-186	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	134-151
3264502-1	1988	Monoclonal antibodies (MAbs) raised to rat liver cytochrome P-450s induced by phenobarbital, 3-methylcholanthrene, and pregnenolone-16 alpha-carbonitrile were used to detect these epitope specific P-450s in human abortion fetuses 14-24 weeks of age.	Phenobarbital	78-91	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	49-65
2462160-5	1988	Treatment with phenobarbital resulted in enhancement of cytochrome P-450 that was visualized in hepatocytes in all regions of the lobule.	Phenobarbital	15-28	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	56-72
2845109-2	1988	MDR-1 (also known as PGY1) was induced following administration of aflatoxin B1, 2-(acetylamino)fluorene (AAF), N-hydroxy-2-(acetylamino)fluorene, isosafrole, phenothiazine, and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), but not after phenobarbital or 7-hydroxy-2-(acetylamino)fluorene treatment.	Phenobarbital	236-249	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-5
2845109-2	1988	MDR-1 (also known as PGY1) was induced following administration of aflatoxin B1, 2-(acetylamino)fluorene (AAF), N-hydroxy-2-(acetylamino)fluorene, isosafrole, phenothiazine, and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), but not after phenobarbital or 7-hydroxy-2-(acetylamino)fluorene treatment.	Phenobarbital	236-249	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	21-25
2845109-3	1988	Cytochrome P-450 isoform d was induced by TCDD, isosafrole, phenothiazine, and AAF, while cytochrome P-450 isoform b was induced by phenobarbital, and to a lesser extent by isosafrole.	Phenobarbital	132-145	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	90-106
2846197-5	1988	Pretreatment of fetuses with phenobarbital potentiated the inducing effect of MC upon P-450c and P-450d mRNA accumulation in relation to the duration of pretreatment, as well as increasing the hepatic content in TCDD-binding protein.	Phenobarbital	29-42	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	86-103
2907458-3	1988	Hypoxia or pretreatment with phenobarbital has been reported to enhance the hepatotoxicity of CCl4 in vivo; these treatments also produced an increase in the biliary concentration of the PBN/.CCl3 radical adduct and in the .CCl3-derived PBN/.CO(-)2 radical adduct as well.	Phenobarbital	29-42	C-C motif chemokine ligand 4	Rattus norvegicus	94-98
2907458-3	1988	Hypoxia or pretreatment with phenobarbital has been reported to enhance the hepatotoxicity of CCl4 in vivo; these treatments also produced an increase in the biliary concentration of the PBN/.CCl3 radical adduct and in the .CCl3-derived PBN/.CO(-)2 radical adduct as well.	Phenobarbital	29-42	C-C motif chemokine ligand 3	Rattus norvegicus	192-196
2907458-3	1988	Hypoxia or pretreatment with phenobarbital has been reported to enhance the hepatotoxicity of CCl4 in vivo; these treatments also produced an increase in the biliary concentration of the PBN/.CCl3 radical adduct and in the .CCl3-derived PBN/.CO(-)2 radical adduct as well.	Phenobarbital	29-42	C-C motif chemokine ligand 3	Rattus norvegicus	224-228
2907568-1	1988	The liver alcohol dehydrogenase inhibitor, 4-methylpyrazole, has been tested for its ability to change the hypnotic concentrations of phenobarbitone (phenobarbital) in rats.	Phenobarbital	134-148	aldo-keto reductase family 1 member A1	Rattus norvegicus	10-31
2907568-1	1988	The liver alcohol dehydrogenase inhibitor, 4-methylpyrazole, has been tested for its ability to change the hypnotic concentrations of phenobarbitone (phenobarbital) in rats.	Phenobarbital	150-163	aldo-keto reductase family 1 member A1	Rattus norvegicus	10-31
3401014-2	1988	The system was used to study effects of the hepatotoxin carbon tetrachloride (CCl4) on lipid peroxidation and cell viability in isolated hepatocytes from phenobarbital-pretreated rats at various steady-state PO2.	Phenobarbital	154-167	C-C motif chemokine ligand 4	Rattus norvegicus	78-82
3420613-1	1988	Rats treated with a single 0.5 ml/kg dose (ip) of CCl4 exhibited a threefold increase in liver microsomal phospholipase C (PLC) activity that was enhanced by phenobarbital and diminished by metyrapone pretreatment, respectively.	Phenobarbital	158-171	C-C motif chemokine ligand 4	Rattus norvegicus	50-54
2971014-1	1988	Phenobarbital is a potent inducer of hepatic cytochrome P-450 and is a tumor promoter in the two-stage model of liver carcinogenesis.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	45-61
3240989-8	1988	P450 PB-1 was induced twofold with phenobarbital in male rats.	Phenobarbital	35-48	cytochrome P450, family 2, subfamily c, polypeptide 12	Rattus norvegicus	0-9
3240989-9	1988	P450 PB-1 was purified from untreated male rats and identified as P450 PB-1 from phenobarbital-treated rats by its NH2-terminal sequence, peptide mapping, and immunochemistry.	Phenobarbital	81-94	cytochrome P450, family 2, subfamily c, polypeptide 12	Rattus norvegicus	0-9
3240989-9	1988	P450 PB-1 was purified from untreated male rats and identified as P450 PB-1 from phenobarbital-treated rats by its NH2-terminal sequence, peptide mapping, and immunochemistry.	Phenobarbital	81-94	cytochrome P450, family 2, subfamily c, polypeptide 12	Rattus norvegicus	66-75
3418515-4	1988	Immunochemical analysis confirmed that the level of immunoreactive P-450j protein was increased in PY-induced microsomes as compared to preparations from control, phenobarbital- or beta-naphthoflavone-induced animals.	Phenobarbital	163-176	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	67-73
3219345-1	1988	The constitutive expression of phenobarbital-inducible mouse cytochrome P-450 (I-P-450(16 alpha) at the mRNA level and its associated testosterone 16 alpha-hydroxylase activity in liver microsomes was a female characteristic in many inbred mice, including BALB/cJ, A/HeJ, and C57BL/6J.	Phenobarbital	31-44	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	61-95
3219345-1	1988	The constitutive expression of phenobarbital-inducible mouse cytochrome P-450 (I-P-450(16 alpha) at the mRNA level and its associated testosterone 16 alpha-hydroxylase activity in liver microsomes was a female characteristic in many inbred mice, including BALB/cJ, A/HeJ, and C57BL/6J.	Phenobarbital	31-44	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	134-167
3219345-5	1988	We propose Rip (regulation of sex-dependent, constitutive expression of phenobarbital-inducible P-450) as the name of this sex-limited locus.	Phenobarbital	72-85	regulation of phenobarbitol-inducible P450	Mus musculus	11-14
3144720-2	1988	In this study phenobarbital, 50 mg at bedtime for ten days, increased serum HDL cholesterol, HDL2 cholesterol and HDL cholesterol/cholesterol and HDL cholesterol/apolipoprotein A-I ratios.	Phenobarbital	14-27	junctophilin 3	Homo sapiens	93-97
3144720-2	1988	In this study phenobarbital, 50 mg at bedtime for ten days, increased serum HDL cholesterol, HDL2 cholesterol and HDL cholesterol/cholesterol and HDL cholesterol/apolipoprotein A-I ratios.	Phenobarbital	14-27	apolipoprotein A1	Homo sapiens	162-180
3058117-0	1988	Regulation of phenobarbital-inducible cytochrome P-450s in rat and mouse liver following dexamethasone administration and hypophysectomy.	Phenobarbital	14-27	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	38-54
3058117-3	1988	To examine the role of constitutive factors in cytochrome P-450 regulation, the levels of three distinct groups of phenobarbital-inducible hepatic cytochrome P-450s were studied following dexamethasone-treatment or hypophysectomy.	Phenobarbital	115-128	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	147-163
3177220-6	1988	A concentration-response relationship also was demonstrated between exposure to CS2 in rats that had been treated with PB and decreased hepatic cholesterol synthesis, increased hepatic cholesterol concentration, increased relative liver weight, increased hepatic water content, and histopathological damage.	Phenobarbital	119-121	calsyntenin 2	Rattus norvegicus	80-83
3177220-7	1988	Treatment with PB lowered the concentration of CS2 required to alter hepatic cholesterol metabolism.	Phenobarbital	15-17	calsyntenin 2	Rattus norvegicus	47-50
3181265-4	1988	Experiments on the binding to cytochrome P-450 in Pb-induced microsomes led to the following findings: (a) the presence of the polycyclic skeleton is necessary for binding; (b) the presence of the sugar moiety gives a further extension of binding, and changes in the sugar moiety affect binding; (c) binding increases on elevation of hydrophobicity; (d) the E-ring itself does not bind.	Phenobarbital	50-52	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	30-46
3042808-0	1988	Demonstration by in situ hybridization of the zonal modulation of rat liver cytochrome P-450b and P-450e gene expression after phenobarbital.	Phenobarbital	127-140	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	76-93
3042808-3	1988	The objective of this study was to determine whether transcriptional or posttranscriptional zonal modulation of cytochromes P-450b,e gene expression was responsible for the heterogeneous induction of the P-450 proteins, which is observed after phenobarbital (PB) administration.	Phenobarbital	244-257	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	124-130
3042808-3	1988	The objective of this study was to determine whether transcriptional or posttranscriptional zonal modulation of cytochromes P-450b,e gene expression was responsible for the heterogeneous induction of the P-450 proteins, which is observed after phenobarbital (PB) administration.	Phenobarbital	259-261	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	124-130
3042808-4	1988	The exact localization in liver tissue of hepatocytes responding to PB with induction of either P-450b,e mRNA or proteins was established by in situ hybridization and by immunofluorescence, respectively.	Phenobarbital	68-70	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	96-102
3042808-5	1988	As demonstrated by quantitative assessment of autoradiographs of approximately 20 hepatocytes located between a terminal portal venule and a hepatic venule, PB induced the P-450b,e mRNA up to sixfold in the 12-15 hepatocytes located closer to the hepatic venules (zones 2 and 3).	Phenobarbital	157-159	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	172-178
3042808-7	1988	Quantitative immunofluorescence using an MAb showed that the acinar distribution of PB-induced P-450b,e proteins was similar to that of the mRNA.	Phenobarbital	84-86	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	95-101
3042808-10	1988	Experiments in which the induction of cytochromes P-450b,e genes was studied after administration of either PB or para-hydroxyphenobarbital, a main hepatic metabolite of PB, suggested that the species involved in the inductive process is the parent PB molecule rather than para-hydroxyphenobarbital.	Phenobarbital	108-110	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	50-56
3042808-10	1988	Experiments in which the induction of cytochromes P-450b,e genes was studied after administration of either PB or para-hydroxyphenobarbital, a main hepatic metabolite of PB, suggested that the species involved in the inductive process is the parent PB molecule rather than para-hydroxyphenobarbital.	Phenobarbital	170-172	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	50-56
3042808-10	1988	Experiments in which the induction of cytochromes P-450b,e genes was studied after administration of either PB or para-hydroxyphenobarbital, a main hepatic metabolite of PB, suggested that the species involved in the inductive process is the parent PB molecule rather than para-hydroxyphenobarbital.	Phenobarbital	170-172	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	50-56
3406955-1	1988	Simultaneous administration of caffeine (100 mg/kg, i.p., 3 days) and phenobarbital (80 mg/kg, i.p., 3 days) to adult male rats resulted in a significant decrease in hepatic cytochrome P-450 and acetanilide hydroxylase activity, compared to phenobarbital administration alone.	Phenobarbital	70-83	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	174-190
3132464-0	1988	Expression of cytochrome P450b and P450e genes in small intestinal mucosa of rats following treatment with phenobarbital, polyhalogenated biphenyls, and organochlorine pesticides.	Phenobarbital	107-120	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	14-30
3148724-2	1988	The major phenobarbital-inducible form of rat liver microsomal cytochrome P-450, designated P-450b, was extremely sensitive to the inhibitory effects of Emulgen 911, which is used in several procedures to purify this and other forms of cytochrome P-450.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	63-79
3148724-2	1988	The major phenobarbital-inducible form of rat liver microsomal cytochrome P-450, designated P-450b, was extremely sensitive to the inhibitory effects of Emulgen 911, which is used in several procedures to purify this and other forms of cytochrome P-450.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	92-98
3148724-2	1988	The major phenobarbital-inducible form of rat liver microsomal cytochrome P-450, designated P-450b, was extremely sensitive to the inhibitory effects of Emulgen 911, which is used in several procedures to purify this and other forms of cytochrome P-450.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	236-252
3261011-5	1988	Monoclonal antibodies raised against 3-methylchloranthrene or phenobarbital induced rat liver cytochrome P-450 were investigated with respect to their inhibiting effects on the rate of O-deethylation of both substrates in human adult liver.	Phenobarbital	62-75	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	94-110
3175344-1	1988	A single acute dose of carbon disulfide (CS2, 5 mmol/kg ip) caused hepatic damage in rats pretreated with phenobarbital.	Phenobarbital	106-119	calsyntenin 2	Rattus norvegicus	41-44
3175344-2	1988	Rats pretreated with phenobarbital and cobaltous chloride (CoCl2, 250 mumol/kg sc) were protected against CS2 induced hepatotoxicity.	Phenobarbital	21-34	calsyntenin 2	Rattus norvegicus	106-109
3220829-1	1988	The effects of phenobarbital (PB), 3-methylcholanthrene (MC), and alpha-naphthoflavone (alpha-NF) on the synthesis of drug-inducible forms of cytochrome P-450, P-450(PB-1), and P-450(MC-1), and sex-specific forms of cytochrome P-450, P-450(M-1), and P-450(F-1), in male and female rats were studied.	Phenobarbital	15-28	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	142-158
3220829-1	1988	The effects of phenobarbital (PB), 3-methylcholanthrene (MC), and alpha-naphthoflavone (alpha-NF) on the synthesis of drug-inducible forms of cytochrome P-450, P-450(PB-1), and P-450(MC-1), and sex-specific forms of cytochrome P-450, P-450(M-1), and P-450(F-1), in male and female rats were studied.	Phenobarbital	30-32	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	142-158
2845535-3	1988	The suppression of p-NP production by CS2 was also observed in livers isolated from phenobarbital (PB)- and 3-methylcholanthrene (3-MC)-treated rats; to a greater extent, in the normal and 3-MC groups.	Phenobarbital	84-97	purine nucleoside phosphorylase	Rattus norvegicus	19-23
2845535-3	1988	The suppression of p-NP production by CS2 was also observed in livers isolated from phenobarbital (PB)- and 3-methylcholanthrene (3-MC)-treated rats; to a greater extent, in the normal and 3-MC groups.	Phenobarbital	84-97	calsyntenin 2	Rattus norvegicus	38-41
2845535-3	1988	The suppression of p-NP production by CS2 was also observed in livers isolated from phenobarbital (PB)- and 3-methylcholanthrene (3-MC)-treated rats; to a greater extent, in the normal and 3-MC groups.	Phenobarbital	99-101	purine nucleoside phosphorylase	Rattus norvegicus	19-23
2845535-3	1988	The suppression of p-NP production by CS2 was also observed in livers isolated from phenobarbital (PB)- and 3-methylcholanthrene (3-MC)-treated rats; to a greater extent, in the normal and 3-MC groups.	Phenobarbital	99-101	calsyntenin 2	Rattus norvegicus	38-41
3175345-5	1988	This increase occurred only when CS2 was given to phenobarbital pretreated rats and was prevented by prior treatment with SKF 525-A.	Phenobarbital	50-63	calsyntenin 2	Rattus norvegicus	33-36
3135288-6	1988	Both cytochrome P-450 (P less than .01) and nicotinamide adenine dinucleotide phosphate (NADPH) cytochrome c reductase (P less than .06) were higher in ewes receiving PB than in controls.	Phenobarbital	167-169	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	5-21
3390203-2	1988	These results indicate that the 3-MC-inducible form of cytochrome P-450 was more susceptible to CS2 than the PB-inducible form.	Phenobarbital	109-111	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	55-71
2456905-1	1988	In rat liver, the two major phenobarbital (PB)-inducible cytochrome P450s, P450b (P450IIB1), and P450e (P450IIB2), are encoded by approximately 2.1-kb mRNAs showing more than 97% nucleotide sequence identity.	Phenobarbital	28-41	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	75-80
2456905-1	1988	In rat liver, the two major phenobarbital (PB)-inducible cytochrome P450s, P450b (P450IIB1), and P450e (P450IIB2), are encoded by approximately 2.1-kb mRNAs showing more than 97% nucleotide sequence identity.	Phenobarbital	43-45	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	75-80
3382400-0	1988	Cytochrome P450 induction by phenobarbital (PB) is inhibited by 12-O-tetradecanoylphorbol-13-acetate (TPA): evidence that protein kinase C regulates induction.	Phenobarbital	29-42	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-15
3382400-0	1988	Cytochrome P450 induction by phenobarbital (PB) is inhibited by 12-O-tetradecanoylphorbol-13-acetate (TPA): evidence that protein kinase C regulates induction.	Phenobarbital	44-46	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-15
3384091-2	1988	We report here that (i) benzanthracene and PB induce P450 c mRNA in differentiated and dedifferentiated cells and (ii) dexamethasone and PB induce P450 b/e and/or P450 PB1 mRNAs in differentiated cells but not in dedifferentiated cells.	Phenobarbital	43-45	cytochrome P450, family 2, subfamily c, polypeptide 12	Rattus norvegicus	163-171
3384091-2	1988	We report here that (i) benzanthracene and PB induce P450 c mRNA in differentiated and dedifferentiated cells and (ii) dexamethasone and PB induce P450 b/e and/or P450 PB1 mRNAs in differentiated cells but not in dedifferentiated cells.	Phenobarbital	137-139	cytochrome P450, family 2, subfamily c, polypeptide 12	Rattus norvegicus	163-171
2837761-3	1988	Furthermore, P-450 15 beta is 47% similar to the major phenobarbital-inducible cytochrome P-450 in rat liver, P-450 b, while its structural similarity to P-450 c, P-450 pregnenolone-16a-carbonitrile, and P-450 lauric acid omega-hydroxylase is less than 30%.	Phenobarbital	55-68	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	79-95
3130800-0	1988	The expression and metabolic activity of cytochrome P-450 isozymes in control and phenobarbital-induced primary cultures of rat hepatocytes.	Phenobarbital	82-95	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	41-57
2837203-2	1988	The catalytic effect of NADPH cytochrome P-450 on the radical formation in the hepatic microsomes obtained from phenobarbital-pretreated rats was also supported by the fact that Hz radical formation was stimulated by flavin adenin dinucleotide or methyl viologen and markedly inhibited by superoxide dismutase, however, carbon monoxide showed no effect.	Phenobarbital	112-125	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	30-46
3377780-1	1988	Oxygen inhibition of CCl4 metabolism by different isoenzymes of cytochrome P-450 was assessed by studying liver microsomes isolated from control rats and rats treated with phenobarbital or isoniazid.	Phenobarbital	172-185	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	64-80
3377780-5	1988	Rats treated with phenobarbital, which increases hepatic cytochrome P-450 content, or isoniazid, which does not increase hepatic cytochrome P-450 content, both metabolized more CCl4 than control rats as indicated by exhalation of greater quantities of CCl4 metabolites and by an increase in CCl4 toxicity.	Phenobarbital	18-31	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	57-73
3377780-5	1988	Rats treated with phenobarbital, which increases hepatic cytochrome P-450 content, or isoniazid, which does not increase hepatic cytochrome P-450 content, both metabolized more CCl4 than control rats as indicated by exhalation of greater quantities of CCl4 metabolites and by an increase in CCl4 toxicity.	Phenobarbital	18-31	C-C motif chemokine ligand 4	Rattus norvegicus	177-181
3259880-2	1988	This study was undertaken into liver microsomal fractions prepared from untreated rabbits or animals treated with drugs known to specifically induce various cytochrome P-450 isozymes such as form LM2 by phenobarbital, LM4 and LM6 by 3-methylcholanthrene and beta-naphthoflavone, LM3a by ethyl alcohol and acetone, and LM3c by macrolide antibiotics (rifampicin, erythromycin and triacetyloleandomycin).	Phenobarbital	203-216	cytochrome P-450	Oryctolagus cuniculus	157-173
3130800-4	1988	P-450b was consistently induced by PB in hepatocytes in T1 and to a lesser extent in Way.	Phenobarbital	35-37	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	0-6
3130800-6	1988	DMBA metabolite formation associated with P-450b and P-450e activity was induced by PB in hepatocytes in T1 and Way and was inhibited by antibodies to P-450b.	Phenobarbital	84-86	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	42-48
3130800-6	1988	DMBA metabolite formation associated with P-450b and P-450e activity was induced by PB in hepatocytes in T1 and Way and was inhibited by antibodies to P-450b.	Phenobarbital	84-86	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	151-157
3130800-7	1988	P-450c was only infrequently expressed in freshly prepared hepatocytes, but was detected in all control and PB-treated cultures although at a much higher level in T1.	Phenobarbital	108-110	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-6
3130800-9	1988	We have demonstrated enzyme induction and increased activity of the major PB-inducible isozymes in hepatocytes in T1; these are also associated with a change in the control of P-450c expression leading to enhanced constitutive expression and inducibility by phenobarbital.	Phenobarbital	74-76	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	176-182
3130800-9	1988	We have demonstrated enzyme induction and increased activity of the major PB-inducible isozymes in hepatocytes in T1; these are also associated with a change in the control of P-450c expression leading to enhanced constitutive expression and inducibility by phenobarbital.	Phenobarbital	258-271	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	176-182
3130803-20	1988	PCNb as well as a third cytochrome P-450 termed PCNc isolated from PB-treated rats both correspond in amino-terminal sequence to the putative protein product of the pP450PCN2/cDNA clone of Gonzalez et al.	Phenobarbital	67-69	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	24-40
3377831-5	1988	The level of the female specific enzyme, P-450-female, slightly decreased in the MSG-treated female rats, whereas higher phenobarbital (PB)-induction of PB-inducible isozymes, P-450b and P-450e, was observed in MSG-treated than in control female rats.	Phenobarbital	121-134	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	176-182
3364973-8	1988	Considered together, these observations strongly suggest that the phenobarbital-inducible cytochrome P-450 isozymes PB-B and PCN-E are present in an inactive complexed state in microsomes from SKF 525-A-induced rat liver.	Phenobarbital	66-79	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	90-106
3377831-5	1988	The level of the female specific enzyme, P-450-female, slightly decreased in the MSG-treated female rats, whereas higher phenobarbital (PB)-induction of PB-inducible isozymes, P-450b and P-450e, was observed in MSG-treated than in control female rats.	Phenobarbital	136-138	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	176-182
3413034-2	1988	A panel of nine inhibitors displaying some P-450 isozyme specificity was used to characterize aryl hydrocarbon hydroxylase (AHH) and 7-ethoxyresorufin 0-deethylase (ERDE) activities in human liver and placenta in vitro in comparison with liver enzymes from control, phenobarbital (PB) and 3-methylcholanthrene (MC) treated rats.	Phenobarbital	266-279	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	124-127
3356011-12	1988	Thus, EPH, a long-acting sedative/anticonvulsant, like the structurally similar PB, promoted hepatocellular and thyroid follicular cell carcinogenesis and induced the PB-inducible form(s) of cytochrome P-450 (P-450b) in rats.	Phenobarbital	167-169	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	191-207
3356011-12	1988	Thus, EPH, a long-acting sedative/anticonvulsant, like the structurally similar PB, promoted hepatocellular and thyroid follicular cell carcinogenesis and induced the PB-inducible form(s) of cytochrome P-450 (P-450b) in rats.	Phenobarbital	167-169	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	209-215
3396451-1	1988	The prototypic members of the rat liver cytochrome P450IIB subfamily, P450b and P450e, have long been the subjects of intense interest, in part because they are highly inducible by phenobarbital (PB).	Phenobarbital	181-194	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	70-75
3396451-1	1988	The prototypic members of the rat liver cytochrome P450IIB subfamily, P450b and P450e, have long been the subjects of intense interest, in part because they are highly inducible by phenobarbital (PB).	Phenobarbital	196-198	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	70-75
3050970-2	1988	The antibodies used in the immunohistochemical analyses were monoclonal antibodies (MAbs) 1-7-1 and 2-66-3, prepared against the 3-methylcholanthrene-induced and phenobarbital-induced rat liver P-450, respectively.	Phenobarbital	162-175	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	194-199
3413034-2	1988	A panel of nine inhibitors displaying some P-450 isozyme specificity was used to characterize aryl hydrocarbon hydroxylase (AHH) and 7-ethoxyresorufin 0-deethylase (ERDE) activities in human liver and placenta in vitro in comparison with liver enzymes from control, phenobarbital (PB) and 3-methylcholanthrene (MC) treated rats.	Phenobarbital	281-283	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	124-127
3135673-2	1988	Five isozymes of cytochrome P-450 were purified from liver microsomes of phenobarbital-pretreated (P-450-SD-I and -II), 3-methylcholanthrene-pretreated (P-450-SD-III) and untreated rats (P-450-SD-IV and -V) to determine their catalytic activities in metabolic reactions of methamphetamine.	Phenobarbital	73-86	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	17-33
3135673-10	1988	The present results indicate that the different extents of the metabolic intermediate complex formation with cytochrome P-450 (455 nm complex) in the microsomes from phenobarbital-, 3-methylcholanthrene-pretreated, and untreated rats is not attributable to the activities of the respective isozymes of cytochrome P-450 to form the precursor of the complex, N-hydroxymethamphetamine.	Phenobarbital	166-179	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	109-125
3368919-7	1988	Induction of cytochrome P-450 isozymes by phenobarbital and beta-naphthoflavone treatment protected the cells against the cytotoxicity of I, while acetone or dexamethasone treatment had no effect.	Phenobarbital	42-55	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
3135673-10	1988	The present results indicate that the different extents of the metabolic intermediate complex formation with cytochrome P-450 (455 nm complex) in the microsomes from phenobarbital-, 3-methylcholanthrene-pretreated, and untreated rats is not attributable to the activities of the respective isozymes of cytochrome P-450 to form the precursor of the complex, N-hydroxymethamphetamine.	Phenobarbital	166-179	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	302-318
3355603-0	1988	Study of deutero-isotopomer-induced inhibition of caffeine and phenobarbitone binding to human serum albumin.	Phenobarbital	63-77	albumin	Homo sapiens	95-108
3355603-1	1988	The present study of inhibition provides confirmation to previously observed deuterium isotope effects on in vitro caffeine and phenobarbitone binding to human serum albumin (HSA).	Phenobarbital	128-142	albumin	Homo sapiens	160-173
3355606-6	1988	Addition of 1 microM dexamethasone or 1 mM phenobarbital gave rise to an induction of cytochrome P-450 (285%).	Phenobarbital	43-56	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	86-102
2451866-8	1988	Expiration of 14CO2 measured during the 6 hr after CCl4 administration was increased in animals pretreated with PB or CD.	Phenobarbital	112-114	C-C motif chemokine ligand 4	Rattus norvegicus	51-55
2451866-0	1988	In vivo metabolism of CCl4 by rats pretreated with chlordecone, mirex, or phenobarbital.	Phenobarbital	74-87	C-C motif chemokine ligand 4	Rattus norvegicus	22-26
3127945-7	1988	About 5 mumol of 18O per gram of dry liver was incorporated in phenobarbital/CCl4-treated rats, of which 60% was in the water-soluble fraction, 17% in the lipids, and 16% in the macromolecules.	Phenobarbital	63-76	C-C motif chemokine ligand 4	Rattus norvegicus	77-81
3128295-3	1988	The degree of UROG-D inhibition observed was: TCBP (39%), Ox-DDC (39%), nifedipine (25%) and phenobarbital (50%).	Phenobarbital	93-106	uroporphyrinogen decarboxylase	Gallus gallus	14-20
3257714-0	1988	Modulation of epidermal growth factor receptors in rat hepatocytes by two liver tumor-promoting regimens, a choline-deficient and a phenobarbital diet.	Phenobarbital	132-145	epidermal growth factor like 1	Rattus norvegicus	14-37
2830813-3	1988	Phenobarbital (PB), which is essentially active in the hepatic microsomal cytochrome P-450, was less effective in counteracting oxygen toxicity.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	74-90
2830813-3	1988	Phenobarbital (PB), which is essentially active in the hepatic microsomal cytochrome P-450, was less effective in counteracting oxygen toxicity.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	74-90
3132207-2	1988	A comparison of these forms with cytochromes P-450b and P-450e obtained from phenobarbital-induced rat liver microsomes revealed their similarity in a number of properties, e.g., chromatographic behaviour on 1.8-diaminooctyl-Sepharose 4B and DEAE-Sephacel columns, molecular mass determined by SDS polyacrylamide gel electrophoresis, spectral properties, immunoreactivity, peptide mapping, catalytic activity.	Phenobarbital	77-90	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	45-51
3257910-0	1988	Phenobarbital reduces EGF receptors and the ability of physiological concentrations of calcium to suppress hepatocyte proliferation.	Phenobarbital	0-13	epidermal growth factor like 1	Rattus norvegicus	22-25
2898344-0	1988	N-benzylimidazole, a high magnitude inducer of rat hepatic cytochrome P-450 exhibiting both polycyclic aromatic hydrocarbon- and phenobarbital-type induction of phase I and phase II drug-metabolizing enzymes.	Phenobarbital	129-142	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	59-75
2898344-3	1988	N-Benzylimidazole exhibited mixed type induction of cytochrome P-450, producing both polycyclic aromatic hydrocarbon- and phenobarbital-type induction.	Phenobarbital	122-135	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	52-68
3356413-0	1988	Phenobarbital induction of cytochrome P-450 b,e genes is dependent on protein synthesis.	Phenobarbital	0-13	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	27-43
2451633-3	1988	The aim of this study was to assess the expression of the phenobarbital-inducible cytochrome P-450 b,e genes in hepatocytes of the right and left fetal liver lobes in mice.	Phenobarbital	58-71	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	82-98
3356413-1	1988	Phenobarbital induces liver cytochrome P-450 b,e proteins mainly by increasing the rate of transcription of these genes.	Phenobarbital	0-13	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	28-44
3356413-2	1988	The mechanism responsible for the phenobarbital increment in the rate of transcription of cytochrome P-450 b,e genes is unknown.	Phenobarbital	34-47	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	90-106
3356413-3	1988	The objective of this study was to assess whether active protein synthesis was needed for phenobarbital to induce the liver cytochrome P-450 b,e genes.	Phenobarbital	90-103	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	124-140
3356413-7	1988	While phenobarbital increased cytochrome P-450 b,e mRNAs about 12-fold at 3 hr, this induction was abolished by cycloheximide.	Phenobarbital	6-19	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	30-46
3356413-8	1988	To define whether the absence of protein synthesis in hepatocytes inhibited the phenobarbital induction of cytochrome P-450 at the transcriptional level, in vitro transcription rates using isolated nuclei were measured.	Phenobarbital	80-93	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	107-123
3356413-9	1988	After phenobarbital administration, there was about a 20-fold increment in transcriptional rate of cytochrome P-450 b,e genes.	Phenobarbital	6-19	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	99-115
3356413-11	1988	It is proposed that either preexisting regulatory proteins or transacting factors dependent on active protein synthesis participate in the regulation of liver cytochrome P-450 b,e gene transcription after phenobarbital.	Phenobarbital	205-218	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	159-175
2839467-0	1988	A mutant rat strain deficient in induction of a phenobarbital-inducible form of cytochrome P-450 in liver microsomes.	Phenobarbital	48-61	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	80-96
3410596-6	1988	Phenobarbital induced a decrease in the plasma concentration of TC, HDL-C and LDL-C (with an unchanged HDL-C/LDL-C ratio) and in the plasma activity of LPL.	Phenobarbital	0-13	lipoprotein lipase	Homo sapiens	152-155
2839467-1	1988	Two phenobarbital-inducible forms of cytochrome P-450, P-450(PB-1), and P-450(PB-4), were purified from the liver microsomes of phenobarbital-treated rats and identified with P-450b and P-450e, respectively.	Phenobarbital	4-17	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	37-53
2839467-1	1988	Two phenobarbital-inducible forms of cytochrome P-450, P-450(PB-1), and P-450(PB-4), were purified from the liver microsomes of phenobarbital-treated rats and identified with P-450b and P-450e, respectively.	Phenobarbital	4-17	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	175-181
2839467-1	1988	Two phenobarbital-inducible forms of cytochrome P-450, P-450(PB-1), and P-450(PB-4), were purified from the liver microsomes of phenobarbital-treated rats and identified with P-450b and P-450e, respectively.	Phenobarbital	128-141	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	37-53
3377780-1	1988	Oxygen inhibition of CCl4 metabolism by different isoenzymes of cytochrome P-450 was assessed by studying liver microsomes isolated from control rats and rats treated with phenobarbital or isoniazid.	Phenobarbital	172-185	C-C motif chemokine ligand 4	Rattus norvegicus	21-25
2832723-3	1988	CCl4 or bromotrichloromethane (CBrCl3) was infused into livers from control or phenobarbital-treated rats perfused with either nitrogen- or oxygen-saturated Krebs-Henseleit bicarbonate buffer.	Phenobarbital	79-92	C-C motif chemokine ligand 4	Rattus norvegicus	0-4
3278056-3	1988	It was found in liver sections from phenobarbital-treated rats incubated with anti-P-450b and anti-epoxide hydrolase and from 3-methylcholanthrene-treated rats incubated with anti-P-450c.	Phenobarbital	36-49	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	83-89
3337745-9	1988	Data are also presented showing that none of the reactions catalyzed by human liver microsomes were inhibited by antibodies to a phenobarbital-inducible form of rat cytochrome P-450 (P-450b).	Phenobarbital	129-142	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	165-181
3337745-9	1988	Data are also presented showing that none of the reactions catalyzed by human liver microsomes were inhibited by antibodies to a phenobarbital-inducible form of rat cytochrome P-450 (P-450b).	Phenobarbital	129-142	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	183-189
3337745-10	1988	These results suggest that the human cytochrome P-450 isozyme that is immunochemically similar and, thus, homologous to rat P-450d plays a major role in the metabolic activation of several procarcinogens examined, and that the activation of AFB1 is catalyzed by another and, possibly, not phenobarbital-inducible form(s) of human cytochrome P-450.	Phenobarbital	289-302	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	37-53
3370247-0	1988	[Comparison of cytochrome P-450 forms induced by phenobarbital and 1,4-bis[3,5-dichloropyridyloxy)]benzene in the mouse and rat liver].	Phenobarbital	49-62	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	15-31
3337745-10	1988	These results suggest that the human cytochrome P-450 isozyme that is immunochemically similar and, thus, homologous to rat P-450d plays a major role in the metabolic activation of several procarcinogens examined, and that the activation of AFB1 is catalyzed by another and, possibly, not phenobarbital-inducible form(s) of human cytochrome P-450.	Phenobarbital	289-302	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	124-130
3370247-1	1988	A form of cytochrome P-450 (P-450PB) with a molecular weight of 53.5-54.0 kD possessing a high benzphetamine-N-demethylase activity (100-120 nmol formaldehyde/min/nmol cytochrome) was isolated from liver microsomes of phenobarbital-induced C57Bl/6 mice.	Phenobarbital	218-231	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	10-26
3370247-5	1988	Immunochemical analysis of microsomes with the use of antibodies to cytochromes P-450PB and P-450b revealed the presence on the electrophoregrams of phenobarbital-induced rat liver microsomes of two immunologically identical forms of cytochrome P-450, i.e., P-450b and P-450e (the latter had a low ability to benzphetamine N-demethylation).	Phenobarbital	149-162	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	92-98
3370247-5	1988	Immunochemical analysis of microsomes with the use of antibodies to cytochromes P-450PB and P-450b revealed the presence on the electrophoregrams of phenobarbital-induced rat liver microsomes of two immunologically identical forms of cytochrome P-450, i.e., P-450b and P-450e (the latter had a low ability to benzphetamine N-demethylation).	Phenobarbital	149-162	cytochrome P450, family 2, subfamily c, polypeptide 12	Rattus norvegicus	234-253
3370247-5	1988	Immunochemical analysis of microsomes with the use of antibodies to cytochromes P-450PB and P-450b revealed the presence on the electrophoregrams of phenobarbital-induced rat liver microsomes of two immunologically identical forms of cytochrome P-450, i.e., P-450b and P-450e (the latter had a low ability to benzphetamine N-demethylation).	Phenobarbital	149-162	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	258-264
3337745-10	1988	These results suggest that the human cytochrome P-450 isozyme that is immunochemically similar and, thus, homologous to rat P-450d plays a major role in the metabolic activation of several procarcinogens examined, and that the activation of AFB1 is catalyzed by another and, possibly, not phenobarbital-inducible form(s) of human cytochrome P-450.	Phenobarbital	289-302	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	330-346
3338104-1	1988	The effects of 2-acetylaminofluorene (2-AAF), phenobarbital (PB) and butylated hydroxyanisole (BHA) on the competitive proliferation of glutathione S-transferase (GST-P) positive liver cell foci induced by diethylnitrosamine (DEN) and surrounding hepatocytes were studied.	Phenobarbital	46-59	hematopoietic prostaglandin D synthase	Rattus norvegicus	136-161
3338104-1	1988	The effects of 2-acetylaminofluorene (2-AAF), phenobarbital (PB) and butylated hydroxyanisole (BHA) on the competitive proliferation of glutathione S-transferase (GST-P) positive liver cell foci induced by diethylnitrosamine (DEN) and surrounding hepatocytes were studied.	Phenobarbital	61-63	hematopoietic prostaglandin D synthase	Rattus norvegicus	136-161
3338104-9	1988	In the group treated with PB, proliferation of surrounding hepatocytes was slightly inhibited (LI one day after PH = 16.0) compared with that of control (LI = 24.2), but proliferation of cells in GST-P positive foci was not inhibited (LI one day after PH = 11.3; control value = 11.0).	Phenobarbital	26-28	glutathione S-transferase pi 1	Rattus norvegicus	196-201
3347063-2	1988	The effects of the enzyme inducing agents phenobarbitone and beta-naphthoflavone on microsomal cytochrome P-450-mediated androst-4-ene-3,17-dione hydroxylation and aromatization was investigated in the rat in vitro.	Phenobarbital	42-56	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	95-111
3121722-1	1988	This study examined the possibility of using an immunohistochemical technique to detect the expression of myc and src oncogene proteins (ops) in livers of male Sprague-Dawley rats after treatment with the carcinogen diethylnitrosamine (with or without phenobarbital promotion) or untreated.	Phenobarbital	252-265	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	106-109
3258422-8	1988	The MAb were raised against 3-methylcholanthrene (MAb 1-7-1) or phenobarbital (MAB 2-66-3) induced rat liver microsomal cytochrome P-450.	Phenobarbital	64-77	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	120-136
3335004-3	1988	The feeding of phenobarbital (0.05%) itself led to a 65% decrease in the level of epidermal growth factor receptor RNA, but no major change in the level of c-myc, H-ras, rat leukemia virus, or 30S RNAs, in the control rat livers.	Phenobarbital	15-28	epidermal growth factor receptor	Rattus norvegicus	82-114
2828114-0	1988	Surface enhanced resonance Raman study of phenobarbital-induced rabbit liver cytochrome P-450 LM2.	Phenobarbital	42-55	cytochrome P450 2B4	Oryctolagus cuniculus	77-97
3335004-4	1988	There was a considerable increase (4- to 5-fold) in the level of c-myc transcripts, at 12 and 48 h after partial hepatectomy in the phenobarbital-treated rats, and at 12 and 24 h in the rats on the control diet.	Phenobarbital	132-145	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	65-70
3335004-6	1988	A slight increase (about 1.5-fold) in the level of c-H-ras transcripts was seen at 24 h, which returned to normal levels by 168 h, in the regenerating livers of both the phenobarbital-treated and control diet rats.	Phenobarbital	170-183	HRas proto-oncogene, GTPase	Rattus norvegicus	51-58
3335004-7	1988	The regenerating livers displayed a marked decrease (3- to 4-fold) in the level of epidermal growth factor receptor RNA in both the phenobarbital and control diet rats.	Phenobarbital	132-145	epidermal growth factor receptor	Rattus norvegicus	83-115
3164963-3	1988	Furthermore, either of these two cytochromes has a homology of about 50% with the major phenobarbital inducible form, cytochrome P-450b, while the homology with the major carcinogen inducible form, cytochrome P-450c, is less than 30%.	Phenobarbital	88-101	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	118-135
2831965-0	1988	Comparison of primary structures deduced from cDNA nucleotide sequences for various forms of liver microsomal cytochrome P-450 from phenobarbital-treated rabbits.	Phenobarbital	132-145	cytochrome P-450	Oryctolagus cuniculus	110-126
2831965-1	1988	cDNA clones, termed pHP2, b32-3, b43, and b43-1, encoding cytochromes P-450 that are expressed in the liver of phenobarbital- (PB-) treated rabbits were isolated, and their nucleotide sequences were determined.	Phenobarbital	111-124	cytochrome P450 2C2	Oryctolagus cuniculus	20-24
3124747-1	1988	Incorporation of detergent-solubilized cytochrome b5 into phenobarbital-induced rabbit liver microsomal fractions decelerates hexobarbital-dependent reduction of ferric cytochrome P-450; this is accompanied by retardation of NADPH utilization and H2O2 formation in the assay media.	Phenobarbital	58-71	cytochrome b5	Oryctolagus cuniculus	39-52
3124747-1	1988	Incorporation of detergent-solubilized cytochrome b5 into phenobarbital-induced rabbit liver microsomal fractions decelerates hexobarbital-dependent reduction of ferric cytochrome P-450; this is accompanied by retardation of NADPH utilization and H2O2 formation in the assay media.	Phenobarbital	58-71	cytochrome P-450	Oryctolagus cuniculus	169-185
3358961-0	1988	[Isolation and comparative analysis of multiple isoenzymes of glutathione-S-transferase from the liver of intact rats and rats administered phenobarbital, 3-methylcholanthrene and butylhydroxytoluene].	Phenobarbital	140-153	hematopoietic prostaglandin D synthase	Rattus norvegicus	62-87
3190440-1	1988	Purified phenobarbital-induced rat liver cytochrome P-450 was incorporated in a reconstituted system containing NADPH-cytochrome P-450 reductase, dilauroyl phosphatidyl choline and sodium cholate.	Phenobarbital	9-22	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	41-57
3190440-1	1988	Purified phenobarbital-induced rat liver cytochrome P-450 was incorporated in a reconstituted system containing NADPH-cytochrome P-450 reductase, dilauroyl phosphatidyl choline and sodium cholate.	Phenobarbital	9-22	cytochrome p450 oxidoreductase	Rattus norvegicus	112-144
3358961-3	1988	Phenobarbital (PB) induced isozymes GST 1-1(A), 1-1(B) (2-fold) and 3-3 (1.5-fold).	Phenobarbital	0-13	glutathione S-transferase alpha 2	Rattus norvegicus	36-43
3248121-1	1988	Two phenobarbital-induced isoenzymes of the rat cytochrome P-450 have been isolated using a modification of a method described earlier.	Phenobarbital	4-17	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	48-64
3358961-3	1988	Phenobarbital (PB) induced isozymes GST 1-1(A), 1-1(B) (2-fold) and 3-3 (1.5-fold).	Phenobarbital	15-17	glutathione S-transferase alpha 2	Rattus norvegicus	36-43
3358961-6	1988	A conclusion was drawn that BHT and PB induced the GST subunits 1 and 3, whereas MC--subunits 2 and 4.	Phenobarbital	36-38	hematopoietic prostaglandin D synthase	Rattus norvegicus	51-54
2894946-3	1988	The treatment of Suncus murinus with phenobarbital and 3-methylcholanthrene elevated the level of cytochrome P-450 and the activity of drug-metabolizing enzymes, but not the level of cytochrome b5.	Phenobarbital	37-50	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	98-114
3121205-8	1988	of revertants induced/nmol cytochrome P-450) for the activation of MeIQx was observed with a high-spin form of cytochrome P-450, P-448-H, followed by the low-spin form, P-448-L, and to a lesser extent by PB-inducible forms, P-450b and P-450e.	Phenobarbital	204-206	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	27-44
3121205-8	1988	of revertants induced/nmol cytochrome P-450) for the activation of MeIQx was observed with a high-spin form of cytochrome P-450, P-448-H, followed by the low-spin form, P-448-L, and to a lesser extent by PB-inducible forms, P-450b and P-450e.	Phenobarbital	204-206	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	27-43
3121205-8	1988	of revertants induced/nmol cytochrome P-450) for the activation of MeIQx was observed with a high-spin form of cytochrome P-450, P-448-H, followed by the low-spin form, P-448-L, and to a lesser extent by PB-inducible forms, P-450b and P-450e.	Phenobarbital	204-206	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	224-230
3164672-2	1988	Treatment of phenobarbital at the oral dose of 120 mg/kg induced significant increases in the contents of cytochrome P-450, cytochrome b5 and NADPH-cytochrome P-450 reductase and in the activity of ethoxycoumarin O-deethylase, and significant decreases in the activities of benzphetamine N-demethylase and aniline hydroxylase.	Phenobarbital	13-26	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	106-137
3164672-2	1988	Treatment of phenobarbital at the oral dose of 120 mg/kg induced significant increases in the contents of cytochrome P-450, cytochrome b5 and NADPH-cytochrome P-450 reductase and in the activity of ethoxycoumarin O-deethylase, and significant decreases in the activities of benzphetamine N-demethylase and aniline hydroxylase.	Phenobarbital	13-26	cytochrome p450 oxidoreductase	Rattus norvegicus	142-174
3168083-4	1988	For comparative reasons, three different drug-metabolizing enzyme systems were used, namely microsomes from control and phenobarbital-treated rats, and a reconstituted system containing the main phenobarbital-induced form of cytochrome P-450 from rat liver.	Phenobarbital	195-208	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	225-241
2839467-1	1988	Two phenobarbital-inducible forms of cytochrome P-450, P-450(PB-1), and P-450(PB-4), were purified from the liver microsomes of phenobarbital-treated rats and identified with P-450b and P-450e, respectively.	Phenobarbital	128-141	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	175-181
2970986-7	1988	Phenobarbital treatment increased the activities of three NADPH generating enzymes, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase and malic enzyme, suggesting that MPA and PB differ in their effects on the liver NADPH-producing system.	Phenobarbital	0-13	glucose-6-phosphate dehydrogenase	Rattus norvegicus	84-117
3243187-3	1988	Our data show also that phenobarbital not only enhances both the direct and metabolism-mediated interaction of most tested PHH with microsomal cytochrome P-450, but also increases the affinity of hexachlorobutadiene, chloroform and carbon tetrachloride for the mitochondrial sites resulting in respiration inhibition.	Phenobarbital	24-37	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	143-159
3220422-4	1988	On the contrary, FF administration decreased the inductive effect of PB on bilirubin UDP-GT activity.	Phenobarbital	69-71	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	85-91
3410874-1	1988	Hepatic microsomal monooxygenase was reconstituted by incorporating cytochrome P-450 and NADPH-cytochrome P-450 reductase, which had been purified from phenobarbital-pretreated rabbit liver microsomes, into phospholipid liposomal membranes.	Phenobarbital	152-165	NADPH--cytochrome P450 reductase	Oryctolagus cuniculus	89-121
3410744-4	1988	In liver cells exhibiting an overall hypertrophy of smooth endoplasmic reticulum (SER) induced by the treatment of fasted rats with phenobarbital, the peripheral localization of FABP immunoreactivity remained unchanged compared with that obtained in the case of fasting alone, and the immunoreactivity did not occur in association with the proliferated SER in the central cytoplasm.	Phenobarbital	132-145	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	178-182
3184783-6	1988	Induction of cytochrome P-450 by pretreatment of the rats with phenobarbital caused an eightfold increase of the nicotine clearance in isolated livers, whereas the pulmonary nicotine clearance was almost doubled.	Phenobarbital	63-76	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
20702341-5	1988	The cytochrome P-450 contents of the hepatocytes from phenobarbital-induced rats were decreased by halothane.	Phenobarbital	54-67	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	4-20
3336347-3	1988	Enzyme inactivation and antibody inhibition studies show that microsomes from both phenobarbital- and non-phenobarbital-treated rats are needed to accurately monitor the inactivation of the major phenobarbital-inducible cytochrome P-450 isozyme (PB-B) and of the major constitutive androstenedione 16 alpha-hydroxylase (UT-A).	Phenobarbital	83-96	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	220-236
3336347-3	1988	Enzyme inactivation and antibody inhibition studies show that microsomes from both phenobarbital- and non-phenobarbital-treated rats are needed to accurately monitor the inactivation of the major phenobarbital-inducible cytochrome P-450 isozyme (PB-B) and of the major constitutive androstenedione 16 alpha-hydroxylase (UT-A).	Phenobarbital	106-119	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	220-236
3406035-2	1988	In a reconstituted enzyme system containing phenobarbital-inducible P-450 form 2, NADPH-cytochrome P-450 reductase, and NADPH, the corresponding alcohols are not produced, but instead carbonyl compounds and hydrocarbons.	Phenobarbital	44-57	cytochrome p450 oxidoreductase	Homo sapiens	82-114
3406035-2	1988	In a reconstituted enzyme system containing phenobarbital-inducible P-450 form 2, NADPH-cytochrome P-450 reductase, and NADPH, the corresponding alcohols are not produced, but instead carbonyl compounds and hydrocarbons.	Phenobarbital	44-57	2,4-dienoyl-CoA reductase 1	Homo sapiens	82-87
3120777-0	1987	Purification and characterization of two constitutive cytochromes P-450 (F-1 and F-2) from adult female rats: identification of P-450F-1 as the phenobarbital-inducible cytochrome P-450 in male rat liver.	Phenobarbital	144-157	coagulation factor II	Rattus norvegicus	66-84
3354230-5	1988	The FAD-containing mono-oxygenase catalysed the formation of (-)-phorate sulphoxide, while two cytochrome P-450 isozymes (cytochrome P-450-B2, a constitutive form, and cytochrome P-450-PB, the principal form induced by phenobarbital) produced (+)-phorate sulphoxide.	Phenobarbital	219-232	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	95-111
2894840-5	1987	Intron insertion sites of the P-450(M-1) gene are located at equivalent positions to those of cytochrome P-450b and P-450e, which are phenobarbital-inducible.	Phenobarbital	134-147	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	30-39
2894840-5	1987	Intron insertion sites of the P-450(M-1) gene are located at equivalent positions to those of cytochrome P-450b and P-450e, which are phenobarbital-inducible.	Phenobarbital	134-147	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	94-111
3120777-0	1987	Purification and characterization of two constitutive cytochromes P-450 (F-1 and F-2) from adult female rats: identification of P-450F-1 as the phenobarbital-inducible cytochrome P-450 in male rat liver.	Phenobarbital	144-157	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	168-184
3120777-10	1987	The NH2-terminal sequence of cytochrome P-450F-1 was identical to that of cytochrome P-450PB-2 purified from hepatic microsomes of male rats treated with phenobarbital.	Phenobarbital	154-167	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	74-94
3120777-12	1987	Furthermore, the antibody to phenobarbital-inducible cytochrome P-450PB-2 gave a single immunoprecipitin band with cytochrome P-450F-1 by Ouchterlony double-diffusion analysis.	Phenobarbital	29-42	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	53-73
3689455-2	1987	In contrast, hepatic cytochrome P-450 concentration was not changed significantly after infusion of perfluorotributylamine, but subsequent administration of phenobarbital caused the usual increase of cytochrome P-450.	Phenobarbital	157-170	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	200-216
3680282-1	1987	2-Allylisopropylacetamide, a porphyrinogen which decreases the microsomal and cytosolic heme pools, is a phenobarbitone-like inducer of cytochrome P-450(b + e) messenger RNAs in rat liver.	Phenobarbital	105-119	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	136-154
3424383-7	1987	Induction of cytochrome P-450 by phenobarbital resulted in enhanced in vivo covalent binding in liver and kidney.	Phenobarbital	33-46	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
2825716-0	1987	Differential induction of human liver UDP-glucuronosyltransferase activities by phenobarbital-type inducers.	Phenobarbital	80-93	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	38-65
3439888-3	1987	When liver microsomes isolated from phenobarbital-pretreated rats were incubated with 35S-CS2, NADPH and glutathione, almost 60% decrease in sulfur binding to microsomal protein was observed under the experimental conditions.	Phenobarbital	36-49	calsyntenin 2	Rattus norvegicus	90-93
2825716-2	1987	(2) UDP-GT activities were differentially induced in liver microsomes from patients treated with the phenobarbital-type inducers phenytoin or pentobarbital.	Phenobarbital	101-114	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	4-10
3427076-4	1987	The D(V/K) isotope effects of the cytochrome P-450 dependent ethanol oxidation were about 4 with liver microsomes from imidazole-, phenobarbital- or acetone-treated rabbits or with microsomes from acetone- or ethanol-treated rats.	Phenobarbital	131-144	cytochrome P-450	Oryctolagus cuniculus	34-50
3315287-1	1987	The effect of the monoclonal antibody MAb 2-66-3, directed against the major rat liver phenobarbital (PB)-induced cytochrome P-450 (P-450), on the S9-mediated mutagenicity of N-nitrosodimethylamine (DMN) in Salmonella typhimurium strain TA1530 was studied using liver S9 from PB-treated mice.	Phenobarbital	87-100	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	114-130
3315287-1	1987	The effect of the monoclonal antibody MAb 2-66-3, directed against the major rat liver phenobarbital (PB)-induced cytochrome P-450 (P-450), on the S9-mediated mutagenicity of N-nitrosodimethylamine (DMN) in Salmonella typhimurium strain TA1530 was studied using liver S9 from PB-treated mice.	Phenobarbital	102-104	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	114-130
3325193-2	1987	Phenobarbital (PB) increases hepatic synthesis of triglyceride but lowers its serum concentration in rats due to increased postheparin plasma activities of lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL); these changes are accompanied by increased activity of these lipolytic enzymes in adipose tissue and liver.	Phenobarbital	0-13	lipoprotein lipase	Rattus norvegicus	156-174
3325193-2	1987	Phenobarbital (PB) increases hepatic synthesis of triglyceride but lowers its serum concentration in rats due to increased postheparin plasma activities of lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL); these changes are accompanied by increased activity of these lipolytic enzymes in adipose tissue and liver.	Phenobarbital	0-13	lipoprotein lipase	Rattus norvegicus	176-179
3325193-2	1987	Phenobarbital (PB) increases hepatic synthesis of triglyceride but lowers its serum concentration in rats due to increased postheparin plasma activities of lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL); these changes are accompanied by increased activity of these lipolytic enzymes in adipose tissue and liver.	Phenobarbital	15-17	lipoprotein lipase	Rattus norvegicus	156-174
3325193-2	1987	Phenobarbital (PB) increases hepatic synthesis of triglyceride but lowers its serum concentration in rats due to increased postheparin plasma activities of lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL); these changes are accompanied by increased activity of these lipolytic enzymes in adipose tissue and liver.	Phenobarbital	15-17	lipoprotein lipase	Rattus norvegicus	176-179
3325193-8	1987	PB (0.5 mM) resulted in marked enhancement of conversion of adipocytes characterized by a two- to threefold increase in extracellular LPL and a 10-fold increase in intracellular enzyme.	Phenobarbital	0-2	lipoprotein lipase	Rattus norvegicus	134-137
3120728-6	1987	Treatment of rats with phenobarbital or chlordane caused a relatively small increase in cytochrome P-450p and UDP-GT-dt1 activity.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	88-105
3427076-5	1987	Similar isotope effects were reached with reconstituted membranes containing the rabbit ethanol-inducible cytochrome P-450 (LMeb), whereas control rat microsomes and membranes containing rabbit phenobarbital-inducible P-450 LM2 oxidized the alcohol with D(V/K) of about 2.8 and 1.8, respectively.	Phenobarbital	194-207	cytochrome P450 2B4	Oryctolagus cuniculus	218-227
3427059-10	1987	Results of microsomal metabolism in conjunction with antibody inhibition experiments indicated that cytochromes P-450a and P-450h were the sole 7 alpha- and 2 alpha-hydroxylases, respectively, and that P-450k or an immunochemically related isozyme contributed greater than 80% of the 21-hydroxylase activity observed in microsomes from phenobarbital-induced rats.	Phenobarbital	336-349	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	112-129
3500724-0	1987	Monoclonal antibody characterization of hepatic and extrahepatic cytochrome P-450 activities in rats treated with phenobarbital or methylcholanthrene and fed various cholesterol diets.	Phenobarbital	114-127	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	65-81
3500724-1	1987	Monoclonal antibodies (MAb) against 3-methylcholanthrene (MC)- and phenobarbital (PB)-inducible forms of cytochrome P-450 isozyme were used to characterize changes in aryl hydrocarbon hydroxylase (AHH) and ethoxycoumarin O-deethylase (ECDE) activities modulated by dietary cholesterol.	Phenobarbital	67-80	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	105-121
3500724-1	1987	Monoclonal antibodies (MAb) against 3-methylcholanthrene (MC)- and phenobarbital (PB)-inducible forms of cytochrome P-450 isozyme were used to characterize changes in aryl hydrocarbon hydroxylase (AHH) and ethoxycoumarin O-deethylase (ECDE) activities modulated by dietary cholesterol.	Phenobarbital	82-84	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	105-121
3689389-2	1987	Administration of cycloheximide blocks the induction of cytochrome P-450 (c+d) messenger RNAs by 3-methylcholanthrene as well as cytochrome P-450 (b+e) messenger RNAs by Phenobarbitone.	Phenobarbital	170-184	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	129-145
3122827-1	1987	NADPH-cytochrome P-450 reductase and cytochrome P-450, both purified from liver microsomes of phenobarbital-treated rabbits, were incorporated into dimyristoylphosphatidylcholine vesicles.	Phenobarbital	94-107	NADPH--cytochrome P450 reductase	Oryctolagus cuniculus	0-32
3122827-1	1987	NADPH-cytochrome P-450 reductase and cytochrome P-450, both purified from liver microsomes of phenobarbital-treated rabbits, were incorporated into dimyristoylphosphatidylcholine vesicles.	Phenobarbital	94-107	cytochrome P-450	Oryctolagus cuniculus	6-22
3118810-7	1987	The levels of expression of P-450b were increased by PB in all sets of adrenal, lung, and intestinal microsomes and in three out of six sets of kidney microsomes.	Phenobarbital	53-55	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	28-34
3118810-11	1987	The high constitutive level of P-450b in the lung (approximately 40 pmol/mg), was remarkably inactive in DMBA metabolism and was only slightly increased by PB treatment (50%).	Phenobarbital	156-158	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	31-37
3118810-12	1987	In contrast, PB treatment caused a 2.5- to 10-fold increase in 12-methyl hydroxylation of DMBA that was highly sensitive to anti-P-450b/e.	Phenobarbital	13-15	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	129-135
3499217-1	1987	Both 12-O-tetradecanoylphorbol-13-acetate (TPA) and phenobarbital (PB) enhanced hepatocyte DNA synthesis stimulated with epidermal growth factor (EGF) by 60 to 80% in primary culture when measured by the incorporation of [3H]thymidine.	Phenobarbital	52-65	epidermal growth factor like 1	Rattus norvegicus	121-144
3674884-3	1987	DDEP-mediated cytochrome P-450 destruction may be reproduced in vitro, is most prominent after pretreatment of rats with dexamethasone, pregnenolone 16 alpha-carbonitrile or phenobarbital, and is blocked by triacetyloleandomycin.	Phenobarbital	174-187	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	14-30
2894963-6	1988	The addition of EC, EGC, ECG, and EGCG to microsomes prepared from control, PB- or 3-methylcholanthrene-treated rats resulted in a dose-dependent inhibition of cytochrome P-450-dependent aryl hydrocarbon hydroxylase, 7-ethoxycoumarin O-deethylase, and 7-ethoxyresorufin O-deethylase activities.	Phenobarbital	76-78	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	160-176
2893707-1	1987	Biotransformation of the trichothecene mycotoxin T-2 by the hepatic S-9 fraction prepared from phenobarbital-treated rats yielded a new metabolic product designated RLM-3.	Phenobarbital	95-108	brachyury 2	Rattus norvegicus	49-52
2893713-0	1987	Selective inactivation by chloramphenicol of the major phenobarbital-inducible isozyme of dog liver cytochrome P-450.	Phenobarbital	55-68	Cytochrome P450 1A1	Canis lupus familiaris	100-116
2893713-1	1987	Chloramphenicol (CAP) is a potent and effective mechanism-based inactivator of the major phenobarbital (PB)-inducible isozyme of dog liver cytochrome P-450 (PBD-2) in vitro.	Phenobarbital	89-102	Cytochrome P450 1A1	Canis lupus familiaris	139-162
2893713-1	1987	Chloramphenicol (CAP) is a potent and effective mechanism-based inactivator of the major phenobarbital (PB)-inducible isozyme of dog liver cytochrome P-450 (PBD-2) in vitro.	Phenobarbital	104-106	Cytochrome P450 1A1	Canis lupus familiaris	139-162
3692389-0	1987	Comparative in vitro metabolism of T-2 toxin by hepatic microsomes prepared from phenobarbital-induced or control rats, mice, rabbits and chickens.	Phenobarbital	81-94	brachyury 2	Rattus norvegicus	35-38
3692389-4	1987	In microsomes isolated from PB-treated chickens, 3"-hydroxy T-2 was the major metabolite, but 30 and 79% of the added T-2 toxin remained unmetabolized at 60 min in incubations from PB-induced and control birds, respectively.	Phenobarbital	28-30	brachyury 2	Rattus norvegicus	60-63
3692389-4	1987	In microsomes isolated from PB-treated chickens, 3"-hydroxy T-2 was the major metabolite, but 30 and 79% of the added T-2 toxin remained unmetabolized at 60 min in incubations from PB-induced and control birds, respectively.	Phenobarbital	28-30	brachyury 2	Rattus norvegicus	118-121
3692389-7	1987	In the rabbit microsomal preparations, 3"-hydroxy T-2, which was not detected in the absence of PA, represented 11% of the added substrate in the PB/PA incubation samples.	Phenobarbital	146-148	brachyury 2	Rattus norvegicus	50-53
2963808-1	1987	P-450 human-2 is a human cytochrome P-450 that is immunochemically related to a constitutive male-specific cytochrome P-450 (P-450-male) and the phenobarbital-inducible P-450b/e in rat liver.	Phenobarbital	145-158	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-5
2963808-1	1987	P-450 human-2 is a human cytochrome P-450 that is immunochemically related to a constitutive male-specific cytochrome P-450 (P-450-male) and the phenobarbital-inducible P-450b/e in rat liver.	Phenobarbital	145-158	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	36-41
2963808-1	1987	P-450 human-2 is a human cytochrome P-450 that is immunochemically related to a constitutive male-specific cytochrome P-450 (P-450-male) and the phenobarbital-inducible P-450b/e in rat liver.	Phenobarbital	145-158	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	36-41
3499217-1	1987	Both 12-O-tetradecanoylphorbol-13-acetate (TPA) and phenobarbital (PB) enhanced hepatocyte DNA synthesis stimulated with epidermal growth factor (EGF) by 60 to 80% in primary culture when measured by the incorporation of [3H]thymidine.	Phenobarbital	52-65	epidermal growth factor like 1	Rattus norvegicus	146-149
3499217-1	1987	Both 12-O-tetradecanoylphorbol-13-acetate (TPA) and phenobarbital (PB) enhanced hepatocyte DNA synthesis stimulated with epidermal growth factor (EGF) by 60 to 80% in primary culture when measured by the incorporation of [3H]thymidine.	Phenobarbital	67-69	epidermal growth factor like 1	Rattus norvegicus	121-144
3499217-1	1987	Both 12-O-tetradecanoylphorbol-13-acetate (TPA) and phenobarbital (PB) enhanced hepatocyte DNA synthesis stimulated with epidermal growth factor (EGF) by 60 to 80% in primary culture when measured by the incorporation of [3H]thymidine.	Phenobarbital	67-69	epidermal growth factor like 1	Rattus norvegicus	146-149
3499217-5	1987	The binding of EGF was transiently down-regulated by TPA, then restored to control values 6 h later, whereas the binding of this factor was significantly increased at both the 12th and 24th h after PB addition.	Phenobarbital	198-200	epidermal growth factor like 1	Rattus norvegicus	15-18
2823418-12	1987	These data suggest that the inhibition of mouse hepatocyte intercellular communication by PB and DDT at the highest concentrations tested may be mediated by transient decreases in intercellular cAMP levels.	Phenobarbital	90-92	cathelicidin antimicrobial peptide	Mus musculus	194-198
3681696-2	1987	Induction of the hepatic cytochrome P-450 system with phenobarbital is known to enhance acetaminophen hepatotoxicity.	Phenobarbital	54-67	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	25-41
2823419-7	1987	In the DEN/PB and BZ/PB groups the parenchyma showed increases (even before PB treatment started) in G-6PD and in gamma-glutamyl transpeptidase (gamma-GT) and decreases in GSH.	Phenobarbital	11-13	glucose-6-phosphate dehydrogenase	Rattus norvegicus	101-106
3433801-2	1987	The imidazole antifungal agents, ketoconazole, miconazole and clotrimazole have been shown to be potent inhibitors of the phenobarbital-induced cytochromes P-450 and the 3-methylcholanthrene-induced cytochromes P-448-dependent rat hepatic microsomal mixed-function oxidases.	Phenobarbital	122-135	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	211-216
3445541-2	1987	Phenobarbital-induced cytochrome P-450 was especially sensitive to the influence of all the agents studied, while cytochrome P-450 from untreated animals was the least sensitive; the 3-methyl-cholanthrene-induced cytochrome P-448 exhibited the least sensitivity to guanidine.	Phenobarbital	0-13	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	22-38
2823419-7	1987	In the DEN/PB and BZ/PB groups the parenchyma showed increases (even before PB treatment started) in G-6PD and in gamma-glutamyl transpeptidase (gamma-GT) and decreases in GSH.	Phenobarbital	11-13	gamma-glutamyltransferase 1	Rattus norvegicus	114-143
2823419-7	1987	In the DEN/PB and BZ/PB groups the parenchyma showed increases (even before PB treatment started) in G-6PD and in gamma-glutamyl transpeptidase (gamma-GT) and decreases in GSH.	Phenobarbital	21-23	glucose-6-phosphate dehydrogenase	Rattus norvegicus	101-106
2823419-7	1987	In the DEN/PB and BZ/PB groups the parenchyma showed increases (even before PB treatment started) in G-6PD and in gamma-glutamyl transpeptidase (gamma-GT) and decreases in GSH.	Phenobarbital	21-23	gamma-glutamyltransferase 1	Rattus norvegicus	114-143
2823419-10	1987	Both initiators caused a high incidence of foci positive for G-6PD and for gamma-GT; nodules induced by DEN/PB were mainly positive for gamma-GT and showed an erratic response to the other parameters.	Phenobarbital	108-110	gamma-glutamyltransferase 1	Rattus norvegicus	136-144
3675573-1	1987	Elimination of nicotine by isolated rat livers was increased eightfold after pretreatment with phenobarbital (PB) as an inducer of cytochrome P-450 while it was only marginally influenced after pretreatment with 5,6-benzoflavone (BF) as an inducer of cytochrome P-448.	Phenobarbital	95-108	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	131-147
3675602-0	1987	Synergy of phenobarbital and 3-methylcholanthrene in "superinduction" of cytochrome P-450c mRNA but not enzyme activity.	Phenobarbital	11-24	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	73-90
3675602-1	1987	The combination of phenobarbital and 3-methylcholanthrene in the inductive process of the rat hepatic cytochrome P-450c gene was evaluated.	Phenobarbital	19-32	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	102-119
3675602-5	1987	Four daily injections of phenobarbital followed by a single dose of 3-methylcholanthrene produced 5-24 times more poly (A)+ RNA coding for P-450c than 3-methylcholanthrene treatment alone.	Phenobarbital	25-38	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	139-145
3675573-1	1987	Elimination of nicotine by isolated rat livers was increased eightfold after pretreatment with phenobarbital (PB) as an inducer of cytochrome P-450 while it was only marginally influenced after pretreatment with 5,6-benzoflavone (BF) as an inducer of cytochrome P-448.	Phenobarbital	95-108	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	251-267
3675573-1	1987	Elimination of nicotine by isolated rat livers was increased eightfold after pretreatment with phenobarbital (PB) as an inducer of cytochrome P-450 while it was only marginally influenced after pretreatment with 5,6-benzoflavone (BF) as an inducer of cytochrome P-448.	Phenobarbital	110-112	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	131-147
3675573-1	1987	Elimination of nicotine by isolated rat livers was increased eightfold after pretreatment with phenobarbital (PB) as an inducer of cytochrome P-450 while it was only marginally influenced after pretreatment with 5,6-benzoflavone (BF) as an inducer of cytochrome P-448.	Phenobarbital	110-112	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	251-267
3130250-2	1987	Conversely, a phenobarbital treatment resulted in an induction of the microsomal cytochrome P450 only.	Phenobarbital	14-27	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	81-96
3663241-2	1987	The inhibitory effectiveness of these agents was increased in microsomes isolated from rats treated chronically with ethanol as compared to microsomes from pair-fed controls or from rats treated with other cytochrome P-450 inducers such as phenobarbital or 3-methylcholanthrene.	Phenobarbital	240-253	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	206-222
3621189-6	1987	Similarly, 1 alpha (OH)D3 treatment of rats markedly inhibited the induction of ODC in the colon mucosa by deoxycholate, a tumor promoter of colon carcinogenesis, and of ODC in the liver by phenobarbital, a promoter of liver carcinogenesis.	Phenobarbital	190-203	ornithine decarboxylase 1	Rattus norvegicus	170-173
3621474-0	1987	Phenobarbital induction of cytochrome P-450 in normal and preneoplastic rat liver: comparison of enzyme and mRNA expression as detected by immunohistochemistry and in situ hybridization.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	27-43
3670281-3	1987	Phenobarbital increased aminopyrine N-demethylase, microsomal epoxide hydrolase, and cytosolic glutathione transferase activities, whereas 3-methylcholanthrene enhanced ethoxyresorufin O-deethylase, epoxide hydrolase, and glutathione transferase activities in the three cell populations.	Phenobarbital	0-13	epoxide hydrolase 1	Rattus norvegicus	51-79
3670281-3	1987	Phenobarbital increased aminopyrine N-demethylase, microsomal epoxide hydrolase, and cytosolic glutathione transferase activities, whereas 3-methylcholanthrene enhanced ethoxyresorufin O-deethylase, epoxide hydrolase, and glutathione transferase activities in the three cell populations.	Phenobarbital	0-13	glutathione S-transferase alpha 4	Rattus norvegicus	95-118
3670281-3	1987	Phenobarbital increased aminopyrine N-demethylase, microsomal epoxide hydrolase, and cytosolic glutathione transferase activities, whereas 3-methylcholanthrene enhanced ethoxyresorufin O-deethylase, epoxide hydrolase, and glutathione transferase activities in the three cell populations.	Phenobarbital	0-13	glutathione S-transferase alpha 4	Rattus norvegicus	222-245
3629598-5	1987	Phenobarbital pretreatment of mice induced hepatic cytochrome P-450 content, as well as microsomal activation of azinphos-methyl in vitro, yet antagonized the acute toxicity of this pesticide in vivo.	Phenobarbital	0-13	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	51-67
3113486-0	1987	Influence of N,N-dimethylaniline on the association of phenobarbital-induced cytochrome P-450 and NADPH-cytochrome c(P-450) reductase in a reconstituted rabbit liver microsomal enzyme system.	Phenobarbital	55-68	cytochrome P450 2B4	Oryctolagus cuniculus	88-93
3113486-0	1987	Influence of N,N-dimethylaniline on the association of phenobarbital-induced cytochrome P-450 and NADPH-cytochrome c(P-450) reductase in a reconstituted rabbit liver microsomal enzyme system.	Phenobarbital	55-68	cytochrome P450 2B4	Oryctolagus cuniculus	117-122
3113486-1	1987	N,N-Dimethylaniline when added to reaction mixtures provokes deviation from Michaelis-Menten law of the interaction kinetics of NADPH-cytochrome c(P-450) reductase (NADPH:ferrihaemoprotein oxidoreductase, EC 1.6.2.4) with highly purified phenobarbital-induced rabbit liver microsomal cytochrome P-450 (P-450LM2).	Phenobarbital	238-251	cytochrome P450 2B4	Oryctolagus cuniculus	147-152
3621474-7	1987	These findings demonstrate that phenobarbital induction of cytochrome P-450 enzymes occurs in neoplastic liver tissue as it does in normal liver and, in addition, suggest that the increase in the levels of the major phenobarbital-inducible P-450s in normal and neoplastic liver is mediated by an enhancement of the steady-state concentrations of their mRNAs.	Phenobarbital	32-45	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	59-75
3621474-7	1987	These findings demonstrate that phenobarbital induction of cytochrome P-450 enzymes occurs in neoplastic liver tissue as it does in normal liver and, in addition, suggest that the increase in the levels of the major phenobarbital-inducible P-450s in normal and neoplastic liver is mediated by an enhancement of the steady-state concentrations of their mRNAs.	Phenobarbital	216-229	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	59-75
3606656-16	1987	Our results reveal that aldrin epoxidation is a reaction indicative of male specific and of phenobarbital-inducible cytochrome P-450 isozymes in rat liver.	Phenobarbital	92-105	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	116-132
2441590-4	1987	Lower T4 and higher RBP were found among children who received diphenylhydantoin (DPH), phenobarbital, or AC combinations, but vitamin A was higher only among those who received DPH.	Phenobarbital	88-101	retinol binding protein 4	Homo sapiens	20-23
3113333-0	1987	Differential expression and function of three closely related phenobarbital-inducible cytochrome P-450 isozymes in untreated rat liver.	Phenobarbital	62-75	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	86-102
3113333-1	1987	The levels of expression of cytochromes P-450b and P-450e (both inducible by phenobarbital (PB) and differing by only 14 of 491 amino acids) in liver microsomes from untreated male rats were separately quantitated by Western blotting with a polyclonal antibody raised against P-450b that is equally effective against P-450e (anti P-450b/e).	Phenobarbital	77-90	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	40-46
3113333-1	1987	The levels of expression of cytochromes P-450b and P-450e (both inducible by phenobarbital (PB) and differing by only 14 of 491 amino acids) in liver microsomes from untreated male rats were separately quantitated by Western blotting with a polyclonal antibody raised against P-450b that is equally effective against P-450e (anti P-450b/e).	Phenobarbital	92-94	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	40-46
3113333-13	1987	Following PB induction, P-450b was induced to about double the level of P-450e in most rat strains examined.	Phenobarbital	10-12	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	24-30
3619446-0	1987	Multiple constitutive but phenobarbital-inducible rat hepatic nuclear RNA species homologous to a novel cytochrome P-450 cDNA.	Phenobarbital	26-39	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	104-120
3447587-1	1987	Two-dimensional gel electrophoresis of hepatic microsomes from phenobarbital-treated animals was used to analyze electrophoretic/regulatory polymorphisms for cytochromes P-450b, P-450e, P-450g, and P-450h in 28 inbred strains of rat.	Phenobarbital	63-76	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	170-176
3447587-1	1987	Two-dimensional gel electrophoresis of hepatic microsomes from phenobarbital-treated animals was used to analyze electrophoretic/regulatory polymorphisms for cytochromes P-450b, P-450e, P-450g, and P-450h in 28 inbred strains of rat.	Phenobarbital	63-76	cytochrome P450, family 2, subfamily c, polypeptide 13	Rattus norvegicus	186-192
3447587-1	1987	Two-dimensional gel electrophoresis of hepatic microsomes from phenobarbital-treated animals was used to analyze electrophoretic/regulatory polymorphisms for cytochromes P-450b, P-450e, P-450g, and P-450h in 28 inbred strains of rat.	Phenobarbital	63-76	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	198-204
3619446-1	1987	A cDNA clone, pPB8, representing partial information for a phenobarbital-inducible rat hepatic cytochrome P-450, immunochemically related to cytochrome P-450b and/or P-450e, hybridized to multiple hepatic nuclear RNA species.	Phenobarbital	59-72	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	95-111
3619446-1	1987	A cDNA clone, pPB8, representing partial information for a phenobarbital-inducible rat hepatic cytochrome P-450, immunochemically related to cytochrome P-450b and/or P-450e, hybridized to multiple hepatic nuclear RNA species.	Phenobarbital	59-72	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	141-158
3663765-1	1987	Using the previously obtained data on the substrate-type induction of monooxygenase by xenobiotics of phenobarbital type, the method of conversion of typical substrates for cytochrome P-450 into inducers of biosynthesis of this enzymatic system by blocking in the substrate molecule of the position subjected to oxidative conversion in the enzyme active center was tested.	Phenobarbital	102-115	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	173-189
3623351-2	1987	Phenobarbital given orally in two doses each of 110 mg/kg 21 and 4 hr before the rats were killed caused large increases in hepatic ornithine decarboxylase (ODC) activity and cytochrome P-450 content.	Phenobarbital	0-13	ornithine decarboxylase 1	Rattus norvegicus	132-155
3623351-2	1987	Phenobarbital given orally in two doses each of 110 mg/kg 21 and 4 hr before the rats were killed caused large increases in hepatic ornithine decarboxylase (ODC) activity and cytochrome P-450 content.	Phenobarbital	0-13	ornithine decarboxylase 1	Rattus norvegicus	157-160
3623351-2	1987	Phenobarbital given orally in two doses each of 110 mg/kg 21 and 4 hr before the rats were killed caused large increases in hepatic ornithine decarboxylase (ODC) activity and cytochrome P-450 content.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	175-191
3302670-1	1987	In vivo administration of the porphyrogenic agent allylisopropylacetamide (AIA) to phenobarbital-pretreated rats results in marked loss of hepatic cytochrome P-450 content.	Phenobarbital	83-96	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	147-163
3110162-7	1987	UDPGTr-3 and a related phenobarbital-inducible form of UDP-glucuronosyltransferase (designated UDPGTr-2) were both expressed in COS cells and their capacities to glucuronidate 13 commonly used substrates were analyzed.	Phenobarbital	23-36	UDP glucuronosyltransferase family 2 member B15	Rattus norvegicus	0-8
3118583-7	1987	The inhibitory effect of deprenyl on monoamine oxidase (MAO) B activity of liver was decreased and increased by pretreatment of rats with PB and SKF 525-A, respectively.	Phenobarbital	138-140	monoamine oxidase A	Rattus norvegicus	37-54
3118583-7	1987	The inhibitory effect of deprenyl on monoamine oxidase (MAO) B activity of liver was decreased and increased by pretreatment of rats with PB and SKF 525-A, respectively.	Phenobarbital	138-140	monoamine oxidase A	Rattus norvegicus	56-59
3453118-4	1987	In contrast to the constitutive isozyme, cytochrome P450IIC5, mRNA in the liver that hybridized to the 3" untranslated region of cytochrome P450IIC4 cDNA was increased about 8-fold 24 hours after a single injection of phenobarbital.	Phenobarbital	218-231	cytochrome P450 2C5	Oryctolagus cuniculus	41-60
3453118-4	1987	In contrast to the constitutive isozyme, cytochrome P450IIC5, mRNA in the liver that hybridized to the 3" untranslated region of cytochrome P450IIC4 cDNA was increased about 8-fold 24 hours after a single injection of phenobarbital.	Phenobarbital	218-231	cytochrome P450 2C4	Oryctolagus cuniculus	129-148
3110162-7	1987	UDPGTr-3 and a related phenobarbital-inducible form of UDP-glucuronosyltransferase (designated UDPGTr-2) were both expressed in COS cells and their capacities to glucuronidate 13 commonly used substrates were analyzed.	Phenobarbital	23-36	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	55-82
3110162-7	1987	UDPGTr-3 and a related phenobarbital-inducible form of UDP-glucuronosyltransferase (designated UDPGTr-2) were both expressed in COS cells and their capacities to glucuronidate 13 commonly used substrates were analyzed.	Phenobarbital	23-36	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	95-103
3298908-6	1987	The activities of liver microsomes from untreated male and female rats and rats treated with phenobarbital, 3-methylcholanthrene or polychlorinated biphenyl were expressed dependent on the activities of forms of cytochrome P-450 examined.	Phenobarbital	93-106	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	212-228
3110162-11	1987	These data show that at least two forms of UDP-glucuronosyltransferase found predominantly in the liver have evolved to glucuronidate the same endogenous steroid substrates and that the phenobarbital-inducible form also has some activity towards foreign compounds.	Phenobarbital	186-199	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	43-70
2820183-0	1987	The influence of theophylline and phenobarbital on rat brain 5"-nucleotidase.	Phenobarbital	34-47	5' nucleotidase, ecto	Rattus norvegicus	61-76
2820183-2	1987	Since the xanthine theophylline is known to inhibit the enzyme 5"-nucleotidase, and thus endogenic adenosine release, an in vitro experiment was conducted on the assumption that theophylline and phenobarbital may have an opposing effect on 5"-nucleotidase activity.	Phenobarbital	195-208	5' nucleotidase, ecto	Rattus norvegicus	63-78
2820183-2	1987	Since the xanthine theophylline is known to inhibit the enzyme 5"-nucleotidase, and thus endogenic adenosine release, an in vitro experiment was conducted on the assumption that theophylline and phenobarbital may have an opposing effect on 5"-nucleotidase activity.	Phenobarbital	195-208	5' nucleotidase, ecto	Rattus norvegicus	240-255
3663750-0	1987	[Phenobarbital-type induction of cytochrome P-450 in liver microsomes by perfluorodecalin].	Phenobarbital	1-14	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	33-49
3663750-2	1987	It was shown that perfluorodecalin injection as well as the phenobarbital one cause an increase in the cytochrome P-450 content, NADPH-cytochrome c reductase activity, the rates of benzphetamine N-demethylation and aldrin epoxidation in the microsomes.	Phenobarbital	60-73	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	103-119
3663750-3	1987	Using the Ouchterlony double immunodiffusion test with antibodies against cytochrome P-450b, an immunological identity of cytochrome P-450 isoforms during perfluorodecalin and phenobarbital inductions was shown.	Phenobarbital	176-189	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	74-91
3663750-3	1987	Using the Ouchterlony double immunodiffusion test with antibodies against cytochrome P-450b, an immunological identity of cytochrome P-450 isoforms during perfluorodecalin and phenobarbital inductions was shown.	Phenobarbital	176-189	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	74-90
3621980-0	1987	Induction of cytochrome P-450 in the rabbit eye by phenobarbital, as detected immunohistochemically.	Phenobarbital	51-64	cytochrome P-450	Oryctolagus cuniculus	13-29
3621980-3	1987	We showed immunohistochemically that cytochrome P-450 was induced in the cornea, conjunctiva and ciliary epithelium of rabbits after four days of intraperitoneal administration of phenobarbital at a dose of 80 mg per kg per day.	Phenobarbital	180-193	cytochrome P-450	Oryctolagus cuniculus	37-53
2888631-6	1987	In addition, M79175 was found to induce cytochrome P-450 which is immunochemically related to one of the major forms of phenobarbital-inducible cytochrome P-450 (P-450(PB-1], but not cytochrome P-450 which is immunochemically related to the major form of 3-methylcholanthrene-inducible cytochrome P-450 (P-450(MC-1].	Phenobarbital	120-133	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	40-56
2888631-6	1987	In addition, M79175 was found to induce cytochrome P-450 which is immunochemically related to one of the major forms of phenobarbital-inducible cytochrome P-450 (P-450(PB-1], but not cytochrome P-450 which is immunochemically related to the major form of 3-methylcholanthrene-inducible cytochrome P-450 (P-450(MC-1].	Phenobarbital	120-133	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	144-160
2888631-6	1987	In addition, M79175 was found to induce cytochrome P-450 which is immunochemically related to one of the major forms of phenobarbital-inducible cytochrome P-450 (P-450(PB-1], but not cytochrome P-450 which is immunochemically related to the major form of 3-methylcholanthrene-inducible cytochrome P-450 (P-450(MC-1].	Phenobarbital	120-133	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	144-160
2888631-6	1987	In addition, M79175 was found to induce cytochrome P-450 which is immunochemically related to one of the major forms of phenobarbital-inducible cytochrome P-450 (P-450(PB-1], but not cytochrome P-450 which is immunochemically related to the major form of 3-methylcholanthrene-inducible cytochrome P-450 (P-450(MC-1].	Phenobarbital	120-133	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	144-160
3574292-2	1987	Transplacental induction by phenobarbital of P-450b and P-450e mRNAs was not detectable in fetal rat livers prior to day 21 of gestation.	Phenobarbital	28-41	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	45-51
3671445-2	1987	From the elimination velocity of these model substances conclusions concerning the activity of 3-methylcholanthrene (caffeine elimination) and phenobarbital inducible isoenzymes (metamizol elimination) of cytochrome P-450 are drawn.	Phenobarbital	143-156	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	205-221
3113479-11	1987	An apparent correlation between P-450 aggregation state and NADPH-supported hydroxylation was also observed with phenobarbital-inducible P-450LM2 in the presence of detergents [Dean, W.L., & Gray, R.D.	Phenobarbital	113-126	cytochrome P450 2B4	Oryctolagus cuniculus	137-145
2886233-0	1987	Differential time-course of induction of rat liver gamma-glutamyltransferase and drug-metabolizing enzymes in the endoplasmic reticulum, Golgi and plasma membranes after a single phenobarbital injection.	Phenobarbital	179-192	gamma-glutamyltransferase 1	Rattus norvegicus	51-76
2886233-2	1987	This study was conducted to follow as a function of time the activity of gamma-glutamyltransferase in the various membranes of rat liver cells after a single dose of phenobarbital (PB) (75 mg kg-1 body weight).	Phenobarbital	166-179	gamma-glutamyltransferase 1	Rattus norvegicus	73-98
2886233-2	1987	This study was conducted to follow as a function of time the activity of gamma-glutamyltransferase in the various membranes of rat liver cells after a single dose of phenobarbital (PB) (75 mg kg-1 body weight).	Phenobarbital	181-183	gamma-glutamyltransferase 1	Rattus norvegicus	73-98
2886233-3	1987	Gamma-glutamyltransferase induction was maximal 24 h after PB treatment in both the rough endoplasmic reticulum and the plasma membranes.	Phenobarbital	59-61	gamma-glutamyltransferase 1	Rattus norvegicus	0-25
2886233-10	1987	Five days of continuous PB treatment induced by appearance of new gamma-glutamyltransferase isoforms in plasma membranes.	Phenobarbital	24-26	gamma-glutamyltransferase 1	Rattus norvegicus	66-91
2886233-11	1987	We demonstrate that after a single injection of PB, gamma-glutamyltransferase activity increases simultaneously with some drug-metabolizing enzymes, such as total cytochrome P-450 but not with others, such as UDP-glucuronosyltransferases.	Phenobarbital	48-50	gamma-glutamyltransferase 1	Rattus norvegicus	52-77
2886233-11	1987	We demonstrate that after a single injection of PB, gamma-glutamyltransferase activity increases simultaneously with some drug-metabolizing enzymes, such as total cytochrome P-450 but not with others, such as UDP-glucuronosyltransferases.	Phenobarbital	48-50	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	163-179
2888623-5	1987	In phenobarbital-induced hepatic microsomes, TFE inactivated up to 67% of the cytochrome P-450, whereas DFE inactivated only up to 17%.	Phenobarbital	3-16	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	78-94
3622636-2	1987	The addition of phenobarbital, 3-methylcholanthrene, or nafenopin from Day 3 to Day 6 increased the contents of cytochrome P-450 to 128, 239, and 251%, respectively, compared to untreated controls at Day 3.	Phenobarbital	16-29	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	112-128
3109323-3	1987	Upon treatment with phenobarbital (PB), at least two cytochrome P-450 isozymes are induced in the dog, and the hepatic microsomal metabolism of 245-HCB is increased on both a per nanomole P-450 basis (twofold) and a per milligram protein basis (fivefold).	Phenobarbital	20-33	Cytochrome P450 1A1	Canis lupus familiaris	53-69
3109323-3	1987	Upon treatment with phenobarbital (PB), at least two cytochrome P-450 isozymes are induced in the dog, and the hepatic microsomal metabolism of 245-HCB is increased on both a per nanomole P-450 basis (twofold) and a per milligram protein basis (fivefold).	Phenobarbital	35-37	Cytochrome P450 1A1	Canis lupus familiaris	53-69
3113708-8	1987	Polychlorinated biphenyls, phenobarbital, nifedipine, and a large number of structurally different chemicals which are porphyrinogenic in chick embryo liver cells inhibit uroporphyrinogen decarboxylase by an unknown mechanism.	Phenobarbital	27-40	uroporphyrinogen decarboxylase	Gallus gallus	171-201
3508583-0	1987	Differences in cytochrome P-450 levels between isolated hepatocytes and hepatic microsomes from phenobarbital treated rats.	Phenobarbital	96-109	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	15-31
3584119-0	1987	Suppression of levels of phenobarbital-inducible rat liver cytochrome P-450 by pituitary hormone.	Phenobarbital	25-38	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	59-75
3584119-1	1987	The effect of pituitary factor on the constitutive and inducible levels of hepatic phenobarbital (PB)-inducible major cytochrome P-450, P-450b and P-450e, in male and female rat livers was studied by immunoblot analyses.	Phenobarbital	83-96	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	118-134
3584119-1	1987	The effect of pituitary factor on the constitutive and inducible levels of hepatic phenobarbital (PB)-inducible major cytochrome P-450, P-450b and P-450e, in male and female rat livers was studied by immunoblot analyses.	Phenobarbital	98-100	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	118-134
3584119-4	1987	Treatment with PB increased more effectively the hepatic contents of P-450b and P-450e, but their contents were still 4-fold higher in the male than the female.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	69-75
3584119-5	1987	Treatment of hypophysectomized female rats with PB increased the contents of P-450b and P-450e 4-fold higher than the contents in PB-treated nonhypophysectomized female rats.	Phenobarbital	48-50	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	77-83
3579981-4	1987	The fluorographic pattern of the protein labeling was cytochrome P-450-dependent, as was demonstrated by CO and metyrapone inhibition as well as by pretreatment of rats with inducing drugs such as 3-methylcholanthrene, benzo(a)pyrene, phenobarbitone and Aroclor 1254.	Phenobarbital	235-249	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	54-70
2439424-6	1987	If administered in anticonvulsively effective concentrations, phenobarbital and benzodiazepines enhance the GABAerg inhibition by direct attachment to the GABA receptor chloride ionophore complex of the postsynaptic neuronal membrane.	Phenobarbital	62-75	GABA type A receptor-associated protein	Homo sapiens	155-168
2820951-0	1987	Cytochrome P-450 related to P-4504 from phenobarbital-treated rabbit liver: molecular cloning of cDNA and characterization of cytochrome P-450 obtained by its expression in yeast cells.	Phenobarbital	40-53	cytochrome P-450	Oryctolagus cuniculus	0-16
2820951-0	1987	Cytochrome P-450 related to P-4504 from phenobarbital-treated rabbit liver: molecular cloning of cDNA and characterization of cytochrome P-450 obtained by its expression in yeast cells.	Phenobarbital	40-53	cytochrome P-450	Oryctolagus cuniculus	126-142
2820951-1	1987	cDNA complementary to mRNA coding for a minor form of cytochrome P-450 from phenobarbital-treated rabbit liver (pHP3) was isolated using cDNA for the major phenobarbital-inducible cytochrome P-450 of rat liver as a probe in the first screening of a cDNA library.	Phenobarbital	76-89	cytochrome P-450	Oryctolagus cuniculus	54-70
2820951-1	1987	cDNA complementary to mRNA coding for a minor form of cytochrome P-450 from phenobarbital-treated rabbit liver (pHP3) was isolated using cDNA for the major phenobarbital-inducible cytochrome P-450 of rat liver as a probe in the first screening of a cDNA library.	Phenobarbital	76-89	cytochrome P450 2C14	Oryctolagus cuniculus	112-116
2820951-1	1987	cDNA complementary to mRNA coding for a minor form of cytochrome P-450 from phenobarbital-treated rabbit liver (pHP3) was isolated using cDNA for the major phenobarbital-inducible cytochrome P-450 of rat liver as a probe in the first screening of a cDNA library.	Phenobarbital	76-89	cytochrome P-450	Oryctolagus cuniculus	180-196
2820951-1	1987	cDNA complementary to mRNA coding for a minor form of cytochrome P-450 from phenobarbital-treated rabbit liver (pHP3) was isolated using cDNA for the major phenobarbital-inducible cytochrome P-450 of rat liver as a probe in the first screening of a cDNA library.	Phenobarbital	156-169	cytochrome P-450	Oryctolagus cuniculus	54-70
2820951-1	1987	cDNA complementary to mRNA coding for a minor form of cytochrome P-450 from phenobarbital-treated rabbit liver (pHP3) was isolated using cDNA for the major phenobarbital-inducible cytochrome P-450 of rat liver as a probe in the first screening of a cDNA library.	Phenobarbital	156-169	cytochrome P450 2C14	Oryctolagus cuniculus	112-116
2820951-1	1987	cDNA complementary to mRNA coding for a minor form of cytochrome P-450 from phenobarbital-treated rabbit liver (pHP3) was isolated using cDNA for the major phenobarbital-inducible cytochrome P-450 of rat liver as a probe in the first screening of a cDNA library.	Phenobarbital	156-169	cytochrome P-450	Oryctolagus cuniculus	180-196
2820951-3	1987	The deduced amino acid sequence of pHP3 protein exhibited about 50% homology with the major cytochrome P-450 from phenobarbital-treated rabbit liver, while the homology was as high as 80% between two minor cytochrome forms, pHP2 and pHP3.	Phenobarbital	114-127	cytochrome P450 2C14	Oryctolagus cuniculus	35-39
2820951-3	1987	The deduced amino acid sequence of pHP3 protein exhibited about 50% homology with the major cytochrome P-450 from phenobarbital-treated rabbit liver, while the homology was as high as 80% between two minor cytochrome forms, pHP2 and pHP3.	Phenobarbital	114-127	cytochrome P-450	Oryctolagus cuniculus	92-108
3106362-1	1987	We have investigated the degradation in rat liver of two typical endoplasmic reticulum (ER) membrane proteins, phenobarbital (PB)-inducible cytochrome P-450 (P-450[PB]) and NADPH-cytochrome P-450 reductase (FP2).	Phenobarbital	111-124	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	140-156
3106362-1	1987	We have investigated the degradation in rat liver of two typical endoplasmic reticulum (ER) membrane proteins, phenobarbital (PB)-inducible cytochrome P-450 (P-450[PB]) and NADPH-cytochrome P-450 reductase (FP2).	Phenobarbital	126-128	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	140-156
2435723-3	1987	Heme-dependent activators of guanylate cyclase elicited a greater -fold increase in hepatic cyclic GMP levels in slices from phenobarbital-pretreated than control mice.	Phenobarbital	125-138	5'-nucleotidase, cytosolic II	Mus musculus	99-102
3109500-1	1987	Studies with monospecific antibodies to individual forms of monooxygenases P-450b (phenobarbital-induced) and P-450c (3-methylcholanthrene-induced) by immunochemical, kinetic and spectral methods revealed differences in the dynamics of xenobiotic-induced changes in the content and monooxygenase activity of the total microsomal CO-binding hemoprotein and of its molecular forms.	Phenobarbital	83-96	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	75-81
3109500-3	1987	Since consecutive injection of phenobarbital and 3-methylcholanthrene (or vice versa) is accompanied by selective induction of the corresponding isoforms and the redistribution of the relative content of P-450b and P-450c in the total pool of cytochrome P-450 in rat liver microsomes, a conclusion was drawn that these molecular forms are induced by different populations of hepatocytes.	Phenobarbital	31-44	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	204-210
3109500-3	1987	Since consecutive injection of phenobarbital and 3-methylcholanthrene (or vice versa) is accompanied by selective induction of the corresponding isoforms and the redistribution of the relative content of P-450b and P-450c in the total pool of cytochrome P-450 in rat liver microsomes, a conclusion was drawn that these molecular forms are induced by different populations of hepatocytes.	Phenobarbital	31-44	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	215-221
3109500-3	1987	Since consecutive injection of phenobarbital and 3-methylcholanthrene (or vice versa) is accompanied by selective induction of the corresponding isoforms and the redistribution of the relative content of P-450b and P-450c in the total pool of cytochrome P-450 in rat liver microsomes, a conclusion was drawn that these molecular forms are induced by different populations of hepatocytes.	Phenobarbital	31-44	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	243-259
3569474-4	1987	Hepatic microsomal cytochrome P-450 content was significantly decreased in infected rats compared to untreated phenobarbital treated groups.	Phenobarbital	111-124	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	19-35
3545456-2	1987	Western blots of total lung microsomes demonstrated that about 40 pmol P-450b/mg protein (and no detectable P-450e) were present in lungs from control or MC treated rats and that pretreatment with PB caused a small but significant (P less than 0.05) increase in the expression of P-450b.	Phenobarbital	197-199	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	71-77
3545456-2	1987	Western blots of total lung microsomes demonstrated that about 40 pmol P-450b/mg protein (and no detectable P-450e) were present in lungs from control or MC treated rats and that pretreatment with PB caused a small but significant (P less than 0.05) increase in the expression of P-450b.	Phenobarbital	197-199	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	280-286
3545456-3	1987	Microsomes from control and PB treated lung contained minimal levels of P-450c, and MC induced this isozyme to 185 pmol/mg.	Phenobarbital	28-30	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	72-78
3545456-6	1987	Type II alveolar cells showed distinct immunoreactivity to P-450b and weak immunoreactivity to P-450c in control or PB treated rats.	Phenobarbital	116-118	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	95-101
3582092-10	1987	The db1 and db2 proteins are differentially regulated: during development db2 is present at birth while db1 is absent, and db1 increases by 1 week of age; in addition, db1 is slightly induced by phenobarbital, 3-methyl-cholanthrene, and dexamethasone whereas db2 is marginally increased by these latter two agents.	Phenobarbital	195-208	RT1 class II, locus Db1	Rattus norvegicus	4-7
3582092-10	1987	The db1 and db2 proteins are differentially regulated: during development db2 is present at birth while db1 is absent, and db1 increases by 1 week of age; in addition, db1 is slightly induced by phenobarbital, 3-methyl-cholanthrene, and dexamethasone whereas db2 is marginally increased by these latter two agents.	Phenobarbital	195-208	RT1 class II, locus Db2	Rattus norvegicus	12-15
3582092-10	1987	The db1 and db2 proteins are differentially regulated: during development db2 is present at birth while db1 is absent, and db1 increases by 1 week of age; in addition, db1 is slightly induced by phenobarbital, 3-methyl-cholanthrene, and dexamethasone whereas db2 is marginally increased by these latter two agents.	Phenobarbital	195-208	RT1 class II, locus Db2	Rattus norvegicus	74-77
3582092-10	1987	The db1 and db2 proteins are differentially regulated: during development db2 is present at birth while db1 is absent, and db1 increases by 1 week of age; in addition, db1 is slightly induced by phenobarbital, 3-methyl-cholanthrene, and dexamethasone whereas db2 is marginally increased by these latter two agents.	Phenobarbital	195-208	RT1 class II, locus Db2	Rattus norvegicus	74-77
2885770-1	1987	The activity of gamma-glutamyltransferase localized in isolated brain synaptic membranes- and microvessels-enriched fractions was assayed after treatment of rats with either phenobarbital or ethanol.	Phenobarbital	174-187	gamma-glutamyltransferase 1	Rattus norvegicus	16-41
2885770-2	1987	Phenobarbital increased the activity of gamma-glutamyltransferase in microvessels, without alteration of synaptic membranes activity.	Phenobarbital	0-13	gamma-glutamyltransferase 1	Rattus norvegicus	40-65
3031564-0	1987	Brain neurotransmitter receptor alterations in offspring of rats exposed to phenobarbital, phenytoin or their combination during pregnancy.	Phenobarbital	76-89	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	6-31
3564013-3	1987	Phenobarbital not only significantly induced hepatic microsomal cytochrome P-450 (p less than 0.05) but also increased microsomal carboxylesterase activity (p less than 0.05).	Phenobarbital	0-13	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	64-80
3106923-0	1987	The effect of hydrocortisone, thyroxine, and phenobarbital on diamine oxidase activity in newborn rat intestine.	Phenobarbital	45-58	amine oxidase, copper containing 1	Rattus norvegicus	62-77
3108693-2	1987	Activated microsomes from the brain of the rat conjugated 1-naphthol with an apparent Km of 95 microM and a Vmax of 5.47 nmol/hr mg protein at 30 degrees C. Microsomal uridine diphosphate (UDP)-glucuronosyltransferase activity in brain towards 1-naphthol was not significantly induced by pretreatment of animals with 3-methylcholanthrene or phenobarbital.	Phenobarbital	341-354	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	168-217
3105540-1	1987	This study demonstrates that the exposure of phenobarbitone-treated rats to halothane at an oxygen concentration of either 10% or 14% results in marked decreases in cytochrome P-450 content and aminopyrine demethylase activity in animals sacrificed from 1 to 48 hr post-exposure.	Phenobarbital	45-59	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	165-181
2881548-12	1987	The observed effects of induction on the apparent equilibrium constants and maximum extents of binding and metabolism of prizidilol indicate that the forms of cytochrome P-450 induced by phenobarbital, pregnenolone-16 alpha-carbonitrile or beta-naphthoflavone do not play a major role in the metabolism of prizidilol.	Phenobarbital	187-200	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	159-175
3034390-5	1987	Phenobarbital (0.04-0.12 mM) produced only depression of synaptic responses in CA 1 and dentate pathways.	Phenobarbital	0-13	carbonic anhydrase 1	Homo sapiens	79-83
3592860-7	1987	The discrepancies between these results observed in vivo and those obtained by others in the isolated perfused rat liver suggest: a) that a metabolite formed (under normal conditions) via the phenobarbital- or butanediol-inducible forms of cytochrome P-450 is not a likely part of the hepatotoxic sequence of events; b) that the isolated perfused rat liver model in this case is not representative of the in vivo situation.	Phenobarbital	192-205	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	240-256
3495296-1	1987	The effects of exogenous phospholipase A2, oleic acid and lysolecithines on oxidative NADPH-dependent O-dealkylation of 7-ethoxycumarin in liver microsomes of phenobarbital- and 3-methylcholanthrene-induced and non-induced rats were studied.	Phenobarbital	159-172	phospholipase A2 group IB	Rattus norvegicus	25-41
3495296-6	1987	In 3-methylcholanthrene-induced microsomes the sensitivity of O-deethylation of 7-ethoxycumarin to the inhibiting effect of phospholipase A2 or lysolecithine is lower than that in non-induced or phenobarbital-induced microsomes.	Phenobarbital	195-208	phospholipase A2 group IB	Rattus norvegicus	124-140
3028267-0	1987	Phenobarbital-induced alterations in the activities of the transport and hydrolytic components of the glucose-6-phosphatase system in smooth and rough subfractions of the rat hepatic endoplasmic reticulum.	Phenobarbital	0-13	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	102-123
2882982-0	1987	In vivo and in vitro biotransformation of theobromine by phenobarbital- and 3-methylcholanthrene-inducible cytochrome P-450 monooxygenases in rat liver.	Phenobarbital	57-70	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	107-123
2882982-2	1987	A new in vitro method was developed and applied to establish the role of the hepatic cytochrome P-450 monooxygenases in theobromine biotransformation by control and phenobarbital (PB)- and 3-methylcholanthrene (3MC)-induced Sprague-Dawley rats.	Phenobarbital	165-178	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	85-101
2882982-2	1987	A new in vitro method was developed and applied to establish the role of the hepatic cytochrome P-450 monooxygenases in theobromine biotransformation by control and phenobarbital (PB)- and 3-methylcholanthrene (3MC)-induced Sprague-Dawley rats.	Phenobarbital	180-182	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	85-101
3805049-15	1987	Consequently, P-450(M-1) could be structurally classified into the phenobarbital-inducible type of P-450 gene family.	Phenobarbital	67-80	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	14-23
3299136-1	1987	The presence of cytochrome P-450 in rat brain was studied by immunohistochemistry, using antibodies to cytochrome P-450 purified from livers of phenobarbital- or 3-methylcholanthrene-treated rats.	Phenobarbital	144-157	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	16-32
3299136-3	1987	This immunoreactivity was abolished by preabsorption of the antibody with highly purified rat liver cytochrome P-450c, the major cytochrome P-450 isozyme induced by 3-methylcholanthrene, but was not affected by other cytochrome P-450 isozymes induced by phenobarbital, isosafrole or pregnenolone-16 alpha-carbonitrile.	Phenobarbital	254-267	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	100-117
3299136-3	1987	This immunoreactivity was abolished by preabsorption of the antibody with highly purified rat liver cytochrome P-450c, the major cytochrome P-450 isozyme induced by 3-methylcholanthrene, but was not affected by other cytochrome P-450 isozymes induced by phenobarbital, isosafrole or pregnenolone-16 alpha-carbonitrile.	Phenobarbital	254-267	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	100-116
3299136-3	1987	This immunoreactivity was abolished by preabsorption of the antibody with highly purified rat liver cytochrome P-450c, the major cytochrome P-450 isozyme induced by 3-methylcholanthrene, but was not affected by other cytochrome P-450 isozymes induced by phenobarbital, isosafrole or pregnenolone-16 alpha-carbonitrile.	Phenobarbital	254-267	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	129-145
3030329-3	1987	The formation of DHVP-16 was cytochrome P-450-mediated as indicated by its dependence on NADPH, its increased production following treatment of mice with phenobarbital, and its marked inhibition by SKF-525A and piperonyl butoxide.	Phenobarbital	154-167	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	29-45
3028267-1	1987	We have examined the influence of the phenobarbital-induced proliferation of the hepatic endoplasmic reticulum (ER) on the activities of the components of the glucose-6-phosphatase system, i.e., the enzyme, the glucose-6-P translocase (T1), and the phosphate translocase (T2).	Phenobarbital	38-51	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	159-180
2433292-0	1987	Determination of the membrane topology of the phenobarbital-inducible rat liver cytochrome P-450 isoenzyme PB-4 using site-specific antibodies.	Phenobarbital	46-59	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	80-96
3814176-2	1987	In microsomes, CS2 metabolism was increased by phenobarbital pretreatment of the rats and decreased with pretreatment of the rats with cobaltous chloride.	Phenobarbital	47-60	calsyntenin 2	Rattus norvegicus	15-18
2433292-1	1987	Fifteen peptides, ranging in length from 6 to 31 amino acids and corresponding in sequence to portions of the major phenobarbital-inducible form of rat liver cytochrome P-450 (P-450 PB-4), were previously synthesized chemically and used to prepare site-specific rabbit antibodies (Frey, A.	Phenobarbital	116-129	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	158-174
3806412-1	1987	Pretreatment of mice with multiple doses of phenobarbital (PB) potentiates N-acetyl-para-aminophenol (APAP) hepatotoxicity through induction of cytochrome P-450, thus increasing the formation of APAP-reactive metabolites.	Phenobarbital	44-57	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	144-160
3027320-6	1987	Treatment with PB induced NADPH-cytochrome c reductase, glutathione transferase, cytochrome P-450 and UDP-glucuronosyltransferase but the degree of induction was found to be at least as strong in pp cells as in pv cells.	Phenobarbital	15-17	glutathione S-transferase alpha 4	Rattus norvegicus	56-79
3027320-6	1987	Treatment with PB induced NADPH-cytochrome c reductase, glutathione transferase, cytochrome P-450 and UDP-glucuronosyltransferase but the degree of induction was found to be at least as strong in pp cells as in pv cells.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	81-97
3027320-6	1987	Treatment with PB induced NADPH-cytochrome c reductase, glutathione transferase, cytochrome P-450 and UDP-glucuronosyltransferase but the degree of induction was found to be at least as strong in pp cells as in pv cells.	Phenobarbital	15-17	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	102-129
3806412-1	1987	Pretreatment of mice with multiple doses of phenobarbital (PB) potentiates N-acetyl-para-aminophenol (APAP) hepatotoxicity through induction of cytochrome P-450, thus increasing the formation of APAP-reactive metabolites.	Phenobarbital	59-61	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	144-160
3602065-3	1987	The characterisation of three phenobarbital modifications by thermic examination procedures (DSC, DTA) is being described.	Phenobarbital	30-43	desmocollin 3	Homo sapiens	93-96
3105185-0	1987	Difference in the effects of phenobarbital and 3-methylcholanthrene treatment on subunit composition of hepatic glutathione S-transferase in male and female rats.	Phenobarbital	29-42	hematopoietic prostaglandin D synthase	Rattus norvegicus	112-137
3426683-5	1987	Induction of the cytochrome P-450 enzymes by phenobarbital (PB) pretreatment doubled the yield of cyanide, while SKF-525A blocked this PB-induced increase.	Phenobarbital	45-58	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	17-33
3426683-5	1987	Induction of the cytochrome P-450 enzymes by phenobarbital (PB) pretreatment doubled the yield of cyanide, while SKF-525A blocked this PB-induced increase.	Phenobarbital	60-62	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	17-33
3426683-5	1987	Induction of the cytochrome P-450 enzymes by phenobarbital (PB) pretreatment doubled the yield of cyanide, while SKF-525A blocked this PB-induced increase.	Phenobarbital	135-137	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	17-33
3426683-7	1987	These results suggest that while catalase is responsible in major part for the oxidation of cyanamide to cyanide by uninduced microsomes, the participation of the hepatic cytochrome P-450 enzymes cannot be ruled out in PB-induced microsomes.	Phenobarbital	219-221	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	171-187
3126696-10	1987	Some chemicals, such as phenobarbital and nifedipine, cause the accumulation of these porphyrins in chick embryo liver cell culture, and this is explained by inhibition of UROD.	Phenobarbital	24-37	uroporphyrinogen decarboxylase	Gallus gallus	172-176
3566772-9	1987	Inducibility of AHH by 3-methylcholanthrene (MCA) or phenobarbital (PB) was largely reduced due to AA feeding.	Phenobarbital	53-66	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	16-19
3566772-9	1987	Inducibility of AHH by 3-methylcholanthrene (MCA) or phenobarbital (PB) was largely reduced due to AA feeding.	Phenobarbital	68-70	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	16-19
2833324-2	1987	The results showed that PB treatment increased the amount of liver total cytochrome P450 (cytP450), a drug metabolizing monooxygenase enzyme in genetically obese, hyperglycemic (ob/ob) mice 6-fold and the total activities of other monooxygenase enzymes NADPH cytP450 reductase and 7-ethoxyresorufin O-deethylase (ERDE) 2- and 6.5-fold, respectively.	Phenobarbital	24-26	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	73-88
2833324-2	1987	The results showed that PB treatment increased the amount of liver total cytochrome P450 (cytP450), a drug metabolizing monooxygenase enzyme in genetically obese, hyperglycemic (ob/ob) mice 6-fold and the total activities of other monooxygenase enzymes NADPH cytP450 reductase and 7-ethoxyresorufin O-deethylase (ERDE) 2- and 6.5-fold, respectively.	Phenobarbital	24-26	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	90-97
2833324-2	1987	The results showed that PB treatment increased the amount of liver total cytochrome P450 (cytP450), a drug metabolizing monooxygenase enzyme in genetically obese, hyperglycemic (ob/ob) mice 6-fold and the total activities of other monooxygenase enzymes NADPH cytP450 reductase and 7-ethoxyresorufin O-deethylase (ERDE) 2- and 6.5-fold, respectively.	Phenobarbital	24-26	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	259-266
2833324-4	1987	The data further showed that PB treatment decreased the high hepatic G6Pase activity in obese mice.	Phenobarbital	29-31	glucose-6-phosphatase, catalytic	Mus musculus	69-75
3802391-0	1987	Inhibition by indomethacin and 5,8,11,14-eicosatetraynoic acid of the induction of rat hepatic ornithine decarboxylase by the tumor promoters phenobarbital and 12-O-tetradecanoylphorbol-13-acetate in vivo.	Phenobarbital	142-155	ornithine decarboxylase 1	Rattus norvegicus	95-118
3802391-1	1987	The involvement of arachidonate metabolism in the induction of rat hepatic ornithine decarboxylase (ODC) activity by the tumor promoters 12-O-tetradecanoylphorbol-13-acetate (TPA) and phenobarbital (PB) was investigated.	Phenobarbital	184-197	ornithine decarboxylase 1	Rattus norvegicus	75-98
3802391-1	1987	The involvement of arachidonate metabolism in the induction of rat hepatic ornithine decarboxylase (ODC) activity by the tumor promoters 12-O-tetradecanoylphorbol-13-acetate (TPA) and phenobarbital (PB) was investigated.	Phenobarbital	184-197	ornithine decarboxylase 1	Rattus norvegicus	100-103
3802391-1	1987	The involvement of arachidonate metabolism in the induction of rat hepatic ornithine decarboxylase (ODC) activity by the tumor promoters 12-O-tetradecanoylphorbol-13-acetate (TPA) and phenobarbital (PB) was investigated.	Phenobarbital	199-201	ornithine decarboxylase 1	Rattus norvegicus	100-103
3690723-1	1987	Distinct and different molecular structural features are manifested by substrates, inhibitors and inducers of the two families of liver microsomal enzymes, the phenobarbital-induced cytochromes P-450 and the 3-methylcholanthrene-induced cytochromes P-448.	Phenobarbital	160-173	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	194-199
3690723-4	1987	The implications are that the binding sites of cytochromes P-448 contain a number of hydrophobic aromatic amino acid residues orientated so as to allow occupation by similar substrates containing co-planar aromatic rings, whereas those of the phenobarbital-induced cytochromes P-450 contain hydrophilic amino acid residues capable of hydrogen bonding to greater than C = O moieties and at least one leucine or valine residue, as these contain the complementary isopropyl function.	Phenobarbital	243-256	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	277-282
3106031-2	1987	After chronic ethanol consumption, microsomal ethanol-oxidizing system (MEOS) activity increases with an associated rise in microsomal cytochrome P-450, including a form different from that induced by phenobarbital and methylcholanthrene and which has a high affinity for ethanol, as shown in reconstituted systems.	Phenobarbital	201-214	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	135-151
3679343-5	1987	P450ac was also active in the metabolism of N-nitrosoethylmethylamine (NEMA), but was less active than phenobarbital-inducible cytochrome P450 (P450b) in the metabolism of N-nitrosobutylmethylamine (NBMA), especially in catalysing the debutylation reaction.	Phenobarbital	103-116	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	144-149
2831173-1	1987	The effect of acute phenobarbitone treatment on the distribution of endogenous bound folates in three specific cytosolic folate-binding proteins (FBP-C), has been studied in rat liver.	Phenobarbital	20-34	far upstream element binding protein 1	Rattus norvegicus	146-149
2831173-3	1987	As it is well known that FBP"s preferentially bind longer-chain polyglutamates, the content of which is markedly lower in phenobarbitone-treated rat liver, it might be suggested that shorter chain folates also bind to FBP"s in these animals.	Phenobarbital	122-136	far upstream element binding protein 1	Rattus norvegicus	25-28
2831173-3	1987	As it is well known that FBP"s preferentially bind longer-chain polyglutamates, the content of which is markedly lower in phenobarbitone-treated rat liver, it might be suggested that shorter chain folates also bind to FBP"s in these animals.	Phenobarbital	122-136	far upstream element binding protein 1	Rattus norvegicus	218-221
3104258-3	1987	High-spin forms of cytochrome P-450 purified from 3-methylcholanthrene-pretreated rats (MC-P-448-H) or hamsters (P-488 ham-II) showed higher catalytic activity for N-hydroxylation of phenetidine than three other low-spin forms of cytochrome P-450 purified from the same animals or from phenobarbital-pretreated rats.	Phenobarbital	286-299	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	19-35
2435023-0	1987	Comparative changes in hepatic DNA, RNA, protein, lipid, and glycogen induced by a subtoxic dose of CCl4 in chlordecone, mirex, and phenobarbital pretreated rats.	Phenobarbital	132-145	C-C motif chemokine ligand 4	Rattus norvegicus	100-104
2833324-0	1987	Hepatic drug metabolism and the activities of NADPH generating enzymes and glucose-6-phosphatase in phenobarbital treated genetically obese (ob/ob) mice.	Phenobarbital	100-113	glucose-6-phosphatase, catalytic	Mus musculus	75-96
2966657-6	1987	By contrast tocopherol strongly potentiated the inductive effect of phenobarbital toward UDPGT activity (group I substrates) in rats fed the peroxidized fish oil.	Phenobarbital	68-81	UDP glucuronosyltransferase family 2 member B15	Rattus norvegicus	89-94
2966657-7	1987	The modification of the inductive effect of phenobarbital in combination with tocopherol on UDPGT activities was concomitant with an increase in seric transaminase activity and with a reverse effect as revealed from the study of the rate of fluorescent probes penetration in microsomes.	Phenobarbital	44-57	UDP glucuronosyltransferase family 2 member B15	Rattus norvegicus	92-97
3492311-4	1987	The latter two substrates have been shown to be preferentially metabolized by the major phenobarbital-inducible form of cytochrome(s) P-450 (P-450b), and were employed since they offered a means of differentiating more clearly varying levels of P-450 induction.	Phenobarbital	88-101	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	141-147
3802399-3	1987	As compared with basal diet, a diet containing 0.05% of PB and 0.1% of OZ enhanced, in both models, the development of gamma-glutamyltransferase-positive lesions in early stages.	Phenobarbital	56-58	gamma-glutamyltransferase 1	Rattus norvegicus	119-144
2890493-6	1987	GST substrate activities in response to phenobarbital, butylated hydroxy-anisole or 5,5"-diphenylhydantoin treatment were increased more often in mouse and rat as compared to the hamster.	Phenobarbital	40-53	hematopoietic prostaglandin D synthase	Rattus norvegicus	0-3
3114017-1	1987	Cytochrome P-450 reductase and cytochrome P-450 fractions have been separated and partially purified from colonic mucosal microsomes of rat pretreated with phenobarbital or beta-naphthoflavone.	Phenobarbital	156-169	cytochrome p450 oxidoreductase	Rattus norvegicus	0-26
3031081-2	1987	Phosphatase treatment of microsomes isolated from phenobarbital-pretreated rabbits and rats caused a marked decrease of monooxygenase activity which was paralleled by a comparable decrease of NADPH-cytochrome P-450 reductase activity while the second essential component of the system, cytochrome P-450, remained unaltered.	Phenobarbital	50-63	cytochrome p450 oxidoreductase	Rattus norvegicus	192-224
3031081-2	1987	Phosphatase treatment of microsomes isolated from phenobarbital-pretreated rabbits and rats caused a marked decrease of monooxygenase activity which was paralleled by a comparable decrease of NADPH-cytochrome P-450 reductase activity while the second essential component of the system, cytochrome P-450, remained unaltered.	Phenobarbital	50-63	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	198-214
2956667-6	1987	PB increased G6PD activity and GGT-positive liver.	Phenobarbital	0-2	glucose-6-phosphate dehydrogenase	Rattus norvegicus	13-17
3798451-7	1987	Pretreatment with phenobarbital also tended to increase hepatic injury as judged by changes in serum GPT.	Phenobarbital	18-31	glutamic pyruvic transaminase, soluble	Mus musculus	101-104
3628472-0	1987	Mechanisms of phenobarbital-type induction of cytochrome P-450 isozymes.	Phenobarbital	14-27	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	46-62
3810888-4	1987	A model is suggested which shows the phenobarbital participation in the formation of the specific configuration of the active site of cytochrome P-450 synthesized; the latter catalyzes the oxidation of a number of substrates by the way typical of inducer itself.	Phenobarbital	37-50	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	134-150
3576079-2	1987	Further experiments with these cells on the expression of different forms of cytochrome P-450, inducible not only by phenobarbital (PB) and 3-methylcholanthrene (MC), but also by metyrapone (MP), ethanol (E), and beta-naphthoflavone (BNF) are reported here.	Phenobarbital	117-130	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	77-93
3576079-2	1987	Further experiments with these cells on the expression of different forms of cytochrome P-450, inducible not only by phenobarbital (PB) and 3-methylcholanthrene (MC), but also by metyrapone (MP), ethanol (E), and beta-naphthoflavone (BNF) are reported here.	Phenobarbital	132-134	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	77-93
3539120-3	1986	The use of antibody titration enabled the effects of phenobarbitone, beta-naphthoflavone and clofibrate on the content and distribution of immunoreactive cytochrome P-450 to be studied in both the liver and in the other organs discussed.	Phenobarbital	53-67	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	154-170
3577066-1	1987	Content of cytochrome P-450 was decreased in rat liver microsomes, pretreated with phenobarbital, after incubation with acrylamide, methyl methacrylate and butyl methacrylate in presence of NADPH in vitro.	Phenobarbital	83-96	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	11-27
3825173-1	1987	From the hepatic cytochrome P-450 isozymes b and c isolated from rats treated with phenobarbital and 3-methylcholanthrene respectively, only cytochrome P-450c was found to be active in the oxidation of paracetamol, in the presence of glutathione ultimately leading to the formation of the 3-glutathionyl conjugate.	Phenobarbital	83-96	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	141-158
2431694-1	1986	Phenobarbital and tetrachlorodibenzo-p-dioxin (TCDD) induce two different forms of aldehyde dehydrogenase (EC 1.2.1.3, ALDH), designated phi and tau respectively, in the rat liver cytosol.	Phenobarbital	0-13	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	119-123
2431694-4	1986	A 10-fold increase in phi-ALDH produced by phenobarbital treatment resulted in small increases in the formation of 3,4-dihydroxyphenylacetic acid and 3,4-dihydroxymandelic acid from the biogenic amines.	Phenobarbital	43-56	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	26-30
3790162-2	1986	Cytochrome b5 was purified to electrophoretic homogeneity from the liver microsomes of untreated rats and reincorporated into liver microsomes from phenobarbital-treated rats, resulting in an approximate three-fold enrichment of the cytochrome b5 specific content (1.5 nmol haemoprotein X mg-1 protein).	Phenobarbital	148-161	cytochrome b5 type A	Rattus norvegicus	0-13
3539120-4	1986	Phenobarbitone induces epitope-specific cytochrome P-450 in the centrilobular cells of the liver but has no effect in any of the other tissues studied.	Phenobarbital	0-14	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	40-56
3801454-1	1986	Rat hepatic cytochrome P-450 PB-1 is a prominent constitutive P-450 form whose levels increase approximately 2-3 fold upon phenobarbital administration.	Phenobarbital	123-136	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	12-33
3099430-7	1986	Further, these findings suggest a discrepancy between 4,4"-DCB and PB in cytochrome P-450 inducing activity, as 4,4"-DCB mimics 3-MC in the induction of phenacetin O-deethylase.	Phenobarbital	67-69	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	73-89
3099430-8	1986	The difference between 4,4"-DCB and PB is discussed in relation to the multiplicity and induction of cytochrome P-450 isoenzymes.	Phenobarbital	36-38	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	101-117
3780743-7	1986	The rabbit enzyme metabolized the hydrocarbon with an apparent Vmax of 4 nmol nmol-1 min-1 and a Km of 8 microM, By contrast, phenobarbital-inducible P-450 LM2 or 3-methylcholanthrene-inducible P-450 LM4 from rabbit liver were quite ineffective catalysts of n-pentane metabolism.	Phenobarbital	126-139	cytochrome P450 2B4	Oryctolagus cuniculus	150-203
3096339-2	1986	UDPGT activities tested could be divided in four groups on the basis of their tissue distribution and induction by PB or 3MC in liver microsomes.	Phenobarbital	115-117	UDP glucuronosyltransferase family 2 member B15	Rattus norvegicus	0-5
3022748-2	1986	The effect of various ratios of cytochrome P-450 (phenobarbital-inducible isozyme)/reductase on the oxidation of ethanol and KMBA was determined: There was essentially no increase in KMBA oxidation over the range of ratios from 0.5 to 5 as compared to the reductase-catalyzed rate.	Phenobarbital	50-63	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	32-48
3096339-5	1986	UDPGT activity towards bilirubin, although induced by PB, can be detected in hepatic, intestinal and renal microsomes.	Phenobarbital	54-56	UDP glucuronosyltransferase family 2 member B15	Rattus norvegicus	0-5
3811968-0	1986	Phenobarbital enhances the aldehyde dehydrogenase activity of rat hepatocytes in vitro and in vivo.	Phenobarbital	0-13	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	27-49
3782137-7	1986	Amino acid alignment also revealed that P450j was 48% similar to P450b and P450e, the major phenobarbital-inducible forms, and 54% similar to P450PB1 and P450f, two developmentally regulated forms.	Phenobarbital	92-105	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	40-45
3782137-7	1986	Amino acid alignment also revealed that P450j was 48% similar to P450b and P450e, the major phenobarbital-inducible forms, and 54% similar to P450PB1 and P450f, two developmentally regulated forms.	Phenobarbital	92-105	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	65-80
3811968-6	1986	Treatment of Long-Evans animals with PB (1 mg/ml, in drinking water for 2 weeks) leads to similar relative increases of the ALDH activity.	Phenobarbital	37-39	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	124-128
3811968-8	1986	These results show that ALDH activity can be greatly enhanced by PB in primary hepatocyte cultures, free from any indirect endogenous influences.	Phenobarbital	65-67	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	24-28
3801548-0	1986	[Identification and characteristics of mRNA for cytochrome P-450 in the rat liver induced by phenobarbital and 3-methylcholanthrene].	Phenobarbital	93-106	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	48-64
3828107-1	1986	The effect of phenobarbital upon the differentiation of two preadipocyte cell lines, 3T3 F442A and 3T3 L-1, was examined by measuring the synthesis and secretion of lipoprotein lipase.	Phenobarbital	14-27	lipoprotein lipase	Mus musculus	165-183
3828107-4	1986	Addition of phenobarbital with insulin enhanced total lipoprotein lipase, protein, and triglyceride content.	Phenobarbital	12-25	lipoprotein lipase	Mus musculus	54-72
3828107-5	1986	The activity of lipoprotein lipase accumulated in the heparin-releasable fraction during differentiation was increased 2- to 3-fold and the intracellular enzyme was enhanced 15- to 20-fold by the addition of phenobarbital.	Phenobarbital	208-221	lipoprotein lipase	Mus musculus	16-34
3828107-8	1986	Phenobarbital also stimulated lipoprotein lipase in differentiating 3T3 L-1 cells in the presence of insulin, although lipoprotein lipase activity was moderately enhanced by phenobarbital alone in these cells.	Phenobarbital	0-13	lipoprotein lipase	Mus musculus	30-48
3778502-3	1986	Cytochrome P-450-PB-B, the major cytochrome P-450 isozyme induced in rat liver by phenobarbital, appeared to be responsible for the formation of 2- and 3-hexanol in lung microsomes from untreated rats as judged by antibody inhibition studies.	Phenobarbital	82-95	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
3096336-9	1986	PB, 3-MC and PCN increased F-UDP-GT activity to 208%, 282% and 342% of vehicle-treated animals, respectively, while F pretreatment did not affect the conjugation of F. In comparison, 1-naphthol glucuronidation was preferentially induced by 3-MC (4.4-fold of control) while estrone glucuronidation was induced by PB and PCN (4.9- and 2.5-fold of control, respectively).	Phenobarbital	0-2	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	29-35
3801548-2	1986	During translation of the PB-induced mRNA in the reticulocyte lysate cell-free protein-synthesizing system, a single polypeptide with an apparent molecular weight of 50,000 was synthesized which was specifically immunoprecipitated by antibodies to major PB-inducible cytochrome P-450 PB-3.	Phenobarbital	26-28	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	267-283
3778502-3	1986	Cytochrome P-450-PB-B, the major cytochrome P-450 isozyme induced in rat liver by phenobarbital, appeared to be responsible for the formation of 2- and 3-hexanol in lung microsomes from untreated rats as judged by antibody inhibition studies.	Phenobarbital	82-95	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	33-49
3791183-0	1986	Ornithine decarboxylase activity and DNA synthesis in rats after long term treatment with butylated hydroxyanisole, sodium saccharin or phenobarbital.	Phenobarbital	136-149	ornithine decarboxylase 1	Rattus norvegicus	0-23
3827818-3	1986	is described for the fractionation and purification to homogeneity of several membrane-bound rat hepatic phenobarbital (PB)-inducible cytochrome P-450 isoenzymes, including the major PB-inducible species.	Phenobarbital	120-122	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	134-150
3827818-3	1986	is described for the fractionation and purification to homogeneity of several membrane-bound rat hepatic phenobarbital (PB)-inducible cytochrome P-450 isoenzymes, including the major PB-inducible species.	Phenobarbital	183-185	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	134-150
3827818-6	1986	Accordingly, we have exploited this particular feature to identify not only the PB-inducible cytochrome P-450 isoenzymes destroyed in vivo by allylisopropylacetamide, a suicide inactivator of cytochrome P-450, but also to distinguish those that are reparable by exogenous haemin from those that are irreparably damaged.	Phenobarbital	80-82	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	93-109
3827818-6	1986	Accordingly, we have exploited this particular feature to identify not only the PB-inducible cytochrome P-450 isoenzymes destroyed in vivo by allylisopropylacetamide, a suicide inactivator of cytochrome P-450, but also to distinguish those that are reparable by exogenous haemin from those that are irreparably damaged.	Phenobarbital	80-82	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	192-208
3827818-0	1986	Fractionation and purification of hepatic microsomal cytochrome P-450 isoenzymes from phenobarbital-pretreated rats by h.p.l.c.	Phenobarbital	86-99	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	53-69
3827818-3	1986	is described for the fractionation and purification to homogeneity of several membrane-bound rat hepatic phenobarbital (PB)-inducible cytochrome P-450 isoenzymes, including the major PB-inducible species.	Phenobarbital	105-118	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	134-150
3809724-1	1986	The pretreatment of calves with a single dose of 10 mg kg-1 dieldrin or 21 daily doses of 10 mg kg-1 phenobarbitone increased the toxicity of diazinon as reflected by the development of more severe clinical signs and greater depression in whole blood cholinesterase activity in the pretreated calves.	Phenobarbital	101-115	butyrylcholinesterase	Bos taurus	251-265
2877820-2	1986	However, the increased rate of metabolism cannot be completely accounted for by the activity of the purified phenobarbital-inducible cytochrome P-450 isozyme 2, even in the presence of cytochrome b5.	Phenobarbital	109-122	cytochrome P450 2B4	Oryctolagus cuniculus	133-159
2877820-3	1986	The discovery of a second hepatic phenobarbital-inducible cytochrome P-450, isozyme 5, led us to undertake experiments to determine in hepatic and pulmonary preparations the portion of microsomal metabolism of methoxyflurane catalyzed by cytochrome P-450 isozymes 2 and 5.	Phenobarbital	34-47	cytochrome P450 4B1	Oryctolagus cuniculus	58-85
2877820-3	1986	The discovery of a second hepatic phenobarbital-inducible cytochrome P-450, isozyme 5, led us to undertake experiments to determine in hepatic and pulmonary preparations the portion of microsomal metabolism of methoxyflurane catalyzed by cytochrome P-450 isozymes 2 and 5.	Phenobarbital	34-47	cytochrome P450 2B4	Oryctolagus cuniculus	238-271
2877820-5	1986	Results for isozyme 5 indicate that it catalyzes 19% and 27% of methoxyflurane metabolism in control and phenobarbital-induced liver, and 47% of O-demethylation in the lung.	Phenobarbital	105-118	cytochrome P450 4B1	Oryctolagus cuniculus	12-21
3557278-0	1986	Phenobarbital treatment increased the astroglia-specific enzyme, glutathione S-transferase in rat brain.	Phenobarbital	0-13	hematopoietic prostaglandin D synthase	Rattus norvegicus	65-90
3095627-0	1986	Evidence for increased membrane permeability of plasmalemmal vesicles from livers of phenobarbital-induced CCl4-intoxicated rats.	Phenobarbital	85-98	C-C motif chemokine ligand 4	Rattus norvegicus	107-111
3095627-1	1986	We have observed a marked increase in Ca2+ permeability of plasma membranes isolated from rats treated in vivo with CCl4 (2 ml/kg), after phenobarbital induction and overnight fast.	Phenobarbital	138-151	C-C motif chemokine ligand 4	Rattus norvegicus	116-120
3488743-5	1986	Of the eleven MAbs, three also bound strongly to the phenobarbital-inducible rat liver cytochrome P-450 PB-4.	Phenobarbital	53-66	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	87-108
3787627-5	1986	PB enhanced cytochrome P-450 activity in all three species; however, a significant increase (p less than 0.05) in aminopyrine N-demethylase activity was observed only in rats and mice.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	12-28
3021733-3	1986	The covalent complex had almost completely blocked the electron transfer from NADPH to exogenous cytochrome c or the rabbit liver microsomal cytochrome P-450 induced by phenobarbital, indicating that the cross-linked cytochrome c covers the electron-accepting site of the reductase.	Phenobarbital	169-182	cytochrome c	Oryctolagus cuniculus	97-109
3021733-3	1986	The covalent complex had almost completely blocked the electron transfer from NADPH to exogenous cytochrome c or the rabbit liver microsomal cytochrome P-450 induced by phenobarbital, indicating that the cross-linked cytochrome c covers the electron-accepting site of the reductase.	Phenobarbital	169-182	cytochrome c	Oryctolagus cuniculus	217-229
3768039-6	1986	The aminoazo dye-induced enzymes differ in their substrate specificities from those induced with 3-methylcholanthrene or phenobarbital, and the induced enzyme was identified to be cytochrome P-448H, as determined by an enzyme-linked immunosorbent assay and immunoblotting with use of anti-cytochrome P-448 monoclonal antibodies.	Phenobarbital	121-134	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	180-196
3780149-9	1986	In patients who are receiving phenytoin, phenobarbital, or other drugs metabolized by the cytochrome P-450 system, serum concentrations of these drugs may increase as a result of influenza vaccination, and dosage adjustments may be necessary.	Phenobarbital	41-54	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	90-106
3780371-4	1986	The intron locations in these genes are identical to those in the genes for rat cytochrome P-450b/e, members of the other phenobarbital-inducible subfamily, but completely different from those in the 3-methylcholanthrene-inducible cytochrome P-450 genes.	Phenobarbital	122-135	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	80-97
3094515-2	1986	This species of cytochrome P-450, having its absorption maximum at 448.5 nm in carbon monoxide-complex of reduced form and low spin ferric ion, is of molecular weight of 56,000 and distinctly different in physicochemical and catalytic properties from major forms of cytochrome P-450 purified from phenobarbital- or 3-methylcholanthrene-treated rat liver.	Phenobarbital	297-310	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	16-32
3491762-3	1986	The mechanism responsible for the protective effect of diphenylhydantoin and phenobarbital against DA neurotoxicity of MPTP is unknown but some previously available findings suggest that they may act, in part, via inhibition of MAO-B and/or DA reuptake in the striatum.	Phenobarbital	77-90	monoamine oxidase B	Mus musculus	228-233
2877820-6	1986	In summary, we demonstrate that methoxyflurane O-demethylation in lung, phenobarbital-induced liver, and control liver microsomes is catalyzed by cytochrome P-450 isozymes 2 and 5.	Phenobarbital	72-85	cytochrome P450 2B4	Oryctolagus cuniculus	146-179
2875809-7	1986	Furthermore, PB caused a 3-fold increase in the number of foci expressing cytochrome P450-PB, gamma-GT or both.	Phenobarbital	13-15	gamma-glutamyltransferase 1	Rattus norvegicus	94-102
3582423-7	1986	Pb inducible cytochrome P-450 drug metabolizing enzymes do not appear to play a major role in the biotransformation of thioridazine to the ring sulfoxide.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
3095295-3	1986	Animals given 1 or 2 g PB for 3 d had higher concentrations of microsomal protein cytochrome b5 and P-450 and NADPH cytochrome c reductase than control animals (P less than .01).	Phenobarbital	23-25	cytochrome b5 type A	Rattus norvegicus	82-95
3095295-6	1986	In a study of the time course of induction all animals given PB had higher levels of microsomal protein, cytochrome P-450 and reductase in 24 h than controls; however, cytochrome b5 was depressed on d 1 and was elevated by d 3.	Phenobarbital	61-63	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	105-135
3095295-6	1986	In a study of the time course of induction all animals given PB had higher levels of microsomal protein, cytochrome P-450 and reductase in 24 h than controls; however, cytochrome b5 was depressed on d 1 and was elevated by d 3.	Phenobarbital	61-63	cytochrome b5 type A	Rattus norvegicus	168-181
3095295-8	1986	Levels of cytochrome P-450 were higher in gilts than in barrows on all days following PB treatment (P less than .04).	Phenobarbital	86-88	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	10-26
3764930-2	1986	Daily pretreatment of mice with phenobarbital (80 mg/kg, ip) for 4 days induced hepatic cytochrome P-450 content, as well as oxidative activation and oxidative detoxification of parathion, as measured in vitro.	Phenobarbital	32-45	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	88-104
3764930-5	1986	These results indicate that phenobarbital pretreatment clearly induces that form(s) of cytochrome P-450 catalyzing conversion of parathion to PO.	Phenobarbital	28-41	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	87-103
3271881-2	1986	The involvement of cytochrome P-450 (P-450) as the catalyst in 2NP denitrification was revealed by the induction of nitrite-releasing activity following phenobarbital (PB) pretreatment, by a decrease in activity with carbon tetrachloride pretreatment, by the inhibition of the reaction with classical P-450 inhibitors, and by the observation of a type I binding spectrum.	Phenobarbital	153-166	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	19-35
3758946-0	1986	Heterogeneous expression of phenobarbital-inducible cytochrome P-450 genes within the hepatic acinus in the rat.	Phenobarbital	28-41	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	52-68
3758946-1	1986	Within the hepatic acinus, the functional unit of liver parenchyma, the induction of cytochrome P-450 protein by phenobarbital is manifested primarily in hepatocytes located closer to the hepatic venule, i.e., distal hepatocytes.	Phenobarbital	113-126	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	85-101
3758946-8	1986	Hepatocytes of the distal half of the hepatic acinus responded to phenobarbital with higher levels of cytochromes P-450b and P-450e mRNAs than proximal hepatocytes.	Phenobarbital	66-79	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	114-120
3094931-0	1986	Polychlorinated biphenyls, classified as either phenobarbital- or 3-methylcholanthrene-type inducers of cytochrome P-450, are both hepatic tumor promoters in diethylnitrosamine-initiated rats.	Phenobarbital	48-61	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	104-120
3021190-1	1986	Thioacetamide, a hepatocarcinogen and an inhibitor of heme synthesis, blocks the phenobarbitone-mediated increase in the transcription of cytochrome P-450b+e messenger RNA in rat liver.	Phenobarbital	81-95	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	138-155
3271881-2	1986	The involvement of cytochrome P-450 (P-450) as the catalyst in 2NP denitrification was revealed by the induction of nitrite-releasing activity following phenobarbital (PB) pretreatment, by a decrease in activity with carbon tetrachloride pretreatment, by the inhibition of the reaction with classical P-450 inhibitors, and by the observation of a type I binding spectrum.	Phenobarbital	168-170	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	19-35
3462728-8	1986	Furthermore, the expression of esterase D was enhanced 3-fold in a promonocytic cell line treated with phenobarbital but not with phorbol myristate acetate, suggesting that esterase D may have a role in detoxification.	Phenobarbital	103-116	esterase D	Homo sapiens	31-41
3462728-8	1986	Furthermore, the expression of esterase D was enhanced 3-fold in a promonocytic cell line treated with phenobarbital but not with phorbol myristate acetate, suggesting that esterase D may have a role in detoxification.	Phenobarbital	103-116	esterase D	Homo sapiens	173-183
3768313-0	1986	3-(Trifluoromethyl)-3-(m-[125I]iodophenyl)diazirine photolabels a substrate-binding site of rat hepatic cytochrome P-450 form PB-4.	Phenobarbital	126-128	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	104-120
3768313-3	1986	The major hepatic microsomal cytochrome P-450 forms inducible by PB and 3-MC, respectively designated P-450s PB-4 and BNF-B, were shown to be the principal polypeptides labeled by [125I]TID in the correspondingly induced microsomes.	Phenobarbital	65-67	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	29-45
3768313-7	1986	In the absence of photoactivation, TID inhibited competitively about 80% of the cytochrome P-450-dependent 7-ethoxycoumarin O-deethylation catalyzed by PB-induced microsomes with a Ki of 10 microM; TID was a markedly less effective inhibitor of the corresponding activity catalyzed by microsomes isolated from uninduced or beta-naphthoflavone-induced livers.	Phenobarbital	152-154	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	80-96
3768314-1	1986	Hexachlorobenzene (HCB) elicits concentration-dependent and saturable type 1 binding spectra when added to oxidized (Fe3+) cytochrome P-450 (CYT P-450) in control, phenobarbital- (PB) induced, and beta-naphthoflavone- (BNF) induced male Sprague-Dawley rat liver microsomes.	Phenobarbital	180-182	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	141-150
3768314-2	1986	The spectral binding constants (Ks) for HCB in control and PB-induced microsomes are 180 microM and 83 microM, respectively, and correlate inversely with the specific content of CYT P-450 (0.9 and 2.1 nmol/mg) in the two microsomal preparations.	Phenobarbital	59-61	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	178-187
2873904-6	1986	PB or alpha-HCH treatment further decreased expression of L-PK in foci, but not in normal liver.	Phenobarbital	0-2	pyruvate kinase L/R	Rattus norvegicus	58-62
3756062-3	1986	Enzyme inhibitory monoclonal antibodies (MAb) to a 3-methylcholanthrene-induced (MAb 1-7-1) and phenobarbitone-induced (MAb 2-66-3) rat hepatic cytochrome P-450 were used to measure the contribution of MAb-defined, epitope-specific cytochromes P-450 to the total reaction measured for each of the above activities.	Phenobarbital	96-110	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	144-160
3726888-15	1986	Thus, pretreatment with phenobarbital, an inducer of cytochrome P-450, enhanced both covalent binding and toxicity while prior treatment with N-octylimidazole, an inhibitor of cytochrome P-450 decreased covalent binding and prevented hepatotoxicity of 2-MF.	Phenobarbital	24-37	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	53-69
3775859-0	1986	[Detection of cells resistant to the cytotoxic action of CCl4 in rat hepatocyte populations following a single exposure to diethylnitrosamine and subsequent injections of phenobarbital].	Phenobarbital	171-184	C-C motif chemokine ligand 4	Rattus norvegicus	57-61
3785219-16	1986	P450PCN1 mRNA was induced by PCN, dexamethasone, and phenobarbital in both male and female rats.	Phenobarbital	53-66	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	0-8
3785219-17	1986	P450PCN2 mRNA was not significantly induced by PCN or dexamethasone but was readily induced by phenobarbital.	Phenobarbital	95-108	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	0-8
3785219-18	1986	Testosterone 6 beta-hydroxylase activity was also induced severalfold by PCN, dexamethasone, and phenobarbital.	Phenobarbital	97-110	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	0-31
3726888-15	1986	Thus, pretreatment with phenobarbital, an inducer of cytochrome P-450, enhanced both covalent binding and toxicity while prior treatment with N-octylimidazole, an inhibitor of cytochrome P-450 decreased covalent binding and prevented hepatotoxicity of 2-MF.	Phenobarbital	24-37	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	176-192
3481957-1	1986	A phenobarbitone inducible cytochrome P-450 gene family (CYP1) has recently been localized to chromosome 19q13.1-qter.	Phenobarbital	2-16	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	27-43
2425812-6	1986	Direct evidence for the presence of mRNA transcript coding for a phenobarbital-inducible cytochrome P-450 was demonstrated in HepG2 cells by Northern blot analysis.	Phenobarbital	65-78	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	89-105
2424910-0	1986	The cDNA and protein sequence of a phenobarbital-induced chicken cytochrome P-450.	Phenobarbital	35-48	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	76-81
2424910-1	1986	Several cDNA clones complementary to a chicken phenobarbital-inducible cytochrome P-450 have been isolated and sequenced, representing the first non-mammalian eukaryotic cytochrome P-450 sequence to be analyzed.	Phenobarbital	47-60	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	82-87
2424910-1	1986	Several cDNA clones complementary to a chicken phenobarbital-inducible cytochrome P-450 have been isolated and sequenced, representing the first non-mammalian eukaryotic cytochrome P-450 sequence to be analyzed.	Phenobarbital	47-60	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	181-186
2424910-6	1986	The chicken cytochrome P-450 shows an overall homology of 45-54% compared with the mammalian phenobarbital-induced cytochrome P-450s.	Phenobarbital	93-106	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	23-28
3015147-6	1986	Phenobarbital caused a small but statistically insignificant increase in gamma-glutamyl transferase activity: density gradient centrifugation studies indicated that the increased activity was predominantly in the biliary canalicular elements.	Phenobarbital	0-13	gamma-glutamyltransferase 1	Rattus norvegicus	73-99
3481957-1	1986	A phenobarbitone inducible cytochrome P-450 gene family (CYP1) has recently been localized to chromosome 19q13.1-qter.	Phenobarbital	2-16	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	57-61
3015147-7	1986	In contrast, cytosolic gamma-glutamyl hydrolase activity was strikingly reduced by phenobarbital treatment.	Phenobarbital	83-96	gamma-glutamyl hydrolase	Rattus norvegicus	23-47
3720920-0	1986	NADPH-dependent and -independent loss of cytochrome P-450 in control and phenobarbital-induced rat hepatic microsomes incubated with carbon tetrachloride.	Phenobarbital	73-86	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	41-57
3729978-1	1986	Twelve homologous and regioisomeric pyridylalkanamides were examined spectrally for their binding affinity to cytochrome P-450 in phenobarbital- and 3-methylcholanthrene-induced rat liver microsomes.	Phenobarbital	130-143	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	110-126
3013443-2	1986	It was found that human HGPRT+/HGPRT- SK-HEP-1 cells only, showed a metabolic cooperation capacity that was inhibited by tumour promoters 12-O-tetradecanoylphorbol-13-acetate (TPA) and phenobarbital, and was not inhibited by the non-promoter 4-O-methyl TPA, provided suitable experimental conditions (short exposure times) were used.	Phenobarbital	185-198	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	24-29
3013443-2	1986	It was found that human HGPRT+/HGPRT- SK-HEP-1 cells only, showed a metabolic cooperation capacity that was inhibited by tumour promoters 12-O-tetradecanoylphorbol-13-acetate (TPA) and phenobarbital, and was not inhibited by the non-promoter 4-O-methyl TPA, provided suitable experimental conditions (short exposure times) were used.	Phenobarbital	185-198	hypoxanthine phosphoribosyltransferase 1	Homo sapiens	31-36
3087771-1	1986	The administration to rats of either t-butyl hydroperoxide or phenobarbital, compounds that are metabolized through detoxification processes, produces an increase in specific activity of the NADPH-consuming enzymes, glutathione reductase and NADPH-cytochrome c reductase.	Phenobarbital	62-75	glutathione-disulfide reductase	Rattus norvegicus	216-237
3742647-1	1986	When cytochrome P-450 in phenobarbital-induced rat liver microsomes was destroyed by 2-isopropyl-4-pentenamide (AIA) in vitro, 50% of the degraded heme was recovered as heme-derived products irreversibly bound to microsomal proteins.	Phenobarbital	25-38	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	5-21
2425856-0	1986	[Induction of the phenobarbital form of cytochrome P-450 by chemically unrelated compounds].	Phenobarbital	18-31	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	40-56
2425856-1	1986	The induction of the phenobarbital form of cytochrome P-450 by xenobiotics (phenobarbital, PB, hexachlorobenzene, HCB; hexachlorocyclohexane.	Phenobarbital	21-34	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	43-59
2425856-1	1986	The induction of the phenobarbital form of cytochrome P-450 by xenobiotics (phenobarbital, PB, hexachlorobenzene, HCB; hexachlorocyclohexane.	Phenobarbital	76-89	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	43-59
2425856-4	1986	Using monospecific antibodies against the cytochrome P-450 form isolated from PB-induced microsomes (PB-cytochrome P-450), a double immunodiffusion test revealed immunological identity of cytochrome P-450 forms induced by phenobarbital and other xenobiotics.	Phenobarbital	222-235	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	42-58
2425856-4	1986	Using monospecific antibodies against the cytochrome P-450 form isolated from PB-induced microsomes (PB-cytochrome P-450), a double immunodiffusion test revealed immunological identity of cytochrome P-450 forms induced by phenobarbital and other xenobiotics.	Phenobarbital	222-235	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	104-120
2425856-4	1986	Using monospecific antibodies against the cytochrome P-450 form isolated from PB-induced microsomes (PB-cytochrome P-450), a double immunodiffusion test revealed immunological identity of cytochrome P-450 forms induced by phenobarbital and other xenobiotics.	Phenobarbital	222-235	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	104-120
3724741-1	1986	Twenty dichloromethyl compounds have been tested as potential mechanism-based inactivators of the major phenobarbital-inducible isozyme of rat liver cytochrome P-450 (PB-B) in a reconstituted system.	Phenobarbital	104-117	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	149-171
3011803-1	1986	DNA sequence analysis of a Yb2 cDNA clone and regulation of the Yb1 and Yb2 mRNAs by phenobarbital.	Phenobarbital	85-98	Y box binding protein 3	Rattus norvegicus	27-30
3011803-1	1986	DNA sequence analysis of a Yb2 cDNA clone and regulation of the Yb1 and Yb2 mRNAs by phenobarbital.	Phenobarbital	85-98	Y box binding protein 1	Rattus norvegicus	64-67
3011803-1	1986	DNA sequence analysis of a Yb2 cDNA clone and regulation of the Yb1 and Yb2 mRNAs by phenobarbital.	Phenobarbital	85-98	Y box binding protein 3	Rattus norvegicus	72-75
3011803-10	1986	We have utilized the divergent 3" untranslated regions of three rat liver glutathione S-transferase cDNA clones as specific probes to determine the effect of phenobarbital on the level of Yb1, Yb2, and Yc mRNAs.	Phenobarbital	158-171	Y box binding protein 1	Rattus norvegicus	188-191
3011803-11	1986	Our results clearly show that the Yb1 and Yb2 mRNAs are elevated approximately 5-6-fold by phenobarbital administration; whereas the Yc mRNA is only modestly elevated by this xenobiotic.	Phenobarbital	91-104	Y box binding protein 1	Rattus norvegicus	34-37
3011803-11	1986	Our results clearly show that the Yb1 and Yb2 mRNAs are elevated approximately 5-6-fold by phenobarbital administration; whereas the Yc mRNA is only modestly elevated by this xenobiotic.	Phenobarbital	91-104	Y box binding protein 3	Rattus norvegicus	42-45
3730555-0	1986	[Induction of cytochrome P-450 and b5 in hepatocyte subpopulations with phenobarbital].	Phenobarbital	72-85	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	14-37
3730555-4	1986	Phenobarbital induced cytochrome P-450 in all subpopulations, with a more pronounced increase observed in light hepatocytes.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	22-38
3013548-0	1986	cDNA clones for liver cytochrome P-450s from individual aroclor-treated rats: constitutive expression of a new P-450 gene related to phenobarbital-inducible forms.	Phenobarbital	133-146	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	22-38
3013548-12	1986	The PB24 cDNA most likely represents a constitutive cytochrome P-450, related to phenobarbital-inducible forms.	Phenobarbital	81-94	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	52-68
3720920-5	1986	Residual cytochrome P-450 at these concentrations was similar in untreated and phenobarbital-treated microsomes.	Phenobarbital	79-92	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	9-25
3523833-4	1986	The data obtained suggest the involvement of a PB-inducible form of cytochrome P-450 in the activation of IP and TP to mutagenic species.	Phenobarbital	47-49	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	68-84
3718496-6	1986	Xenobiotics such as phenobarbital, 3-methylcholanthrene, and trans-stilbene oxide induce rat liver GSH S-transferase activities, especially the Ya- and Yb-subunit containing isozymes.	Phenobarbital	20-33	glutathione synthetase	Rattus norvegicus	99-104
3707601-3	1986	Purified phenobarbital-induced cytochrome P-450 produced more oxide per nmole enzyme than any of the purified uninduced cytochrome P-450s.	Phenobarbital	9-22	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	31-47
3707601-5	1986	Diethylphenylphosphine bound to oxidized purified phenobarbital-induced cytochrome P-450 and uninduced cytochrome P-450 with Ks values of 16 microM and 11-18 microM respectively.	Phenobarbital	50-63	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	72-88
3707601-5	1986	Diethylphenylphosphine bound to oxidized purified phenobarbital-induced cytochrome P-450 and uninduced cytochrome P-450 with Ks values of 16 microM and 11-18 microM respectively.	Phenobarbital	50-63	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	103-119
3705085-2	1986	The ratio of side chain to aromatic hydroxylation was found to be approximately 1:1 in lung microsomes from untreated rats and in a reconstituted system containing the major cytochrome P-450 isozyme induced in rat liver by phenobarbital, cytochrome P-450-PB-B2, as compared to 8:1 in liver microsomes.	Phenobarbital	223-236	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	174-190
3718496-8	1986	Our results clearly demonstrate that GSH S-transferase expression in seminal vesicles and pituitary glands can be suppressed by phenobarbital and diethylstilbestrol, respectively.	Phenobarbital	128-141	glutathione synthetase	Rattus norvegicus	37-42
3707601-6	1986	Diethylphenylphosphine was also a competitive inhibitor of p-nitroanisole O-demethylation catalyzed by a reconstituted phenobarbital-induced cytochrome P-450-dependent monooxygenase system, with a Ki value of 5 microM.	Phenobarbital	119-132	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	141-157
3719856-1	1986	A hepatic cytochrome P-450 isolated in an electrophoretically homogeneous form from phenobarbital-treated rats, exists predominantly in the low spin configuration (82% at 20 degrees C).	Phenobarbital	84-97	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	10-26
3084479-2	1986	The cDNA encoding a phenobarbital-inducible form of rat liver UDP-glucuronosyltransferase has been isolated, sequenced, and expressed to yield a catalytically active enzyme.	Phenobarbital	20-33	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	62-89
3707616-7	1986	These findings indicate that cytochrome P450 species induced with 3MC as well as PB are highly susceptible to CHCl3 intoxication, whereas the administration of CCl4 depletes the PB-induced species without affecting the 3MC-induced species.	Phenobarbital	178-180	C-C motif chemokine ligand 4	Rattus norvegicus	160-164
2872200-10	1986	However, they differed in their basal ALDH activities and in ALDH inducibility by 3-methylcholanthrene, benzo(a)pyrene, and phenobarbital.	Phenobarbital	124-137	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	61-65
3720941-1	1986	The study of the inducing effect of phenobarbital on the activity of N-demethylase of aminopyrine in the rat liver microsomes revealed the correlation of the rate of enzymic reaction with the changes in the maximum binding of aminopyrine by cytochrome P-450 rather than with the content of hemoprotein itself.	Phenobarbital	36-49	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	241-257
2872038-10	1986	Monoclonal antibodies directed against cytochrome P-448 inhibited ERDE activities induced by BA and PB to a similar extent.	Phenobarbital	100-102	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	50-55
2422427-1	1986	In vivo treatment of randombred Swiss Webster mice with polyriboinosinic-polyribocytidylic acid (poly l X poly C) inhibited the induction of cytochrome P-450"s by both 3-methylcholanthrene [(MCA) CAS: 56-49-5] and phenobarbitol [(PB) CAS: 50-06-6].	Phenobarbital	214-227	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	141-157
3009786-9	1986	These results suggest that 1) in vitro interactions between barbiturates and GABAa receptor agonists may not be the same in vivo, 2) GABAa receptors may play a minor role in the minimal neurotoxicity and anticonvulsant activity of barbiturates and 3) inhibition of glutamate-induced excitation by baclofen may be an important action in potentiating the anti-MES activity of phenobarbital.	Phenobarbital	374-387	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	133-138
2872669-1	1986	Plasma levels of gamma-glutamyl transpeptidase were measured prospectively in 75 epileptic patients treated with one of the following drugs: phenobarbitone (n = 20), phenytoin (n = 23), carbamazepine (n = 18) or sodium valproate (n = 14).	Phenobarbital	141-155	inactive glutathione hydrolase 2	Homo sapiens	17-46
3007463-1	1986	Electron spin resonance spectroscopy has been used to monitor free radicals formed during CCl4 metabolism by perfused livers from phenobarbital-treated rats.	Phenobarbital	130-143	C-C motif chemokine ligand 4	Rattus norvegicus	90-94
3715917-2	1986	Corticosterone inhibited aryl hydrocarbon hydroxylase (AHH) activity nonlinearly in hepatic microsomes from uninduced, phenobarbital-induced, or 3-methylcholanthrene-induced rats.	Phenobarbital	119-132	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	25-53
3083888-0	1986	[Cytochrome P-450 isoforms in the liver of rats treated with phenobarbital, 3-methylcholanthrene and Aroclor 1254 studied by monoclonal antibodies].	Phenobarbital	61-74	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	1-17
3085962-6	1986	Using specific antibodies to isolated cytochromes P-450 and P-448 (anti-P-450 and anti-P-448) it has been found by rocket immunoelectrophoresis that in HCB-treated microsomes 20% of the total cytochrome P-450 consist of PB-form and about 10% comprise cytochrome P-488.	Phenobarbital	220-222	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	50-92
3085962-8	1986	The data presented give direct proof that HCB exemplifies an individual chemical compound which is able to initiate the synthesis of both PB-form and MC-form of the cytochrome P-450.	Phenobarbital	138-140	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	165-181
3458196-1	1986	The mRNAs encoding the two major phenobarbital-inducible forms of cytochrome P-450 of rat liver, P-450b and P-450e, are remarkably similar (98% homologous) in nucleotide sequence, but the distribution of differences within them is not random.	Phenobarbital	33-46	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	97-103
3754327-3	1986	On the basis of experiments involving cell-free translation and hybridization to the cloned probe, it was shown that prototype inducers of cytochrome P-450 such as phenobarbitone and 3-methylcholanthrene as well as inhibitors such as CoCl2 and 3-amino-1,2,4-triazole enhanced the glutathione transferase (Ya+Yc) messenger RNA contents in rat liver.	Phenobarbital	164-178	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	139-155
3754327-3	1986	On the basis of experiments involving cell-free translation and hybridization to the cloned probe, it was shown that prototype inducers of cytochrome P-450 such as phenobarbitone and 3-methylcholanthrene as well as inhibitors such as CoCl2 and 3-amino-1,2,4-triazole enhanced the glutathione transferase (Ya+Yc) messenger RNA contents in rat liver.	Phenobarbital	164-178	glutathione S-transferase alpha 4	Rattus norvegicus	280-303
3754327-4	1986	A comparative study with the induction of cytochrome P-450 (b+e) by phenobarbitone revealed that the drug manifested a striking increase in the nuclear pre-messenger RNAs for the cytochrome at 12 hr, but did not significantly affect the same in the case of glutathione transferase (Ya+Yc).	Phenobarbital	68-82	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	42-58
3754327-5	1986	3-Amino-1,2,4-triazole and CoCl2 blocked the phenobarbitone mediated increase in cytochrome P-450 (b+e) nuclear pre-messenger RNAs.	Phenobarbital	45-59	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	81-97
3754327-7	1986	The polysomal, poly (A)- containing messenger RNAs for cytochrome P-450 (b+e) increased by 12-15 fold after phenobarbitone administration, reached a maximum around 16 hr and then decreased sharply.	Phenobarbital	108-122	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	55-71
3754327-9	1986	Run-off transcription rates for cytochrome P-450 (b+e) increased by nearly 15 fold in 4 hr after phenobarbitone administration, whereas the increase for glutathione transferase (Ya+Yc) was only 2.0 fold.	Phenobarbital	97-111	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	32-48
3754327-11	1986	Administration of 3-amino-1,2,4-triazole and CoCl2 blocked the phenobarbitone-mediated increase in the transcription of cytochrome P-450 (b+e) messenger RNAs.	Phenobarbital	63-77	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	120-136
3754327-14	1986	Administration of phenobarbitone enhanced the half-life of glutathione transferase (Ya+Yc) messenger RNA by nearly two fold.	Phenobarbital	18-32	glutathione S-transferase alpha 4	Rattus norvegicus	59-82
3083864-0	1986	Regulation of cytochrome P-450p by phenobarbital and phenobarbital-like inducers in adult rat hepatocytes in primary monolayer culture and in vivo.	Phenobarbital	35-48	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	14-31
3947671-1	1986	We have recently shown that the administration of phenobarbital to rats leads to an increased serum alpha 1-acid glycoprotein content with alterations in the relative proportion of the sugar moiety.	Phenobarbital	50-63	orosomucoid 1	Rattus norvegicus	100-125
3947671-2	1986	Therefore, alpha 1-acid glycoprotein was purified from normal (alpha 1-acid glycoproteine N) and phenobarbital-treated rats (alpha 1-acid glycoprotein PB) Glycans were separated by AX-10 chromatography and analysed by gas chromatography.	Phenobarbital	97-110	orosomucoid 1	Rattus norvegicus	11-36
3083864-0	1986	Regulation of cytochrome P-450p by phenobarbital and phenobarbital-like inducers in adult rat hepatocytes in primary monolayer culture and in vivo.	Phenobarbital	53-66	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	14-31
3083864-1	1986	Treatment of rats with phenobarbital increases the hepatic concentration of P-450p, a form of cytochrome P-450 believed to be controlled primarily by a mechanism that stereospecifically recognizes glucocorticoids like dexamethasone and anti-glucocorticoids like pregnenolone-16 alpha-carbonitrile [Schuetz, E.G., & Guzelian, P.S.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	94-110
2872903-0	1986	Effects of in utero administration of phenobarbital on gamma-glutamyl transpeptidase.	Phenobarbital	38-51	gamma-glutamyltransferase 1	Rattus norvegicus	55-84
2872903-1	1986	The present study was undertaken to determine the effects of the in utero administration of phenobarbital (Pb) on gamma glutamyl transpeptidase (gamma-GTP) in rats.	Phenobarbital	92-105	gamma-glutamyltransferase 1	Rattus norvegicus	114-143
2872903-1	1986	The present study was undertaken to determine the effects of the in utero administration of phenobarbital (Pb) on gamma glutamyl transpeptidase (gamma-GTP) in rats.	Phenobarbital	92-105	gamma-glutamyltransferase 1	Rattus norvegicus	145-154
2872903-1	1986	The present study was undertaken to determine the effects of the in utero administration of phenobarbital (Pb) on gamma glutamyl transpeptidase (gamma-GTP) in rats.	Phenobarbital	107-109	gamma-glutamyltransferase 1	Rattus norvegicus	114-143
2872903-1	1986	The present study was undertaken to determine the effects of the in utero administration of phenobarbital (Pb) on gamma glutamyl transpeptidase (gamma-GTP) in rats.	Phenobarbital	107-109	gamma-glutamyltransferase 1	Rattus norvegicus	145-154
2872903-8	1986	Brain gamma-GTP activity was found to be 0.00807 u in the Pb group and 0.00670 u in the control group.	Phenobarbital	58-60	gamma-glutamyltransferase 1	Rattus norvegicus	6-15
3731348-0	1986	Different depressing effects of lentinan on the increases of cytochrome P-450-dependent monooxygenase activities induced in mice by phenobarbital and by 3-methylcholanthrene.	Phenobarbital	132-145	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	61-77
3717918-7	1986	Phenobarbital is a more strong and selective inductor of this form of cytochrome P-450 than 3-methylcholanthrene.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	70-86
3956453-0	1986	Prolactin secretion in epileptic subjects treated with phenobarbital: sex differences and circadian periodicity.	Phenobarbital	55-68	prolactin	Homo sapiens	0-9
3715917-2	1986	Corticosterone inhibited aryl hydrocarbon hydroxylase (AHH) activity nonlinearly in hepatic microsomes from uninduced, phenobarbital-induced, or 3-methylcholanthrene-induced rats.	Phenobarbital	119-132	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	55-58
3956453-3	1986	Circadian PRL secretion, studied in six male epileptic patients on PB monotherapy and in nine normal subjects, showed comparable 24-h PRL mean values and a preserved PRL surge during the night in both groups; however, a statistically significant additional peak was found in male epileptic subjects during the late afternoon.	Phenobarbital	67-69	prolactin	Homo sapiens	10-13
3956453-5	1986	These results indicate that central and/or peripheral mechanisms involved in PRL secretion control are more sensitive to PB alone or in combination with other antiepileptic drugs in male than in female subjects.	Phenobarbital	121-123	prolactin	Homo sapiens	77-80
3086298-0	1986	Effects of phenobarbital, 3-methylcholanthrene and polychlorinated biphenyls on sex-specific forms of cytochrome P-450 in liver microsomes of rats.	Phenobarbital	11-24	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	102-118
3086298-1	1986	The effects of treatment with phenobarbital, 3-methylcholanthrene or polychlorinated biphenyls (PCB) on the amounts of sex-specific forms of cytochrome P-450, namely P-450-male and P-450-female, in male and female rats were studied.	Phenobarbital	30-43	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	141-157
3086298-2	1986	Although treatment with phenobarbital, 3-methylcholanthrene or PCB markedly increased the total amount of hepatic cytochrome P-450, P-450-male and P-450-female were rather decreased or not significantly changed.	Phenobarbital	24-37	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	114-130
3484995-15	1986	AVP-induced BR in sensitized rats: phenytoin, diazepam, valproic acid and phenobarbital; all drugs reduced the proportion of rats with BR and prolonged the latency.	Phenobarbital	74-87	arginine vasopressin	Rattus norvegicus	0-3
3754047-4	1986	In contrast, mRNAs homologous to the P-450b oligomer were detected at low levels in control and inducer pretreated lung and testis, and at high levels in PB induced liver.	Phenobarbital	154-156	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	37-43
3947639-3	1986	The results demonstrated that P-450b and epoxide hydrolase were present in the lungs of male and female rats and that their expression in this tissue was independent of phenobarbital treatment.	Phenobarbital	169-182	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	30-36
3753840-1	1986	Using specific testosterone 16 alpha-hydroxylase activity as the basis for selection of fractions during purification, the cytochrome P-450 ("I"-P-450(16)alpha) has been isolated from livers of phenobarbital-treated 129/J female mice [K. Devore, N. Harada, and M. Negishi (1985) Biochemistry, 24, 5632-5637].	Phenobarbital	194-207	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	123-159
3947732-1	1986	The effect of liver monooxygenase system substrates upon the rate of cytochrome P-450 isoform degradation was investigated by measuring the half-life of liver microsomal proteins in C57BL/6 mice injected with phenobarbital and then 24 hours later with aminopyrine every 6 hours.	Phenobarbital	209-222	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	69-85
3947732-2	1986	The rate of phenobarbital-induced degradation of cytochrome P-450 isoform (mol weight 56000 daltons) was shown to be increased two-fold.	Phenobarbital	12-25	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	49-65
3955788-1	1986	Approximately 90% of the NADPH- and NADH-dependent O-demethylation of p-nitroanisole (PNA) in the hepatic microsomal fraction from phenobarbital (PB)-treated rabbits and in the pulmonary microsomal fraction from untreated rabbits is catalyzed by the same isozyme of cytochrome P-450.	Phenobarbital	146-148	cytochrome P-450	Oryctolagus cuniculus	266-282
2868808-2	1986	An increase in the incidence of gamma-glutamyltransferase (GGT)-positive hepatocytes was found in rats fed PB or DDT, while CPIB strikingly decreased the incidence.	Phenobarbital	107-109	gamma-glutamyltransferase 1	Rattus norvegicus	32-57
3512116-6	1986	These results demonstrate a correlation between the mutagenicity of nine N-nitrosopropylamines mediated by liver S9 from three animal species and their known carcinogenicity in rodent in vivo experiments, and that the PB-inducible major cytochrome P-450 is selectively involved in the mutagenic activation.	Phenobarbital	218-220	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	237-253
3295745-7	1986	LIF production of lymphocytes was inhibited by INDO, ASA, PhB, CHINOIN 127 and CHINOIN 105.	Phenobarbital	63-70	LIF interleukin 6 family cytokine	Homo sapiens	0-3
3082822-8	1986	These results demonstrated that the phenobarbital-inducible major cytochrome P-450 in animal and human livers is involved in the mutagenic activation of the N-nitrosopropylamines.	Phenobarbital	36-49	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	66-82
3007551-1	1986	Cytochrome P-450 from rat liver microsomes treated with phenobarbital (PB) was separated into six fractions, as was cytochrome P-450 treated with 3-methylcholanthrene (MC), by high-performance liquid chromatography (HPLC) with an anion-exchange column.	Phenobarbital	56-69	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
3007551-1	1986	Cytochrome P-450 from rat liver microsomes treated with phenobarbital (PB) was separated into six fractions, as was cytochrome P-450 treated with 3-methylcholanthrene (MC), by high-performance liquid chromatography (HPLC) with an anion-exchange column.	Phenobarbital	71-73	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
3007551-2	1986	PB and MC induced three forms and one form of cytochrome P-450, respectively.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	46-62
3082610-1	1986	A full-length cDNA for rat NADPH-cytochrome P-450 reductase was cloned by the procedure of Okayama and Berg (1982) from hepatic poly(A)RNA prepared from phenobarbital-induced rats.	Phenobarbital	153-166	cytochrome p450 oxidoreductase	Rattus norvegicus	27-59
3456067-6	1986	In the presence of beta-glucuronidase (beta G), increased numbers of TA98 revertants were noted in the urine of rats pretreated with PB, saline, or corn oil.	Phenobarbital	133-135	glucuronidase, beta	Rattus norvegicus	19-37
3456067-6	1986	In the presence of beta-glucuronidase (beta G), increased numbers of TA98 revertants were noted in the urine of rats pretreated with PB, saline, or corn oil.	Phenobarbital	133-135	glucuronidase, beta	Rattus norvegicus	39-45
3699630-8	1986	However, gomisin A is distinctly different from phenobarbital in the finding that phenobarbital lessened the survival ratio of CCl4-intoxicated mice, but gomisin A did not.	Phenobarbital	82-95	chemokine (C-C motif) ligand 4	Mus musculus	127-131
3083608-7	1986	The inhibitory effect of the drug on hepatic MAO-B activity was annulled by pretreatment of rats with PB, but not 3-MC, and augmented by pretreatment with SKF 525-A.	Phenobarbital	102-104	monoamine oxidase B	Rattus norvegicus	45-50
3295745-7	1986	LIF production of lymphocytes was inhibited by INDO, ASA, PhB, CHINOIN 127 and CHINOIN 105.	Phenobarbital	79-86	LIF interleukin 6 family cytokine	Homo sapiens	0-3
3947068-1	1986	When CCl4 was incubated with rat liver microsomes from phenobarbital-treated rats in an aerobic or anaerobic atmosphere, over 69% of the heme moiety of cytochrome P-450 was destroyed.	Phenobarbital	55-68	C-C motif chemokine ligand 4	Rattus norvegicus	5-9
3947068-1	1986	When CCl4 was incubated with rat liver microsomes from phenobarbital-treated rats in an aerobic or anaerobic atmosphere, over 69% of the heme moiety of cytochrome P-450 was destroyed.	Phenobarbital	55-68	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	152-168
3539534-10	1986	When drugs such as phenobarbital are administered to animals, there is a rapid induction in the liver of both cytochrome P-450 and ALV-synthase.	Phenobarbital	19-32	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	110-143
3944090-2	1986	We conducted solution hybridization and Northern blot experiments utilizing synthetic 18"-mer oligodeoxyribonucleotides complementary to two major rat hepatic phenobarbital-inducible cytochrome P-450s, P-450b and P-450e, to assess their mRNA expression during rat development.	Phenobarbital	159-172	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	202-208
3944090-8	1986	The age-dependent increase in responsiveness to phenobarbital was associated with an age-dependent decrease in the ratio of P-450b to P-450e mRNA levels.	Phenobarbital	48-61	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	124-130
3944090-10	1986	Maximal levels of phenobarbital-induced hepatic RNA for both isozymes occurred 24 days after birth (day 46 of development), at which time P-450b and P-450e mRNAs accumulated to levels 2.4- and 1.8-fold greater, respectively, than levels found in comparably induced adult rat liver.	Phenobarbital	18-31	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	138-144
3468920-8	1986	As the age course of H2O2 production is similar to that of ethylmorphine N-demethylation, it is concluded that the phenobarbital-inducible cytochrome P-450 subspecies predominantly catalyse H2O2 production.	Phenobarbital	115-128	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	139-155
2867834-4	1986	Withdrawing PB for 10 days resulted in a decrease in the number and volume of AHF, particularly those which stained positively for gamma-glutamyltranspeptidase (GGT).	Phenobarbital	12-14	gamma-glutamyltransferase 1	Rattus norvegicus	131-159
2871955-6	1986	The co-administration of other potentially nephrotoxic agents (e.g., gentamicin), the diuretic frusemide, or inhibitors or suppressors of hepatic drug metabolism increases the degree of NAG enzymuria, whilst inducers of drug metabolism (e.g., phenobarbitone) have the reverse effect.	Phenobarbital	243-257	O-GlcNAcase	Rattus norvegicus	186-189
2869885-0	1986	Kinetic constant determination of liver microsomal and purified UDP-glucuronosyltransferase after phenobarbital and 3-methylcholanthrene treatments in rats.	Phenobarbital	98-111	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	64-91
2869885-1	1986	After induction by phenobarbital and 3-methylcholanthrene, UDP-glucuronosyltransferase involved mainly in the conjugation of planar substrates was purified.	Phenobarbital	19-32	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	59-86
3556453-6	1986	Total cytochrome P-450 content was induced at all age groups in all tissues by beta-naphthoflavone and in all tissues except lung by phenobarbital.	Phenobarbital	133-146	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	6-22
3792215-10	1986	The specific activity of cytochrome P-450 for the metabolism of DMN and B(a)P, however, was significantly reduced in menhaden oil-fed animals by phenobarbital.	Phenobarbital	145-158	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	25-41
3556453-7	1986	Induction of cytochrome P-450 in kidney by phenobarbital was only observed in 24 and 78 week old rats.	Phenobarbital	43-56	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
3758228-3	1986	Radial immunodiffusion analysis of rat liver microsomes indicate that cytochrome P-450 Forms 1 and 2 respond to induction by beta-naphthoflavone or phenobarbital less well in aging rats than in young rats.	Phenobarbital	148-161	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	70-86
3514588-4	1986	In the microsomal preparation, the DBE-debromination rate per nmol cytochrome P-450 was enhanced by phenobarbital-pretreatment of rabbits compared with the untreated microsomes, whereas it was diminished by 3-methylcholanthrene-pretreatment.	Phenobarbital	100-113	cytochrome P-450	Oryctolagus cuniculus	67-83
3514588-5	1986	The debromination reaction was reconstituted in a purified enzyme system containing phenobarbital-inducible rabbit liver microsomal cytochrome P-450 (P-450PB), NADPH-cytochrome P-450 reductase, and NADPH.	Phenobarbital	84-97	cytochrome P-450	Oryctolagus cuniculus	132-148
3514588-5	1986	The debromination reaction was reconstituted in a purified enzyme system containing phenobarbital-inducible rabbit liver microsomal cytochrome P-450 (P-450PB), NADPH-cytochrome P-450 reductase, and NADPH.	Phenobarbital	84-97	NADPH--cytochrome P450 reductase	Oryctolagus cuniculus	160-192
3082968-0	1986	The distribution of cytochrome P-450-mediated drug oxidation and glutathione in periportal and perivenous rat hepatocytes after phenobarbital treatment.	Phenobarbital	128-141	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	20-36
3082968-7	1986	A 3-day treatment with phenobarbital equalized the pp-pv difference by producing more induction of the periportal cytochrome P-450-mediated drug and ethanol oxidation capacities in microsomes derived from periportally enriched hepatocytes.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	114-130
3723330-4	1986	None of the drugs affected nocturnal HIOMT levels, and only phenobarbitone affected NAT levels, apparently causing a shift in the nocturnal peak later in the dark phase.	Phenobarbital	60-74	N-acetyltransferase 1	Rattus norvegicus	84-87
3012058-11	1986	The metabolic rate (per nmol cytochrome P-450) of CBD was also increased significantly by phenobarbital-treatment but not by 3-methylcholanthrene-treatment.	Phenobarbital	90-103	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	29-45
3012058-12	1986	These results suggest that CBD metabolites rather than CBD itself, play some role in the decreasing effect on cytochrome P-450 content in the hepatic microsomes in vitro, and that the microsomal formation of reactive metabolite of CBD is increased by phenobarbital-treatment.	Phenobarbital	251-264	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	110-126
3531907-7	1986	In the second experiment, OVX phenobarbital-pretreated rats were given 1.25 ng LH-RH/100 g b.w.	Phenobarbital	30-43	gonadotropin releasing hormone 1	Rattus norvegicus	79-84
3941398-0	1986	Cytochrome P-450 isoenzyme content and monooxygenase activities in rat liver: effect of ontogenesis and pretreatment by phenobarbital and 3-methylcholanthrene.	Phenobarbital	120-133	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
3942013-3	1986	A non-hepatotoxic dose of CCl4 did not cause a significant increase in ethane production except in PB-induced rats but did enhance n-pentane elimination, whereas an hepatotoxic dose increased the emission of both hydrocarbons.	Phenobarbital	99-101	C-C motif chemokine ligand 4	Rattus norvegicus	26-30
3489949-5	1986	PB induced soluble glutathione S-transferase, a detoxifying enzyme, only in rats fed dietary fats.	Phenobarbital	0-2	hematopoietic prostaglandin D synthase	Rattus norvegicus	19-44
3596751-4	1986	In contrast to HCB, the lower chlorinated benzenes did not induce significant amounts of P-450c or P-450d in the rat, but were phenobarbital-type inducers, inducing P-450b and P-450e.	Phenobarbital	127-140	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	165-171
3942013-4	1986	No interaction between CM and CCl4 could be shown but, as expected, PB potentiated the effect of CCl4.	Phenobarbital	68-70	C-C motif chemokine ligand 4	Rattus norvegicus	97-101
3877725-0	1985	The structure of phenobarbital-inducible rat liver cytochrome P-450 isoenzyme PB-4.	Phenobarbital	17-30	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	51-67
3739442-0	1986	Effect of phenobarbital on the contents of microsomal cytochrome P-450 and levels of glutathione (GSH) in the liver of various animal species.	Phenobarbital	10-23	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	54-70
3877725-2	1985	Fifteen peptides corresponding in sequence to segments of the major phenobarbital-inducible forms of rat hepatic cytochrome P-450 (termed P-450 PB-4 and P-450 PB-5) were chemically synthesized, conjugated to carrier proteins, and used to prepare site-specific rabbit and/or mouse antipeptide antibodies.	Phenobarbital	68-81	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	113-129
4074780-7	1985	Treatment of rabbit with phenobarbital, which induces the cytochrome P-450 isozyme specific to benzphetamine results in a 2-fold increase in the degree of coupling of NADPH and benzphetamine oxidation.	Phenobarbital	25-38	cytochrome P-450	Oryctolagus cuniculus	58-74
4064252-1	1985	The effect of the liver tumor promoter, phenobarbital, on the level of the asialoglycoprotein receptor (ASGP-R) was examined in adult rat liver.	Phenobarbital	40-53	mucin 4, cell surface associated	Rattus norvegicus	104-108
2866045-6	1985	An increase in ornithine decarboxylase activity, associated with a decrease in the liver S-adenosyl-L-methionine pool, also occurred in normal animals on the first day following a partial hepatectomy and was enhanced by phenobarbital.	Phenobarbital	220-233	ornithine decarboxylase 1	Rattus norvegicus	15-38
2866045-11	1985	Phenobarbital stimulated polyamine synthesis and cell growth and further prolonged the period of time during which a high ornithine decarboxylase activity and labeling index were present.	Phenobarbital	0-13	ornithine decarboxylase 1	Rattus norvegicus	122-145
4064252-8	1985	Treatment with a single dose of chemical carcinogen one day after birth combined with promotion by phenobarbital resulted in a significant reduction of ASGP-Rs in pre-neoplastic and neoplastic areas of livers.	Phenobarbital	99-112	mucin 4, cell surface associated	Rattus norvegicus	152-156
3904978-6	1985	Hepatocytes from a male F344 donor rat that had received a 70% hepatectomy and 30 mg of diethylnitrosamine per kg and had been maintained on 0.05% PB for 12 mo formed GGT-positive colonies and hepatocellular carcinomas in both male and female recipients.	Phenobarbital	147-149	gamma-glutamyltransferase 1	Rattus norvegicus	167-170
2998479-2	1985	The inducing effect exerted by phenobarbital on cytochrome P-450, delta-aminolevulinic acid synthase and ferrochelatase biosynthesis and cyclic AMP content in diabetic hepatic cells is markedly greater than that observed in normal hepatocytes.	Phenobarbital	31-44	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	48-64
2866268-6	1985	These levels were responsive to phenobarbital induction, although the induced levels in the GGT-positive cells were much lower than the induced levels in GGT-negative hepatocytes.	Phenobarbital	32-45	gamma-glutamyltransferase 1	Rattus norvegicus	92-95
2866268-6	1985	These levels were responsive to phenobarbital induction, although the induced levels in the GGT-positive cells were much lower than the induced levels in GGT-negative hepatocytes.	Phenobarbital	32-45	gamma-glutamyltransferase 1	Rattus norvegicus	154-157
2998479-2	1985	The inducing effect exerted by phenobarbital on cytochrome P-450, delta-aminolevulinic acid synthase and ferrochelatase biosynthesis and cyclic AMP content in diabetic hepatic cells is markedly greater than that observed in normal hepatocytes.	Phenobarbital	31-44	ferrochelatase	Rattus norvegicus	105-119
3933421-2	1985	In the present study, an array of 12 different monoclonal antibodies produced against cytochrome P-450b has been used to distinguish among these closely related phenobarbital-inducible rat hepatic cytochromes P-450.	Phenobarbital	161-174	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	86-103
2865013-5	1985	Results showed that immunohistochemical demonstration of GSTs A, B and C for detection of foci were only effective when the administration of 2-FAA, PB, BHA or BHT in the diet was discontinued, because these GSTs were induced in surrounding hepatocytes by these compounds in the diet.	Phenobarbital	149-151	glutathione S-transferase pi 1	Rattus norvegicus	57-61
4063404-0	1985	[Induction of cytochrome P-450 forms in liver microsomes of rats in the early neonatal period after administration of phenobarbital and 3-methylcholanthrene].	Phenobarbital	118-131	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	14-30
4063404-1	1985	The activity of cytochrome P-450 dependent monooxygenase system from rat liver microsomes after induction by phenobarbital and 3-methylcholantrene in early neonatal period (3-16 days after birth) was studied.	Phenobarbital	109-122	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	16-32
2865013-6	1985	gamma-GT was induced in periportal hepatocytes strongly by BHA and BHT and slightly by PB, and gamma-GT positive foci in periportal areas were not distinguishable from gamma-GT positive periportal hepatocytes.	Phenobarbital	87-89	gamma-glutamyltransferase 1	Rattus norvegicus	0-8
4063404-4	1985	Immunochemical analysis involving the use of antibodies specifically directed against cytochrome P-450 of adult rats revealed that the level of cytochrome P-450 in the case of 3-methylcholantrene induction increases from 5 to 50%, whereas that of cytochrome P-450 upon phenobarbital induction increases from 5 to 40% in liver microsomes of 3- and 16-day-old rats.	Phenobarbital	269-282	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	86-102
3002843-1	1985	EPR spectroscopy was used to study phenobarbital influence on the kinetics of paramagnetic complexes variability of metal proteins--cytochrome P-450 and iron-sulfur proteins of rat liver in acute oral poisoning with the dinitrophenol pesticides DNOK and dinoseb.	Phenobarbital	35-48	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	132-148
4063404-4	1985	Immunochemical analysis involving the use of antibodies specifically directed against cytochrome P-450 of adult rats revealed that the level of cytochrome P-450 in the case of 3-methylcholantrene induction increases from 5 to 50%, whereas that of cytochrome P-450 upon phenobarbital induction increases from 5 to 40% in liver microsomes of 3- and 16-day-old rats.	Phenobarbital	269-282	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	144-160
4063404-4	1985	Immunochemical analysis involving the use of antibodies specifically directed against cytochrome P-450 of adult rats revealed that the level of cytochrome P-450 in the case of 3-methylcholantrene induction increases from 5 to 50%, whereas that of cytochrome P-450 upon phenobarbital induction increases from 5 to 40% in liver microsomes of 3- and 16-day-old rats.	Phenobarbital	269-282	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	144-160
4063404-6	1985	The participation of phenobarbital-induced cytochrome P-450 in the metabolism of benzphetamine and aldrin in neonatal rats is much lower than in the adult ones.	Phenobarbital	21-34	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	43-59
4063404-8	1985	The age-dependent differences in inhibition of metabolism and the increase in the benz(a)pyrene hydroxylase activity in phenobarbital-induced rats suggest that the spectrum of inducible forms of cytochrome P-450 in neonatal rats differ from that in adult animals.	Phenobarbital	120-133	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	195-211
3930218-7	1985	Phenobarbital increased pituitary LH responses to LHRH, but did not alter the FSH responses.	Phenobarbital	0-13	gonadotropin releasing hormone 1	Rattus norvegicus	50-54
3002843-3	1985	It is discussed that phenobarbital may act both as an inducer of cytochrome P-450 and iron-sulfur proteins involved in electron transport of the mitochondria.	Phenobarbital	21-34	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	65-81
4069149-2	1985	Upon metabolic activation by liver microsomes from phenobarbital-treated rats or by isolated rat hepatocytes co-cultured with the V79 cells, hydroxyurea caused a concentration-dependent increase in the frequency of HGPRT-deficient mutants.	Phenobarbital	51-64	hypoxanthine-guanine phosphoribosyltransferase	Cricetulus griseus	215-220
4079340-1	1985	Radioactive methadone, phenytoin, phenobarbital, and diazepam were easily and efficiently removed from human urine samples by adsorption on C18 bonded silica phases.	Phenobarbital	34-47	Bardet-Biedl syndrome 9	Homo sapiens	140-143
3903473-3	1985	Its major trifluoroacetylated component was immunochemically identified as a phenobarbital-inducible form of cytochrome P-450 (54 kDa), whereas the other observed trifluoroacetylated protein fraction (59 kDa) was not identified.	Phenobarbital	77-90	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	109-125
3934534-6	1985	These data suggest that 3-MeO-AAB is a unique carcinogenic aromatic amine as a substrate for mutagenic activation via catalysis of those cytochrome P-450s that are induced by PB pretreatment.	Phenobarbital	175-177	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	137-153
4095132-1	1985	Caffeine is mainly metabolized by 3-methylcholanthrene-inducible cytochrome P-450 (P-450MC) and metamizol (noramidopyrine methanesulfonate sodium) is mainly metabolized by phenobarbital-inducible cytochrome P-450 (P-450PB).	Phenobarbital	172-185	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	76-81
4095131-2	1985	From the elimination velocity of these model substances conclusions concerning the activity of 3-methylcholanthrene inducible (caffeine elimination) and of phenobarbital inducible (metamizol elimination) isoenzymes of cytochrome P-450 are drawn.	Phenobarbital	156-169	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	218-234
2867151-3	1985	Fascioliasis provoked decreases in aminopyrine N-demethylase, aniline hydroxylase, the mutagenic activity of cyclophosphamide and cytochrome P-450 concentration in untreated or phenobarbitone or Arochlor pretreated rats.	Phenobarbital	177-191	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	130-146
3937306-0	1985	[Detection of cells resistant to the cytotoxic action of CCl4 in the hepatocyte populations of rats following a single exposure to 4-dimethylaminoazobenzene combined with subsequent injections of the tumor promoter phenobarbital].	Phenobarbital	215-228	C-C motif chemokine ligand 4	Rattus norvegicus	57-61
2413863-11	1985	Induction of cytochrome P-450 by phenobarbital (PB) and 3-methylcholanthrene (MC) under fed and fasted conditions was also investigated in male and female rats.	Phenobarbital	33-46	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
2413863-11	1985	Induction of cytochrome P-450 by phenobarbital (PB) and 3-methylcholanthrene (MC) under fed and fasted conditions was also investigated in male and female rats.	Phenobarbital	48-50	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
3000277-1	1985	We have recently isolated a cloned cDNA coding for a cytochrome P-450 of human liver microsomal membranes, which corresponds to a major phenobarbital-inducible cytochrome P-450 of rat liver.	Phenobarbital	136-149	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	53-69
3000277-1	1985	We have recently isolated a cloned cDNA coding for a cytochrome P-450 of human liver microsomal membranes, which corresponds to a major phenobarbital-inducible cytochrome P-450 of rat liver.	Phenobarbital	136-149	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	160-176
2862989-3	1985	In contrast the livers of rats fed an equimolar concentration of phenobarbital displayed increases in cytosolic glutathione transferase activities and enhancement of gamma-glutamyl transpeptidase activity but no changes in glutathione peroxidase activities.	Phenobarbital	65-78	gamma-glutamyltransferase 1	Rattus norvegicus	166-195
4043084-4	1985	This increase was much higher than that caused by phenobarbital, the only well known inducer of coumarin 7-hydroxylase.	Phenobarbital	50-63	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	96-118
4051505-3	1985	The phenobarbital-induced form (P-450b) was ineffective in NDMA metabolism but was active in catalyzing the demethylation of N-nitrosomethylaniline, with an estimated Km of 0.08 mM and a Vmax of 7.2 nmol min-1 nmol-1.	Phenobarbital	4-17	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	32-38
2865001-0	1985	Promoting effects of phenobarbital and 3"-methyl-4-dimethylaminoazobenzene on the appearance of gamma-glutamyltranspeptidase positive foci in rat liver pretreated with varying doses of diethylnitrosamine.	Phenobarbital	21-34	gamma-glutamyltransferase 1	Rattus norvegicus	96-124
3001883-2	1985	This was seen here as increased aryl hydrocarbon hydroxylase (AHH) activity after therapy with MPA or PB in rats with a chemical liver injury, produced by dimethylnitrosamine (DMN).	Phenobarbital	102-104	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	32-60
3001883-2	1985	This was seen here as increased aryl hydrocarbon hydroxylase (AHH) activity after therapy with MPA or PB in rats with a chemical liver injury, produced by dimethylnitrosamine (DMN).	Phenobarbital	102-104	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	62-65
4074718-0	1985	Characterization of testosterone 16 alpha-hydroxylase (I-P-450(16) alpha) induced by phenobarbital in mice.	Phenobarbital	85-98	cytochrome P450, family 2, subfamily d, polypeptide 10	Mus musculus	20-53
4074718-1	1985	Cytochrome P-450 (I-P-450(16) alpha), which is associated with phenobarbital-induced testosterone 16 alpha-hydroxylation activity, was purified from livers of phenobarbital-treated female 129/J mice on the basis of the specific hydroxylation activity in fractions eluted from columns of octylamino-Sepharose 4B, hydroxylapatite, DEAE-Bio-Gel A, and isobutyl-Sepharose 4B.	Phenobarbital	63-76	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	0-35
4074718-1	1985	Cytochrome P-450 (I-P-450(16) alpha), which is associated with phenobarbital-induced testosterone 16 alpha-hydroxylation activity, was purified from livers of phenobarbital-treated female 129/J mice on the basis of the specific hydroxylation activity in fractions eluted from columns of octylamino-Sepharose 4B, hydroxylapatite, DEAE-Bio-Gel A, and isobutyl-Sepharose 4B.	Phenobarbital	159-172	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	0-35
3840372-1	1985	Mechanistic mode for the oxygenation of sulfides with the pig liver microsomal FAD-containing monooxygenase(EC 1.14.13.8) has been conveniently distinguished from that with the phenobarbital induced liver microsomal cytochrome P-450 by analyzing products of the oxygenation of phenacyl phenyl sulfide.	Phenobarbital	177-190	cytochrome P450 family 2 subfamily D member 6	Sus scrofa	216-232
3896900-1	1985	The reduction in blood glucose in non-insulin-dependent diabetes mellitus (NIDDM) brought about by the use of phenobarbital (PB), a hepatic microsomal enzyme inducer, suggests an improvement in insulin sensitivity.	Phenobarbital	110-123	insulin	Homo sapiens	38-45
2936317-6	1985	When the S-9 fraction was prepared from mice pretreated with phenobarbital, the inhibitory potency was not different from that of the control.	Phenobarbital	61-74	proteasome (prosome, macropain) 26S subunit, non-ATPase, 11	Mus musculus	9-12
2863006-5	1985	Rats receiving PB had significantly increased numbers and volumes of eosinophilic and GGT-positive FHPL while the numbers and volumes of the common basophilic FHPL seen in controls were not affected by PB exposure.	Phenobarbital	15-17	gamma-glutamyltransferase 1	Rattus norvegicus	86-89
2863006-7	1985	An uncommon GGT-positive FHPL found in control rats was detected in zone 1 of the hepatic acinus, a similar location of the GGT-positive eosinophilic FHPL seen in PB-exposed rats, while the common basophilic FHPL was observed in zones 1-3.	Phenobarbital	163-165	gamma-glutamyltransferase 1	Rattus norvegicus	12-15
2863006-7	1985	An uncommon GGT-positive FHPL found in control rats was detected in zone 1 of the hepatic acinus, a similar location of the GGT-positive eosinophilic FHPL seen in PB-exposed rats, while the common basophilic FHPL was observed in zones 1-3.	Phenobarbital	163-165	gamma-glutamyltransferase 1	Rattus norvegicus	124-127
2863006-8	1985	These findings suggest that PB does not promote the growth or development of the common naturally occurring basophilic FHPL but either promotes the uncommon GGT-positive FHPL or induces new FHPL de novo.	Phenobarbital	28-30	gamma-glutamyltransferase 1	Rattus norvegicus	157-160
2863007-4	1985	The use of three markers in the present study confirmed the findings of our earlier study, which showed the maximal response of GGT+ AHF to PB administration following PH/DEN initiation and the stability of GGT+/AHF induced by the PH/DEN/PB regimen after the withdrawal of PB.	Phenobarbital	140-142	gamma-glutamyltransferase 1	Rattus norvegicus	128-131
4037796-2	1985	Utilizing this new extinction coefficient, the increased cytochrome P-450 present after phenobarbital induction was almost exclusively that which is able to both bind to metyrapone and form a metabolic-intermediate complex from norbenzphetamine.	Phenobarbital	88-101	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	57-73
4037796-4	1985	Thus, neither technique alone can be used to quantitate the "phenobarbital-induced form" of cytochrome P-450.	Phenobarbital	61-74	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	92-108
4041913-0	1985	Early phenobarbital-induced alterations in hippocampal acetylcholinesterase activity and behavior.	Phenobarbital	6-19	acetylcholinesterase	Mus musculus	55-75
3896900-1	1985	The reduction in blood glucose in non-insulin-dependent diabetes mellitus (NIDDM) brought about by the use of phenobarbital (PB), a hepatic microsomal enzyme inducer, suggests an improvement in insulin sensitivity.	Phenobarbital	125-127	insulin	Homo sapiens	38-45
3896900-3	1985	The addition of PB to sulfonylurea therapy, concurrently for 6 wk, reduced fasting blood glucose (BG, from 12.8 +/- 1.6 to 10.2 +/- 3.2 mmol/L, P less than 0.01) and immunoreactive insulin (IRI) levels (from 32.4 +/- 13.6 to 24.7 +/- 9.8 mU/L, P less than 0.01), whereas body weight remained unaltered.	Phenobarbital	16-18	insulin	Homo sapiens	181-188
4045338-11	1985	injection of diethyldithiocarbamate, a noradrenaline synthesis inhibitor, or phenobarbitone was effective in raising blood oxytocin levels only in rats older than 10 and 20 days of age respectively.	Phenobarbital	77-91	oxytocin/neurophysin I prepropeptide	Homo sapiens	123-131
4065181-2	1985	Metabolic activation by cytochrome P-450 was found to play a role in the covalent binding of VP 16-213 to rat liver microsomal proteins, as shown by the need of NADPH cofactor, the increased binding after phenobarbital pretreatment and the inhibition by SFK-525A.	Phenobarbital	205-218	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	24-40
4033629-4	1985	P-450PB-C, an isozyme which is present in significant amounts in untreated rats and which is induced approximately 2-fold by phenobarbital, was the most susceptible cytochrome P-450 to inhibition by chloramphenicol both in vivo and in vitro.	Phenobarbital	125-138	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	165-181
4026325-4	1985	In contrast, phospholipid caused only a minor change in the strength of cimetidine binding by the predominant liver cytochrome P-450 from phenobarbitone-pretreated rats.	Phenobarbital	138-152	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	116-132
3937330-2	1985	After administration of phenobarbital into the neonatal rats content of cytochrome P-450 and activity of NADPH-cytochrome c reductase were increased in liver microsomes.	Phenobarbital	24-37	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	72-88
3937330-4	1985	Immunochemical studies with antibodies towards some forms of cytochrome P-450 showed that enzymatic forms of cytochrome P-450 PB were induced; this enzymatic form is predominant in adult animals treated with phenobarbital.	Phenobarbital	208-221	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	61-77
3937330-4	1985	Immunochemical studies with antibodies towards some forms of cytochrome P-450 showed that enzymatic forms of cytochrome P-450 PB were induced; this enzymatic form is predominant in adult animals treated with phenobarbital.	Phenobarbital	208-221	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	109-125
2990571-0	1985	Effect of glucose on induction of delta-aminolevulinic acid synthase, ferrochelatase and cytochrome P-450 hemoproteins in isolated rat hepatocytes by phenobarbital and lead.	Phenobarbital	150-163	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	89-105
2990571-1	1985	In the present work we have been able to demonstrate that phenobarbital and lead exert an inducing effect on the biosynthesis of delta-aminolevulinic acid synthase, ferrochelatase and cytochrome P-450 hemoproteins in isolated rat hepatocytes of normal adult rats.	Phenobarbital	58-71	ferrochelatase	Rattus norvegicus	165-179
2990571-1	1985	In the present work we have been able to demonstrate that phenobarbital and lead exert an inducing effect on the biosynthesis of delta-aminolevulinic acid synthase, ferrochelatase and cytochrome P-450 hemoproteins in isolated rat hepatocytes of normal adult rats.	Phenobarbital	58-71	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	184-200
3928374-2	1985	We have studied the induction of cytochrome P-450b,e-type antigen and mRNA by phenobarbital, 4,4"-dichlorobiphenyl and 2,4,5,2",4",5"-hexachlorobiphenyl in male Wistar rat liver.	Phenobarbital	78-91	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	33-50
3928374-4	1985	Treatment of rats with phenobarbital or 2,4,5,2",4",5"-hexachlorobiphenyl results in a faster and more pronounced increase of cytochrome P-450b,e-type antigen and mRNA levels.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	126-143
3928374-5	1985	Analysis of clones from cDNA banks showed that two types of sequences are induced by phenobarbital corresponding to cytochrome P-450b and cytochrome P-450e respectively.	Phenobarbital	85-98	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	116-133
3928374-5	1985	Analysis of clones from cDNA banks showed that two types of sequences are induced by phenobarbital corresponding to cytochrome P-450b and cytochrome P-450e respectively.	Phenobarbital	85-98	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	138-155
3935002-1	1985	A simple and sensitive assay has been developed that is capable of detecting as little as 0.2 ng of the major isozyme of cytochrome P-450 (P-450b) isolated from the livers of phenobarbital-induced rats.	Phenobarbital	175-188	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	121-137
3935002-1	1985	A simple and sensitive assay has been developed that is capable of detecting as little as 0.2 ng of the major isozyme of cytochrome P-450 (P-450b) isolated from the livers of phenobarbital-induced rats.	Phenobarbital	175-188	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	139-145
2411220-0	1985	Transcriptional regulation of rat liver glutathione S-transferase genes by phenobarbital and 3-methylcholanthrene.	Phenobarbital	75-88	hematopoietic prostaglandin D synthase	Rattus norvegicus	40-65
3924914-0	1985	On the mechanism of the inactivation of the major phenobarbital-inducible isozyme of rat liver cytochrome P-450 by chloramphenicol.	Phenobarbital	50-63	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	95-111
2864416-0	1985	Effects of saikosaponin-d on enhanced CCl4-hepatotoxicity by phenobarbitone.	Phenobarbital	61-75	C-C motif chemokine ligand 4	Rattus norvegicus	38-42
3930452-3	1985	The interaction was enhanced by pretreatment in vivo with phenobarbitone but was suppressed by addition of 2-diethylaminoethyl-2,2-diphenylvalerate HC1 in vitro.	Phenobarbital	58-72	Hypercalciuria QTL 1	Rattus norvegicus	148-151
2991008-1	1985	The phenobarbital-inducible form of cytochrome P-450 purified from rabbit liver microsomes is phosphorylated by cAMP-dependent protein kinase at a single site, the serine residue in position 128 of the amino acid sequence.	Phenobarbital	4-17	cytochrome P-450	Oryctolagus cuniculus	36-52
2991008-2	1985	The serine is located in a characteristic recognition sequence for cAMP-dependent protein kinase and is part of a primary structure which is conserved during evolution, present also in phenobarbital-inducible rat cytochrome and cytochrome P-450 CAM from Pseudomonas putida.	Phenobarbital	185-198	cytochrome P-450	Oryctolagus cuniculus	228-244
2996591-4	1985	The majority of the microsomal oxidation was inhibited by an antibody raised against the major isozyme of cytochrome P-450 purified from livers of phenobarbital-pretreated rats.	Phenobarbital	147-160	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	106-122
3924914-1	1985	The mechanism of the inactivation of the major phenobarbital-inducible isozyme of rat liver cytochrome P-450 (P-450 PB-B2) by chloramphenicol has been investigated.	Phenobarbital	47-60	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	92-108
4015689-0	1985	Induction of cytochrome P-450 by phenobarbital is mediated at the level of transcription.	Phenobarbital	33-46	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
2989270-0	1985	Gene structure of a major form of phenobarbital-inducible cytochrome P-450 in rat liver.	Phenobarbital	34-47	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	58-74
4015689-1	1985	We have previously shown that the 43-fold induction by phenobarbital of the major phenobarbital-inducible cytochrome P-450 of rat liver microsomal membranes (PB P-450) is mediated by a 20-fold increase in the amount of its mRNA in the cytoplasm.	Phenobarbital	55-68	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	106-122
4015689-1	1985	We have previously shown that the 43-fold induction by phenobarbital of the major phenobarbital-inducible cytochrome P-450 of rat liver microsomal membranes (PB P-450) is mediated by a 20-fold increase in the amount of its mRNA in the cytoplasm.	Phenobarbital	82-95	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	106-122
2989270-1	1985	The gene structure of cytochrome P-450b, a major form of phenobarbital-inducible cytochrome P-450 in rat livers was elucidated by sequence analysis of the cloned genomic DNAs and was compared with the previously determined gene structures of cytochrome P-450e, a minor form of phenobarbital-inducible cytochrome P-450 and two forms of 3-methylcholanthrene-inducible cytochrome P-450 (P-450c and -d).	Phenobarbital	57-70	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	22-39
2989270-1	1985	The gene structure of cytochrome P-450b, a major form of phenobarbital-inducible cytochrome P-450 in rat livers was elucidated by sequence analysis of the cloned genomic DNAs and was compared with the previously determined gene structures of cytochrome P-450e, a minor form of phenobarbital-inducible cytochrome P-450 and two forms of 3-methylcholanthrene-inducible cytochrome P-450 (P-450c and -d).	Phenobarbital	57-70	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	22-38
2989270-9	1985	The nucleotide sequences in all 9 exons and their flanking regions in introns show very close homology between the two phenobarbital-inducible cytochrome P-450 genes.	Phenobarbital	119-132	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	143-159
2989270-18	1985	The close sequence homology between the two phenobarbital-inducible cytochrome P-450 genes is also found to extend to the promoter region with one notable exception.	Phenobarbital	44-57	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	68-84
2989270-19	1985	The simple repeated sequences of (CA)n which is present at -254 position in cytochrome P-450e gene is also observed at the equivalent position in cytochrome P-450b gene, but the repetitiveness is greatly reduced in cytochrome P-450b gene ((CA)5 for P-450b versus (CA)19 for P-450e), and this may somehow be related to the difference in the level of cytochrome P-450b and P-450e in the inductive phase of phenobarbital administration.	Phenobarbital	404-417	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	76-93
2989270-19	1985	The simple repeated sequences of (CA)n which is present at -254 position in cytochrome P-450e gene is also observed at the equivalent position in cytochrome P-450b gene, but the repetitiveness is greatly reduced in cytochrome P-450b gene ((CA)5 for P-450b versus (CA)19 for P-450e), and this may somehow be related to the difference in the level of cytochrome P-450b and P-450e in the inductive phase of phenobarbital administration.	Phenobarbital	404-417	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	146-163
2989270-19	1985	The simple repeated sequences of (CA)n which is present at -254 position in cytochrome P-450e gene is also observed at the equivalent position in cytochrome P-450b gene, but the repetitiveness is greatly reduced in cytochrome P-450b gene ((CA)5 for P-450b versus (CA)19 for P-450e), and this may somehow be related to the difference in the level of cytochrome P-450b and P-450e in the inductive phase of phenobarbital administration.	Phenobarbital	404-417	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	215-232
4041439-0	1985	Effects of detergent on substrate binding and spin state of purified liver microsomal cytochrome P-450LM2 from phenobarbital-treated rabbits.	Phenobarbital	111-124	cytochrome P450 2B4	Oryctolagus cuniculus	86-105
2989270-19	1985	The simple repeated sequences of (CA)n which is present at -254 position in cytochrome P-450e gene is also observed at the equivalent position in cytochrome P-450b gene, but the repetitiveness is greatly reduced in cytochrome P-450b gene ((CA)5 for P-450b versus (CA)19 for P-450e), and this may somehow be related to the difference in the level of cytochrome P-450b and P-450e in the inductive phase of phenobarbital administration.	Phenobarbital	404-417	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	157-163
4041439-1	1985	Spectral changes accompanying the binding of the nonionic detergent n-octyl beta-D-glucopyranoside (n-octyl glucoside) to cytochrome P-450LM2 purified from liver microsomes of phenobarbital-treated rabbits have been compared to changes in catalytic activity obtained in a reconstituted system consisting of various levels of detergent, P-450LM2, and NADPH-cytochrome P-450 reductase.	Phenobarbital	176-189	cytochrome P450 2B4	Oryctolagus cuniculus	122-141
4041439-1	1985	Spectral changes accompanying the binding of the nonionic detergent n-octyl beta-D-glucopyranoside (n-octyl glucoside) to cytochrome P-450LM2 purified from liver microsomes of phenobarbital-treated rabbits have been compared to changes in catalytic activity obtained in a reconstituted system consisting of various levels of detergent, P-450LM2, and NADPH-cytochrome P-450 reductase.	Phenobarbital	176-189	cytochrome P450 2B4	Oryctolagus cuniculus	133-141
2989270-19	1985	The simple repeated sequences of (CA)n which is present at -254 position in cytochrome P-450e gene is also observed at the equivalent position in cytochrome P-450b gene, but the repetitiveness is greatly reduced in cytochrome P-450b gene ((CA)5 for P-450b versus (CA)19 for P-450e), and this may somehow be related to the difference in the level of cytochrome P-450b and P-450e in the inductive phase of phenobarbital administration.	Phenobarbital	404-417	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	215-232
3925953-8	1985	In guinea pigs, we confirmed that phenobarbital selectively increased the activities of UDPGT towards twenty monoterpenoid alcohols without affecting other typical phenobarbital-induced activities such as those for conjugation of morphine.	Phenobarbital	34-47	beta-1,3-glucuronyltransferase 2	Rattus norvegicus	88-93
2864416-2	1985	Saikosaponin-d showed protection against the CCl4-hepatotoxicity enhanced by phenobarbitone.	Phenobarbital	77-91	C-C motif chemokine ligand 4	Rattus norvegicus	45-49
4038266-0	1985	Turnover of messenger RNA, apoprotein and haem of cytochrome P-450b + e induced by phenobarbitone in rat liver.	Phenobarbital	83-97	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	50-67
2864416-4	1985	The rate of microsomal lipid peroxidation by NADPH and CCl4 was significantly lowered in-vitro in rats pretreated with phenobarbitone and saikosaponin-d compared with those pretreated with phenobarbitone alone.	Phenobarbital	119-133	C-C motif chemokine ligand 4	Rattus norvegicus	55-59
4015676-1	1985	Immunochemical evidence with antibody against phenobarbital-inducible cytochrome P-450.	Phenobarbital	46-59	cytochrome P450 3A14	Cavia porcellus	70-86
4015676-3	1985	PB-inducible cytochrome P-450 (PB-P-450) was purified to homogeneity from liver microsomes of PB-treated guinea pigs.	Phenobarbital	0-2	cytochrome P450 3A14	Cavia porcellus	13-29
4015676-3	1985	PB-inducible cytochrome P-450 (PB-P-450) was purified to homogeneity from liver microsomes of PB-treated guinea pigs.	Phenobarbital	31-33	cytochrome P450 3A14	Cavia porcellus	13-29
4038266-1	1985	A single injection of phenobarbitone elicits asynchronous behaviour in the pattern of induction of mRNA, apoprotein and haem of cytochrome P-450b + e. The mRNA content reaches a maximum around 16h, the apoprotein content reaches a maximum around 30-36h, and the holoprotein content shows biphasic behaviour, with maxima around 16h and 30-36h.	Phenobarbital	22-36	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	128-145
2863157-9	1985	PB treatment decreased efficiently the falling rate of total cytochrome P-450 content, but did not induce P-450PB, which is the specific form of cytochrome P-450 induced by PB, in primary cultured hepatocytes.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	61-77
2863118-7	1985	Debrisoquine 4-hydroxylase activity was inducible by both 3-methylcholanthrene and phenobarbital in DA and Fischer rats.	Phenobarbital	83-96	cytochrome P450, family 2, subfamily d, polypeptide 2	Rattus norvegicus	0-26
4005852-9	1985	Pretreatment of rats with enzyme inducers (phenobarbital and 3-methylcholanthrene) stimulated the activity of DT-diaphorase in liver cytosolic fractions.	Phenobarbital	43-56	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	110-123
4017102-1	1985	Heteroassociation of O- and N-isopropyl derivatives of barbital and phenobarbital with 9-ethyladenine (9-EA) in CCl4 solutions were studied by infrared spectroscopy.	Phenobarbital	68-81	C-C motif chemokine ligand 4	Homo sapiens	112-116
4015658-1	1985	Cytochrome P-450 was isolated from liver microsomes of phenobarbital treated rats by an essentially single step immunopurification with a monoclonal antibody (MAb).	Phenobarbital	55-68	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
4015658-2	1985	The amino terminal sequence of the isolated cytochrome P-450 displayed a microheterogeneity of isozymes related to previously identified phenobarbital induced forms, indicating that each of these isozymes possess the MAb-specific epitope.	Phenobarbital	137-150	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	44-60
4015648-1	1985	1-Ethynylpyrene, trans-, & cis-1-(2-bromovinyl)pyrene, methyl 1-pyrenyl acetylene, and phenyl 1-pyrenyl acetylene are substrates for cytochrome P-450 dependent monooxygenases and also inhibitors of cytochrome P-450 dependent benzo[a]pyrene hydroxylase activities in liver microsomes from 5,6-benzoflavone or phenobarbital pretreated rats.	Phenobarbital	312-325	cytokine inducible SH2-containing protein	Rattus norvegicus	31-36
4015648-3	1985	Incubation with NADPH and 1-ethynylpyrene, trans-, or cis-1-(2-bromovinyl)pyrene causes a loss of the P-450 content in the microsomes from 5,6-benzoflavone or phenobarbital pretreated rats, but incubations with methyl 1-pyrenyl acetylene or phenyl 1-pyrenyl acetylene did not cause a loss of the P-450 content of either microsomal preparation.	Phenobarbital	159-172	cytokine inducible SH2-containing protein	Rattus norvegicus	54-59
3988762-5	1985	The constitutive form is only 46% homologous to the phenobarbital-induced cytochrome P-450 (Heinemann, F. S., and Ozols, J.	Phenobarbital	52-65	cytochrome P-450	Oryctolagus cuniculus	74-90
3922304-9	1985	They are also inhibited to varying degrees by aldose reductase inhibitors such as sorbinil, alrestatin, quercetrin, tetramethylene glutaric acid, and sodium phenobarbital.	Phenobarbital	150-170	aldo-keto reductase family 1 member B	Homo sapiens	46-62
4021556-3	1985	Continuous hexachlorobenzene administration with, or without, phenobarbitone pretreatment has different effects on the deactivation/activation kinetics of porphyrinogen carboxylase, delta-aminolaevulinate synthase and delta-aminolaevulinate dehydratase.	Phenobarbital	62-76	uroporphyrinogen decarboxylase	Rattus norvegicus	155-180
3994378-3	1985	The maintenance studies have been expanded to demonstrate the in vitro induction of cytochrome P-450 by phenobarbital treatment.	Phenobarbital	104-117	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	84-100
3994759-6	1985	In both untreated and phenobarbital-treated animals, cytochrome P-450 content and 7-ethoxycoumarin O-deethylase activity rose significantly from fraction 1 to fraction 5.	Phenobarbital	22-35	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	53-69
3994759-9	1985	The cytochrome P-450 content in phenobarbital-plus-allylisopropylacetamide-treated animals was decreased in all fractions but more extensively in fraction 5 than in fraction 1.	Phenobarbital	32-45	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	4-20
3986141-3	1985	The dechlorination of haloethanes catalysed by a vesicular reconstituted system of cytochrome P-450 enzymes from rabbit liver was also studied and found to be similar to that catalysed by microsomes: both reductase and a phenobarbital inducible form of cytochrome P-450 were essential.	Phenobarbital	221-234	cytochrome P-450	Oryctolagus cuniculus	83-99
3994764-9	1985	In vitro treatment of hepatocytes with trans-stilbene oxide and phenobarbital increased microsomal epoxide hydrolase, while this activity was refractory to 2-acetylaminofluorene treatment.	Phenobarbital	64-77	epoxide hydrolase 1	Rattus norvegicus	88-116
4036165-1	1985	A series of eight 4-n-alkoxymethylenedioxybenzene (AMDB) derivatives were evaluated for their inhibitory effects on several mono-oxygenase reactions and their capacity to form metabolite complexes with cytochrome P-450 in vitro in hepatic microsomes from phenobarbital (PB)-and Beta-naphthoflavone (Beta NF)-induced rats.	Phenobarbital	255-268	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	202-218
2861996-4	1985	The administration of the inducers, phenobarbital or the polychlorinated biphenyl mixture Aroclor 1254, resulted in significant increases in cytochrome P-450 and ethylmorphine N-demethylase activity and minimal changes in benzo(a)pyrene hydroxylase activity in both strains.	Phenobarbital	36-49	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	141-157
2861996-9	1985	The latter strain appeared to be more responsive to the inducing properties of the phenobarbital class of inducers, as reflected in the inducibility of cytochrome P-450 and the associated enzymic activities in the liver.	Phenobarbital	83-96	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	152-168
3888809-8	1985	When specific isozymes of cytochrome P-450 were induced with phenobarbital or 3-methylcholanthrene, the constitutive cytochrome P-450 was localized predominantly in the periportal region.	Phenobarbital	61-74	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	26-42
3888809-8	1985	When specific isozymes of cytochrome P-450 were induced with phenobarbital or 3-methylcholanthrene, the constitutive cytochrome P-450 was localized predominantly in the periportal region.	Phenobarbital	61-74	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	117-133
4036165-1	1985	A series of eight 4-n-alkoxymethylenedioxybenzene (AMDB) derivatives were evaluated for their inhibitory effects on several mono-oxygenase reactions and their capacity to form metabolite complexes with cytochrome P-450 in vitro in hepatic microsomes from phenobarbital (PB)-and Beta-naphthoflavone (Beta NF)-induced rats.	Phenobarbital	270-272	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	202-218
3921402-5	1985	However, phenobarbital-inducible proteins were identified on "Western blots" using antibodies to a rat liver phenobarbital inducible P-450 form.	Phenobarbital	9-22	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	133-138
2985574-5	1985	The similarity of the gene organization between cytochrome P-450d and P-450c as well as their homology in the deduced amino acid and the nucleotide sequences suggests that these two genes of MC-inducible cytochromes P-450 constitute a different subfamily than those of the phenobarbital-inducible one in the cytochrome P-450 gene family.	Phenobarbital	273-286	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	59-64
2985574-5	1985	The similarity of the gene organization between cytochrome P-450d and P-450c as well as their homology in the deduced amino acid and the nucleotide sequences suggests that these two genes of MC-inducible cytochromes P-450 constitute a different subfamily than those of the phenobarbital-inducible one in the cytochrome P-450 gene family.	Phenobarbital	273-286	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	70-75
3921402-5	1985	However, phenobarbital-inducible proteins were identified on "Western blots" using antibodies to a rat liver phenobarbital inducible P-450 form.	Phenobarbital	109-122	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	133-138
3921029-2	1985	The ability of phenobarbital (PB) to neonatally "imprint" or "program" the hepatic microsomal cytochrome P-450-dependent monooxygenase system (MOS) was investigated.	Phenobarbital	15-28	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	94-110
3985997-12	1985	These results suggest the following: NDMA demethylation is catalyzed by PB-induced cytochrome P-450 species (P450-PB) and MC-induced cytochrome P-450 species (P448-MC).	Phenobarbital	72-74	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	83-99
3985997-12	1985	These results suggest the following: NDMA demethylation is catalyzed by PB-induced cytochrome P-450 species (P450-PB) and MC-induced cytochrome P-450 species (P448-MC).	Phenobarbital	114-116	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	83-99
3986002-0	1985	Altered induction response of hepatic cytochrome P-450 to phenobarbital, 3-methylcholanthrene, and beta-naphthoflavone in organotin-treated animals.	Phenobarbital	58-71	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	38-54
3986002-1	1985	The effects of tricyclohexyltin hydroxide on the induction of cytochrome P-450 in liver by phenobarbital, 3-methylcholanthrene and beta-naphthoflavone were studied.	Phenobarbital	91-104	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	62-78
3986002-2	1985	A single dose of the organotin (15 mg/kg body wt) prevented the full extent of phenobarbital induction of cytochrome P-450 from occurring; this was the case whether tricyclohexyltin was given 48 hr preceeding a single injection of phenobarbital, or administered simultaneously with the first of three daily doses of the drug.	Phenobarbital	79-92	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	106-122
3986002-6	1985	The electrophoretic profiles illustrate clearly that the apoprotein moieties of the various cytochrome P-450 subspecies are affected to a considerable extent by treatment with tricyclohexyltin hydroxide alone, and staining in these bands was noticeably reduced even when phenobarbital was administered together with the organotin.	Phenobarbital	271-284	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	92-108
3994685-1	1985	Administration of allylisopropylacetamide (AIA) to phenobarbital-pretreated rats results in the destruction of several phenobarbital-inducible cytochrome P-450 isoenzymes and a correspondingly marked loss of benzphetamine N-demethylase and ethylmorphine N-demethylase activities.	Phenobarbital	51-64	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	143-159
3921270-2	1985	The enzymes investigated were two phenobarbital-inducible cytochrome P-450 (cyt.	Phenobarbital	34-47	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	58-74
3988004-1	1985	The real-time interactions of 1,1,1-trichloroethane (TCE) and 1,1,2-TCE with cytochrome P-450 were observed using in vivo optical methods to measure the spectral changes of cytochrome P-450 and the reduction-oxidation transition of pyridine nucleotides in the perfused liver of rats treated with phenobarbital.	Phenobarbital	296-309	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	77-93
3992601-4	1985	Acute toxicity of OCT A was reduced by simultaneous administration of phenylalanine or by pretreatment with phenobarbital (PB) for 1 week and the LD50 increased to 1.5-2.0 times control.	Phenobarbital	108-121	plexin A2	Mus musculus	18-21
3992601-4	1985	Acute toxicity of OCT A was reduced by simultaneous administration of phenylalanine or by pretreatment with phenobarbital (PB) for 1 week and the LD50 increased to 1.5-2.0 times control.	Phenobarbital	123-125	plexin A2	Mus musculus	18-21
3992601-5	1985	Chromatographic analyses of OCT A and the metabolite, OCT alpha, extracted from urine and bile after administration of OCT A, indicated that amounts of OCT A and OCT alpha decreased in the urine and increased in the bile of PB-pretreated mice, suggesting that a change in metabolism of OCT A could cause the decrease in the toxicity of OCT A in PB-pretreated mice.	Phenobarbital	224-226	plexin A2	Mus musculus	54-57
3992601-5	1985	Chromatographic analyses of OCT A and the metabolite, OCT alpha, extracted from urine and bile after administration of OCT A, indicated that amounts of OCT A and OCT alpha decreased in the urine and increased in the bile of PB-pretreated mice, suggesting that a change in metabolism of OCT A could cause the decrease in the toxicity of OCT A in PB-pretreated mice.	Phenobarbital	224-226	plexin A2	Mus musculus	54-57
3992601-5	1985	Chromatographic analyses of OCT A and the metabolite, OCT alpha, extracted from urine and bile after administration of OCT A, indicated that amounts of OCT A and OCT alpha decreased in the urine and increased in the bile of PB-pretreated mice, suggesting that a change in metabolism of OCT A could cause the decrease in the toxicity of OCT A in PB-pretreated mice.	Phenobarbital	224-226	plexin A2	Mus musculus	54-57
3992601-5	1985	Chromatographic analyses of OCT A and the metabolite, OCT alpha, extracted from urine and bile after administration of OCT A, indicated that amounts of OCT A and OCT alpha decreased in the urine and increased in the bile of PB-pretreated mice, suggesting that a change in metabolism of OCT A could cause the decrease in the toxicity of OCT A in PB-pretreated mice.	Phenobarbital	224-226	plexin A2	Mus musculus	54-57
3992601-5	1985	Chromatographic analyses of OCT A and the metabolite, OCT alpha, extracted from urine and bile after administration of OCT A, indicated that amounts of OCT A and OCT alpha decreased in the urine and increased in the bile of PB-pretreated mice, suggesting that a change in metabolism of OCT A could cause the decrease in the toxicity of OCT A in PB-pretreated mice.	Phenobarbital	224-226	plexin A2	Mus musculus	54-57
3992601-5	1985	Chromatographic analyses of OCT A and the metabolite, OCT alpha, extracted from urine and bile after administration of OCT A, indicated that amounts of OCT A and OCT alpha decreased in the urine and increased in the bile of PB-pretreated mice, suggesting that a change in metabolism of OCT A could cause the decrease in the toxicity of OCT A in PB-pretreated mice.	Phenobarbital	224-226	plexin A2	Mus musculus	54-57
4024668-1	1985	The formation of ligand complexes between hepatic microsomal cytochrome P-450 and safrole, isosafrole and other methylenedioxyphenyl compounds was studied in vivo and in vitro in rats pretreated with either phenobarbital or 3-methylcholanthrene.	Phenobarbital	207-220	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	61-77
4024668-2	1985	Both the phenobarbital-induced cytochrome P-450 and the 3-methylcholanthrene-induced cytochrome P-448 metabolically convert safrole, isosafrole, and those metabolites possessing an intact methylenedioxy group, to reactive metabolites which then interact with the cytochromes to form ligand complexes.	Phenobarbital	9-22	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	31-101
2994255-1	1985	The in vitro metabolism of polybrominated biphenyl (PBB) congeners by cytochrome P-450-dependent monooxygenases was investigated using hepatic microsomes isolated from immature male rats pretreated with 3-methylcholanthrene (MC) or phenobarbital (PB).	Phenobarbital	232-245	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	70-86
2994255-1	1985	The in vitro metabolism of polybrominated biphenyl (PBB) congeners by cytochrome P-450-dependent monooxygenases was investigated using hepatic microsomes isolated from immature male rats pretreated with 3-methylcholanthrene (MC) or phenobarbital (PB).	Phenobarbital	52-54	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	70-86
3972824-0	1985	Phenobarbital induction of rat liver cytochromes P-450b and P-450e.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	49-55
3972824-2	1985	Cytochromes P-450b and P-450e are extremely homologous and immunochemically indistinguishable proteins that are coordinately induced by phenobarbital in rat liver.	Phenobarbital	136-149	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	12-18
3972824-4	1985	Our data demonstrate that phenobarbital administration to rats resulted in marked increases in levels of hepatic mRNA for both cytochrome P-450b and cytochrome P-450e, with a 4- to 5-fold greater accumulation of P-450b mRNA vis a vis P-450e mRNA.	Phenobarbital	26-39	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	127-144
3972824-4	1985	Our data demonstrate that phenobarbital administration to rats resulted in marked increases in levels of hepatic mRNA for both cytochrome P-450b and cytochrome P-450e, with a 4- to 5-fold greater accumulation of P-450b mRNA vis a vis P-450e mRNA.	Phenobarbital	26-39	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	149-166
3972824-4	1985	Our data demonstrate that phenobarbital administration to rats resulted in marked increases in levels of hepatic mRNA for both cytochrome P-450b and cytochrome P-450e, with a 4- to 5-fold greater accumulation of P-450b mRNA vis a vis P-450e mRNA.	Phenobarbital	26-39	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	138-144
3972824-5	1985	The level of hepatic mRNA increased from less than 3 molecules/cell of each mRNA in untreated rats, to 630 and 130 molecules/cell for P-450b and P-450e, respectively, in phenobarbital-treated rats.	Phenobarbital	170-183	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	134-140
4035663-3	1985	Induction of hepatic cytochrome P-450 following 2,5-hexanedione and SKF 525-A pretreatment of animals showed an induction pattern in the five-fraction "handprint" similar to that produced by phenobarbital.	Phenobarbital	191-204	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	21-37
3921029-2	1985	The ability of phenobarbital (PB) to neonatally "imprint" or "program" the hepatic microsomal cytochrome P-450-dependent monooxygenase system (MOS) was investigated.	Phenobarbital	30-32	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	94-110
3921029-7	1985	However, at 140 days of age rats of both sexes that had received neonatal phenobarbital showed increased levels of cytochrome P-450, as well as both P-450 and cytochrome c reductase, ethoxycoumarin O-deethylation, glucuronyl transferase activity, in vitro covalent binding of benzo[a]pyrene to DNA and in vivo covalent binding of aflatoxin B1 to hepatic macromolecular fractions.	Phenobarbital	74-87	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	115-131
3995102-7	1985	Neither of the four cytochrome P-450 forms interacted with the antibodies raised against cytochrome P-450 isolated from liver microsomes of rats induced with phenobarbital.	Phenobarbital	158-171	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	89-105
3884171-6	1985	Metyrapone, a specific inhibitor of PB-inducible major cytochrome P-450, considerably inhibited mutagenicity, whereas 7,8-benzoflavone, a specific inhibitor of 3-MC-inducible major cytochrome P-448, was totally lacking this effect.	Phenobarbital	36-38	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	55-71
3884171-7	1985	These results demonstrate a correlation between rat liver S9 dependent mutagenicity of six N-nitrosopropylamines and their known carcinogenicity in rat in vivo experiments, and that the PB-inducible major cytochrome P-450 is involved in the mutagenic activation.	Phenobarbital	186-188	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	205-221
3918791-1	1985	Rabbit antibodies raised against the major isozymes of cytochrome P-450 isolated from hepatic microsomes of beta-naphthoflavone- (BNF) and phenobarbital-treated rats (cytochrome P-450 BNF-B2 and cytochrome P-450 PB-B2, respectively) and against rat liver NADPH-cytochrome P-450 reductase were used to localize these enzymes immunohistochemically in the rat ventral prostate.	Phenobarbital	139-152	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	55-71
3918791-1	1985	Rabbit antibodies raised against the major isozymes of cytochrome P-450 isolated from hepatic microsomes of beta-naphthoflavone- (BNF) and phenobarbital-treated rats (cytochrome P-450 BNF-B2 and cytochrome P-450 PB-B2, respectively) and against rat liver NADPH-cytochrome P-450 reductase were used to localize these enzymes immunohistochemically in the rat ventral prostate.	Phenobarbital	139-152	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	167-183
3918791-1	1985	Rabbit antibodies raised against the major isozymes of cytochrome P-450 isolated from hepatic microsomes of beta-naphthoflavone- (BNF) and phenobarbital-treated rats (cytochrome P-450 BNF-B2 and cytochrome P-450 PB-B2, respectively) and against rat liver NADPH-cytochrome P-450 reductase were used to localize these enzymes immunohistochemically in the rat ventral prostate.	Phenobarbital	139-152	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	167-183
3918791-2	1985	Using the unlabeled antibody peroxidase-antiperoxidase technique, NADPH-cytochrome P-450 reductase was detected exclusively in the epithelial cells of the gland to the same magnitude in untreated, phenobarbital-, and BNF-treated rats.	Phenobarbital	197-210	cytochrome p450 oxidoreductase	Rattus norvegicus	66-98
2859164-1	1985	The possible role of free hydroxyl radicals in the oxidation of cyclohexanol to cyclohexanone and of benzene to phenol was examined in a reconstituted system containing rabbit phenobarbital-inducible P-450LM2.	Phenobarbital	176-189	cytochrome P450 2B4	Oryctolagus cuniculus	200-208
3889686-1	1985	The effect of short-term administration of chlorpromazine and phenobarbital on cytoplasmic alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) was studied in distinct brain regions of the male rat.	Phenobarbital	62-75	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	123-145
3889686-1	1985	The effect of short-term administration of chlorpromazine and phenobarbital on cytoplasmic alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) was studied in distinct brain regions of the male rat.	Phenobarbital	62-75	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	147-151
3919279-0	1985	Phenobarbital induces rat liver apolipoprotein A-I mRNA.	Phenobarbital	0-13	apolipoprotein A1	Rattus norvegicus	32-50
3919279-1	1985	The effect of phenobarbital on the level of rat liver apolipoprotein A-I (apo-A-I) mRNA was studied.	Phenobarbital	14-27	apolipoprotein A1	Rattus norvegicus	54-72
3919279-1	1985	The effect of phenobarbital on the level of rat liver apolipoprotein A-I (apo-A-I) mRNA was studied.	Phenobarbital	14-27	apolipoprotein A1	Rattus norvegicus	74-81
3919279-2	1985	Poly(A+)-RNA isolated from livers of control or phenobarbital-treated rats was translated in vitro in the rabbit reticulocyte lysate system and immunoprecipitated with rabbit antiserum against rat apo-A-I.	Phenobarbital	48-61	apolipoprotein A1	Rattus norvegicus	197-204
3919279-6	1985	To study the effect of phenobarbital on the level of rat liver apo-A-I mRNA, a recombinant plasmid which contained a cDNA insert corresponding to rat liver apo-A-I mRNA was isolated and used to hybridize total liver poly(A+)-RNA from control and phenobarbital-treated rats.	Phenobarbital	23-36	apolipoprotein A1	Rattus norvegicus	63-70
3919279-8	1985	Thus, phenobarbital increases the level of rat liver apo-A-I mRNA.	Phenobarbital	6-19	apolipoprotein A1	Rattus norvegicus	53-60
4002661-4	1985	Electrophoresis in SDS-polyacrylamide gel showed that HCB, as phenobarbital does, induced appearance of the protein with a molecular mass 52,000 (cytochrome P-450) but not of the protein of molecular mass 56,000, which is the main isozyme of cytochrome P-450 in 3-MC microsomes (P-448).	Phenobarbital	62-75	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	146-162
4002661-4	1985	Electrophoresis in SDS-polyacrylamide gel showed that HCB, as phenobarbital does, induced appearance of the protein with a molecular mass 52,000 (cytochrome P-450) but not of the protein of molecular mass 56,000, which is the main isozyme of cytochrome P-450 in 3-MC microsomes (P-448).	Phenobarbital	62-75	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	242-258
3838174-2	1985	A cDNA clone for cytochrome P-450e, a phenobarbitone-inducible species in rat liver, has been isolated and characterized.	Phenobarbital	38-52	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	17-34
3838174-4	1985	Inhibitors of heme synthesis such as cobalt chloride and 3-amino-1,2,4-triazole block the induction of cytochrome P-450e by phenobarbitone at the level of transcription.	Phenobarbital	124-138	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	103-120
3918537-6	1985	Phenobarbital (80 mg/kg daily for 3 days) was a poor inducer of renal cytochrome P-450 in sham-operated rats but became a potent inducer of renal cytochrome P-450 in rats with two-thirds hepatectomy.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	70-86
3918537-6	1985	Phenobarbital (80 mg/kg daily for 3 days) was a poor inducer of renal cytochrome P-450 in sham-operated rats but became a potent inducer of renal cytochrome P-450 in rats with two-thirds hepatectomy.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	146-162
3918538-1	1985	Microsomal NADPH-cytochrome c (P-450) reductase and cytochrome P-450 were purified from the livers of phenobarbitone-treated rats.	Phenobarbital	102-116	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	52-68
3967237-5	1985	Cytochrome P-450LM2, which is induced by pretreatment with phenobarbital, exhibited the highest activity for the metabolism of cis-NNDM.	Phenobarbital	59-72	cytochrome P450 2B4	Oryctolagus cuniculus	0-19
3965334-1	1985	Immunochemical characterization of the increase in cytochrome P450 caused by phenobarbital.	Phenobarbital	77-90	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	51-66
3965334-2	1985	We have studied total cytochrome P450 and the major form of cytochrome P450 increased by phenobarbital in small intestinal epithelial cells and livers of male Sprague-Dawley rats.	Phenobarbital	89-102	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	60-75
3965334-4	1985	In untreated rats, less than 5% of total cytochrome P450 of liver or intestinal epithelium is the form induced by phenobarbital, as measured by rocket immunoelectrophoresis.	Phenobarbital	114-127	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	41-56
3965334-6	1985	In the small intestine of phenobarbital-treated rats, the concentrations of total cytochrome P450 and of the major phenobarbital-induced form increase concurrently as epithelial cells mature from crypt to upper villus.	Phenobarbital	26-39	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	82-97
3965334-7	1985	Concentrations of total cytochrome P450 and of the major phenobarbital-induced form in the proximal two-thirds of the rat small intestine are twofold higher than in the distal third.	Phenobarbital	57-70	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	24-39
3965334-8	1985	Immunoblotting performed with a monoclonal antibody to the major phenobarbital-induced form of cytochrome P450 from rat liver revealed a subtle difference between this form in liver and intestine.	Phenobarbital	65-78	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	95-110
3856261-1	1985	A previously reported cDNA clone [pP450(1)] coding for a phenobarbital-inducible cytochrome P-450 variant of rat liver microsomal membranes, designated P-450e(U.C.	Phenobarbital	57-70	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	81-97
3917669-5	1985	Studies on the effects of pretreatment of animals with either phenobarbital or Aroclor 1254 suggest that cytochrome P-450 isozymes catalyzed both N-deethylation and hydroxylation reactions.	Phenobarbital	62-75	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	105-121
3917920-0	1985	Resolution by high-pressure liquid chromatography and partial characterization of multiple forms of cytochrome P-450 from hepatic microsomes of phenobarbital-treated rats.	Phenobarbital	144-157	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	100-116
3917920-1	1985	Seven cytochromes P-450 (A, B, C, D, E1, E2 and F) were isolated from hepatic microsomes of phenobarbital-induced rats by a modification of the procedure of Guengerich and Martin [Arch.	Phenobarbital	92-105	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	18-49
2988654-8	1985	Phenobarbital, injected intraperitoneally at 15 mg/kg/day for 6 consecutive days to 8- to 13-day-old puppies (n = 3), produced induction of P-450 (235% of age-matched controls) and bilirubin GT activity (160%), diminished G6P activity (81%), and failed to modify p-nitrophenol GT activity (102%).	Phenobarbital	0-13	glucose-6-phosphatase catalytic subunit 1	Canis lupus familiaris	222-225
3966918-4	1985	After oral applications of 120 mg/kg warfarin once daily for three days SDS-PAGE analysis of the partially purified cytochrome P-450 fraction revealed a protein pattern in the 50 Kd region that is practically indistinguishable from that after conventional phenobarbitone pretreatment.	Phenobarbital	256-270	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	116-132
3966972-4	1985	This protection appears to be, at least in part, related to phenobarbital induction of hepatic cytochrome P-450 isozyme(s) that metabolizes CP to a new metabolite tentatively identified as didechlorodihydroxycyclophosphamide.	Phenobarbital	60-73	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	95-111
3933372-0	1985	Effect of serum albumin on free fractions of phenobarbital and valproic acid in patients with convulsive seizures.	Phenobarbital	45-58	albumin	Homo sapiens	16-23
3978310-3	1985	HACU was inhibited by drugs which have in common the ability to facilitate gamma-aminobutyric acid (GABA) transmission, pentobarbitone, phenobarbitone, barbitone, diazepam, chloridiazepoxide, and valproic acid.	Phenobarbital	136-150	high affinity choline uptake	Mus musculus	0-4
4043714-1	1985	Chromatofocusing between pH 7.4 and 5.0 was introduced as a final step for the resolution of multiple forms of cytochrome P-450 from control, phenobarbital and 3-methylcholanthrene-pretreated rat liver microsomal fractions.	Phenobarbital	142-155	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	111-127
3868365-3	1985	Such a "booster"-phenomenon was also observed with different cytochrome P-450 (P-450)-dependent N-demethylation reactions after repeated phenobarbital (PB) administrations.	Phenobarbital	137-150	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	61-77
3868365-3	1985	Such a "booster"-phenomenon was also observed with different cytochrome P-450 (P-450)-dependent N-demethylation reactions after repeated phenobarbital (PB) administrations.	Phenobarbital	152-154	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	61-77
2858353-5	1985	For instance, GST activity toward EA at birth is mature in guinea pigs but not in the other species; phenobarbital treatment increased GST activities in mice and rats but not in rabbits and guinea-pigs; treatment with trans-stilbene oxide enhanced GST activity for TPBO 4.5-fold in mice but not at all in rats.	Phenobarbital	101-114	hematopoietic prostaglandin D synthase	Mus musculus	135-138
2858353-5	1985	For instance, GST activity toward EA at birth is mature in guinea pigs but not in the other species; phenobarbital treatment increased GST activities in mice and rats but not in rabbits and guinea-pigs; treatment with trans-stilbene oxide enhanced GST activity for TPBO 4.5-fold in mice but not at all in rats.	Phenobarbital	101-114	hematopoietic prostaglandin D synthase	Mus musculus	135-138
2858378-10	1985	Losses of cytochrome P-450 were also observed after incubation of microsomes from phenobarbital- (31%) of beta-naphthoflavone-pretreated rats (44%) with NADPH and methimazole.	Phenobarbital	82-95	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	10-26
2858378-12	1985	These results indicate that both phenobarbital and beta-naphthoflavone induce isozymes of cytochrome P-450 capable of directly activating methimazole.	Phenobarbital	33-46	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	90-106
3881283-11	1985	Phenobarbital and other anticonvulsants are inducers of cytochrome P-450 and the mixed-function oxidase system.	Phenobarbital	0-13	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	56-72
3000845-2	1985	NADPH-cytochrome P-450 reductase was purified from phenobarbital-induced mouse liver and from human placenta and was combined with cytochrome P-450 and dilauroylphosphatidylcholine to reconstitute the cytochrome P-450 monooxygenase system.	Phenobarbital	51-64	cytochrome p450 oxidoreductase	Mus musculus	0-32
3996731-2	1985	An excellent direct correlation (r = 0.95) has been observed between ethoxyresorufin O-deethylase and the metabolic activation of benzo[a]pyrene to mutagens when the fraction of cytochromes P-450 present as cytochrome P-448 was altered by the administration of phenobarbitone and 3-methylcholanthrene alone or in combination with 9-hydroxyellipticine.	Phenobarbital	261-275	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	207-223
3000845-2	1985	NADPH-cytochrome P-450 reductase was purified from phenobarbital-induced mouse liver and from human placenta and was combined with cytochrome P-450 and dilauroylphosphatidylcholine to reconstitute the cytochrome P-450 monooxygenase system.	Phenobarbital	51-64	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	6-22
3000845-2	1985	NADPH-cytochrome P-450 reductase was purified from phenobarbital-induced mouse liver and from human placenta and was combined with cytochrome P-450 and dilauroylphosphatidylcholine to reconstitute the cytochrome P-450 monooxygenase system.	Phenobarbital	51-64	cytochrome P450 family 20 subfamily A member 1	Homo sapiens	201-231
2867096-10	1985	Furthermore, in the carcinogen-treated cultures, PB treatment caused a dose-dependent increase in the number of GGT positive cultures and in the percentage of GGT positive cells in each culture, and also caused a dose-dependent increase in the number of cultures with chromosomal abnormalities.	Phenobarbital	49-51	gamma-glutamyltransferase 1	Rattus norvegicus	112-115
2867096-10	1985	Furthermore, in the carcinogen-treated cultures, PB treatment caused a dose-dependent increase in the number of GGT positive cultures and in the percentage of GGT positive cells in each culture, and also caused a dose-dependent increase in the number of cultures with chromosomal abnormalities.	Phenobarbital	49-51	gamma-glutamyltransferase 1	Rattus norvegicus	159-162
4020114-5	1985	PB effects were manifested by the persistent decrease in rats" body weight, increase in the liver weight, increase in the cytoplasmatic activity of glutathione S-transferase in the liver and increase in TDGA urinary excretion.	Phenobarbital	0-2	hematopoietic prostaglandin D synthase	Rattus norvegicus	148-173
2984438-10	1985	In vitro incubation of hepatic microsomes prepared from either BNF-, PB-, or PCB-pretreated rats with an atmosphere of 20% propylene/80% air produced in NADPH-dependent decrease in cytochrome P-450 content.	Phenobarbital	69-71	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	181-197
3965924-4	1985	In cultures prepared from untreated rats or from rats treated with phenobarbital or with 3-methylcholanthrene, individual forms of cytochrome P-450 declined at markedly differing rates.	Phenobarbital	67-80	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	131-147
3877941-5	1985	Medicarpin and maackiain and two of their biosynthetic precursors inhibit the constitutive and phenobarbital (PB)-induced types of AHH, but have little effect on the 3-methylcholanthrene (MC)-induced type of AHH.	Phenobarbital	95-108	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	131-134
3885070-1	1985	The effect of postnatal administration of phenobarbital on enzymes degrading enkephalin was examined.	Phenobarbital	42-55	proenkephalin	Rattus norvegicus	77-87
3885070-6	1985	The treatment of the rats with phenobarbital resulted in a significant inhibition of enkephalinase A when measured in vitro, using methionine enkephalin as substrate.	Phenobarbital	31-44	membrane metallo-endopeptidase	Rattus norvegicus	85-98
3885070-6	1985	The treatment of the rats with phenobarbital resulted in a significant inhibition of enkephalinase A when measured in vitro, using methionine enkephalin as substrate.	Phenobarbital	31-44	proenkephalin	Rattus norvegicus	85-95
3160048-6	1985	Phenobarbital and pentobarbital inhibited aldehyde dehydrogenase (ALDH) activities in vitro in a noncompetitive fashion; Ki were 29 and 37 mM, respectively.	Phenobarbital	0-13	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	42-64
3160048-6	1985	Phenobarbital and pentobarbital inhibited aldehyde dehydrogenase (ALDH) activities in vitro in a noncompetitive fashion; Ki were 29 and 37 mM, respectively.	Phenobarbital	0-13	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	66-70
3877941-5	1985	Medicarpin and maackiain and two of their biosynthetic precursors inhibit the constitutive and phenobarbital (PB)-induced types of AHH, but have little effect on the 3-methylcholanthrene (MC)-induced type of AHH.	Phenobarbital	110-112	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	131-134
3975258-1	1985	Rats were pretreated with phenobarbital to induce hepatic cytochrome P-450.	Phenobarbital	26-39	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	58-74
6439217-2	1984	Cytochrome P-450 (termed MC P-4481 and MC P-4482) purified from liver microsomes of 3-methyl-cholanthrene-treated rats was active in both 2- and 4-hydroxylation of biphenyl but cytochrome P-450 (termed PB P-450) purified from liver microsomes of phenobarbital-treated rats was active in 4-hydroxylation of biphenyl only.	Phenobarbital	246-259	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
4023043-1	1985	Pretreatment of rabbits with phenobarbital caused significant increases in total pulmonary cytochrome P-450 content, benzo(a)pyrene hydroxylase and 7-ethoxycoumarin O-deethylase activities and to a lesser extent in benzphetamine N-demethylase activity in lung microsomes.	Phenobarbital	29-42	cytochrome P-450	Oryctolagus cuniculus	91-107
4023043-4	1985	Column chromatography of the pulmonary monooxygenases demonstrated that in untreated and phenobarbital-treated rabbits, cytochromes P-450I and P-450II constituted the major forms of cytochrome P-450 isozymes.	Phenobarbital	89-102	cytochrome P-450	Oryctolagus cuniculus	182-198
3991787-1	1985	Caffeine is mainly metabolized by 3-methylcholanthrene-inducible cytochrome P-450 (P-450MC) and noramidopyrine-methanesulfonate sodium (metamizol, Analgin) is mainly metabolized by phenobarbital-inducible cytochrome P-450 (P-450PB).	Phenobarbital	181-194	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	76-81
3920836-5	1985	PB, PCB and MC treatments enhanced the activity of enzymes involved in conjugation reactions, UDP-glucuronyltransferase and glutathione S-transferase, whereas the dietary manipulation and ethanol consumption produced no significant effect on these enzymes.	Phenobarbital	0-2	hematopoietic prostaglandin D synthase	Rattus norvegicus	124-149
6334605-7	1984	(b) MAb-PB-sensitive AHH, ECDE and AE activities were also observed in untreated and phenobarbital-treated cells.	Phenobarbital	85-98	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	21-24
6334605-12	1984	The results show that the hepatoma cells examined express to various degrees phenobarbital-inducible cytochrome P-450 and/or 3-methylcholanthrene-inducible cytochrome P-450.	Phenobarbital	77-90	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	101-117
6099695-3	1984	The enzymatic mitochondrial CCl4 activation operates more efficiently under anaerobic conditions; it requires NADPH, is CO sensitive, is inducible by phenobarbital pretreatment and is only weakly inhibited by high concentrations of cyanide or azide.	Phenobarbital	150-163	C-C motif chemokine ligand 4	Rattus norvegicus	28-32
6096035-0	1984	Phenobarbital induces cytochrome P-450- and cytochrome P-448-dependent monooxygenases in rat hepatoma cells.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	22-60
6096035-1	1984	The induction by phenobarbital (PB) of aldrin epoxidase (AE) and aryl hydrocarbon hydroxylase (AHH), markers of cytochrome P-450- and cytochrome P-448-dependent monooxygenases, was studied in cell lines derived from Reuber H35 rat hepatoma which differ widely in their degree of differentiation.	Phenobarbital	17-30	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	112-150
6096035-6	1984	Thus, the flavonoid had only a slight inhibitory effect on PB-induced AHH in C2Rev7 cells, but strongly inhibited PB-induced AHH in H5 cells.	Phenobarbital	59-61	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	70-73
6096035-6	1984	Thus, the flavonoid had only a slight inhibitory effect on PB-induced AHH in C2Rev7 cells, but strongly inhibited PB-induced AHH in H5 cells.	Phenobarbital	114-116	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	125-128
6096035-7	1984	The induction of AE and of 7,8-benzoflavone-inhibitable AHH in 2sFou cells indicated that PB is capable of inducing cytochromes P-450 and cytochrome P-448 in the same cell.	Phenobarbital	90-92	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	56-59
6096035-7	1984	The induction of AE and of 7,8-benzoflavone-inhibitable AHH in 2sFou cells indicated that PB is capable of inducing cytochromes P-450 and cytochrome P-448 in the same cell.	Phenobarbital	90-92	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	138-154
6442209-7	1984	When microsomes from untreated, phenobarbital-treated (3 days), or TCDD-treated (1 or 3 weeks) rats were compared, iron release correlated most closely with the cytochrome P-450 concentration.	Phenobarbital	32-45	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	161-177
6152472-2	1984	FTA-induced tonic extensor convulsion was markedly suppressed by anticonvulsant, e.g. phenobarbital, phenytoin.	Phenobarbital	86-99	farnesyltransferase, CAAX box, alpha	Mus musculus	0-3
6152472-3	1984	Phenobarbital, trimethadione, valproic acid and mephenesin decreased the occurrence of abnormal behaviors induced by FTA.	Phenobarbital	0-13	farnesyltransferase, CAAX box, alpha	Mus musculus	117-120
6392865-1	1984	We present and evaluate a dual assay, the CYPIA (Cytochrome P-450 induction assay) for the detection and the simultaneous identification of chemicals belonging either to the 3-methylcholanthrene or phenobarbital classes of cytochrome P-450 monooxygenase inducers.	Phenobarbital	198-211	cytochrome P450, family 2, subfamily j, polypeptide 3	Rattus norvegicus	223-253
6095901-0	1984	Stereochemical studies on the cytochrome P-450 and hydroxyl radical dependent pathways of 2-butanol oxidation by microsomes from chow-fed, phenobarbital-treated, and ethanol-treated rats.	Phenobarbital	139-152	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	30-46
6436023-1	1984	Phenobarbital-induced coumarin 7-hydroxylase is high in DBA/2J and low in C57BL/6N inbred mice; this genetic difference is encoded by the Coh locus on chromosome 7.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	22-44
6436023-3	1984	P-450 fractions, highly specific for phenobarbital-inducible coumarin 7-hydroxylase activity, were purified from DBA/2J and C57BL/6N mouse liver microsomes.	Phenobarbital	37-50	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	61-83
6488182-8	1984	Benzo(a)pyrene, 3-methylcholanthrene, and phenobarbital induce hepatic ALDH activity after treatment in vivo.	Phenobarbital	42-55	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	71-75
6488182-13	1984	Only marginal increases in NADP-dependent ALDH are observed after phenobarbital treatment in 4 of 5 cell lines.	Phenobarbital	66-79	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	42-46
6435683-1	1984	The soluble, cytochrome P-450-dependent fatty acid monooxygenase of Bacillus megaterium ATCC 14581 is induced by phenobarbital and at least twelve other barbiturates (Kim, B.-H. and Fulco, A.J.	Phenobarbital	113-126	cytochrome P450	Bacillus megaterium NBRC 15308 = ATCC 14581	13-29
6149821-0	1984	Effect of chronic phenobarbital administration on the gamma-glutamyl transpeptidase activity of hyperplastic liver lesions induced in rats by the Solt/Farber initiation: selection process of hepatocarcinogenesis.	Phenobarbital	18-31	gamma-glutamyltransferase 1	Rattus norvegicus	54-83
6149821-1	1984	A chronic 8 to 11 week administration of the hepatic tumor promoter phenobarbital (0.05% in drinking water) to rats previously subjected to the initiation:selection process of Solt and Farber was found to further increase the gamma-glutamyl transpeptidase activity of individual hyperplastic liver nodules of 4.0-10.0 mm in diameter over comparably sized nodules from control livers.	Phenobarbital	68-81	gamma-glutamyltransferase 1	Rattus norvegicus	226-255
6149821-3	1984	In addition, random tissue samples of non-nodular liver taken from the 11 week phenobarbital-treated rats exhibited a gamma-glutamyl transpeptidase mean specific activity which was approximately 3 times higher than that of control non-nodular liver samples.	Phenobarbital	79-92	gamma-glutamyltransferase 1	Rattus norvegicus	118-147
6149821-4	1984	In contrast, there was a 1.5-fold increase in the mean % gamma-glutamyl transpeptidase-positive area (cm2), as determined histochemically, in cryostat sections made from non-nodular samples of the 11 week phenobarbital-treated rats when compared with that of control liver sections.	Phenobarbital	205-218	gamma-glutamyltransferase 1	Rattus norvegicus	57-86
6149821-5	1984	Interruption of the chronic phenobarbital administration at 8 weeks followed by 3 weeks of control treatment resulted in a reversal of the gamma-glutamyl transpeptidase activity response shown by the hyperplastic liver nodules and non-nodular liver tissue samples.	Phenobarbital	28-41	gamma-glutamyltransferase 1	Rattus norvegicus	139-168
6149821-6	1984	Thus, phenobarbital can quantitatively modulate gamma-glutamyl transpeptidase activity in carcinogen-induced hyperplastic liver lesions in the rat during the early stages of hepatocarcinogenesis.	Phenobarbital	6-19	gamma-glutamyltransferase 1	Rattus norvegicus	48-77
6506083-4	1984	Administration of nickel ions at a dose of 60 mg/kg body wt to female rats did not reduce to a significant level the content or the activity of any of the hepatic microsomal enzymes mentioned above, but did interfere in the de novo synthesis of cytochrome P-450 following phenobarbital treatment.	Phenobarbital	272-285	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	245-261
6436235-3	1984	Both phenobarbital (PB) and 3-methylcholanthrene (3-MC) induce the level of mitochondrial cytochrome P-450 by 2.0- to 2.5-fold above the level of control mitoplasts.	Phenobarbital	5-18	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	90-106
6436235-3	1984	Both phenobarbital (PB) and 3-methylcholanthrene (3-MC) induce the level of mitochondrial cytochrome P-450 by 2.0- to 2.5-fold above the level of control mitoplasts.	Phenobarbital	20-22	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	90-106
6436235-8	1984	The activity, however, was restored to preparations from both PB-induced and 3-MC-induced mitochondrial enzymes (AFB1 activation, ethylmorphine, and benzphetamine deamination and BaP metabolism) by addition of purified rat liver cytochrome P-450 reductase, and beef adrenodoxin and adrenodoxin reductase.	Phenobarbital	62-64	cytochrome p450 oxidoreductase	Rattus norvegicus	229-255
6436235-11	1984	Anti-P-450b and anti-P-450c provided Ouchterlony precipitin bands against PB- and 3-MC induced mitoplasts, respectively.	Phenobarbital	74-76	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	5-11
6436235-11	1984	Anti-P-450b and anti-P-450c provided Ouchterlony precipitin bands against PB- and 3-MC induced mitoplasts, respectively.	Phenobarbital	74-76	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	21-27
6487651-7	1984	Whereas hepatic ligandin concentration could be increased at all stages of development by phenobarbital induction, no induction occurred in the endocrine tissues.	Phenobarbital	90-103	glutathione S-transferase alpha 2	Rattus norvegicus	16-24
2985574-3	1985	The insertion sites of the introns in this gene are well-conserved as compared with those of another MC-inducible cytochrome P-450c gene, but are completely different from those of a phenobarbital-inducible cytochrome P-450e gene.	Phenobarbital	183-196	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	114-131
2985574-3	1985	The insertion sites of the introns in this gene are well-conserved as compared with those of another MC-inducible cytochrome P-450c gene, but are completely different from those of a phenobarbital-inducible cytochrome P-450e gene.	Phenobarbital	183-196	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	207-224
2985574-5	1985	The similarity of the gene organization between cytochrome P-450d and P-450c as well as their homology in the deduced amino acid and the nucleotide sequences suggests that these two genes of MC-inducible cytochromes P-450 constitute a different subfamily than those of the phenobarbital-inducible one in the cytochrome P-450 gene family.	Phenobarbital	273-286	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	59-65
2985574-5	1985	The similarity of the gene organization between cytochrome P-450d and P-450c as well as their homology in the deduced amino acid and the nucleotide sequences suggests that these two genes of MC-inducible cytochromes P-450 constitute a different subfamily than those of the phenobarbital-inducible one in the cytochrome P-450 gene family.	Phenobarbital	273-286	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	70-76
6489239-10	1984	Benzo[a]pyrene hydroxylase activity of trout liver microsomes was similar to that of rat and quail microsomes, whereas hydroxylation of substrates which in rat liver are preferentially metabolized by phenobarbital-inducible forms of cytochrome P-450 was much lower in trout microsomes.	Phenobarbital	200-213	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	233-249
6548384-9	1984	Similarly, PB pretreatment reversed the decline in hepatic ALA-S activity after CCNU administration but had no effect on the decline in splenic ALA-S activity.	Phenobarbital	11-13	5'-aminolevulinate synthase 1	Rattus norvegicus	59-64
6380709-1	1984	The hepatic cytochrome P-450-mediated metabolism and metabolic activation of [chloroethyl-3H]cyclophosphamide [( chloroethyl-3H]CP) and [4-14C]cyclophosphamide [( 4-14C]CP) were investigated in vitro in the reconstituted system containing cytochrome P-450 isolated from phenobarbital-treated rats.	Phenobarbital	270-283	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	12-28
6207173-1	1984	UDP-glucuronosyltransferase (transferase) clones were isolated from a cDNA bank constructed in pBR322 using transferase-enriched mRNA from the livers of phenobarbital-treated rats.	Phenobarbital	153-166	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	0-27
6491971-10	1984	The covalent binding is completely inhibited by antibodies to the major phenobarbital-induced isozyme of rat liver cytochrome P-450.	Phenobarbital	72-85	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	115-131
6207184-2	1984	At 0.1 microgram/ml, TPA depressed the specific activities of lactate dehydrogenase and gamma-glutamyl transpeptidase, whereas 2 mM PB depressed gamma-glutamyl transpeptidase and alkaline phosphatase.	Phenobarbital	132-134	gamma-glutamyltransferase 1	Rattus norvegicus	145-174
6207184-7	1984	The depression of gamma-glutamyl transpeptidase activity by PB is contradictory to that observed histochemically in hepatocytes in vivo, but such discrepancy may be related to the differences in cell type, growth conditions, or duration of exposure.	Phenobarbital	60-62	gamma-glutamyltransferase 1	Rattus norvegicus	18-47
6592385-3	1984	A significantly decreased level of activity of L-PK was observed during continuous feedings of the hepatocarcinogen 3"-methyl-4-dimethylaminoazobenzene [(3"-MeDAB) CAS: 55-80-1], which initiates and promotes hepatocarcinogenesis, and of the known hepatic promoters phenobarbital [(PB) CAS: 50-06-6] and dichlorodiphenyltrichloroethane (CAS: 50-29-3) for at least 4 weeks.	Phenobarbital	265-278	pyruvate kinase L/R	Rattus norvegicus	47-51
6239340-3	1984	PB improved hepatic glycogen and cytP450 contents and NADPH cytP450 reductase activity in DMN pretreated rats.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	33-40
6239340-3	1984	PB improved hepatic glycogen and cytP450 contents and NADPH cytP450 reductase activity in DMN pretreated rats.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	60-67
6437438-2	1984	The anaerobic reduction kinetics of purified rat liver ferric cytochrome P-450 from phenobarbital-treated rat liver microsomes, reconstituted with saturating NADPH-cytochrome P-450 reductase, have been investigated and were shown not to be monophasic.	Phenobarbital	84-97	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	62-78
6506750-7	1984	Administration of 3-methylcholanthrene and phenobarbital to pigeons resulted in the induction of demethylase and benzo[a]pyrene hydroxylase activities and in cytochrome P-450 levels.	Phenobarbital	43-56	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	158-174
6206064-2	1984	Analysis of the levels of mRNA in liver revealed that (a) cytochrome P-450PBc1 mRNA was not detectable in livers from control animals but was present in livers from animals treated with phenobarbital, (b) cytochrome P-450PBc2 was present in control tissue and was increased by about 3-fold 24 h after phenobarbital treatment, and (c) the levels of cytochrome P-450PBc3 mRNA was the same in livers from control and treated animals.	Phenobarbital	186-199	cytochrome P450 2C1	Oryctolagus cuniculus	58-78
6545996-0	1984	Effects of phenobarbitone and short-term exposure to heat on microsomal cytochrome P-450 and associated monooxygenases in rat liver.	Phenobarbital	11-25	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	72-88
6206064-2	1984	Analysis of the levels of mRNA in liver revealed that (a) cytochrome P-450PBc1 mRNA was not detectable in livers from control animals but was present in livers from animals treated with phenobarbital, (b) cytochrome P-450PBc2 was present in control tissue and was increased by about 3-fold 24 h after phenobarbital treatment, and (c) the levels of cytochrome P-450PBc3 mRNA was the same in livers from control and treated animals.	Phenobarbital	186-199	cytochrome P450 2C2	Oryctolagus cuniculus	216-225
6206064-2	1984	Analysis of the levels of mRNA in liver revealed that (a) cytochrome P-450PBc1 mRNA was not detectable in livers from control animals but was present in livers from animals treated with phenobarbital, (b) cytochrome P-450PBc2 was present in control tissue and was increased by about 3-fold 24 h after phenobarbital treatment, and (c) the levels of cytochrome P-450PBc3 mRNA was the same in livers from control and treated animals.	Phenobarbital	186-199	cytochrome P450 2C3	Oryctolagus cuniculus	348-368
6206064-2	1984	Analysis of the levels of mRNA in liver revealed that (a) cytochrome P-450PBc1 mRNA was not detectable in livers from control animals but was present in livers from animals treated with phenobarbital, (b) cytochrome P-450PBc2 was present in control tissue and was increased by about 3-fold 24 h after phenobarbital treatment, and (c) the levels of cytochrome P-450PBc3 mRNA was the same in livers from control and treated animals.	Phenobarbital	301-314	cytochrome P450 2C1	Oryctolagus cuniculus	58-78
6206064-3	1984	In the kidney, only P-450PBc2 mRNA was detected at a level 15% of that in the liver, and the levels increased about 3-fold after phenobarbital treatment.	Phenobarbital	129-142	cytochrome P450 2C2	Oryctolagus cuniculus	20-29
6334430-0	1984	Ethanol-inducible cytochrome P-450 is more susceptible to in vitro carbon tetrachloride-mediated destruction than phenobarbital-inducible and beta-naphthoflavone-inducible cytochromes P-450.	Phenobarbital	114-127	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	18-34
6334430-4	1984	Microsomes from control and phenobarbital-pretreated rats lost between 30 and 35% of their cytochrome P-450 and between 65 and 50% of the ethoxycoumarin 0-deethylase activity.	Phenobarbital	28-41	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	91-107
6545996-1	1984	Short-term exposure of the control and phenobarbitone-treated rats to high ambient temperature caused a different response of the hepatic microsomal cytochrome P-450-dependent monooxygenase system participating in the oxidation of aniline, aminopyrine and p-nitroanisole.	Phenobarbital	39-53	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	149-165
6433897-4	1984	Androsterone UDP-glucuronosyltransferase activity was induced by phenobarbital in rats with the high-activity phenotype, but not in rats with the low-activity phenotype.	Phenobarbital	65-78	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	13-40
6494651-5	1984	Not only the microsomal monooxygenase but also amidase was strongly induced by pretreatment with phenobarbital, 3-methylcholanthrene and rifampicin, respectively.	Phenobarbital	97-110	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	13-37
6477526-0	1984	Formation of cytochrome P-450 containing haem or cobalt-protoporphyrin in liver homogenates of rats treated with phenobarbital and allylisopropylacetamide.	Phenobarbital	113-126	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
6477526-2	1984	This decrease occurs particularly in phenobarbital-induced cytochrome P-450 and is caused by suicidal breakdown of the haem of cytochrome P-450.	Phenobarbital	37-50	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	59-75
6477526-2	1984	This decrease occurs particularly in phenobarbital-induced cytochrome P-450 and is caused by suicidal breakdown of the haem of cytochrome P-450.	Phenobarbital	37-50	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	127-143
6477526-3	1984	Quantitative rocket immunoelectrophoresis showed that the protein moiety of the major phenobarbital-inducible form of hepatic cytochrome P-450 was not diminished up to 1 h, but was markedly decreased (to 43% of that of the phenobarbital-treated control) at 20 h after allylisopropylacetamide treatment.	Phenobarbital	86-99	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	126-142
6477526-3	1984	Quantitative rocket immunoelectrophoresis showed that the protein moiety of the major phenobarbital-inducible form of hepatic cytochrome P-450 was not diminished up to 1 h, but was markedly decreased (to 43% of that of the phenobarbital-treated control) at 20 h after allylisopropylacetamide treatment.	Phenobarbital	223-236	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	126-142
6477526-7	1984	Incubation with haem increased spectrophotometrically measurable cytochrome P-450 to 69%, ethylmorphine demethylase to 64% and benzphetamine demethylase to 93% of the activities in rats treated with phenobarbital alone.	Phenobarbital	199-212	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	65-81
6384000-3	1984	Other studies in isolated perfused rat liver revealed that selectively increased cytosolic ligandin concentration, following phenobarbital treatment or thyroidectomy, directly correlated with net bilirubin uptake which resulted from reduced bilirubin efflux.	Phenobarbital	125-138	glutathione S-transferase alpha 2	Rattus norvegicus	91-99
6434390-2	1984	A concomitant maintenance of the amino-pyrine N-demethylase activity and a high aflatoxin B1-induced cytotoxicity was observed, and addition of phenobarbital to the culture medium produced about a 2-fold increase in cytochrome P-450 level.	Phenobarbital	144-157	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	216-232
6438379-1	1984	Cytochrome P-450-dependent oxidative cleavage of 1-(tetrahydro-2-furanyl)-5-fluorouracil (FT) was investigated in a reconstituted system containing purified phenobarbital-inducible cytochrome P-450 (P-450(1)) or 3-methylcholanthrene-inducible cytochrome P-450 (P-448(1)).	Phenobarbital	157-170	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-16
6438379-1	1984	Cytochrome P-450-dependent oxidative cleavage of 1-(tetrahydro-2-furanyl)-5-fluorouracil (FT) was investigated in a reconstituted system containing purified phenobarbital-inducible cytochrome P-450 (P-450(1)) or 3-methylcholanthrene-inducible cytochrome P-450 (P-448(1)).	Phenobarbital	157-170	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	11-16
6469956-2	1984	The substrates hexobarbital and ethylbenzene have been shown to compete for the spectral binding site of phenobarbital-induced rat hepatic microsomal cytochrome p-450.	Phenobarbital	105-118	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	150-166
6435285-3	1984	The HCBP, a PB-type inducer of cytochrome P-450, resembled phenobarbitone (PB) in its ability to increase susceptibility of hepatocytes to bromobenzene (0.5 to 1.6 mM) and acetaminophen (1 to 16 mM).	Phenobarbital	12-14	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	31-47
6440322-3	1984	The treatment of rats with phenobarbital (6 PhB injections 7 days after DAB application) blocked the restoration of the normal glycogen distribution.	Phenobarbital	27-40	prohibitin 1	Rattus norvegicus	44-47
6469958-1	1984	The hypothesis of a preferential biosynthesis of a major phenobarbital inducible form of hepatic cytochrome P-450 (P-450b) in mitochondria-associated rough endoplasmic reticulum (RERmito) was tested by measuring incorporation rates of [35S]methionine and delta-amino[3H]levulinate into the hemoprotein in adult rats.	Phenobarbital	57-70	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	97-113
6469958-1	1984	The hypothesis of a preferential biosynthesis of a major phenobarbital inducible form of hepatic cytochrome P-450 (P-450b) in mitochondria-associated rough endoplasmic reticulum (RERmito) was tested by measuring incorporation rates of [35S]methionine and delta-amino[3H]levulinate into the hemoprotein in adult rats.	Phenobarbital	57-70	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	115-121
6490752-6	1984	The lambda max of the reduced CO-complex spectra and molecular weights were found to be 450 nm and 53,000, respectively, for all the three HPLC-resolved cytochrome P-450s from PB-induced rats; and 448 nm and 56,000, respectively, for the HPLC-isolated cytochrome P-450 from 3MC-induced rats.	Phenobarbital	176-178	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	153-169
6433911-1	1984	Antibody to mouse UDP glucuronosyltransferase, previously shown to cross-react with rat transferase [1], immunoadsorbed 3 electrophoretically distinct transferase forms from the microsomes of untreated and phenobarbital-treated rats and 4 forms from 3-methylcholanthrene treated animals.	Phenobarbital	206-219	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	18-45
6430587-0	1984	Characterization, localization and regulation of a novel phenobarbital-inducible form of cytochrome P450, compared with three further P450-isoenzymes, NADPH P450-reductase, glutathione transferases and microsomal epoxide hydrolase.	Phenobarbital	57-70	epoxide hydrolase 1	Rattus norvegicus	202-230
6437140-5	1984	The cytochrome P-450 inducer phenobarbital moderately (PER 152%) increased the rate of 14CO2-formation from PCDD II, whereas 3-methylcholanthrene and several technical grade chlorinated paraffins generally gave less or no inductive effects.	Phenobarbital	29-42	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	4-20
6490752-1	1984	The major forms of cytochrome P-450 in the hepatic microsomes of rats pretreated with phenobarbital (PB) or 3-methylcholanthrene (3MC) were isolated by sequential chromatography on n-octylamino-Sepharose 4B and DEAE-cellulose columns.	Phenobarbital	86-99	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	19-35
6490752-1	1984	The major forms of cytochrome P-450 in the hepatic microsomes of rats pretreated with phenobarbital (PB) or 3-methylcholanthrene (3MC) were isolated by sequential chromatography on n-octylamino-Sepharose 4B and DEAE-cellulose columns.	Phenobarbital	101-103	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	19-35
6490752-3	1984	High-performance liquid chromatography (HPLC) of these preparations on an anion-exchange column yielded three peaks from the PB-induced major cytochrome P-450 and a single peak from the 3MC-induced major cytochrome P-450.	Phenobarbital	125-127	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	142-158
6147167-1	1984	Phenazepam (I) and 3-hydroxymetabolite (II) interacting with cytochrome P-450 of the liver of rats administered phenobarbital and 3-methylcholantrene demonstrated the 2nd type of spectral changes in hemoprotein.	Phenobarbital	112-125	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	61-77
6430544-6	1984	The microsomal activity was induced by the pretreatment of rats with 3-methylcholanthrene, sodium phenobarbital, or polychlorinated biphenyl, and the increments of the activity correlated well with those of the specific contents of cytochrome P-450 in microsomes.	Phenobarbital	91-111	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	232-248
6465891-13	1984	Translatable cytochrome P-450 mRNA was increased as early as 4 h after phenobarbital treatment, peaked between 24 and 36 h, and dropped back to control levels by 120 h. The induction of AHH lagged behind the increase in translatable mRNA, remaining at control levels well after levels of translatable mRNA began to increase but then decreasing roughly in parallel with translatable mRNA.	Phenobarbital	71-84	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
6465891-13	1984	Translatable cytochrome P-450 mRNA was increased as early as 4 h after phenobarbital treatment, peaked between 24 and 36 h, and dropped back to control levels by 120 h. The induction of AHH lagged behind the increase in translatable mRNA, remaining at control levels well after levels of translatable mRNA began to increase but then decreasing roughly in parallel with translatable mRNA.	Phenobarbital	71-84	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	186-189
6430587-1	1984	Two cytochromes P450 (PB1 and PB2) have been isolated from the livers of rats treated with phenobarbital.	Phenobarbital	91-104	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	22-25
6430587-6	1984	PB1 and PB2 were induced by phenobarbital, Aroclor 1254, trans-stilbene oxide and to a lesser extent by isosafrole.	Phenobarbital	28-41	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	0-3
6209127-0	1984	Perturbation of calcium homeostasis by CCl4 in rats pretreated with chlordecone and phenobarbital.	Phenobarbital	84-97	C-C motif chemokine ligand 4	Rattus norvegicus	39-43
6209127-3	1984	Induction of cytochrome P-450 was greater with phenobarbital treatment than with chlordecone, but the CCl4-induced destruction of P-450 was similar in both groups and was progressive with the dose of CCl4 and with time after CCl4 administration.	Phenobarbital	47-60	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
6498796-4	1984	BHA enhanced forestomach and urinary bladder carcinogenesis as did SA also for the urinary bladder, whereas PB enhanced the induction of gamma-glutamyl transpeptidase positive (gamma-GT+) foci in the liver and also the incidence of thyroid carcinoma and forestomach carcinoma.	Phenobarbital	108-110	gamma-glutamyltransferase 1	Rattus norvegicus	137-166
6209127-5	1984	These findings are consistent with greater bioactivation of CCl4 after the above two pretreatments There was a massive accumulation of Ca2+ in CD- and PB-pretreated animals after CCl4 administration, CD being more effective in this regard.	Phenobarbital	151-153	C-C motif chemokine ligand 4	Rattus norvegicus	60-64
6209127-5	1984	These findings are consistent with greater bioactivation of CCl4 after the above two pretreatments There was a massive accumulation of Ca2+ in CD- and PB-pretreated animals after CCl4 administration, CD being more effective in this regard.	Phenobarbital	151-153	C-C motif chemokine ligand 4	Rattus norvegicus	179-183
6087814-1	1984	Rats fed a synthetic diet containing 0.25% benzamide, 0.1% phenobarbital, separately or in combination, for two weeks showed a significant augmentation in the activity of nuclear poly(ADP-ribose) polymerase as well as changes in various nuclear, microsomal and cytosolic liver enzymes involved in the metabolism of xenobiotics.	Phenobarbital	59-72	poly (ADP-ribose) polymerase 1	Rattus norvegicus	179-206
6206609-1	1984	The effects of chlordecone (CD), mirex or phenobarbital (PB) treatment of male Mongolian gerbils on CCl4-hepatotoxicity were determined.	Phenobarbital	42-55	C-C motif chemokine ligand 4	Rattus norvegicus	100-104
6206609-1	1984	The effects of chlordecone (CD), mirex or phenobarbital (PB) treatment of male Mongolian gerbils on CCl4-hepatotoxicity were determined.	Phenobarbital	57-59	C-C motif chemokine ligand 4	Rattus norvegicus	100-104
6378929-7	1984	Exposure of confluent monolayers to either phenobarbital or 3-methylcholanthrene resulted in an induction of cytochrome P-450(PB) or cytochrome P-450(MC), respectively.	Phenobarbital	43-56	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	109-129
6378929-7	1984	Exposure of confluent monolayers to either phenobarbital or 3-methylcholanthrene resulted in an induction of cytochrome P-450(PB) or cytochrome P-450(MC), respectively.	Phenobarbital	43-56	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	133-153
6089174-0	1984	Distinct organization of methylcholanthrene- and phenobarbital-inducible cytochrome P-450 genes in the rat.	Phenobarbital	49-62	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	73-89
6089174-3	1984	Comparison of the gene with that of the phenobarbital-inducible cytochrome P-450e showed that the gene structures for the two types of cytochrome P-450 differ greatly; the location, number, and size of intervening sequences are very dissimilar.	Phenobarbital	40-53	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	64-81
6089174-3	1984	Comparison of the gene with that of the phenobarbital-inducible cytochrome P-450e showed that the gene structures for the two types of cytochrome P-450 differ greatly; the location, number, and size of intervening sequences are very dissimilar.	Phenobarbital	40-53	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	64-80
6331457-0	1984	Monoclonal antibodies to phenobarbital-induced rat liver cytochrome P-450.	Phenobarbital	25-38	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	57-73
6331321-1	1984	Uninduced rat liver microsomes and NADPH-Cytochrome P-450 reductase, purified from phenobarbital-treated rats, catalyzed an NADPH-dependent oxidation of hydroxyl radical scavenging agents.	Phenobarbital	83-96	cytochrome p450 oxidoreductase	Rattus norvegicus	35-67
6204978-4	1984	The MAb 1-7-1-sensitive cytochrome P-450 is a major contributor to aryl hydrocarbon hydroxylase in rat liver, lung, and kidney of 3-methylcholanthrene-treated rats, C57BL/6 mice, guinea pigs, and hamsters; this type is also present in lesser amounts in the extrahepatic tissues of the control and PB-treated animals, and in the lungs of the relatively "noninducible" DBA/2 mice treated with 3-methylcholanthrene.	Phenobarbital	297-299	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	24-40
6430240-0	1984	Rat liver DT-diaphorase: regulation of functional mRNA levels by 3-methylcholanthrene, trans-stilbene oxide, and phenobarbital.	Phenobarbital	113-126	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	10-23
6331457-1	1984	Somatic cell hybrids were made between mouse myeloma cells and spleen cells derived from BALB/c female mice immunized with purified phenobarbital-induced rat liver cytochrome P-450 (PB-P-450).	Phenobarbital	132-145	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	164-190
6548043-12	1984	When PB was given alone, hepatic cytochrome P-450 was increased 96% at 16 hours, whereas when combined with cimetidine a similar increase of hepatic cytochrome P-450 was observed.	Phenobarbital	5-7	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	33-49
6589592-7	1984	Comparison with phenobarbital-induced rabbit cytochrome P-450 isozyme 2 indicated about 25% homology.	Phenobarbital	16-29	cytochrome P450 2B4	Oryctolagus cuniculus	45-71
6548043-12	1984	When PB was given alone, hepatic cytochrome P-450 was increased 96% at 16 hours, whereas when combined with cimetidine a similar increase of hepatic cytochrome P-450 was observed.	Phenobarbital	5-7	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	149-165
6743320-1	1984	Treatment of rats with phenobarbital for three days greatly increases the activity of 2,5 oligoadenylate synthetase in liver nuclei.	Phenobarbital	23-36	2'-5' oligoadenylate synthetase 1A	Rattus norvegicus	86-115
6740677-5	1984	The experiments reported herein were designed to identify the relationship between metabolism and toxicity of CHCl3 in the kidney of rabbits, a species in which renal cytochrome P-450 is induced by phenobarbital.	Phenobarbital	198-211	cytochrome P-450	Oryctolagus cuniculus	167-183
6723583-6	1984	The enzyme activities were stimulated by treatment of the rats with phenobarbital, beta-naphthoflavone, 5 alpha-androstane-3 beta,17 beta-diol,5 alpha-dihydrotestosterone, and methyltrienolone, whereas the activities were suppressed by ovine PRL, human GH, estradiol benzoate, cholesterol, andrenalectomy , hypophysectomy, and castration.	Phenobarbital	68-81	prolactin	Rattus norvegicus	242-245
6744241-4	1984	With anthralin a slow decrease of ODC back to control level is observed approximately within 22 h. In contrast, ODC induction mediated by other tumor promoters like TPA and PB decreased to control levels within 4-6 hours.	Phenobarbital	173-175	ornithine decarboxylase 1	Rattus norvegicus	112-115
6587354-1	1984	Insertion of newly synthesized P-450(1), the major phenobarbital-inducible form of rabbit liver microsomal cytochrome P-450, into microsomal membranes was studied in a wheat germ cell-free translation system programed with total RNA from the liver of a phenobarbital-treated rabbit.	Phenobarbital	51-64	cytochrome P450 2C5	Oryctolagus cuniculus	31-39
6587354-1	1984	Insertion of newly synthesized P-450(1), the major phenobarbital-inducible form of rabbit liver microsomal cytochrome P-450, into microsomal membranes was studied in a wheat germ cell-free translation system programed with total RNA from the liver of a phenobarbital-treated rabbit.	Phenobarbital	51-64	cytochrome P-450	Oryctolagus cuniculus	107-123
6331534-0	1984	[Isolation and characterization of the basic forms of cytochrome P-450 from liver microsomes of C57BL mice after phenobarbital and 3-methylcholanthrene induction].	Phenobarbital	113-126	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	54-70
6722175-2	1984	Phenobarbital-inducible isozyme cytochrome P-450 LM2 (RH, reduced-flavoprotein:oxygen oxidoreductase (RH-hydroxylating), EC 1.14.14.1) from rabbit liver microsomes has been modified with N-acetylimidazole and tetranitromethane.	Phenobarbital	0-13	cytochrome P450 2B4	Oryctolagus cuniculus	32-52
6327095-6	1984	No binding occurred when the beta-naphthoflavone-induced isozyme of cytochrome P-450 was replaced by the major isozyme induced by phenobarbital, but both cytochromes incorporated benzo[a]pyrene to approximately the same extent when they were incubated together in the presence of the reductase and NADPH.	Phenobarbital	130-143	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	68-84
6430886-1	1984	A unique form of cytochrome P-450 (called P-450(2] with high affinity for 7-alkoxycoumarins was purified from liver microsomes of phenobarbital-treated rabbits with an overall yield of about 0.6%.	Phenobarbital	130-143	cytochrome P-450	Oryctolagus cuniculus	17-33
6377421-0	1984	Phenobarbital treatment enhances insulin mediated glucose metabolism in man.	Phenobarbital	0-13	insulin	Homo sapiens	33-40
6089451-3	1984	All H2 blockers except for ranitidine (up to 400 microM) produced a concentration-dependent inhibitory effect of the metabolic intermediate (MI)-cytochrome P-450 complex formation which is displayed during metabolism of tofenacine in PB hepatic microsomes in vitro.	Phenobarbital	234-236	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	145-161
6089451-6	1984	In liver microsomes of phenobarbital-pretreated rats, substrate-dependent inhibition of H2O2 production correlates with inhibition of MI-cytochrome P-450 complex formation of tofenacine.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	137-153
6732764-0	1984	Metabolism of cyclophosphamide by purified cytochrome P-450 from microsomes of phenobarbital-treated rats.	Phenobarbital	79-92	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	43-59
6732764-2	1984	These results indicate that phenobarbital-inducible cytochrome P-450 is able to dechlorinate CPA and may account, in part, for the inability of phenobarbital to enhance the therapeutic activity and toxicity of this important anticancer and immunosuppressive agent.	Phenobarbital	28-41	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	52-68
6732764-2	1984	These results indicate that phenobarbital-inducible cytochrome P-450 is able to dechlorinate CPA and may account, in part, for the inability of phenobarbital to enhance the therapeutic activity and toxicity of this important anticancer and immunosuppressive agent.	Phenobarbital	144-157	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	52-68
6325423-1	1984	Complete nucleotide sequence of a glutathione S-transferase mRNA and the regulation of the Ya, Yb, and Yc mRNAs by 3-methylcholanthrene and phenobarbital.	Phenobarbital	140-153	hematopoietic prostaglandin D synthase	Rattus norvegicus	34-59
6712731-10	1984	Fetal hepatic cytochrome P-450 and monooxygenase activities were increased by tilorone in PB- and PCN-induced rats but not in non-induced or MC-induced animals.	Phenobarbital	90-92	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	14-30
6743236-2	1984	Treatment of rats with phenobarbital induces the level of glutathione S-transferase D in testis with no increase in the activities of glutathione S-transferases A and C. This result indicates a specific induction of the Yb2 subunit in testis, in contrast with the situation in rat liver, where phenobarbital specifically induces the Yb1 subunit.	Phenobarbital	23-36	Y box binding protein 3	Rattus norvegicus	220-223
6743236-2	1984	Treatment of rats with phenobarbital induces the level of glutathione S-transferase D in testis with no increase in the activities of glutathione S-transferases A and C. This result indicates a specific induction of the Yb2 subunit in testis, in contrast with the situation in rat liver, where phenobarbital specifically induces the Yb1 subunit.	Phenobarbital	23-36	Y box binding protein 1	Rattus norvegicus	333-336
6743236-2	1984	Treatment of rats with phenobarbital induces the level of glutathione S-transferase D in testis with no increase in the activities of glutathione S-transferases A and C. This result indicates a specific induction of the Yb2 subunit in testis, in contrast with the situation in rat liver, where phenobarbital specifically induces the Yb1 subunit.	Phenobarbital	294-307	Y box binding protein 3	Rattus norvegicus	220-223
6611263-3	1984	Phenobarbital, but not beta-naphthoflavone induced additional cytochrome P-450, which with specific esters could be complexed to about 60%.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	62-78
6547716-0	1984	Induction of mRNA coding for phenobarbital-inducible form of microsomal cytochrome P-450 in rat liver by administration of 1,1-Di(p-chlorophenyl)-2,2-dichloroethylene and phenobarbital.	Phenobarbital	29-42	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	72-88
6547716-0	1984	Induction of mRNA coding for phenobarbital-inducible form of microsomal cytochrome P-450 in rat liver by administration of 1,1-Di(p-chlorophenyl)-2,2-dichloroethylene and phenobarbital.	Phenobarbital	171-184	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	72-88
6746601-0	1984	Induction of a phenobarbital-inducible form of cytochrome P-450 in rat liver microsomes by 1,1-di(p-chlorophenyl)-2,2-dichloroethylene.	Phenobarbital	15-28	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	47-63
6537216-10	1984	Both ethanol and phenobarbital elevated cytochrome P-450; ethanol also elevated cytochrome b5 measured as NADH-reducible cytochrome.	Phenobarbital	17-30	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	40-56
6537216-10	1984	Both ethanol and phenobarbital elevated cytochrome P-450; ethanol also elevated cytochrome b5 measured as NADH-reducible cytochrome.	Phenobarbital	17-30	cytochrome b5 type A	Rattus norvegicus	80-93
6712620-2	1984	The drug blocks the phenobarbitone-mediated induction of cytochrome P-450b.	Phenobarbital	20-34	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	57-74
6713597-9	1984	Although phenobarbital treatment of rats increased the rate of liver microsomal metabolism of precocene I by approximately 50% (nmol products/nmol cytochrome P-450/min) compared to liver microsomes from control rats, hepatic damage caused by precocene I was not significantly affected.	Phenobarbital	9-22	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	147-167
6427199-3	1984	PB-1 and MC-1 were the major cytochrome P-450 components inducible by phenobarbital (PB) and 3-methylcholanthrene (MC), respectively.	Phenobarbital	70-83	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	0-4
6427199-3	1984	PB-1 and MC-1 were the major cytochrome P-450 components inducible by phenobarbital (PB) and 3-methylcholanthrene (MC), respectively.	Phenobarbital	70-83	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	29-45
6427199-3	1984	PB-1 and MC-1 were the major cytochrome P-450 components inducible by phenobarbital (PB) and 3-methylcholanthrene (MC), respectively.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	29-45
6427199-9	1984	The quantity of each form of cytochrome P-450 in microsomes was determined by quantitative immunoprecipitation, and selective induction of PB-1 and MC-1 by PB and MC, respectively, was confirmed.	Phenobarbital	139-141	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	29-45
6700577-5	1984	A reconstituted form of cytochrome P-450 from phenobarbital-pretreated rats metabolized CCl4 to COCl2.	Phenobarbital	46-59	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	24-40
6700577-5	1984	A reconstituted form of cytochrome P-450 from phenobarbital-pretreated rats metabolized CCl4 to COCl2.	Phenobarbital	46-59	C-C motif chemokine ligand 4	Rattus norvegicus	88-92
6701911-1	1984	Vinylcyclooctane (VCO), which binds to the active site of cytochrome P-450 (P-450) giving a type I difference spectrum, has been found to form the corresponding epoxide as the main metabolite on treatment with liver microsomal monooxygenase obtained from phenobarbital-treated or untreated mice.	Phenobarbital	255-268	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	58-74
6710543-2	1984	The inhibition of delta-aminolevulinic acid dehydratase (ALA-D) was examined in liver, blood and bone marrow of naive and phenobarbital pretreated animals exposed to TRI.	Phenobarbital	122-135	aminolevulinate dehydratase	Rattus norvegicus	18-55
6710543-2	1984	The inhibition of delta-aminolevulinic acid dehydratase (ALA-D) was examined in liver, blood and bone marrow of naive and phenobarbital pretreated animals exposed to TRI.	Phenobarbital	122-135	aminolevulinate dehydratase	Rattus norvegicus	57-62
6710543-4	1984	In addition to this finding, significant interaction between TRI exposure and phenobarbital treatment was observed in the inhibition of ALA-D in liver and blood.	Phenobarbital	78-91	aminolevulinate dehydratase	Rattus norvegicus	136-141
6421810-1	1984	The zwitterionic detergent 3-(3-cholamidopropyl)-dimethylammonio-1-propanesulfonate (CHAPS) supports reconstituted cyclohexane hydroxylase activity of cytochrome P-450LM2 and NADPH-cytochrome reductase purified from phenobarbital-induced rabbit liver.	Phenobarbital	216-229	cytochrome P450 2B4	Oryctolagus cuniculus	151-170
6698172-2	1984	Moreover, dinemorphan N-demethylation is inhibited by CO, SKF-525A, metyrapone and it is specifically catalyzed by a phenobarbital-inducible form of cytochrome P-450.	Phenobarbital	117-130	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	149-165
6701906-4	1984	There was a concommitant time-dependent decline in cytochrome P-450 levels in the phenobarbital pretreated animals, but not controls.	Phenobarbital	82-95	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	51-67
6421617-3	1984	The steroid 21-hydroxylase activity of liver microsomes decreased with treatment by sodium phenobarbital or beta-naphthoflavone and was inhibited by anti-cytochrome b5 immunoglobulin, although that of adrenocortical microsomes was not.	Phenobarbital	84-104	LOC107131127	Bos taurus	4-26
6546728-0	1984	Regulation of glutathione S-transferase mRNAs by phenobarbital and 3-methylcholanthrene: analysis using cDNA probes.	Phenobarbital	49-62	glutathione S-transferase kappa 1	Homo sapiens	14-39
6697440-0	1984	Relation between induction of rat hepatic ornithine decarboxylase activity by tumor promoters 12-O-tetradecanoylphorbol-13-acetate and phenobarbital and levels of the polyamines putrescine, spermidine and spermine, in vivo; differential effects of retinyl-acetate.	Phenobarbital	135-148	ornithine decarboxylase 1	Rattus norvegicus	42-65
6366529-2	1984	Upon incubating emodin with the hepatic S9 derived from PCB-pretreated rats, this anthraquinone exhibited mutagenicity in the presence of NADPH or NADH, and this enzymatic activation, maximal at pH 7.0 and occurring in the microsomes, was induced by the pretreatment of rats with PCB, 3-methyl-cholanthrene or phenobarbital and was inhibited by alpha-naphthoflavone, SKF 525A and carbon monoxide.	Phenobarbital	310-323	pyruvate carboxylase	Rattus norvegicus	56-59
6693395-3	1984	Microsomal epoxide hydrolase was purified to homogeneity from phenobarbital-induced rabbit liver for the purpose of determining the complete amino acid sequence.	Phenobarbital	62-75	epoxide hydrolase 1	Oryctolagus cuniculus	0-28
6546520-0	1984	Isolation and sequence analysis of three cloned cDNAs for rabbit liver proteins that are related to rabbit cytochrome P-450 (form 2), the major phenobarbital-inducible form.	Phenobarbital	144-157	cytochrome P-450	Oryctolagus cuniculus	107-131
6546520-9	1984	These cDNAs are part of a family of genes that are related to rabbit liver cytochrome P-450 (form 2) and rat liver cytochrome P-450b which are the major phenobarbital-inducible forms.	Phenobarbital	153-166	cytochrome P-450	Oryctolagus cuniculus	75-91
6546520-9	1984	These cDNAs are part of a family of genes that are related to rabbit liver cytochrome P-450 (form 2) and rat liver cytochrome P-450b which are the major phenobarbital-inducible forms.	Phenobarbital	153-166	cytochrome P-450	Oryctolagus cuniculus	93-99
6546520-9	1984	These cDNAs are part of a family of genes that are related to rabbit liver cytochrome P-450 (form 2) and rat liver cytochrome P-450b which are the major phenobarbital-inducible forms.	Phenobarbital	153-166	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	115-132
6330937-4	1984	Pretreatment of C57 and DBA mice with phenobarbital (PB) markedly increased hepatic AHH activity and hepatotoxicity of CHCl3 in both strains but did not affect renal AHH or nephrotoxicity of CHCl3.	Phenobarbital	38-51	aryl-hydrocarbon receptor	Mus musculus	84-87
6330937-4	1984	Pretreatment of C57 and DBA mice with phenobarbital (PB) markedly increased hepatic AHH activity and hepatotoxicity of CHCl3 in both strains but did not affect renal AHH or nephrotoxicity of CHCl3.	Phenobarbital	53-55	aryl-hydrocarbon receptor	Mus musculus	84-87
6144610-9	1984	Administration of phenobarbital after N-2-fluorenylacetamide resulted in an elevation of liver and plasma gamma-glutamyltranspeptidase, but none of the benzodiazepines produced this effect and thus no biochemical evidence of a promoting effect on the liver was observed.	Phenobarbital	18-31	gamma-glutamyltransferase 1	Rattus norvegicus	106-134
6724188-4	1984	Isozyme 3a, 4, and 6, the three major forms of cytochrome P-450 present in liver microsomes from rabbits chronically treated with ethanol, exhibited the highest activities in the reconstituted enzyme system, whereas isozymes 3b and 3c were 10- to 20-fold less effective and phenobarbital-inducible isozyme 2 was essentially inactive, even in the presence of cytochrome b5.	Phenobarbital	274-287	cytochrome P-450	Oryctolagus cuniculus	47-63
6547716-3	1984	95, 937-947), we reported that 1,1-di(p-chlorophenyl)-2,2-dichloro-ethylene (DDE) induced the phenobarbital (PB)-inducible form of microsomal cytochrome P-450 (P-450(PB-1) in rat liver.	Phenobarbital	94-107	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	142-158
6547716-3	1984	95, 937-947), we reported that 1,1-di(p-chlorophenyl)-2,2-dichloro-ethylene (DDE) induced the phenobarbital (PB)-inducible form of microsomal cytochrome P-450 (P-450(PB-1) in rat liver.	Phenobarbital	94-107	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	160-170
6547716-3	1984	95, 937-947), we reported that 1,1-di(p-chlorophenyl)-2,2-dichloro-ethylene (DDE) induced the phenobarbital (PB)-inducible form of microsomal cytochrome P-450 (P-450(PB-1) in rat liver.	Phenobarbital	109-111	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	142-158
6547716-3	1984	95, 937-947), we reported that 1,1-di(p-chlorophenyl)-2,2-dichloro-ethylene (DDE) induced the phenobarbital (PB)-inducible form of microsomal cytochrome P-450 (P-450(PB-1) in rat liver.	Phenobarbital	109-111	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	160-170
6547716-4	1984	In order to study more precisely the molecular events responsible for the induction of this particular form of cytochrome P-450 by the two chemical compounds, we determined the amounts of the mRNA coding for P-450(PB-1) in the liver of rats given a single dose of PB or DDE.	Phenobarbital	214-216	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	111-127
6464499-0	1984	Induction of cytosolic glutathione transferase and microsomal epoxide hydrolase activities in extrahepatic organs of the rat by phenobarbital, 3-methylcholanthrene and trans-stilbene oxide.	Phenobarbital	128-141	epoxide hydrolase 1	Rattus norvegicus	51-79
6464499-1	1984	The effects of treating male Sprague-Dawley rats with phenobarbital, 3-methylcholanthrene or trans-stilbene oxide on cytosolic glutathione transferase and microsomal epoxide hydrolase activities in the liver, intestine, kidney, lung, testis, adrenal, spleen, heart and brain have been investigated.	Phenobarbital	54-67	epoxide hydrolase 1	Rattus norvegicus	155-183
6464499-3	1984	Phenobarbital induces both cytosolic glutathione transferase and microsomal epoxide hydrolase activities significantly only in liver and intestine.	Phenobarbital	0-13	epoxide hydrolase 1	Rattus norvegicus	65-93
6712655-0	1984	Preparation and characterization of monoclonal antibodies against phenobarbital-inducible cytochrome P-450.	Phenobarbital	66-79	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	90-106
6712655-1	1984	Monoclonal antibodies against cytochrome P-450 were prepared from phenobarbital-induced rat liver microsomes.	Phenobarbital	66-79	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	30-46
6712655-3	1984	Their specificity was verified by various techniques and seemed to correspond to a single form of cytochrome P-450, the major phenobarbital-inducible form.	Phenobarbital	126-139	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	98-114
6703710-0	1984	Detection of phenobarbital-induced cytochrome P-450 in rat hepatic microsomes using an enzyme-linked immunosorbent assay.	Phenobarbital	13-26	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	35-51
6703710-1	1984	The major phenobarbital-inducible form of cytochrome P-450 (cytochrome P-450 PB) was purified to homogeneity from rat liver microsomes and rabbit antibodies prepared against the purified enzyme.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	42-58
6703710-1	1984	The major phenobarbital-inducible form of cytochrome P-450 (cytochrome P-450 PB) was purified to homogeneity from rat liver microsomes and rabbit antibodies prepared against the purified enzyme.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	60-76
6703710-4	1984	Phenobarbital and Aroclor 1254 pretreatments resulted in several-fold increases in immunoreactive cytochrome P-450 PB over control levels.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	98-114
6703710-10	1984	Concomitant pretreatment with phenobarbital and AT resulted in levels of ELISA-detectable cytochrome P-450 PB which were significantly increased over control levels, while spectrally detectable levels of total holoenzyme remained unchanged.	Phenobarbital	30-43	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	90-106
6721585-0	1984	Effect of phenobarbitol pretreatment on regeneration of plasma cholinesterase activity inhibited by parathion or dichlorovos.	Phenobarbital	10-23	butyrylcholinesterase	Homo sapiens	63-77
6373027-0	1984	A biochemical and electron microscopic study of changes in the content of cytochrome P-450 in rat livers after cessation of treatment with phenobarbital, beta-naphtoflavone or 3-methylcholanthrene.	Phenobarbital	139-152	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	74-90
6427199-0	1984	Purification and characterization of four forms of cytochrome P-450 from liver microsomes of phenobarbital-treated and 3-methylcholanthrene-treated rats.	Phenobarbital	93-106	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	51-67
6142138-0	1984	Effect of coadministration of phenobarbital sodium on N-nitrosodiethylamine-induced gamma-glutamyltransferase-positive foci and hepatocellular carcinoma in rats.	Phenobarbital	30-50	gamma-glutamyltransferase 1	Rattus norvegicus	84-109
6142138-1	1984	The effect of concurrent administration of phenobarbital on the hepatocarcinogenicity of N-nitrosodiethylamine (diethylnitrosamine; DENA) in rats was investigated by determination of the incidence of gamma-glutamyltransferase (gamma-glutamyltranspeptidase) (GGT)-positive foci and liver tumors.	Phenobarbital	43-56	gamma-glutamyltransferase 1	Rattus norvegicus	200-225
6562683-1	1984	Incubation of premitochondrial liver homogenate supernatants of phenobarbital-induced rats with sodium vanadate led to a time- and concentration-dependent formation of malondialdehyde and a parallel release of beta-glucuronidase from lysosomes.	Phenobarbital	64-77	glucuronidase, beta	Rattus norvegicus	210-228
6584898-4	1984	Computer-aided analysis was carried out to compare the complete primary structures of five species of cytochrome P-450, two molecular species of phenobarbital-inducible rat liver cytochrome P-450 (P-450b and P-450e), phenobarbital-inducible rabbit liver cytochrome P-450LM2, 3-methylcholanthrene-inducible rat liver cytochrome P-450d, and camphor-hydroxylating P-450 of Pseudomonas putida (P-450CAM).	Phenobarbital	145-158	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	179-195
6584898-4	1984	Computer-aided analysis was carried out to compare the complete primary structures of five species of cytochrome P-450, two molecular species of phenobarbital-inducible rat liver cytochrome P-450 (P-450b and P-450e), phenobarbital-inducible rabbit liver cytochrome P-450LM2, 3-methylcholanthrene-inducible rat liver cytochrome P-450d, and camphor-hydroxylating P-450 of Pseudomonas putida (P-450CAM).	Phenobarbital	145-158	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	197-203
6741019-2	1984	Administration of phenobarbital leads to cytochrome P-450 induction and activation of monooxygenase of rat liver microsomes, the quality of food protein not affecting cytochrome induction.	Phenobarbital	18-31	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	41-57
6322806-0	1984	Elevated binding of 2,3,7,8-tetrachlorodibenzo-p-dioxin and 3-methylcholanthrene to the Ah receptor in hepatic cytosols from phenobarbital-treated rats and mice.	Phenobarbital	125-138	aryl hydrocarbon receptor	Rattus norvegicus	88-99
6322806-3	1984	Injection of 50-100 mg/kg of phenobarbital (PB) for 3 days more than doubled the concentration of Ah receptor in hepatic cytosol from Sprague-Dawley rats.	Phenobarbital	29-42	aryl hydrocarbon receptor	Rattus norvegicus	98-109
6322806-3	1984	Injection of 50-100 mg/kg of phenobarbital (PB) for 3 days more than doubled the concentration of Ah receptor in hepatic cytosol from Sprague-Dawley rats.	Phenobarbital	44-46	aryl hydrocarbon receptor	Rattus norvegicus	98-109
6322806-4	1984	In C57BL/6J mice, PB injection at 25 mg/kg X 3 days significantly increased (P less than 0.01) the Ah receptor concentration in hepatic cytosol.	Phenobarbital	18-20	aryl-hydrocarbon receptor	Mus musculus	99-110
6322806-6	1984	Although PB significantly elevated Ah receptor in hepatic cytosols of responsive rodents, many previous studies have shown that the maximal level of AHH activity in animals given PB and an "MC-type" inducer simultaneously is additive rather than synergistic.	Phenobarbital	9-11	aryl-hydrocarbon receptor	Mus musculus	35-46
6322806-7	1984	Ah receptor concentrations can be doubled by PB treatment without doubling the subsequent AHH-induction response to "MC-type" compounds.	Phenobarbital	45-47	aryl-hydrocarbon receptor	Mus musculus	0-11
6704114-1	1984	Cytochrome P-450, purified from liver microsomes of phenobarbital-treated rabbits, was incorporated into dimyristoylphosphatidylcholine liposomes.	Phenobarbital	52-65	cytochrome P-450	Oryctolagus cuniculus	0-16
6704172-3	1984	The disappearance of cytochrome P-450 was especially fast in hepatocytes obtained from female phenobarbital-treated rats where only 40% of the original cytochrome P-450 was present after 2 hr in culture and 80% had disappeared in 2 days.	Phenobarbital	94-107	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	21-37
6704172-3	1984	The disappearance of cytochrome P-450 was especially fast in hepatocytes obtained from female phenobarbital-treated rats where only 40% of the original cytochrome P-450 was present after 2 hr in culture and 80% had disappeared in 2 days.	Phenobarbital	94-107	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	152-168
6693411-1	1984	A rapid solid phase radioimmunoassay (RIA) for cytochromes P-450 has been developed utilizing specific monoclonal antibodies to major forms of rat liver cytochrome P-450 that are induced by 3-methylcholanthrene (MC-P-450) and phenobarbital (PB-P-450).	Phenobarbital	226-239	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	153-169
6426342-4	1984	Cytochrome P-450, form 2, was detected and quantitated in microsomal samples containing 0.1 to 0.5 and 0.02 to 0.05 micrograms protein for preparations from untreated and phenobarbital-treated rabbits, respectively.	Phenobarbital	171-184	cytochrome P-450	Oryctolagus cuniculus	0-24
6147962-2	1984	Hyperplastic liver nodules of various size classes from the phenobarbital-treated group exhibited a significant increase in GGT specific activity, as well as 2- to 3-fold higher levels of microsomal cytochrome P-450 than was shown by control nodules.	Phenobarbital	60-73	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	199-215
6328898-6	1984	Therapy with phenobarbital and medroxyprogesterone acetate, known inducers, increased G6Pase activity, shortened antipyrine T/2, reduced BG and did not alter IRI, in four NIDDs .	Phenobarbital	13-26	glucose-6-phosphatase catalytic subunit 1	Homo sapiens	86-92
6422940-13	1984	A genetic variation between the strains was observed after phenobarbital (PB) treatment in the content of cytochrome P-450 and in the various enzyme activities, varying from non-responsiveness to a 4- to 5-fold increase.	Phenobarbital	59-72	Cytochrome P450-9b2	Drosophila melanogaster	106-122
6496222-4	1984	Phenobarbital induction gave 20% of the PCB response and Pregnenolone-16a-carbonitrile and corn oil were inactive.	Phenobarbital	0-13	pyruvate carboxylase	Homo sapiens	40-43
6101050-0	1984	[Effect of phenobarbital on the morphologic, histochemical and ultrastructural picture of the rat liver after chronic administration of CCl4].	Phenobarbital	11-24	C-C motif chemokine ligand 4	Rattus norvegicus	136-140
6534377-1	1984	A method for the isolation of liver microsomal cytochrome P-450 from phenobarbital-treated rats is described which is based on chromatography on 1-adamantane-carbonyl-aminohexyl-Sepharose 4B, subsequent ion exchange chromatography on DEAE-cellulose and detergent removal by adsorption on silica gel G. The method gives preparations with high electrophoretic homogeneity which correspond to a major phenobarbital-inducible form of rat liver microsomal cytochrome P-450.	Phenobarbital	69-82	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	47-63
6422940-13	1984	A genetic variation between the strains was observed after phenobarbital (PB) treatment in the content of cytochrome P-450 and in the various enzyme activities, varying from non-responsiveness to a 4- to 5-fold increase.	Phenobarbital	74-76	Cytochrome P450-9b2	Drosophila melanogaster	106-122
6534377-1	1984	A method for the isolation of liver microsomal cytochrome P-450 from phenobarbital-treated rats is described which is based on chromatography on 1-adamantane-carbonyl-aminohexyl-Sepharose 4B, subsequent ion exchange chromatography on DEAE-cellulose and detergent removal by adsorption on silica gel G. The method gives preparations with high electrophoretic homogeneity which correspond to a major phenobarbital-inducible form of rat liver microsomal cytochrome P-450.	Phenobarbital	69-82	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	451-467
6422942-1	1984	Various substrates of rat liver microsomal UDP-glucuronosyltransferase were classified in vitro as preferred substrates of either 3-methylcholanthrene- or phenobarbital-inducible enzyme forms.	Phenobarbital	155-168	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	43-70
6534377-1	1984	A method for the isolation of liver microsomal cytochrome P-450 from phenobarbital-treated rats is described which is based on chromatography on 1-adamantane-carbonyl-aminohexyl-Sepharose 4B, subsequent ion exchange chromatography on DEAE-cellulose and detergent removal by adsorption on silica gel G. The method gives preparations with high electrophoretic homogeneity which correspond to a major phenobarbital-inducible form of rat liver microsomal cytochrome P-450.	Phenobarbital	398-411	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	47-63
6140087-2	1984	Phenobarbitone induced gamma-glutamyltranspeptidase activity in perilobular hepatocytes.	Phenobarbital	0-14	gamma-glutamyltransferase 1	Rattus norvegicus	23-51
6547088-0	1984	Characterization of a cDNA clone for mouse phenobarbital-inducible cytochrome P-450b.	Phenobarbital	43-56	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	78-84
6547088-9	1984	Two previously reported cDNA clones of phenobarbital-inducible rat P-450, R17 (P- 450e ) and pcP- 450pb4 (P-450b), were compared with mouse p40.	Phenobarbital	39-52	ribonuclease 17	Rattus norvegicus	67-77
6547088-1	1984	p40, a mouse 1040-nucleotide cDNA clone encoding a form of phenobarbital-inducible cytochrome P-450b, was selected by probing a cDNA library derived from phenobarbital-treated DBA/2N mouse liver with a rat 1830-nucleotide cDNA probe complementary to P-450b mRNA.	Phenobarbital	59-72	interleukin 12b	Mus musculus	0-3
6547088-9	1984	Two previously reported cDNA clones of phenobarbital-inducible rat P-450, R17 (P- 450e ) and pcP- 450pb4 (P-450b), were compared with mouse p40.	Phenobarbital	39-52	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	106-112
6547088-1	1984	p40, a mouse 1040-nucleotide cDNA clone encoding a form of phenobarbital-inducible cytochrome P-450b, was selected by probing a cDNA library derived from phenobarbital-treated DBA/2N mouse liver with a rat 1830-nucleotide cDNA probe complementary to P-450b mRNA.	Phenobarbital	59-72	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	94-100
6547088-1	1984	p40, a mouse 1040-nucleotide cDNA clone encoding a form of phenobarbital-inducible cytochrome P-450b, was selected by probing a cDNA library derived from phenobarbital-treated DBA/2N mouse liver with a rat 1830-nucleotide cDNA probe complementary to P-450b mRNA.	Phenobarbital	59-72	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	250-256
6547088-1	1984	p40, a mouse 1040-nucleotide cDNA clone encoding a form of phenobarbital-inducible cytochrome P-450b, was selected by probing a cDNA library derived from phenobarbital-treated DBA/2N mouse liver with a rat 1830-nucleotide cDNA probe complementary to P-450b mRNA.	Phenobarbital	154-167	interleukin 12b	Mus musculus	0-3
6547088-1	1984	p40, a mouse 1040-nucleotide cDNA clone encoding a form of phenobarbital-inducible cytochrome P-450b, was selected by probing a cDNA library derived from phenobarbital-treated DBA/2N mouse liver with a rat 1830-nucleotide cDNA probe complementary to P-450b mRNA.	Phenobarbital	154-167	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	94-100
6141905-0	1984	Correlation between antipyrine clearance and cytochrome P-450 level after phenobarbital induction in rat.	Phenobarbital	74-87	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	45-61
6326415-0	1984	Glucose-6-phosphatase activities in the developing rat liver and kidney and after phenobarbital, 3-methylcholanthrene, and actinomycin D pretreatment.	Phenobarbital	82-95	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	0-21
6150844-0	1984	[Histochemical appearance of gamma-glutamyltranspeptidase in the rat liver after transplacental exposure to diethylnitrosamine and postnatal administration of phenobarbital].	Phenobarbital	159-172	gamma-glutamyltransferase 1	Rattus norvegicus	29-57
6201621-5	1984	In addition, PB protected cultures from the cytotoxic effects of AFB1, as evidenced by a significantly reduced (p less than 0.05) leakage of lactate dehydrogenase into the medium at 51 h. Elevated mixed-function oxidase and glutathione S-transferase activities, as well as higher levels of AFB1-glutathione conjugate were measured in cultures from rats pretreated with PB.	Phenobarbital	13-15	hematopoietic prostaglandin D synthase	Rattus norvegicus	224-249
6326393-17	1984	The corresponding values for purified and microsomal cytochrome P-450 from phenobarbital-pretreated rats are 1 and 6, respectively.	Phenobarbital	75-88	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	53-69
6326393-19	1984	Type I binding spectra with purified yeast cytochrome P-448 were observed with benzo[a]pyrene, lanosterol, ethylmorphine, dimethylnitrosamine, sodium phenobarbitone and perhydrofluorene.	Phenobarbital	143-164	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	43-59
6666162-2	1983	While the frequency of exchange transfusions due to hyperbilirubinaemia and ABO incompatibility could be reduced by 90% by phototherapy and phenobarbital prophylaxis, only 55% reduction was observed in connection with rhesus immunization.	Phenobarbital	140-153	ABO, alpha 1-3-N-acetylgalactosaminyltransferase and alpha 1-3-galactosyltransferase	Homo sapiens	76-79
6654907-3	1983	Cytochrome P-450LM4 from phenobarbital-treated rabbits as well as cytochromes P-450LM4 I and P-450LM4 II from cholestyramine-treated rabbits were able to bind cholesterol.	Phenobarbital	25-38	cytochrome P450 1A2	Oryctolagus cuniculus	0-19
6654907-3	1983	Cytochrome P-450LM4 from phenobarbital-treated rabbits as well as cytochromes P-450LM4 I and P-450LM4 II from cholestyramine-treated rabbits were able to bind cholesterol.	Phenobarbital	25-38	cytochrome P450 1A2	Oryctolagus cuniculus	11-19
6696448-1	1984	Complex formation between the phenobarbital-inducible form of rabbit liver microsomal cytochrome P-450 incorporated into phosphatidylcholine and detergent-solubilized cytochrome b5 is associated with a low-to-high spin transition of the former pigment.	Phenobarbital	30-43	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	86-102
6696448-1	1984	Complex formation between the phenobarbital-inducible form of rabbit liver microsomal cytochrome P-450 incorporated into phosphatidylcholine and detergent-solubilized cytochrome b5 is associated with a low-to-high spin transition of the former pigment.	Phenobarbital	30-43	cytochrome b5	Oryctolagus cuniculus	167-180
6705991-1	1984	Cytochromes P-450b and P-450e are two phenobarbital-inducible rat hepatic microsomal isoenzymes that possess approx.	Phenobarbital	38-51	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	12-18
6419743-10	1983	Cytochrome p-450 content and cytochrome c reductase activity were induced approximately 2.5- and 2.0-fold, respectively, by phenobarbital while aminopyrine demethylase activity was induced about 30% in each strain.	Phenobarbital	124-137	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
6196592-0	1983	Destruction of hepatic mixed-function oxygenase parameters by CCl4 in rats following acute treatment with chlordecone, Mirex, and phenobarbital.	Phenobarbital	130-143	C-C motif chemokine ligand 4	Rattus norvegicus	62-66
6661250-2	1983	Metyrapone (2-methyl-1,2-di-3-pyridyl-1-propanone, MTP) is used as an inhibitor of cytochrome P-450 enzymes, particularly those induced by phenobarbital (PB).	Phenobarbital	139-152	microsomal triglyceride transfer protein	Rattus norvegicus	51-54
6661250-2	1983	Metyrapone (2-methyl-1,2-di-3-pyridyl-1-propanone, MTP) is used as an inhibitor of cytochrome P-450 enzymes, particularly those induced by phenobarbital (PB).	Phenobarbital	154-156	microsomal triglyceride transfer protein	Rattus norvegicus	51-54
6661254-1	1983	Bis(tri-n-butyltin)oxide, an agriculturally important biocidal agent, when added in vitro to liver microsomes containing the phenobarbital-induced form of cytochrome P-450, produced a typical type I binding spectrum (an absorption maximum at 390 nm; an absorption minimum at 420 nm).	Phenobarbital	125-138	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	155-171
6661254-4	1983	The formation of cytochrome P-420 was both time and temperature dependent, and it also occurred to a greater extent in microsomal preparations containing cytochrome P-448 than in microsomes containing the phenobarbital-induced form of cytochrome P-450.	Phenobarbital	205-218	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	235-251
6196592-8	1983	PB caused the greatest increase in total P-450 content and the greatest increase in CCl4-mediated destruction of microsomal protein and APD activity.	Phenobarbital	0-2	C-C motif chemokine ligand 4	Rattus norvegicus	84-88
6651850-1	1983	Several rat liver cytochromes P-450 have been substantially purified in a one-step immunoadsorption procedure using Sepharose-bound monoclonal antibodies (MAbs) to the major forms of rat liver cytochrome P-450 induced by 3-methylcholanthrene and phenobarbital (MC-P-450 and PB-P-450, respectively).	Phenobarbital	246-259	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	193-209
6141764-0	1983	Molecular induction by phenobarbital of a rat hepatic form of cytochrome P-450: expression of a 4-kilobase messenger RNA.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	62-78
6141764-1	1983	A differential screening procedure was employed to isolate a cDNA clone corresponding to a major phenobarbital (PB)-inducible form of rat hepatic cytochrome P-450.	Phenobarbital	97-110	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	146-162
6141764-1	1983	A differential screening procedure was employed to isolate a cDNA clone corresponding to a major phenobarbital (PB)-inducible form of rat hepatic cytochrome P-450.	Phenobarbital	112-114	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	146-162
6141764-9	1983	One cDNA clone, designated PB-8, contained a 600-bp insert partially coding for a PB-inducible cytochrome P-450 species that comigrated on SDS-gel electrophoresis with highly purified P-450b.	Phenobarbital	27-29	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	95-111
6584878-7	1983	Similar changes in steroid delta 4-5 alpha-reduction and cytochrome P-450-dependent chemical oxidations have been observed in circumstances in which the mixed-function oxidase system in liver is induced by agents such as phenobarbital, hexachlorobenzene, dioxin, and polyhalogenated biphenyls.	Phenobarbital	221-234	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	57-73
6661223-1	1983	The major form of cytochrome P-450 isolated and purified from the hepatic microsomes of phenobarbital pretreated rats by sequential chromatography on n-octylamino-Sepharose 4B and DEAE-cellulose columns was found to be homogeneous by sodium dodecyl sulphate-polyacrylamide gel electrophoresis.	Phenobarbital	88-101	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	18-34
6418173-3	1983	We have now shown that at least 4 of these barbiturates (phenobarbital, secobarbital, pentobarbital and methohexital) seem to induce the same active cytochrome P-450-containing enzyme by a non-substrate type mechanism.	Phenobarbital	57-70	cytochrome P450	Bacillus megaterium NBRC 15308 = ATCC 14581	149-165
6418176-4	1983	Cytochrome P-450-dependent S-oxidation of thiobenzamide was induced in the liver by treatment of mice with phenobarbital and slightly increased by treatment with 3-methylcholanthrene, while in rat liver either of these treatments caused only a small increase in metabolism due to cytochrome P-450.	Phenobarbital	107-120	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	0-16
6416256-6	1983	The degree of stimulation was somewhat different when using microsomes from phenobarbital- or beta-naphthoflavone-treated animals, implying a selectivity of the cytosolic effect for various isozymes of cytochrome P-450.	Phenobarbital	76-89	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	202-218
6688781-0	1983	Evidence that 2-allyl-2-isopropylacetamide, phenobarbital and 3,5-diethoxycarbonyl-1,4-dihydrocollidine induce the same cytochrome P450 mRNA in chick embryo liver.	Phenobarbital	44-57	cytochrome P450 709B1	Triticum aestivum	120-135
6201195-1	1983	Phenobarbital treatment and streptozotocin-diabetes both increase, in mouse and rat microsomes, a benzphetamine-N-demethylase activity which can be inhibited by a specific antibody raised against purified rat phenobarbital-induced cytochrome P-450.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	231-247
6201195-1	1983	Phenobarbital treatment and streptozotocin-diabetes both increase, in mouse and rat microsomes, a benzphetamine-N-demethylase activity which can be inhibited by a specific antibody raised against purified rat phenobarbital-induced cytochrome P-450.	Phenobarbital	209-222	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	231-247
6631725-6	1983	CL*int,HB and CL*int,AP were both increased by PB pretreatment, but 3-MC-pretreatment increased CL*int,AP, whereas CL*int,HB was decreased.	Phenobarbital	47-49	clathrin interactor 1	Rattus norvegicus	0-9
6416257-1	1983	Acetone stimulated NADPH-dependent aniline hydroxylation catalysed by cytochrome P-450 purified from phenobarbital-treated rats.	Phenobarbital	101-114	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	70-86
6139159-0	1983	The effect of pre- and post-treatment with phenobarbital on the extent of gamma-glutamyl transpeptidase positive foci induced in rat liver by N-nitrosomorpholine.	Phenobarbital	43-56	gamma-glutamyltransferase 1	Rattus norvegicus	74-103
6139159-3	1983	When given after the carcinogen treatment, phenobarbital enhanced the formation of gamma-GT-positive foci in liver compared with rats treated with NNM alone.	Phenobarbital	43-56	gamma-glutamyltransferase 1	Rattus norvegicus	83-91
6317666-7	1983	In RNA blot analysis with MC-, polychlorinated biphenyls (PCB)-, and phenobarbital (PB)-induced mRNA as well as uninduced mRNA, a longer cDNA (P-34) which had been isolated by hybridization with the insertion of clone 3-9-1, and the previously isolated PB-inducible cytochrome P-450b cDNA (Fujii-Kuriyama et al.	Phenobarbital	69-82	alpha- and gamma-adaptin binding protein	Rattus norvegicus	143-147
6317666-7	1983	In RNA blot analysis with MC-, polychlorinated biphenyls (PCB)-, and phenobarbital (PB)-induced mRNA as well as uninduced mRNA, a longer cDNA (P-34) which had been isolated by hybridization with the insertion of clone 3-9-1, and the previously isolated PB-inducible cytochrome P-450b cDNA (Fujii-Kuriyama et al.	Phenobarbital	253-255	alpha- and gamma-adaptin binding protein	Rattus norvegicus	143-147
6631725-6	1983	CL*int,HB and CL*int,AP were both increased by PB pretreatment, but 3-MC-pretreatment increased CL*int,AP, whereas CL*int,HB was decreased.	Phenobarbital	47-49	clathrin interactor 1	Rattus norvegicus	14-23
6639678-3	1983	Support for such interpretation was provided by the finding that the spectral binding curve for a purified sample of the principal cytochrome P-450 isoenzyme from liver microsomes of phenobarbitone-pretreated rats could be described adequately by a single rectangular hyperbolic relationship, the spectral dissociation constant being indistinguishable experimentally from that for the weaker class of cytochrome P-450 binding site in the corresponding microsomes.	Phenobarbital	183-197	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	131-147
6662113-7	1983	Phenobarbital induces aldrin epoxidase in the absence of dexamethasone in the culture medium, providing that the cells are pretreated with the corticoid for 48 h. The use of antibodies against the main cytochrome P-450 species purified from adult and phenobarbital-treated rats confirms that a similar cytochrome P-450 can be induced in fetal cells in culture.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	202-218
6662113-7	1983	Phenobarbital induces aldrin epoxidase in the absence of dexamethasone in the culture medium, providing that the cells are pretreated with the corticoid for 48 h. The use of antibodies against the main cytochrome P-450 species purified from adult and phenobarbital-treated rats confirms that a similar cytochrome P-450 can be induced in fetal cells in culture.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	302-318
6639678-3	1983	Support for such interpretation was provided by the finding that the spectral binding curve for a purified sample of the principal cytochrome P-450 isoenzyme from liver microsomes of phenobarbitone-pretreated rats could be described adequately by a single rectangular hyperbolic relationship, the spectral dissociation constant being indistinguishable experimentally from that for the weaker class of cytochrome P-450 binding site in the corresponding microsomes.	Phenobarbital	183-197	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	401-417
6604612-1	1983	Certain anticonvulsant drugs, especially phenytoin and phenobarbital, interfere with vitamin K metabolism as indicated by a raised serum osteocalcin level.	Phenobarbital	55-68	bone gamma-carboxyglutamate protein	Homo sapiens	137-148
6414466-1	1983	Three forms of cytochrome P-450 were purified to homogeneity from liver microsomes of Wistar-strain rats treated with phenobarbital.	Phenobarbital	118-131	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	15-31
6309378-10	1983	Phenobarbital increased enzyme activities of EH and UDPGT by about 50%.	Phenobarbital	0-13	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	52-57
6415197-2	1983	Luteinizing hormone releasing hormone was administered by infusion to rats anaesthetized with phenobarbitone.	Phenobarbital	94-108	gonadotropin releasing hormone 1	Rattus norvegicus	0-37
6360828-4	1983	On the other hand, S-9 fractions from rat liver induced with Aroclor 1254 or with a combination of phenobarbital and 5,6-benzoflavone activated both DAA and DAPB, DAA being by far the more mutagenic of the two.	Phenobarbital	99-112	ribosomal protein S9	Homo sapiens	19-22
6360828-5	1983	S-9 preparations from mixed liver, kidney and spleen homogenates from animals pretreated with Aroclor or with phenobarbital and 5,6-benzoflavone were less effective than the liver homogenates.	Phenobarbital	110-123	ribosomal protein S9	Homo sapiens	0-3
6314341-1	1983	To study the relationship between the dose of phenobarbital (PB) and the magnitude of its effects on microsomal enzymes, cytochrome P-450, UDP-glucuronyl transferase (UDPGT), and glucose-6-phosphatase (G6P) activities were determined in liver homogenate and microsome preparations from control rats and rats treated for 6 days with PB at doses ranging from 1 to 125 mg/kg/day.	Phenobarbital	46-59	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	139-165
6630514-6	1983	Treatment of cultures with phenobarbital or 2-propyl-2-isopropylacetamide significantly increased oxidation at C-16 (1.9-fold and 2.6-fold greater than control values, respectively), whereas no significant change in C-16 oxidation was observed after treatment of the cultures with 3-methylcholanthrene, benzo[a]pyrene, or benz[a]anthracene.	Phenobarbital	27-40	galectin 1B	Gallus gallus	111-115
6630514-8	1983	The increase in C-2 oxidation after treatment of cultures with phenobarbital or 2-propyl-2-isopropylacetamide was significantly less than that observed for oxidation at C-16.	Phenobarbital	63-76	complement C2	Gallus gallus	16-19
6314341-1	1983	To study the relationship between the dose of phenobarbital (PB) and the magnitude of its effects on microsomal enzymes, cytochrome P-450, UDP-glucuronyl transferase (UDPGT), and glucose-6-phosphatase (G6P) activities were determined in liver homogenate and microsome preparations from control rats and rats treated for 6 days with PB at doses ranging from 1 to 125 mg/kg/day.	Phenobarbital	46-59	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	179-200
6314341-1	1983	To study the relationship between the dose of phenobarbital (PB) and the magnitude of its effects on microsomal enzymes, cytochrome P-450, UDP-glucuronyl transferase (UDPGT), and glucose-6-phosphatase (G6P) activities were determined in liver homogenate and microsome preparations from control rats and rats treated for 6 days with PB at doses ranging from 1 to 125 mg/kg/day.	Phenobarbital	46-59	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	202-205
6314341-2	1983	Both P-450 and UDPGT activities were enhanced by PB in a dose-related fashion.	Phenobarbital	49-51	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	15-20
6314341-3	1983	However, while the lowest dose of the drug to produce significant induction of both enzymes was the same (3 mg/kg), maximal induction of P-450 (214%) and UDPGT (285%) was obtained with different doses of PB, namely 75 and 125 mg/kg, respectively.	Phenobarbital	204-206	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	154-159
6314341-7	1983	These results indicate that: (I) enzyme induction by PB is dose-related; (ii) induction of both P-450 and UDPGT is obtained in the rat with doses of the drug similar to those given to man; and (iii) observed inhibition of G6P activity by PB does not solely reflect an enzymatic dilution secondary to the proliferated endoplasmic reticulum.	Phenobarbital	53-55	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	106-111
6415870-1	1983	The specificity of two major types of cytochrome P-450 of rat liver microsomes induced by phenobarbital (PB) and 3-methylcholanthrene (MC) toward activation of three 14C-labeled tetrachlorobiphenyl (TCB) isomers to protein-bound metabolites was examined by intact microsomal and reconstituted monooxygenase systems.	Phenobarbital	90-103	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	38-54
6415870-1	1983	The specificity of two major types of cytochrome P-450 of rat liver microsomes induced by phenobarbital (PB) and 3-methylcholanthrene (MC) toward activation of three 14C-labeled tetrachlorobiphenyl (TCB) isomers to protein-bound metabolites was examined by intact microsomal and reconstituted monooxygenase systems.	Phenobarbital	105-107	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	38-54
6314341-7	1983	These results indicate that: (I) enzyme induction by PB is dose-related; (ii) induction of both P-450 and UDPGT is obtained in the rat with doses of the drug similar to those given to man; and (iii) observed inhibition of G6P activity by PB does not solely reflect an enzymatic dilution secondary to the proliferated endoplasmic reticulum.	Phenobarbital	53-55	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	222-225
6314341-7	1983	These results indicate that: (I) enzyme induction by PB is dose-related; (ii) induction of both P-450 and UDPGT is obtained in the rat with doses of the drug similar to those given to man; and (iii) observed inhibition of G6P activity by PB does not solely reflect an enzymatic dilution secondary to the proliferated endoplasmic reticulum.	Phenobarbital	238-240	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	106-111
6314341-7	1983	These results indicate that: (I) enzyme induction by PB is dose-related; (ii) induction of both P-450 and UDPGT is obtained in the rat with doses of the drug similar to those given to man; and (iii) observed inhibition of G6P activity by PB does not solely reflect an enzymatic dilution secondary to the proliferated endoplasmic reticulum.	Phenobarbital	238-240	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	222-225
6413255-1	1983	Cytochrome P450 purified from phenobarbital-induced rat liver microsomes was acetylated at 3 lysyl residues.	Phenobarbital	30-43	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-15
6415870-2	1983	The monooxygenase system containing PB-inducible form(s) of cytochrome P-450 was much more active than those inducible by MC in activating two TCB isomers, i.e., 2,4,2",5"-[14C]TCB, for the binding reaction.	Phenobarbital	36-38	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	60-76
6626536-0	1983	Cytochrome P-450 isozyme 1 from phenobarbital-induced rat liver: purification, characterization, and interactions with metyrapone and cytochrome b5.	Phenobarbital	32-45	cytochrome b5 type A	Rattus norvegicus	134-147
6626536-1	1983	Cytochrome P-450 isozyme 1 (PB-1) (Mr congruent to 53 000) was purified to apparent homogeneity from phenobarbital (PB)-induced rat liver microsomes, and its spectral, structural, immunochemical, and catalytic properties were determined.	Phenobarbital	101-114	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	28-32
6626536-2	1983	PB-1, present in significant amounts in uninduced rat liver microsomes, is induced approximately 2-4-fold by phenobarbital, as compared to the greater than 30-fold induction typical of the major PB isozymes characterized previously.	Phenobarbital	109-122	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	0-4
6688421-2	1983	Phenobarbital (PB) treatment of rats of various strains leads to the accumulation of liver mRNAs which encode two or three immunochemically related but electrophoretically separable cytochrome P-450 polypeptides.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	182-198
6688421-2	1983	Phenobarbital (PB) treatment of rats of various strains leads to the accumulation of liver mRNAs which encode two or three immunochemically related but electrophoretically separable cytochrome P-450 polypeptides.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	182-198
6688421-4	1983	The nucleotide sequence of this cloned cDNA was determined and shown to encode the COOH-terminal 211 amino acids of one of the major cytochrome P-450 isozymes induced in rat liver by PB.	Phenobarbital	183-185	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	133-149
6885818-4	1983	In order to approach the questions of the genetic basis for the existence of multiple cytochrome P-450 isozymes and the molecular mechanisms of the induction process, we have used a cloned cDNA for a major phenobarbital-induced form of cytochrome P-450 to identify and characterize thirteen distinct rat genomic clones containing segments of six different genes.	Phenobarbital	206-219	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	86-102
6885818-4	1983	In order to approach the questions of the genetic basis for the existence of multiple cytochrome P-450 isozymes and the molecular mechanisms of the induction process, we have used a cloned cDNA for a major phenobarbital-induced form of cytochrome P-450 to identify and characterize thirteen distinct rat genomic clones containing segments of six different genes.	Phenobarbital	206-219	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	236-252
6885818-7	1983	Although there are a small number of differences, DNA sequence analysis of the eight exons of the gene present in these genomic clones indicates that they encode residues 58 to 491 (the COOH terminus) of cytochrome P-450e, a major phenobarbital-induced isozyme.	Phenobarbital	231-244	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	204-221
6885818-8	1983	It appears that the other cloned genes may contain only a small region of very strong homology to the cytochrome P-450e gene, a region which includes the exon encoding a tridecapeptide which is also present in two dissimilar forms of rabbit liver cytochrome P-450, one constitutive and one induced by phenobarbital.	Phenobarbital	301-314	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	102-119
6885818-8	1983	It appears that the other cloned genes may contain only a small region of very strong homology to the cytochrome P-450e gene, a region which includes the exon encoding a tridecapeptide which is also present in two dissimilar forms of rabbit liver cytochrome P-450, one constitutive and one induced by phenobarbital.	Phenobarbital	301-314	cytochrome P-450	Oryctolagus cuniculus	102-118
6885818-10	1983	One of these genes is likely to encode cytochrome P-450b, the major phenobarbital induced form of cytochrome P-450 whose mRNA is greater than 95% homologous to that encoding cytochrome P-450e.	Phenobarbital	68-81	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	39-56
6885818-10	1983	One of these genes is likely to encode cytochrome P-450b, the major phenobarbital induced form of cytochrome P-450 whose mRNA is greater than 95% homologous to that encoding cytochrome P-450e.	Phenobarbital	68-81	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-55
6885818-10	1983	One of these genes is likely to encode cytochrome P-450b, the major phenobarbital induced form of cytochrome P-450 whose mRNA is greater than 95% homologous to that encoding cytochrome P-450e.	Phenobarbital	68-81	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	174-191
6326548-2	1983	This experiment was set up to determine if reversal of flow of membrane from the nuclear envelope to the RER would occur during phenobarbital-stimulated increased synthesis of RER.	Phenobarbital	128-141	IK cytokine	Homo sapiens	105-108
6309801-4	1983	The rank order of binding affinities of these chemicals to the cytosolic Ah receptor (2,3,7,8-tetrachlorodibenzo-p-dioxin much greater than benzo[a]pyrene greater than benzo[a]anthracene greater than 6-aminochrysene much greater than phenobarbital) is not correlated with their effects on EGF binding capacity.	Phenobarbital	234-247	aryl-hydrocarbon receptor	Mus musculus	73-84
6326548-2	1983	This experiment was set up to determine if reversal of flow of membrane from the nuclear envelope to the RER would occur during phenobarbital-stimulated increased synthesis of RER.	Phenobarbital	128-141	IK cytokine	Homo sapiens	176-179
6199107-1	1983	The incidence of gamma-glutamyltranspeptidase (GGT)-positive foci induced by 0.3 mmol/kg diethylnitrosamine (DENA) followed by promotion with 500 ppm sodium phenobarbital in drinking water and was the same in Fischer 344, Sprague-Dawley and Wistar-Lewis rats.	Phenobarbital	150-170	gamma-glutamyltransferase 1	Rattus norvegicus	47-50
6636196-5	1983	Cytochrome P-450 isozymes, purified from xylene- and phenobarbital-treated animals, were efficient catalysts of antipyrine metabolism, with turnover numbers of 33.3 and 21.1, respectively.	Phenobarbital	53-66	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
6688415-11	1983	In contrast, cytochrome P-450b mRNA, which is readily induced by phenobarbital, was only slightly elevated (approximately 2-fold) after PCN administration.	Phenobarbital	65-78	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	13-30
6309775-0	1983	Genetic polymorphisms for a phenobarbital-inducible cytochrome P-450 map to the Coh locus in mice.	Phenobarbital	28-41	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	52-68
6309775-1	1983	Southern blot analysis suggests that multiple sequences homologous to a phenobarbital-inducible cytochrome P-450 cDNA are present in the rat and mouse genomes.	Phenobarbital	72-85	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	96-112
6309775-2	1983	A cDNA (pP-450b-5) to a major phenobarbital-inducible cytochrome P-450 mRNA species in the rat detected 6 polymorphic DNA fragments when hybridized to DNA from C57BL/6J and DBA/2J mice restricted with endonucleases EcoRI, BamHI, and PvuII.	Phenobarbital	30-43	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	54-70
6309775-4	1983	The Coh locus has previously been shown to code for a phenobarbital-inducible enzyme, believed to be a cytochrome P-450, which catalyzes the conversion of coumarin to 7-hydroxycoumarin (umbelliferone).	Phenobarbital	54-67	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	103-119
6411467-3	1983	The cytochrome P-450 content and response to induction by 3-methylcholanthrene and phenobarbitone; the distribution of lactate dehydrogenase, glucose-6-phosphatase, pyruvate kinase and tyrosine aminotransferase activities in the sub-populations is also reported.	Phenobarbital	83-97	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	4-20
6311445-4	1983	Pretreatment with phenobarbital (PB), Aroclor 1254 (PCB) or beta-naphthoflavone (BNF) increased the cytochrome P-450 content and the various cytochrome P-450-mediated reactions up to 7-fold in larvae.	Phenobarbital	18-31	Pyruvate carboxylase	Drosophila melanogaster	52-55
6311445-4	1983	Pretreatment with phenobarbital (PB), Aroclor 1254 (PCB) or beta-naphthoflavone (BNF) increased the cytochrome P-450 content and the various cytochrome P-450-mediated reactions up to 7-fold in larvae.	Phenobarbital	18-31	Cytochrome P450-9b2	Drosophila melanogaster	100-116
6311445-4	1983	Pretreatment with phenobarbital (PB), Aroclor 1254 (PCB) or beta-naphthoflavone (BNF) increased the cytochrome P-450 content and the various cytochrome P-450-mediated reactions up to 7-fold in larvae.	Phenobarbital	18-31	Cytochrome P450-9b2	Drosophila melanogaster	141-157
6311445-4	1983	Pretreatment with phenobarbital (PB), Aroclor 1254 (PCB) or beta-naphthoflavone (BNF) increased the cytochrome P-450 content and the various cytochrome P-450-mediated reactions up to 7-fold in larvae.	Phenobarbital	33-35	Cytochrome P450-9b2	Drosophila melanogaster	100-116
6136493-6	1983	Endotoxin administration was also shown to diminish, but not prevent, the induction of cytochrome P--450 and ethylmorphine N-demethylase activity produced by phenobarbital.	Phenobarbital	158-171	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	87-104
6311445-4	1983	Pretreatment with phenobarbital (PB), Aroclor 1254 (PCB) or beta-naphthoflavone (BNF) increased the cytochrome P-450 content and the various cytochrome P-450-mediated reactions up to 7-fold in larvae.	Phenobarbital	33-35	Cytochrome P450-9b2	Drosophila melanogaster	141-157
6614916-0	1983	Effect of cobalt chloride and 3-amino-1,2,4-triazole on the induction of cytochrome P-450 synthesis by phenobarbitone in rat liver.	Phenobarbital	103-117	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	73-89
6614916-1	1983	Administration of cobalt chloride and 3-amino-1,2,4-triazole leads to a suppression of phenobarbitone-mediated increase in total cytochrome P-450 as well as cytochrome P-450b contents of the liver.	Phenobarbital	87-101	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	129-145
6614916-1	1983	Administration of cobalt chloride and 3-amino-1,2,4-triazole leads to a suppression of phenobarbitone-mediated increase in total cytochrome P-450 as well as cytochrome P-450b contents of the liver.	Phenobarbital	87-101	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	168-174
6409115-0	1983	Effect of low-dose phenobarbital on hepatic microsomal UDP-glucuronyl transferase activity.	Phenobarbital	19-32	UDP glucuronosyltransferase family 1 member A5	Rattus norvegicus	55-81
6409115-2	1983	While no significant increases in liver weight and protein content of homogenate and microsomal preparations were observed with either dose of the drug, both UDPGT and P-450 activities were enhanced significantly following administration of phenobarbital at 3 mg per kg per day.	Phenobarbital	241-254	UDP glucuronosyltransferase family 1 member A5	Rattus norvegicus	158-163
6409115-5	1983	These data suggest that the discordant effects of phenobarbital on UDPGT and cytochrome P-450 previously reported in humans and rats may not be attributable solely to differences in the drug doses employed.	Phenobarbital	50-63	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	67-72
6409115-5	1983	These data suggest that the discordant effects of phenobarbital on UDPGT and cytochrome P-450 previously reported in humans and rats may not be attributable solely to differences in the drug doses employed.	Phenobarbital	50-63	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	77-93
6412692-2	1983	Treatment of cultured chick embryo hepatocytes with phenobarbital, polychlorinated biphenyl compounds and 2,3,7,8-tetrachlorodibenzo-p-dioxin resulted in increased delta-aminolaevulinate synthase and decreased uroporphyrinogen decarboxylase activities and porphyrin accumulation; uroporphyrin and heptacarboxyporphyrin predominated.	Phenobarbital	52-65	uroporphyrinogen decarboxylase	Gallus gallus	210-240
6412692-4	1983	Simultaneous treatment of cultures with dioxin and phenobarbital produced a synergistic response in delta-aminolaevulinate synthase induction, uroporphyrinogen decarboxylase inhibition and porphyrin accumulation.	Phenobarbital	51-64	uroporphyrinogen decarboxylase	Homo sapiens	143-173
6408085-0	1983	Transcriptional regulation of rat liver epoxide hydratase, NADPH-Cytochrome P-450 oxidoreductase, and cytochrome P-450b genes by phenobarbital.	Phenobarbital	129-142	epoxide hydrolase 2	Rattus norvegicus	40-57
6408085-0	1983	Transcriptional regulation of rat liver epoxide hydratase, NADPH-Cytochrome P-450 oxidoreductase, and cytochrome P-450b genes by phenobarbital.	Phenobarbital	129-142	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	102-119
6408085-5	1983	Specifically, cytochrome P-450b gene transcription increased 23-fold above control values 6 to 8 h after phenobarbital administration and then slowly declined to 14-fold at 24 h. The increased levels of intranuclear pre-mRNA and cytoplasmic mRNA for each enzyme correlated well with transcriptional activity.	Phenobarbital	105-118	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	14-31
6880567-0	1983	Effects of a single oral dose of phenobarbital on prolactin, growth hormone and luteinizing hormone in normal women.	Phenobarbital	33-46	prolactin	Homo sapiens	50-59
6880567-0	1983	Effects of a single oral dose of phenobarbital on prolactin, growth hormone and luteinizing hormone in normal women.	Phenobarbital	33-46	growth hormone 1	Homo sapiens	61-75
6880567-1	1983	The effects of a single oral dose of phenobarbital (PB) on the 24 h secretion of prolactin, growth hormone and luteinizing hormone have been evaluated in normal women.	Phenobarbital	37-50	prolactin	Homo sapiens	81-90
6880567-1	1983	The effects of a single oral dose of phenobarbital (PB) on the 24 h secretion of prolactin, growth hormone and luteinizing hormone have been evaluated in normal women.	Phenobarbital	37-50	growth hormone 1	Homo sapiens	92-106
6880567-1	1983	The effects of a single oral dose of phenobarbital (PB) on the 24 h secretion of prolactin, growth hormone and luteinizing hormone have been evaluated in normal women.	Phenobarbital	52-54	prolactin	Homo sapiens	81-90
6880567-1	1983	The effects of a single oral dose of phenobarbital (PB) on the 24 h secretion of prolactin, growth hormone and luteinizing hormone have been evaluated in normal women.	Phenobarbital	52-54	growth hormone 1	Homo sapiens	92-106
6872097-3	1983	It is metabolized by microsomes from control rats and by rats treated with phenobarbital or 3-methylcholanthrene at 3.9, 4.2 and 7.8 nmol/nmol cytochrome P-450/min, respectively.	Phenobarbital	75-88	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	143-163
6137336-0	1983	The alteration of hepatic cytochrome P-450 subpopulations of phenobarbital-induced and uninduced rat by regioselective hepatotoxins.	Phenobarbital	61-74	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	26-42
6137342-2	1983	The imidazole derivatives were potent inhibitors of total BaP metabolism in microsomes from control and PB-induced rats (I50 approximately 10(-5) M) but did not affect the proportions of BaP metabolites formed.	Phenobarbital	104-106	prohibitin 2	Rattus norvegicus	58-61
6193935-0	1983	Hepatic microsomal metabolism of CCL4 after pretreatment with chlordecone, mirex, or phenobarbital in male rats.	Phenobarbital	85-98	C-C motif chemokine ligand 4	Rattus norvegicus	33-37
6865923-0	1983	The relationship between increases in the hepatic content of cytochrome P-450, form 5, and in the metabolism of aromatic amines to mutagenic products following treatment of rabbits with phenobarbital.	Phenobarbital	186-199	cytochrome P-450	Oryctolagus cuniculus	61-85
6630164-3	1983	In the livers from fasted, PB-treated rats, 2,4-DNP (50 microM) significantly decreased the amount of reduced (oxygenated) cytochrome P-450 and the drug-induced oxygen uptake by about 50%.	Phenobarbital	27-29	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	123-139
6630164-6	1983	In the livers from PB-treated rats, infusion of sorbitol (4 mM), a glycogenic substrate in fasted rats, stimulated the rate of drug-induced oxygen uptake and the steady-state level of reduced (oxygenated) cytochrome P-450 increased during mixed-function oxidation of hexobarbital.	Phenobarbital	19-21	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	205-221
6865923-1	1983	Treatment of rabbits with phenobarbital is followed by increases in the hepatic microsomal concentration of cytochrome P-450, form 5, and in the hepatic microsomal metabolism of aromatic amines to mutagenic products.	Phenobarbital	26-39	cytochrome P-450	Oryctolagus cuniculus	108-132
6865923-4	1983	The results indicate that phenobarbital increases the hepatic microsomal concentration of cytochrome P-450, form 5, to the same extent that it increases form 5-mediated metabolism of aromatic amines to mutagenic products: 10- to 12-fold.	Phenobarbital	26-39	cytochrome P-450	Oryctolagus cuniculus	90-114
6870906-0	1983	Immunological and enzymatic comparison of hepatic cytochrome P-450 fractions from phenobarbital-, 3-methylcholanthrene-, beta-naphthoflavone- and 2,3,7,8- tetrachlorodibenzo-p-dioxin-treated rats.	Phenobarbital	82-95	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	50-66
6882464-3	1983	These reductions and cytochrome P-450-dependent since they are inhibited by CO and metyrapone, and are increased after pretreatment of rats by phenobarbital and 3-methylcholanthrene.	Phenobarbital	143-156	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	21-37
6872091-2	1983	Anaerobic in vitro incubation of microsomes from phenobarbital(PB)-induced rats with halothane results in an irreversible decrease of measurable cytochrome P-450.	Phenobarbital	49-62	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	145-161
6622816-9	1983	Our data also suggest that MI-complexation is generated on phenobarbital induced cytochrome P-450 species.	Phenobarbital	59-72	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	81-97
6851415-3	1983	These inducers (phenobarbital and medroxyprogesterone acetate) when added as adjuvant therapy to sulfonyl urea regimen, reduced blood glucose and plasma insulin, and increased microsomal enzyme activity (as indicated by increased antipyrine metabolism).	Phenobarbital	16-29	insulin	Homo sapiens	153-160
6631663-2	1983	Phenobarbital (80 mg/kg, daily for 4 d) injected intraperitoneally caused 30% increase of the enzyme activity and 160% increase of the microsomal cytochrome P-450 content.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	146-162
6684702-0	1983	[Effect of chronic ethanol feeding on the amount of phenobarbital inducible form of cytochrome P-450 and its localization in the hepatic lobule of the rat].	Phenobarbital	52-65	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	84-100
6414108-1	1983	Highly purified NADPH-cytochrome P-450 reductase and the major phenobarbital (PB) and beta-naphthoflavone (beta NF) forms of cytochrome P-450 were used in reconstituted systems to study the demethylation and subsequent activation of dimethylnitrosamine (DMN) to mutagenic intermediates.	Phenobarbital	78-80	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	22-38
6414108-2	1983	Both forms of cytochrome P-450 were active in the demethylation of DMN, cytochrome P-450 from PB-treated animals being more efficient, generating nearly twice as much formaldehyde per nmol of haemoprotein.	Phenobarbital	94-96	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	14-30
6414108-2	1983	Both forms of cytochrome P-450 were active in the demethylation of DMN, cytochrome P-450 from PB-treated animals being more efficient, generating nearly twice as much formaldehyde per nmol of haemoprotein.	Phenobarbital	94-96	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	72-88
6612743-9	1983	Polyacrylamide gel electrophoresis of liver microsomes from animals exposed to xylenes in the presence of SDS showed increases in protein bands comigrating with cytochrome P-450 PB-B2 and epoxide hydrolase purified from phenobarbital treated rats.	Phenobarbital	220-233	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	161-177
6405752-3	1983	Measurements of cytochrome P-450 in cultures induced with phenobarbital were always higher after ultracentrifugation.	Phenobarbital	58-71	cytochrome P450	Bacillus megaterium NBRC 15308 = ATCC 14581	16-32
6409093-6	1983	A molar ratio of 15:1 (cytochromes P-450/NADPH: cytochrome P-450 reductase) was calculated for control and phenobarbital-treated animals.	Phenobarbital	107-120	cytochrome p450 oxidoreductase	Rattus norvegicus	35-74
6885729-0	1983	Phenobarbital- and 3-methylcholanthrene-induced synthesis of two different molecular species of microsomal cytochrome P-450 in rat liver.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	107-123
6885729-9	1983	PB and MC induced the syntheses of P-450(PB) and P-450(MC) by bound ribosomes but not by free ribosomes, and the contribution of bound ribosomes to the syntheses of these two species of cytochrome P-450 was predominant in the case of drug-treated animals.	Phenobarbital	0-2	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	49-57
6885729-9	1983	PB and MC induced the syntheses of P-450(PB) and P-450(MC) by bound ribosomes but not by free ribosomes, and the contribution of bound ribosomes to the syntheses of these two species of cytochrome P-450 was predominant in the case of drug-treated animals.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	186-202
6870856-0	1983	Induction and repression of the major phenobarbital-induced cytochrome P-450 measured by radioimmunoassay.	Phenobarbital	38-51	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	60-76
6622818-2	1983	Pretreatment of rats with 3,4-benzpyrene or phenobarbital increased the liver microsomal concentration of cytochrome P-450 (448) and the rate of aminopyrine and p-nitroanisole demethylation and of aniline hydroxylation whereas pretreatment cytochrome P-450 depressor agents such as cadmium or cobalt lowered the concentration of the hemoprotein and decreased the rate of the demethylation reactions.	Phenobarbital	44-57	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	106-122
6622818-2	1983	Pretreatment of rats with 3,4-benzpyrene or phenobarbital increased the liver microsomal concentration of cytochrome P-450 (448) and the rate of aminopyrine and p-nitroanisole demethylation and of aniline hydroxylation whereas pretreatment cytochrome P-450 depressor agents such as cadmium or cobalt lowered the concentration of the hemoprotein and decreased the rate of the demethylation reactions.	Phenobarbital	44-57	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	240-256
6865917-0	1983	Interaction of constitutive and phenobarbital-induced cytochrome P-450 isozymes during the sequential oxidation of benzphetamine.	Phenobarbital	32-45	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	54-70
6865917-15	1983	The current study shows that PB induction of monooxygenase activity need not be due entirely to an increase in the amount of cytochrome P-450 or the substrate selectivity of cytochrome P-450 isozyme(s) responsible for that activity, but that, in at least one case, the metabolism of Bz, PB-induced activity can be due, at least in part, to the induction of a cytochrome P-450 isozyme that relieves substrate inhibition.	Phenobarbital	29-31	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	174-190
6865917-15	1983	The current study shows that PB induction of monooxygenase activity need not be due entirely to an increase in the amount of cytochrome P-450 or the substrate selectivity of cytochrome P-450 isozyme(s) responsible for that activity, but that, in at least one case, the metabolism of Bz, PB-induced activity can be due, at least in part, to the induction of a cytochrome P-450 isozyme that relieves substrate inhibition.	Phenobarbital	29-31	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	174-190
6870856-1	1983	Two independent radioimmunoassay techniques for the major phenobarbital-inducible cytochrome P-450 (PB P-450) of rat liver microsomal membranes are described.	Phenobarbital	58-71	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	82-98
6135606-11	1983	Promotion by phenobarbital stimulated the growth and decreased the time required for the appearance of GGTase-positive foci and liver tumors.	Phenobarbital	13-26	gamma-glutamyltransferase 1	Rattus norvegicus	103-109
6833251-0	1983	The complete amino acid sequence of rabbit phenobarbital-induced liver microsomal cytochrome P-450.	Phenobarbital	43-56	cytochrome P450 2B4	Oryctolagus cuniculus	93-98
6833251-1	1983	The complete amino acid sequence of the major phenobarbital-induced cytochrome P-450 (P-450LM2) from rabbit liver microsomes has been determined.	Phenobarbital	46-59	cytochrome P450 2B4	Oryctolagus cuniculus	79-84
6833251-1	1983	The complete amino acid sequence of the major phenobarbital-induced cytochrome P-450 (P-450LM2) from rabbit liver microsomes has been determined.	Phenobarbital	46-59	cytochrome P450 2B4	Oryctolagus cuniculus	86-94
6833251-3	1983	The sequence was compared with the amino acid sequence of P-450CAM and the nucleotide sequence of cDNA obtained from phenobarbital-induced rat liver cytochrome P-450 mRNA.	Phenobarbital	117-130	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	149-165
6833252-2	1983	Hepatic microsomal cytochrome P-450 from phenobarbital-pretreated rats is inactivated during the metabolism of linear olefins (ethylene, propene, and octene) and acetylenes (acetylene, propyne, and octyne).	Phenobarbital	41-54	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	19-35
6679774-1	1983	The interaction of highly purified liver microsomal cytochrome P-450 from phenobarbital-induced rabbits and cytochrome b5 has been investigated by the difference and second derivative difference spectroscopy.	Phenobarbital	74-87	cytochrome P-450	Oryctolagus cuniculus	52-68
6679774-1	1983	The interaction of highly purified liver microsomal cytochrome P-450 from phenobarbital-induced rabbits and cytochrome b5 has been investigated by the difference and second derivative difference spectroscopy.	Phenobarbital	74-87	cytochrome b5	Oryctolagus cuniculus	108-121
6191977-6	1983	Of the miscellaneous compounds tested, phenobarbital, deoxycholic acid and ethynyl estradiol also induced gamma-glutamyl transpeptidase (gamma-GT) positive foci.	Phenobarbital	39-52	gamma-glutamyltransferase 1	Rattus norvegicus	106-135
6191977-6	1983	Of the miscellaneous compounds tested, phenobarbital, deoxycholic acid and ethynyl estradiol also induced gamma-glutamyl transpeptidase (gamma-GT) positive foci.	Phenobarbital	39-52	gamma-glutamyltransferase 1	Rattus norvegicus	137-145
6830852-1	1983	Cytochrome P-450 substrate interactions were studied with cytochrome P-450 partially purified from livers of untreated, phenobarbital-treated, benzo[a]pyrene-treated and caffeine-treated rats.	Phenobarbital	120-133	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
6834827-5	1983	This conclusion was further supported using inhibitors of cytochrome P-450 (SKF-525A, metyrapone and alpha-naphthoflavone) and with immunoinhibition by antibodies directed towards the phenobarbital-inducible form of cytochrome P-450.	Phenobarbital	184-197	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	58-74
6834827-5	1983	This conclusion was further supported using inhibitors of cytochrome P-450 (SKF-525A, metyrapone and alpha-naphthoflavone) and with immunoinhibition by antibodies directed towards the phenobarbital-inducible form of cytochrome P-450.	Phenobarbital	184-197	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	216-232
6844353-1	1983	Administration of phenobarbital (60 mg/kg) daily for 4 days to male rabbits resulted in induction of renal cytochrome P-450 (3.5-fold) and a corresponding increase in ethoxycoumarin-O-deethylase and benzphetamine-N-demethylase activity (17- and 4-fold, respectively).	Phenobarbital	18-31	cytochrome P-450	Oryctolagus cuniculus	107-123
6131891-4	1983	These two mRNAs do not show detectable sequence homology to the mRNAs coding for the major phenobarbital-induced forms of cytochrome P-450 (P-450b and P-450e) since in Northern blotting experiments they fail to hybridize under conditions of low to moderate stringency to cloned probes for the latter mRNAs.	Phenobarbital	91-104	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	122-138
6617864-2	1983	Succinylacetone potentiated the phenobarbital-mediated induction of delta-aminolevulinate synthase, strongly inhibited porphobilinogen synthase activity, reduced cellular heme concentration and impaired induction of cytochrome P450.	Phenobarbital	32-45	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	216-231
6131891-4	1983	These two mRNAs do not show detectable sequence homology to the mRNAs coding for the major phenobarbital-induced forms of cytochrome P-450 (P-450b and P-450e) since in Northern blotting experiments they fail to hybridize under conditions of low to moderate stringency to cloned probes for the latter mRNAs.	Phenobarbital	91-104	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	140-146
6406101-3	1983	In rats pretreated with phenobarbital (75 mg/kg per 6 days), a 70-90% increase in UDPGT activity was observed with either diazotization procedure, irrespective of whether "native", UDP-N-acetylglucosamine-or digitonin-activated enzyme was employed.	Phenobarbital	24-37	UDP glucuronosyltransferase family 1 member A5	Rattus norvegicus	82-87
6838663-3	1983	The binding of PI to the highly purified, individual cytochrome P-450s that constituted the major forms from the PB- and beta-naphthoflavone (beta NF)-induced rats exhibited affinities similar to the high and low affinity binding sites observed in microsomal suspensions.	Phenobarbital	113-115	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	53-69
6687693-0	1983	Multiplicity of deoxyribonucleic acid sequences with homology to a cloned complementary deoxyribonucleic acid coding for rat phenobarbital-inducible cytochrome P-450.	Phenobarbital	125-138	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	149-165
6829959-9	1983	Phenobarbital treatment increased the microsomal content of cytochrome P-450, while ethanol treatment did not.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	60-76
6409073-12	1983	Typical aldehyde reductase inhibitors, such as phenobarbital and sodium valproate, had the same effect on both enzymes.	Phenobarbital	47-60	aldo-keto reductase family 1 member B	Sus scrofa	8-26
6687693-1	1983	We previously identified cDNA clones for rat cytochrome P-450 of the phenobarbital-inducible type by sequence analysis [Fujii-Kuriyama, Y., Mizukami, Y., Kawajiri, K., Sogawa, K., & Muramatsu, M. (1982) Proc.	Phenobarbital	69-82	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	45-61
6687693-6	1983	With these cloned cDNAs as probe, the multiplicity of phenobarbital-inducible cytochrome P-450 gene in rat genome was investigated by three approaches.	Phenobarbital	54-67	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	78-94
6687693-8	1983	With internal and external markers used as gene-number standards, the reassociation kinetics were studied, which suggested the presence of approximately six genes or gene-like sequences hybridizable to phenobarbital-inducible cytochrome P-450 cDNA per rat haploid genome.	Phenobarbital	202-215	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	226-242
6838626-9	1983	Microsomal monooxygenase oxidized styrene to R-(+)- and S-(-)-phenyloxiranes (ratio 1.3:1), and the ratio was little changed by the pretreatment of the animal with phenobarbital, 3-methylcholanthrene and polychlorinated biphenyls.	Phenobarbital	164-177	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-24
6407528-5	1983	Ouchterlony double diffusion revealed cross-reactivity between anti-P-450LM4 (phenobarbital) IgG and cytochrome P-450 isolated from cholestyramine- or beta-naphthoflavone-treated rabbit liver microsomes.	Phenobarbital	78-91	cytochrome P450 1A2	Oryctolagus cuniculus	68-76
6825202-1	1983	A series of benzimidazole derivatives containing additional fused and non-fused aromatic groupings were effective inhibitors of aryl hydrocarbon hydroxylase (PB/AHH) and aminopyrine N-demethylase (ADPM) activities in hepatic microsomes from phenobarbitone(PB)-induced rats.	Phenobarbital	241-255	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	128-156
6601233-1	1983	Intraperitoneal administration of chloramphenicol (100 mg/kg) to phenobarbital-treated rats causes 50% inhibition of liver microsomal 7-ethoxycoumarin and 1,1,2,2 tetrachloroethane metabolism but has no effect on the level of cytochrome P-450 detectable as its carbon monoxide complex or on the NADPH-cytochrome c reductase (EC 1.6.2.4) activity.	Phenobarbital	65-78	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	226-242
6572377-2	1983	These two phenobarbital-inducible hemoproteins, which are immunochemically indistinguishable with antibody against cytochrome P-450b, have extensive sequence homology.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	115-132
6433923-0	1983	Multiple forms of cytochrome P-450 from kidney cortex microsomes of rabbits treated with phenobarbital.	Phenobarbital	89-102	cytochrome P-450	Oryctolagus cuniculus	18-34
6433923-1	1983	Two distinct forms of cytochrome P-450 (P-450), referred to as P-450a and P-450b, were separated and purified from kidney cortex microsomes of rabbits treated with phenobarbital.	Phenobarbital	164-177	cytochrome P-450	Oryctolagus cuniculus	22-38
6836579-2	1983	The reaction rate was stimulated approximately 2-fold in microsomes from phenobarbital-pretreated rats and was inhibited by addition of SKF-525A, carbon monoxide, metyrapone, and hexobarbital to the microsomal suspension, indicating dependence on cytochrome P-450.	Phenobarbital	73-86	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	247-263
6404899-6	1983	These observations suggested the position specificities of the PB-inducible form (P-450(PB)) and MC-inducible form (P-450(MC)) of cytochrome P-450 in the hydroxylation of n-hexane.	Phenobarbital	88-90	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	130-146
6408471-5	1983	The contents of liver microsomal cytochrome p-450 of mice pretreated with PB or MC were about twice those of non-treated mice.	Phenobarbital	74-76	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	33-49
6830757-5	1983	Three of the cysteine-containing peptides exhibited significant sequence homology with peptides from the major phenobarbital-induced rat liver cytochrome P-450 (P-450b) and two with peptides from cytochrome P-450cam (camphor methylene hydroxylase from Pseudomonas putida).	Phenobarbital	111-124	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	143-159
6823207-0	1983	Liver microsome phospholipids and cytochrome P.450 concentration in phenobarbital treated rats fed on different diets.	Phenobarbital	68-81	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	34-50
6296075-2	1983	Specific immunochemical techniques were used to quantitate the levels of eight isozymes of cytochrome P-450 (P-450) and epoxide hydrolase in liver microsomes of untreated rats and rats treated with phenobarbital, 3-methylcholanthrene, a mixture of these two compounds, nine individual polybrominated biphenyl (PBB) congeners, and a commercial mixture of PBBs.	Phenobarbital	198-211	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	91-107
6830757-5	1983	Three of the cysteine-containing peptides exhibited significant sequence homology with peptides from the major phenobarbital-induced rat liver cytochrome P-450 (P-450b) and two with peptides from cytochrome P-450cam (camphor methylene hydroxylase from Pseudomonas putida).	Phenobarbital	111-124	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	161-167
6414255-8	1983	When phenobarbital was administered to block spontaneous proestrous LH surges it also completely blocked the increase in NE T/R which occur in ME and SCN but did not affect DA T/R.	Phenobarbital	5-18	solute carrier family 6 member 2	Rattus norvegicus	121-125
6307540-3	1983	The following parameters proved to be significantly altered in the livers of rats treated with either NNM or PB or both compared with untreated controls: glycogen content was increased and the activities of glucose-6-phosphatase and glycogen synthetase were decreased.	Phenobarbital	109-111	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	207-228
6679315-2	1983	Measurements of the activities of these components showed that phenobarbital pretreatment prevented the decrease in the specific activity of benzphetamine demethylase, as well as decrease in the contents of cytochrome P-450 and phosphatidyl choline seen in rats given cadmium alone.	Phenobarbital	63-76	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	207-223
6291757-2	1983	This induced cytochrome(s) was characterized and compared to the major forms of cytochrome P-450 induced by phenobarbital and 3-methylcholanthrene.	Phenobarbital	108-121	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	80-96
6291757-4	1983	The results indicate that 2-acetylaminofluorene induces a form(s) of cytochrome P-450 especially effective in the metabolism of this substance itself (i.e., the process can be called substrate induction) and different from the major forms of cytochrome P-450 induced by phenobarbital and 3-methylcholanthrene.	Phenobarbital	270-283	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	69-85
6132789-5	1983	A correlation was observed between the octanol-buffer or heptane-buffer distribution ratios of the compounds and the negative logarithm of the Michaelis constant (pKm) for the enzyme in control microsomes and for each of the enzyme systems in microsomes from phenobarbital-pretreated animals.	Phenobarbital	259-272	pyruvate kinase M1/2	Rattus norvegicus	163-166
6432511-6	1983	Cytochrome P-450 concentration was higher in the microsomes from thiamin-deficient rats and was induced to a greater degree by phenobarbital than in microsomes from rats fed thiamin-supplemented diets ad libitum.	Phenobarbital	127-140	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
6432511-9	1983	The fact that DMN metabolism per unit of microsomal cytochrome P-450 in phenobarbital-treated animals is decreased to about one-half of that in controls indicates that DMN is either metabolized by a non-cytochrome P-450-dependent system or that it is metabolized by a form of P-450 not induced by phenobarbital.	Phenobarbital	72-85	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	52-68
6432511-9	1983	The fact that DMN metabolism per unit of microsomal cytochrome P-450 in phenobarbital-treated animals is decreased to about one-half of that in controls indicates that DMN is either metabolized by a non-cytochrome P-450-dependent system or that it is metabolized by a form of P-450 not induced by phenobarbital.	Phenobarbital	72-85	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	203-219
6678746-4	1983	In marked contrast to the large increases produced by BHA, EQ, and ARO, the feeding of PB, MC, or SE resulted in little or no increase in epoxide hydrolase, UDP-glucuronyl transferase, UDP-glucose dehydrogenase, glutathione reductase, glutathione S-transferase, and glutathione levels.	Phenobarbital	87-89	glutathione reductase	Mus musculus	212-233
6678746-4	1983	In marked contrast to the large increases produced by BHA, EQ, and ARO, the feeding of PB, MC, or SE resulted in little or no increase in epoxide hydrolase, UDP-glucuronyl transferase, UDP-glucose dehydrogenase, glutathione reductase, glutathione S-transferase, and glutathione levels.	Phenobarbital	87-89	hematopoietic prostaglandin D synthase	Mus musculus	235-260
6683666-3	1983	PB administered alone significantly increased hepatic phospholipids and microsomal protein, phospholipid and cytochrome P-450 contents, as well as microsomal aminopyrine-N-demethylase (APDM-ase) activity.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	109-125
6678833-7	1983	The unusual severity of CCl4-induced liver and renal injury observed in this case is best explained by the induction of CCl4 microsomal activation due to phenobarbital therapy.	Phenobarbital	154-167	C-C motif chemokine ligand 4	Homo sapiens	24-28
6678833-7	1983	The unusual severity of CCl4-induced liver and renal injury observed in this case is best explained by the induction of CCl4 microsomal activation due to phenobarbital therapy.	Phenobarbital	154-167	C-C motif chemokine ligand 4	Homo sapiens	120-124
6630281-2	1983	Inhibition by SKF 525 A or dithiocarb as well as induction by pretreatment with phenobarbital or 20-methylcholanthrene suggest participation of cytochrome P-450 in this reaction.	Phenobarbital	80-93	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	144-160
6298436-8	1983	2,2",5,5"-Tetrabromobiphenyl, also a minor component of fireMaster BP-6, is a weak phenobarbital-type inducer of cytochrome P-450.	Phenobarbital	83-96	Blood pressure QTL 6	Rattus norvegicus	67-71
6298436-8	1983	2,2",5,5"-Tetrabromobiphenyl, also a minor component of fireMaster BP-6, is a weak phenobarbital-type inducer of cytochrome P-450.	Phenobarbital	83-96	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	113-129
6408389-4	1983	Utilizing the RIAs, both forms of cytochrome P-448 were found in significant quantities in liver microsomes of rats treated with 3-MC, 3,4,5-HCB, isosafrole, and Aroclor 1254 but only in minute concentrations in untreated and phenobarbital-treated rats.	Phenobarbital	226-239	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	34-50
6865901-2	1983	In order to elucidate the mechanism underlying this synergistic effect, the major liver microsomal cytochrome P-450 isozymes induced by xylene and phenobarbital, respectively, were purified.	Phenobarbital	147-160	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	99-115
6865901-8	1983	We conclude that xylene induces a rat liver microsomal cytochrome P-450 isozyme very similar to the major isozyme induced by phenobarbital and that this induction is the probable explanation for the enhanced formation of 2,5-hexanedione from n-hexane in vivo.	Phenobarbital	125-138	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	55-71
6674910-0	1983	Effect of phenobarbital treatment on erythrocyte glucose-6-phosphate dehydrogenase in human newborns.	Phenobarbital	10-23	glucose-6-phosphate dehydrogenase	Homo sapiens	49-82
6674910-1	1983	The effect of phenobarbital (PB) treatment on erythrocyte glucose-6-phosphate dehydrogenase (G-6-PD) levels was studied in normal and G-6-PD-deficient human newborns.	Phenobarbital	14-27	glucose-6-phosphate dehydrogenase	Homo sapiens	58-91
6674910-1	1983	The effect of phenobarbital (PB) treatment on erythrocyte glucose-6-phosphate dehydrogenase (G-6-PD) levels was studied in normal and G-6-PD-deficient human newborns.	Phenobarbital	14-27	glucose-6-phosphate dehydrogenase	Homo sapiens	93-99
6674910-1	1983	The effect of phenobarbital (PB) treatment on erythrocyte glucose-6-phosphate dehydrogenase (G-6-PD) levels was studied in normal and G-6-PD-deficient human newborns.	Phenobarbital	29-31	glucose-6-phosphate dehydrogenase	Homo sapiens	58-91
6674910-1	1983	The effect of phenobarbital (PB) treatment on erythrocyte glucose-6-phosphate dehydrogenase (G-6-PD) levels was studied in normal and G-6-PD-deficient human newborns.	Phenobarbital	29-31	glucose-6-phosphate dehydrogenase	Homo sapiens	93-99
6186523-0	1982	Differential effect of phenobarbital and beta-naphthoflavone on the mRNAs coding for cytochrome P450 and NADPH cytochrome P450 reductase.	Phenobarbital	23-36	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	85-100
6186523-0	1982	Differential effect of phenobarbital and beta-naphthoflavone on the mRNAs coding for cytochrome P450 and NADPH cytochrome P450 reductase.	Phenobarbital	23-36	cytochrome p450 oxidoreductase	Homo sapiens	105-136
7174657-3	1982	However, our present studies on the primary structure of the phenobarbital-inducible cytochrome from rabbit liver microsomes (P-450LM2) show that this protein is about 80% identical to the corresponding rat protein (P-450b), the sequence of which was recently deduced by others.	Phenobarbital	61-74	cytochrome P450 2B4	Oryctolagus cuniculus	126-134
7174657-3	1982	However, our present studies on the primary structure of the phenobarbital-inducible cytochrome from rabbit liver microsomes (P-450LM2) show that this protein is about 80% identical to the corresponding rat protein (P-450b), the sequence of which was recently deduced by others.	Phenobarbital	61-74	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	216-222
7174680-0	1982	The covalent structure of rabbit phenobarbital-induced cytochrome P-450.	Phenobarbital	33-46	cytochrome P-450	Oryctolagus cuniculus	55-71
7174680-2	1982	The phenobarbital-induced isozyme of cytochrome P-450 was isolated from rabbit liver microsomes and subjected to chemical and proteolytic degradation.	Phenobarbital	4-17	cytochrome P-450	Oryctolagus cuniculus	37-53
7174680-17	1982	The amino acid sequence data were also compared with the amino acid sequence deduced from the nucleotide sequence of phenobarbital-inducible cytochrome P-450 mRNA from rat liver (Kurijama-Fuji, Y., Mizukami, Y., Kawajiri, K., Sogawa, K., Muramatsu, M. (1982) Proc.	Phenobarbital	117-130	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	141-157
6817801-1	1982	The present study describes the purification and characterization of strain variant forms of a major phenobarbital-inducible microsomal hemoprotein, cytochrome P-450b, from Holtzman and Long-Evans rats.	Phenobarbital	101-114	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	149-166
7161973-4	1982	Phenobarbital induced cytochrome P-450 monooxygenase, and the activity was still higher in the median and right lobes even after the pretreatment of rats with phenobarbital.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily j, polypeptide 3	Rattus norvegicus	22-52
6130037-4	1982	Phenobarbital treatment resulted in significant increases in serum GGT activity (p less than 0.05) and urinary d-glucaric acid excretion (p less than 0.005).	Phenobarbital	0-13	inactive glutathione hydrolase 2	Homo sapiens	67-70
7161973-4	1982	Phenobarbital induced cytochrome P-450 monooxygenase, and the activity was still higher in the median and right lobes even after the pretreatment of rats with phenobarbital.	Phenobarbital	159-172	cytochrome P450, family 2, subfamily j, polypeptide 3	Rattus norvegicus	22-52
7150369-3	1982	The simultaneous induction of the PB-inducible and MC-inducible forms of cytochrome P-450 by administering Aroclor 1254 or by coadministering PB with MC increased the proportion of cytochrome P-450 that bound metyrapone to 74 and 78% respectively.	Phenobarbital	34-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	73-89
6758842-1	1982	Eight different forms of cytochrome P-450 (P-450) were purified to electrophoretic homogeneity by a common procedure from liver microsomes of rats treated with phenobarbital or beta-naphthoflavone.	Phenobarbital	160-173	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	25-41
7150369-3	1982	The simultaneous induction of the PB-inducible and MC-inducible forms of cytochrome P-450 by administering Aroclor 1254 or by coadministering PB with MC increased the proportion of cytochrome P-450 that bound metyrapone to 74 and 78% respectively.	Phenobarbital	34-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	181-197
7172093-3	1982	Adipose tissue lipoprotein lipase activity was also increased in the phenobarbital-treated rats.	Phenobarbital	69-82	lipoprotein lipase	Rattus norvegicus	15-33
7150369-3	1982	The simultaneous induction of the PB-inducible and MC-inducible forms of cytochrome P-450 by administering Aroclor 1254 or by coadministering PB with MC increased the proportion of cytochrome P-450 that bound metyrapone to 74 and 78% respectively.	Phenobarbital	142-144	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	73-89
7172093-6	1982	The increased postheparin lipolytic activity of fasting phenobarbital-treated rats seems to be accountable through increased lipoprotein lipase activity of adipose tissue and increased triacylglycerol lipase activity of liver, both of which may contribute to the lowered fasting concentrations of serum triacylglycerol mediated by the drug, as previously reported.	Phenobarbital	56-69	lipoprotein lipase	Rattus norvegicus	125-143
7150369-3	1982	The simultaneous induction of the PB-inducible and MC-inducible forms of cytochrome P-450 by administering Aroclor 1254 or by coadministering PB with MC increased the proportion of cytochrome P-450 that bound metyrapone to 74 and 78% respectively.	Phenobarbital	142-144	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	181-197
6130905-2	1982	UDP-GT activity after 3-methylcholanthrene (3-MC) and phenobarbital (PB) treatment was studied in additional rats for comparative purposes.	Phenobarbital	54-67	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	0-6
6130905-2	1982	UDP-GT activity after 3-methylcholanthrene (3-MC) and phenobarbital (PB) treatment was studied in additional rats for comparative purposes.	Phenobarbital	69-71	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	0-6
6130905-12	1982	Thus, 3-MC, PB, and PCN induce UDP-GT activities toward different groups of acceptors of glucuronic acid.	Phenobarbital	12-14	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	31-37
6820042-2	1982	In kidney microsomes, both contents of cytochrome P-450 (448) and activity of N4-hydroxylase were markedly increased by pretreatment with 3,4,5,3",4"-pentachlorobiphenyl (PenCB) (about 4 times), although neither one was increased by 3-methylcholanthrene (3-MC) and phenobarbital (PB) pretreatments.	Phenobarbital	265-278	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-55
6815045-0	1982	Immunofluorescence of phenobarbital inducible cytochrome P-450 in the hepatic lobule of normal and phenobarbital-treated rats.	Phenobarbital	22-35	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	46-62
6815045-0	1982	Immunofluorescence of phenobarbital inducible cytochrome P-450 in the hepatic lobule of normal and phenobarbital-treated rats.	Phenobarbital	99-112	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	46-62
6815045-1	1982	The localization of the form of cytochrome P-450 that is induced by phenobarbital was studied by direct immunofluorescence in the hepatocytes of rats pretreated with phenobarbital in comparison with saline-treated rats.	Phenobarbital	68-81	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	32-48
6815045-1	1982	The localization of the form of cytochrome P-450 that is induced by phenobarbital was studied by direct immunofluorescence in the hepatocytes of rats pretreated with phenobarbital in comparison with saline-treated rats.	Phenobarbital	166-179	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	32-48
6820042-2	1982	In kidney microsomes, both contents of cytochrome P-450 (448) and activity of N4-hydroxylase were markedly increased by pretreatment with 3,4,5,3",4"-pentachlorobiphenyl (PenCB) (about 4 times), although neither one was increased by 3-methylcholanthrene (3-MC) and phenobarbital (PB) pretreatments.	Phenobarbital	280-282	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-55
6820042-3	1982	In liver microsomes, on the other hand, both N4-hydroxylase activity and cytochrome P-450 (448) contents were increased by either PenCB or 3-MC pretreatment, whereas by PB pretreatment, N4-hydroxylase activity was not changed although cytochrome P-450 contents was increased 2-fold.	Phenobarbital	169-171	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	235-251
6579541-0	1983	Complete amino acid sequence and predicted membrane topology of phenobarbital-induced cytochrome P-450 (isozyme 2) from rabbit liver microsomes.	Phenobarbital	64-77	cytochrome P450 2B4	Oryctolagus cuniculus	86-113
6809749-0	1982	Phenobarbital-induced rat liver cytochrome P-450.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	32-48
6579541-1	1983	The complete amino acid sequence of phenobarbital-induced isozyme 2 of rabbit liver microsomal cytochrome P-450 (P-450LM2) is presented.	Phenobarbital	36-49	cytochrome P450 2B4	Oryctolagus cuniculus	58-67
6579541-1	1983	The complete amino acid sequence of phenobarbital-induced isozyme 2 of rabbit liver microsomal cytochrome P-450 (P-450LM2) is presented.	Phenobarbital	36-49	cytochrome P450 2B4	Oryctolagus cuniculus	106-111
6579541-1	1983	The complete amino acid sequence of phenobarbital-induced isozyme 2 of rabbit liver microsomal cytochrome P-450 (P-450LM2) is presented.	Phenobarbital	36-49	cytochrome P450 2B4	Oryctolagus cuniculus	113-121
7173394-1	1982	The turnover of the heme and apocytochrome moieties of phenobarbital-inducible microsomal cytochrome P450 (P450b) was investigated.	Phenobarbital	55-68	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	107-112
7168193-10	1982	The levels of some of these cytochrome P-450 isozymes have been quantified immunologically in hepatic microsomal preparations from untreated rats and following induction by phenobarbital, 3-methylcholanthrene or Aroclor 1254.	Phenobarbital	173-186	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	28-44
7181861-1	1982	The interaction of substrates of the microsomal mixed-function oxidases with cytochromes P-450 and P-448 was investigated by using liver microsomes from rats pretreated with phenobarbital or 3-methylcholanthrene, and with purified forms of the cytochromes isolated from rabbit liver.	Phenobarbital	174-187	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	89-104
6890504-7	1982	In vitro, the gallates proved to be potent inhibitors of ethoxycoumarin deethylation in liver microsomes from untreated and phenobarbital-treated rats; however, when cytochrome P-448 had been induced by pretreatment with 3-methylcholanthrene, ethoxycoumarin deethylase was less sensitive to the inhibitory action of the gallates.	Phenobarbital	124-137	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	166-182
6809749-2	1982	The "major" phenobarbital (PB)-induced cytochrome P-450 species present in livers of male Sprague-Dawley rats was resolved into two catalytically active heme-protein fractions on diethylaminoethyl cellulose.	Phenobarbital	12-25	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-55
6809749-2	1982	The "major" phenobarbital (PB)-induced cytochrome P-450 species present in livers of male Sprague-Dawley rats was resolved into two catalytically active heme-protein fractions on diethylaminoethyl cellulose.	Phenobarbital	27-29	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-55
6815477-2	1982	In the present study, a reconstituted system which consisted of cytochrome P-450 and NADPH cytochrome P-450 reductase purified from liver microsomes of phenobarbital-induced rabbits was found to oxidize phentermine to N-hydroxyphentermine.	Phenobarbital	152-165	cytochrome P-450	Oryctolagus cuniculus	64-117
6286112-4	1982	Cytochrome P-450 specific content is increased 2- to 3-fold by treatment with phenobarbital plus hydrocortisone and benz(a)anthracene, respectively.	Phenobarbital	78-91	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-16
7132565-3	1982	The effects of the 4"-halo-2,3,4,5-tetrachlorobiphenyls on the microsomal enzyme activities and on the relative peak intensities and spectral shifts of the reduced cytochrome P-450:CO and ethylisocyanide (EIC) binding difference spectra were similar to those observed after coadministration of phenobarbitone (PB) and 3-methylcholanthrene (MC).	Phenobarbital	294-308	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	164-180
7132565-3	1982	The effects of the 4"-halo-2,3,4,5-tetrachlorobiphenyls on the microsomal enzyme activities and on the relative peak intensities and spectral shifts of the reduced cytochrome P-450:CO and ethylisocyanide (EIC) binding difference spectra were similar to those observed after coadministration of phenobarbitone (PB) and 3-methylcholanthrene (MC).	Phenobarbital	310-312	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	164-180
6286155-1	1982	Hexachlorobenzene (HCB) produced increases in ethoxyresorufin (ERR) O-deethylase, aryl hydrocarbon hydroxylase (AHH) and aminopyrine N-demethylase activities in rat liver phenobarbital which were intermediate between those produced by phenobarbital and 3,4-benzpyrene (BP), alpha-Naphthoflavone (ANF) selectivity inhibited ERR activity in BP and HCB-induced microsomes (94% and 88%).	Phenobarbital	171-184	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	112-115
7113725-6	1982	Pretreatment of animals with the cytochrome P-450 inducer phenobarbital did not affect N-OH-pHAA cytotoxicity or covalent binding, whereas the cytochrome P-450 inhibitor metyrapone inhibited both cytotoxicity and binding.	Phenobarbital	58-71	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	33-49
6286155-1	1982	Hexachlorobenzene (HCB) produced increases in ethoxyresorufin (ERR) O-deethylase, aryl hydrocarbon hydroxylase (AHH) and aminopyrine N-demethylase activities in rat liver phenobarbital which were intermediate between those produced by phenobarbital and 3,4-benzpyrene (BP), alpha-Naphthoflavone (ANF) selectivity inhibited ERR activity in BP and HCB-induced microsomes (94% and 88%).	Phenobarbital	235-248	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	112-115
6818357-4	1982	In rats pretreated with phenobarbital (0.05%), Zn (10 mg/l) and Cu (10 mg/l) in tap water and cysteine (200 mg/kg s.c.), fetal toxicity of ASA was reduced, whereas it was enhanced in rats pretreated with SKF-525A (200 mg/kg s.c.) and alpha-naphthyl acetic acid (200 mg/kg p.o.)	Phenobarbital	24-37	nuclear RNA export factor 1	Rattus norvegicus	80-83
6818357-6	1982	The UDPGT activity in hepatic 9000 x g supernate was higher in mice than in rats and the activity of mice was increased by phenobarbital and Cu.	Phenobarbital	123-136	UDP glucuronosyltransferase 1 family, polypeptide A6A	Mus musculus	4-9
6889862-0	1982	3-Methylcholanthrene induces phenobarbital-induced cytochrome P-450 hemoprotein in fetal liver and not cytochrome P-448 hemoprotein induced in maternal liver of rats.	Phenobarbital	29-42	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	51-67
7083399-0	1982	Effects of phenobarbital and sodium salicylate on cytochrome P-450 mixed function oxygenase and glutathione S-transferase activities in rat brain.	Phenobarbital	11-24	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	50-66
7083399-0	1982	Effects of phenobarbital and sodium salicylate on cytochrome P-450 mixed function oxygenase and glutathione S-transferase activities in rat brain.	Phenobarbital	11-24	hematopoietic prostaglandin D synthase	Rattus norvegicus	96-121
7083399-1	1982	The effects of acute and therapeutic doses of phenobarbital and sodium salicylate on cytochrome P-450 mixed function oxygenase (EC 1.14.14.1) and glutathione S-transferase (EC 2.5.1.18) activities have been studied in rat brain and compared with those of rat liver.	Phenobarbital	46-59	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	85-101
7083399-1	1982	The effects of acute and therapeutic doses of phenobarbital and sodium salicylate on cytochrome P-450 mixed function oxygenase (EC 1.14.14.1) and glutathione S-transferase (EC 2.5.1.18) activities have been studied in rat brain and compared with those of rat liver.	Phenobarbital	46-59	hematopoietic prostaglandin D synthase	Rattus norvegicus	146-171
7083399-10	1982	The increase in brain glutathione S-transferase by prolonged treatment of phenobarbital was significant compared to the control values.	Phenobarbital	74-87	hematopoietic prostaglandin D synthase	Rattus norvegicus	22-47
6805966-1	1982	Tritiated 2,2"5,5"-tetrachlorobiphenyl (3H-TCB) was incubated with phenobarbital(PB)-induced rat liver microsomes in the presence of an epoxide hydrase inhibitor and brominated analog (BrAO) of the expected metabolic intermediate, 2,2",5,5"-tetrachlorobiphenyl-3,4-oxide (TCBAO).	Phenobarbital	67-80	T-cell receptor beta chain	Rattus norvegicus	43-46
7115427-6	1982	The binding and metabolism of the 1,2-dichloroethylenes and the 1,2-dichloroethylene-mediated inactivation of cytochrome P-450 were enhanced per mg of microsomal protein, but generally not per nmole of cytochrome P-450 by prior induction with beta-naphthoflavone or phenobarbital.	Phenobarbital	266-279	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	110-126
7109711-0	1982	The quantitation of liver cytochrome P450-LM2 mRNA in rabbits of different ages and after phenobarbital treatment.	Phenobarbital	90-103	cytochrome P450 2B4	Oryctolagus cuniculus	26-45
7097715-2	1982	Effects of benzimidazole and related compounds on aryl hydrocarbon hydroxylase activity from phenobarbitone and 3-methylcholanthrene induced rats.	Phenobarbital	93-107	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	50-78
7097715-3	1982	A series of 2-n-alkylbenzimidazoles inhibited cytochrome P-450 dependent aryl hydrocarbon hydroxylase (AHH) and aminopyrine N-demethylase (APDM) activities in phenobarbitone (PB) induced rat liver microsomes.	Phenobarbital	159-173	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	73-101
7097715-3	1982	A series of 2-n-alkylbenzimidazoles inhibited cytochrome P-450 dependent aryl hydrocarbon hydroxylase (AHH) and aminopyrine N-demethylase (APDM) activities in phenobarbitone (PB) induced rat liver microsomes.	Phenobarbital	175-177	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	73-101
7109711-4	1982	Using a specific assay for translatable cytochrome P450-LM2 mRNA, we show that the age-dependent decrease in control and phenobarbital-induced enzyme activities is due to a decrease in the levels of translatable mRNA specific for cytochrome P450-LM2.	Phenobarbital	121-134	cytochrome P450 2B4	Oryctolagus cuniculus	40-59
7109711-4	1982	Using a specific assay for translatable cytochrome P450-LM2 mRNA, we show that the age-dependent decrease in control and phenobarbital-induced enzyme activities is due to a decrease in the levels of translatable mRNA specific for cytochrome P450-LM2.	Phenobarbital	121-134	cytochrome P450 2B4	Oryctolagus cuniculus	230-249
7104016-1	1982	The in vitro metabolism of biphenyl, 4-fluoro-, 4-chloro-, 4-bromo- and 4-iodobiphenyl by cytochrome P-450-dependent monooxygenases was investigated using hepatic microsomes from immature male rats pretreated with phenobarbitone or 3-methylcholanthrene.	Phenobarbital	214-228	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	90-106
7103956-0	1982	Limitations on the metyrapone assay for the major phenobarbital inducible form of cytochrome P-450.	Phenobarbital	50-63	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	82-98
7093199-11	1982	With sulindac sulfide as substrate, though, both control and phenobarbital-induced microsomes catalyze sulfoxidation to yield the same (+)-sulfoxide enantiomer generated by the purified FAD-containing monoxygenase, suggesting a low degree of participation by the cytochrome P-450 isozymes in sulfoxidation of this compound.	Phenobarbital	61-74	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	263-279
7093200-1	1982	The chirality of sulfoxidation catalyzed by two cytochrome P-450 isozymes purified from phenobarbital-induced rat liver was studied by using 4-tolyl ethyl sulfide as a substrate.	Phenobarbital	88-101	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	48-64
6125358-7	1982	In another set of experiments, R30 values determined in controls and in PB- and CoCl2-pretreated rats demonstrated excellent correlation to changes in hepatic microsomal AP and ethylmorphine N-demethylase and aniline hydroxylase activities and cytochrome P-450 content.	Phenobarbital	72-74	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	244-260
6953431-0	1982	Primary structure of a cytochrome P-450: coding nucleotide sequence of phenobarbital-inducible cytochrome P-450 cDNA from rat liver.	Phenobarbital	71-84	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	23-39
6953431-0	1982	Primary structure of a cytochrome P-450: coding nucleotide sequence of phenobarbital-inducible cytochrome P-450 cDNA from rat liver.	Phenobarbital	71-84	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	95-111
6953431-1	1982	We determined the coding nucleotide sequence of phenobarbital-inducible cytochrome P-450 mRNA of the rat by analysis of three cloned cDNAs and by primer extension methods.	Phenobarbital	48-61	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	72-88
6953431-4	1982	In their 922 overlapping nucleotides, 14 nucleotide substitutions occur, and 7 of them result in 6 amino acid changes, therefore indicating the presence of at least two similar but distinct mRNAs for phenobarbital-inducible cytochrome P-450.	Phenobarbital	200-213	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	224-240
6953437-0	1982	Stimulation of de novo synthesis of cytochrome P-450 by phenobarbital in primary nonproliferating cultures of adult rat hepatocytes.	Phenobarbital	56-69	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	36-52
6953437-1	1982	Primary monolayer cultures of nonproliferating parenchymal cells prepared from adult rat liver and maintained in serum-free medium responded to additions of phenobarbital with concentration-dependent increases in synthesis and accumulation of a cytochrome P-450 protein immunochemically and catalytically indistinguishable from that found in the livers of adult rats treated with phenobarbital.	Phenobarbital	157-170	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	245-261
6953437-1	1982	Primary monolayer cultures of nonproliferating parenchymal cells prepared from adult rat liver and maintained in serum-free medium responded to additions of phenobarbital with concentration-dependent increases in synthesis and accumulation of a cytochrome P-450 protein immunochemically and catalytically indistinguishable from that found in the livers of adult rats treated with phenobarbital.	Phenobarbital	380-393	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	245-261
6953437-6	1982	Contrary to the concept that liver cells placed in culture promptly dedifferentiate with general loss of specialized functions such as cytochrome P-450, our data demonstrate that expression of the phenobarbital-inducible form of cytochrome P-450 is not extinguished in culture, but rather it is masked transiently and is attenuated as the cells adapt to the imperfect conditions of the culture environment.	Phenobarbital	197-210	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	229-245
7068621-1	1982	It was shown previously that four immunochemically identical forms of phenobarbital-induced hepatic cytochrome P-450 exist in unique combinations which characterize different strains and colonies of rats (Vlasuk, G. P., Ghrayeb, J., Ryan, D. E., Reik, L., Thomas, P. E., Levin, W., and Walz, F. G., Jr. (1982) Biochemistry 21, 789-798).	Phenobarbital	70-83	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	100-116
7074142-2	1982	After phenobarbital pretreatment, the specific activity of nicotine oxidase increased while the activity of the enzyme per cytochrome P-450 molecule decreased.	Phenobarbital	6-19	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	123-139
6810877-1	1982	We have defined conditions that permit quantitative and specific measurement of the metabolism of the major phenobarbital-inducible form of cytochrome P-450 protein in primary non-proliferating monolayer cultures of adult rat hepatocytes.	Phenobarbital	108-121	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	140-156
7074142-4	1982	These results show that phenobarbital-induced cytochrome P-450 and constitutive form(s) of the enzyme may be active in hepatic nicotine oxidation.	Phenobarbital	24-37	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	46-62
6810877-6	1982	Basal rates of synthesis of phenobarbital cytochrome P-450 representing as little as 0.02-0.05% of total cellular protein synthesis were reliably and reproducibly detected in hepatocyte culture maintained in serum-free medium for 72h.	Phenobarbital	28-41	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	42-58
6810877-7	1982	Moreover, inclusion of phenobarbital in the culture medium for 96h stimulated not only synthesis de novo of phenobarbital cytochrome P-450 protein, but also accumulation of spectrally and catalytically active cytochrome P-450.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	122-138
6810877-7	1982	Moreover, inclusion of phenobarbital in the culture medium for 96h stimulated not only synthesis de novo of phenobarbital cytochrome P-450 protein, but also accumulation of spectrally and catalytically active cytochrome P-450.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	209-225
6285672-4	1982	One type of human liver microsomal fraction was selectively induced in specimens obtained from patients with known regular drug intake before death and correlated well in molecular weight to the phenobarbital-inducible form of cytochrome P-450 in the rabbit.	Phenobarbital	195-208	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	227-243
6807317-4	1982	Higher doses of phenobarbital (80 mg/kg) induced both UDP-GT1 and UDP-GT2 activities.	Phenobarbital	16-29	solute carrier family 2 (facilitated glucose transporter), member 1	Mus musculus	58-61
7082800-3	1982	The degree of cytochrome P450 induction with phenobarbital was found to be dependent on the diet.	Phenobarbital	45-58	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	14-29
6807317-3	1982	Phenobarbital, however, at low doses (50 mg/kg), selectively induced UDP-GT2 activities.	Phenobarbital	0-13	guanine nucleotide binding protein, alpha transducing 2	Mus musculus	73-76
6807317-4	1982	Higher doses of phenobarbital (80 mg/kg) induced both UDP-GT1 and UDP-GT2 activities.	Phenobarbital	16-29	guanine nucleotide binding protein, alpha transducing 2	Mus musculus	70-73
7037176-0	1982	Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin and phenobarbital on the occurrence and distribution of four cytochrome P-450 isozymes in rabbit kidney, lung, and liver.	Phenobarbital	50-63	cytochrome P-450	Oryctolagus cuniculus	107-123
6217856-5	1982	DAB azoreductase activity was induced by 20-methylcholanthrene and phenobarbital, and increased in streptozotocin-induced diabetes or fasting.	Phenobarbital	67-80	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	4-16
7138085-0	1982	[Serum beta-glucuronidase activity in patients treated with phenobarbital and diphenylhydantoin].	Phenobarbital	60-73	glucuronidase beta	Homo sapiens	7-25
7037176-1	1982	The effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and of phenobarbital (PB) on the distribution and occurrence of four cytochrome P-450 isozymes, Forms 2, 3, 4, and 6, in the kidney, lung, and liver of adult male rabbits was investigated using immunofluorescence.	Phenobarbital	79-81	cytochrome P-450	Oryctolagus cuniculus	126-142
7082331-0	1982	Specificity of a phenobarbital-induced cytochrome P-450 for metabolism of carbon tetrachloride to the trichloromethyl radical.	Phenobarbital	17-30	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-55
7061465-5	1982	Two isozymes of rabbit liver microsomal cytochrome P-450 were examined: the isozyme induced by phenobarbital (P-450LM2), which has a sixth ligand and is low spin and the isozyme induced by 5,6-benzoflavone (P-450LM4), which is without a sixth ligand and is high spin.	Phenobarbital	95-108	cytochrome P450 2B4	Oryctolagus cuniculus	110-118
6276399-1	1982	The 5"-nucleotidase activity of rat liver plasma membranes could be selectively modulated by the anionic drugs phenobarbital and pentobarbital, whereas the corresponding activity of a Lubrol-solubilized preparations remained unaltered.	Phenobarbital	111-124	5' nucleotidase, ecto	Rattus norvegicus	4-19
7062265-1	1982	Subchronic treatment with phenobarbital induces renal cortical microsomal monooxygenase activities (e.g., ethoxycoumarin O-deethylase, benzphetamine N-demethylase and arylhydrocarbon hydroxylase) and cytochrome P-450 content in rabbits but not in rats.	Phenobarbital	26-39	cytochrome P-450	Oryctolagus cuniculus	200-216
6808350-0	1982	Differential inducibility of nuclear envelope epoxide hydratase by trans-stilbene oxide and phenobarbital.	Phenobarbital	92-105	epoxide hydrolase 2	Homo sapiens	46-63
6124393-5	1982	Microsomes from PB-treated animals demethylated and hydroxylated DAB at the same rate as did control microsomes, based on cytochrome P-450 content, whereas microsomes from BNF- or MC-treated animals demethylated more rapidly and hydroxylated more slowly.	Phenobarbital	16-18	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	122-138
6124393-9	1982	Only one of the four cytochrome P-450 fractions isolated from PB-treated animals had significant activity with DAB and the turnover number of one of these (fraction B) was approximately that seen in microsomes.	Phenobarbital	62-64	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	21-37
7099146-3	1982	This reaction was demonstrated to be mediated by cytochrome P-450 as suggested by induction experiments using phenobarbital, which markedly enhanced the production of this nitroxide, and by the inhibition of this monooxygenase by metyrapone, which depressed the formation of this free radical.	Phenobarbital	110-123	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	49-65
6276399-2	1982	The perturbation in the outer half of the bilayer induced by phenobarbital, which lead to a depression in the high temperature onset of the lipid phase separation occurring in this half of the bilayer, concomitantly lowered the break temperature in Arrhenius plots of 5"-nucleotidase activity from 28 degrees C to 16 degrees C. The stimulation of the membrane-bound activity achieved by low anionic drug concentrations was attributed to a preferential fluidization of the outer half of the bilayer.	Phenobarbital	61-74	5' nucleotidase, ecto	Rattus norvegicus	268-283
6799005-2	1982	Two facts ((i) inhibition of the formation of 1-piperidinoanthrahydroquinone (1-PAH) by metyrapone and antibodies to cytochrome P-450, and (ii) increase in the rate of 1-PAH formation upon induction of rats by phenobarbital) indicate that cytochrome P-450 participates in the reduction of 1-PA.	Phenobarbital	210-223	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	117-133
7049121-0	1982	Effect of cadmium and phenobarbital on cerebral aldehyde reductase.	Phenobarbital	22-35	aldo-keto reductase family 1 member A1	Homo sapiens	48-66
6120697-3	1982	Significant destruction of cytochrome P-450 was observed when alclofenac was incubated with microsomes from mice pretreated with PB but not from untreated or 3-MC-treated mice.	Phenobarbital	129-131	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	27-43
7059232-0	1982	Effect of phenobarbitol pretreatment on regeneration of plasma cholinesterase activity inhibited by parathion or dichlorovos.	Phenobarbital	10-23	butyrylcholinesterase	Rattus norvegicus	63-77
7059232-1	1982	Rats were pretreated with phenobarbitol [PB (75 mg/kg, IP)] for 3 days and subsequently injected with parathion, an organophosphorous insecticide, which requires microsomal activation for its anticholinesterase effect or with dichlorovos, a cholinesterase (ChE) inhibitor as such.	Phenobarbital	26-39	butyrylcholinesterase	Rattus norvegicus	196-210
7059232-8	1982	Phenobarbital caused accelerated in vitro ChE regeneration in the case of dichlorovos-inhibited enzyme in the plasma, but not in the case of parathion-inhibited enzyme.	Phenobarbital	0-13	butyrylcholinesterase	Rattus norvegicus	42-45
7054190-0	1982	Effects of 3-methylcholanthrene, beta-naphthoflavone, and phenobarbital on the 3-methylcholanthrene-inducible isozyme of cytochrome P-450 within centrilobular, midzonal, and periportal hepatocytes.	Phenobarbital	58-71	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	121-137
7049121-4	1982	From these results it is concluded, that only in heavily contaminated people will an interaction between Cd and phenobarbital on the aldehyde reductase level in the brain occur.	Phenobarbital	112-125	aldo-keto reductase family 1 member A1	Homo sapiens	133-151
7094216-3	1982	AdoMet levels greater than 100 mug/g liver were noted in rats receiving PB + methionine for 1 week, DDT + methionine for 1 week or methionine alone for 5 weeks.	Phenobarbital	72-74	methionine adenosyltransferase 1A	Rattus norvegicus	0-6
6121634-3	1982	Maximum induction of ODC by phenobarbital was obtained in 18 h. Barbital (500-5000 p.p.m.)	Phenobarbital	28-41	ornithine decarboxylase 1	Rattus norvegicus	21-24
6811264-0	1982	Phenobarbital induction of cytochrome P-450 and UDP-glucuronosyltransferase in rabbit liver plasma membranes.	Phenobarbital	0-13	cytochrome P-450	Oryctolagus cuniculus	27-43
6273441-7	1982	Phenobarbital treatment resulted in a 3.2-fold increase in glutathione S-transferase mRNA over levels found in control rats, while trans-stilbene oxide increased glutathione S-transferase mRNA levels 5.7-fold.	Phenobarbital	0-13	hematopoietic prostaglandin D synthase	Rattus norvegicus	59-84
6811264-0	1982	Phenobarbital induction of cytochrome P-450 and UDP-glucuronosyltransferase in rabbit liver plasma membranes.	Phenobarbital	0-13	UDP-glucuronosyltransferase 2C1	Oryctolagus cuniculus	48-75
6811264-3	1982	Both enzymes were induced by phenobarbital treatment of the animals: administration of the barbiturate for 4 days, produced a 150% increase in the cytochrome P-450 content and in the specific activity of UDP-glucuronosyltransferase.	Phenobarbital	29-42	cytochrome P-450	Oryctolagus cuniculus	147-163
6811264-3	1982	Both enzymes were induced by phenobarbital treatment of the animals: administration of the barbiturate for 4 days, produced a 150% increase in the cytochrome P-450 content and in the specific activity of UDP-glucuronosyltransferase.	Phenobarbital	29-42	UDP-glucuronosyltransferase 2C1	Oryctolagus cuniculus	204-231
7173298-6	1982	Subjects with a normal liver undergoing treatment with enzyme-inducing drugs, such as phenytoin, phenobarbital and primidone, had higher HDL cholesterol, apoproteins A-I and A-II, HDL cholesterol/total cholesterol ratio, cytochrome P-450 and antipyrine clearance rate than subjects not receiving such therapy.	Phenobarbital	97-110	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	221-237
7060925-0	1982	Comparative effects of phenobarbital and picrotoxin on the choline acetyltransferase activity of specific rat brain areas.	Phenobarbital	23-36	choline O-acetyltransferase	Rattus norvegicus	59-84
6300027-1	1982	Complementary (c)DNA clones of phenobarbital-inducible cytochrome P-450 which has a strong activity toward metabolic activation of aflatoxin B1 were identified by a hybridization-arrested translation assay and a positive hybridization-translation assay.	Phenobarbital	31-44	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	55-71
7132955-1	1982	The kinetics and reversibility of the suicide inactivation of rat liver cytochrome P-450 by chloramphenicol have been investigated with the use of a reconstituted monooxygenase system purified from liver microsomes of phenobarbital-treated rats.	Phenobarbital	218-231	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	72-88
6300027-5	1982	Fourteen nucleotide substitutions occur in their 922 overlapping nucleotides and 7 of them result in 6 amino acid replacements, therefore indicating the presence of at least two similar but distinct mRNAs for phenobarbital-inducible cytochrome P-450.	Phenobarbital	209-222	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	233-249
7080062-7	1982	Simultaneous lead and phenobarbital treatment produced a delayed but robust induction of cytochrome P-450, only a moderate rise in U-ALA, and a reduced proliferation of the SER of hepatocytes.	Phenobarbital	22-35	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	89-105
6100830-2	1982	Phenobarbital is known to increase rabbit but not rat renal mixed-function oxidase activities; however, several other compounds such as polybrominated biphenyls (PBB), trans-stilbene oxide (TSO) and beta-naphthoflavone (BNF) have been shown to induce renal enzyme activities in rats.	Phenobarbital	0-13	natriuretic peptide B	Rattus norvegicus	199-224
6124064-14	1982	spectra of cytochrome P-450 from phenobarbital-pretreated rats, in the presence of ranitidine, reveal two types of interaction depending on the ranitidine concentration.	Phenobarbital	33-46	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	11-27
6798990-3	1981	Reconstituted, purified cytochrome P-450 PB-B and BNF-B, the major terminal oxidase isozymes of this system, from phenobarbital (PB)- and beta-naphthoflavone (BNF)-induced rats were used to investigate this metabolism.	Phenobarbital	114-127	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	24-40
6798990-3	1981	Reconstituted, purified cytochrome P-450 PB-B and BNF-B, the major terminal oxidase isozymes of this system, from phenobarbital (PB)- and beta-naphthoflavone (BNF)-induced rats were used to investigate this metabolism.	Phenobarbital	41-43	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	24-40
6800375-0	1981	Specific evidence that schizandrins induce a phenobarbital-like cytochrome P-450 form separated from rat liver.	Phenobarbital	45-58	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	64-80
7309741-7	1981	In fed, sodium phenobarbital-treated rats, the steady state level of reduced (an oxygenated) cytochrome P-450 was dependent on the concentration and the kind of substrates added, and the level correlated well with mixed-function oxidase activity.	Phenobarbital	8-28	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	93-109
7342977-0	1981	The effects of dietary lipid and phenobarbitone on the production and utilization of NADPH in the liver.	Phenobarbital	33-47	2,4-dienoyl-CoA reductase 1	Homo sapiens	85-90
7342977-3	1981	The amount of NADPH, generated by glucose 6-phosphate dehydrogenase, entering Pathways I and II in the centrilobular and periportal regions was measured by quantitative cytochemistry, and the values obtained were compared with biochemical measurements of mixed-function oxidase and fatty acid synthetase activity after the administration of sodium phenobarbitone or by altering the quantity and nature of the dietary lipid.	Phenobarbital	341-362	2,4-dienoyl-CoA reductase 1	Homo sapiens	14-19
7317380-1	1981	Hepatic microsomal cytochrome P-450 from phenobarbital-pretreated rats is destroyed by propyne in a reduced nicotinamide adenine dinucleotide dependent process which also results in vivo in the accumulation of an abnormal green porphyrin.	Phenobarbital	41-54	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	19-35
7080062-8	1982	Therefore, phenobarbital, an inducer of heme synthetic enzymes, is apparently capable of reversing lead-induced inhibition of heme synthesis as measured by hepatic cytochrome P-450 induction and U-ALA content.	Phenobarbital	11-24	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	164-180
6800639-3	1981	The formation of N-hydroxy-Trp-P-2 by nuclei of PCB- or MC-treated rat livers was greater than that by nuclei of untreated or PB-treated rat livers.	Phenobarbital	126-128	polycystin 2, transient receptor potential cation channel	Rattus norvegicus	27-34
7298626-8	1981	When microsomes isolated from incubations metabolizing [4-14C]cyclophosphamide were subjected to gel electrophoresis, the major radioactive band detected by autoradiography was associated with a cytochrome P-450 band at 55,000 daltons, the major band induced by phenobarbital in the rat.	Phenobarbital	262-275	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	195-211
7294161-3	1981	Cells prepared from male rats pretreated with phenobarbital were more sensitive to CCl4 than cells prepared from either male or female rats.	Phenobarbital	46-59	C-C motif chemokine ligand 4	Rattus norvegicus	83-87
6270145-2	1981	Addition of glucose to cultured chick embryo hepatocytes caused a concentration-dependent impairment of phenobarbital-mediated induction of delta-aminolevulinate (ALA) synthase resembling the "glucose effect" observed in rodents in vivo.	Phenobarbital	104-117	5'-aminolevulinate synthase 1	Gallus gallus	140-176
6270145-6	1981	The phenobarbital-mediated induction of cytochrome P-450 hemoprotein(s) and its monooxygenase function were concomitantly diminished by glucose.	Phenobarbital	4-17	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	40-56
6270145-8	1981	Glucagon and dibutyryl cAMP enhanced the induction of ALA synthase and cytochrome P-450 by phenobarbital and partially counteracted the glucose effect on both enzymes suggesting that the glucose effect may be mediated by changes in cAMP levels.	Phenobarbital	91-104	5'-aminolevulinate synthase 1	Gallus gallus	54-66
6270145-8	1981	Glucagon and dibutyryl cAMP enhanced the induction of ALA synthase and cytochrome P-450 by phenobarbital and partially counteracted the glucose effect on both enzymes suggesting that the glucose effect may be mediated by changes in cAMP levels.	Phenobarbital	91-104	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	71-87
6797104-1	1981	Phenobarbital stimulates the induction of liver microsomal drug-metabolizing enzyme, namely, cytochrome P-450, which enhances the rate of conversion of FT-207 to 5-FU, the active substance.	Phenobarbital	0-13	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	93-109
7317837-0	1981	Effect of phenobarbital on sleep and nighttime plasma growth hormone and cortisol levels.	Phenobarbital	10-23	growth hormone 1	Homo sapiens	54-68
6116706-0	1981	Mechanism of induction of cytochrome P-450 by phenobarbital.	Phenobarbital	46-59	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	26-42
6116706-1	1981	Treatment of rats with phenobarbital (PB) leads to a substantial increase in the hepatic levels of translatable polysomal poly(A) + cytochrome P-450 mRNA.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	132-148
7080065-7	1982	Using male genetically heterogeneous stock (HS) mice it was shown that phenobarbital pretreatment potentiated the CCl4-induced decrease in in vivo acetaldehyde oxidation.	Phenobarbital	71-84	chemokine (C-C motif) ligand 4	Mus musculus	114-118
7080065-11	1982	and that this inhibition is enhanced by the cytochrome P-450-inducing agent phenobarbital.	Phenobarbital	76-89	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	44-60
6116706-1	1981	Treatment of rats with phenobarbital (PB) leads to a substantial increase in the hepatic levels of translatable polysomal poly(A) + cytochrome P-450 mRNA.	Phenobarbital	38-40	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	132-148
6797104-2	1981	When FT-207 is administered in combination with phenobarbital to cancer patients, the fluctuation in level of the drug-metabolizing enzyme, cytochrome P-450, should be taken into consideration.	Phenobarbital	48-61	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	140-156
7295776-5	1981	This frequency and those of other structure-sensitive bands implied that the heme iron of oxidized P-450SCC adopts the hexa-coordinate high-spin structure, in contrast with the high-spin type cytochrome P-450 purified from phenobarbital- or 3-methylcholanthrene-treated rabbit liver microsomes which presumably have a penta-coordinate structure.	Phenobarbital	223-236	cholesterol side-chain cleavage enzyme, mitochondrial	Bos taurus	99-107
7298716-1	1981	Induction of cytochrome P-450s by 3-methylcholanthrene (MC) and phenobarbital (PB) and distribution of P-450s in the rat liver nuclear envelope were investigated by biochemical analyses and ferritin immunoelectron microscopy using specific antibodies against the major molecular species of MC- and PB-induced cytochrome P-450.	Phenobarbital	64-77	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
7298716-1	1981	Induction of cytochrome P-450s by 3-methylcholanthrene (MC) and phenobarbital (PB) and distribution of P-450s in the rat liver nuclear envelope were investigated by biochemical analyses and ferritin immunoelectron microscopy using specific antibodies against the major molecular species of MC- and PB-induced cytochrome P-450.	Phenobarbital	79-81	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
18792759-2	1981	The effects of simultaneous phenobarbital (PB) treatment (0.05% in drinking water) on the hepatotoxicity of CCl4 was studied during 16 weeks of treatment.	Phenobarbital	28-41	C-C motif chemokine ligand 4	Rattus norvegicus	108-112
18792759-2	1981	The effects of simultaneous phenobarbital (PB) treatment (0.05% in drinking water) on the hepatotoxicity of CCl4 was studied during 16 weeks of treatment.	Phenobarbital	43-45	C-C motif chemokine ligand 4	Rattus norvegicus	108-112
18792759-5	1981	The potentiating effect of PB on CCl4 hepatotoxicity was also seen in hexobarbital sleeping time, the rate of hexobarbital metabolism, and the cytochrome P-450 content in liver microsomes.	Phenobarbital	27-29	C-C motif chemokine ligand 4	Rattus norvegicus	33-37
18792759-5	1981	The potentiating effect of PB on CCl4 hepatotoxicity was also seen in hexobarbital sleeping time, the rate of hexobarbital metabolism, and the cytochrome P-450 content in liver microsomes.	Phenobarbital	27-29	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	143-159
6788368-0	1981	Apparent differential response of nuclear envelope cytochrome P-450 following phenobarbital induction arising from a preferential loss during gradient purification.	Phenobarbital	78-91	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	51-67
7287694-1	1981	Interaction and electron transfer between highly purified microsomal cytochrome P-450 from phenobarbital-induced rabbits and cytochrome b5 from uninduced rabbits was investigated by difference and stopped-flow spectrophotometry.	Phenobarbital	91-104	cytochrome P-450	Oryctolagus cuniculus	69-85
7287694-1	1981	Interaction and electron transfer between highly purified microsomal cytochrome P-450 from phenobarbital-induced rabbits and cytochrome b5 from uninduced rabbits was investigated by difference and stopped-flow spectrophotometry.	Phenobarbital	91-104	cytochrome b5	Oryctolagus cuniculus	125-138
21043248-5	1981	Hepatocytes prepared from phenobarbital (PB)-pretreated animals exhibited increased AP N-demethylase activity and typical Michaelis-Menten kinetics.	Phenobarbital	26-39	alanyl aminopeptidase, membrane	Rattus norvegicus	84-88
21043248-5	1981	Hepatocytes prepared from phenobarbital (PB)-pretreated animals exhibited increased AP N-demethylase activity and typical Michaelis-Menten kinetics.	Phenobarbital	41-43	alanyl aminopeptidase, membrane	Rattus norvegicus	84-88
7196447-4	1981	The involvement of the cytochrome P-450 system in the activation of 6-thiopurine to the chemically reactive metabolite was supported by the effects of inhibitors of cytochrome P-450 mediated reactions and phenobarbital induction.	Phenobarbital	205-218	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	23-39
7263679-0	1981	Determination of partition ratios for allylisopropylacetamide during suicidal processing by a phenobarbital-induced cytochrome P-450 isozyme from rat liver.	Phenobarbital	94-107	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	116-132
7263679-2	1981	In phenobarbital-induced rat liver microsomes about 70% of the cytochrome P-450-mediated N,N-dimethylaniline N-demethylase activity is sensitive to allylisopropylacetamide inactivation; the residual 30% of the N-demethylase activity is incapable of allylisopropylacetamide turnover and insensitive to allylisopropylacetamide inactivation.	Phenobarbital	3-16	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	63-79
7263679-4	1981	A purified phenobarbital-induced isozyme of cytochrome P-450, when reconstituted with purified rat liver cytochrome P-450 reductase, is also inactivated by allylisopropylacetamide in a suicide fashion with a corrected partition ratio of 184 turnovers of allylisopropylacetamide per inactivation event.	Phenobarbital	11-24	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	44-60
7263679-4	1981	A purified phenobarbital-induced isozyme of cytochrome P-450, when reconstituted with purified rat liver cytochrome P-450 reductase, is also inactivated by allylisopropylacetamide in a suicide fashion with a corrected partition ratio of 184 turnovers of allylisopropylacetamide per inactivation event.	Phenobarbital	11-24	cytochrome p450 oxidoreductase	Rattus norvegicus	105-131
6788368-3	1981	In endoplasmic reticulum preparations, we observed an increase in cytochrome P-450 content following phenobarbital pretreatment, which was reduced by subsequent thioacetamide treatment.	Phenobarbital	101-114	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	66-82
6788368-4	1981	Nuclear envelope cytochrome P-450 was apparently not modulated by these treatments, although nuclear cytochrome P-450 content was increased by phenobarbital.	Phenobarbital	143-156	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	101-117
6788368-5	1981	When endoplasmic reticulum preparations were subjected to treatments paralleling those used in nuclear envelope purification, we found a preferential loss of cytochrome P-450 from phenobarbital-pretreated preparations, with a loss of camphor-binding ability.	Phenobarbital	180-193	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	158-174
7302386-0	1981	Cholesterol HDL in G-6-PD deficient newborn infants following phenobarbital administration.	Phenobarbital	62-75	glucose-6-phosphate dehydrogenase	Homo sapiens	19-25
6791701-0	1981	The effect of phenobarbital and 3"-methyl-N,N-dimethyl-4-aminoazobenzene administration on catalytic, binding and immunological properties of ligandin subunits in rat liver.	Phenobarbital	14-27	glutathione S-transferase alpha 2	Rattus norvegicus	142-150
6791701-1	1981	Following administration of phenobarbital to rats, liver ligandin content, bilirubin binding, glutathione-S-transferase and steroid isomerase activities increased by 150% and the 22000-dalton subunit was selectively increased.	Phenobarbital	28-41	glutathione S-transferase alpha 2	Rattus norvegicus	57-65
6791701-1	1981	Following administration of phenobarbital to rats, liver ligandin content, bilirubin binding, glutathione-S-transferase and steroid isomerase activities increased by 150% and the 22000-dalton subunit was selectively increased.	Phenobarbital	28-41	hematopoietic prostaglandin D synthase	Rattus norvegicus	94-119
6114833-1	1981	One hour after the intraperitoneal administration of CHCl3, CBrCl3, or CCl4 to phenobarbital (PB)-treated rats, hepatic GSH levels decreased to 30, 59, and 88% of control levels, respectively; after 4 hr, the GSH levels had returned to 46, 65, 99%, respectively, of control levels.	Phenobarbital	79-92	C-C motif chemokine ligand 4	Rattus norvegicus	71-75
7028163-0	1981	[Immunohistochemical localization of cytochrome P-450 in rat liver during phenobarbital induction].	Phenobarbital	74-87	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	37-53
7028163-2	1981	Cytochrome P-450 was isolated from the liver of rats preliminarily treated with phenobarbital (PB).	Phenobarbital	80-93	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
7028163-2	1981	Cytochrome P-450 was isolated from the liver of rats preliminarily treated with phenobarbital (PB).	Phenobarbital	95-97	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
6114833-1	1981	One hour after the intraperitoneal administration of CHCl3, CBrCl3, or CCl4 to phenobarbital (PB)-treated rats, hepatic GSH levels decreased to 30, 59, and 88% of control levels, respectively; after 4 hr, the GSH levels had returned to 46, 65, 99%, respectively, of control levels.	Phenobarbital	94-96	C-C motif chemokine ligand 4	Rattus norvegicus	71-75
6792322-2	1981	Induction of cytochrome P-450 and NADPH-cytochrome P-450 reductase activity in microsomes by phenobarbital pretreatment caused a decrease in the apparent chromate-enzyme dissociation constant, Km, and an increase in the apparent second-order rate constant, kcat/Km, but did not affect the kcat of NADPH-mediated microsomal metabolism of chromate.	Phenobarbital	93-106	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
7197229-1	1981	Phenobarbital in a dose of 20 mg/kg administered for 3 days lowered renal sodium excretion after an increase in the amount of extracellular liquid induced by different methods: by intravenous injection chloride isotonic solution in an amount of 3% of body mass, by warmed tap water or salt (0.45% solution) loads given in the same quantity.	Phenobarbital	0-13	nuclear RNA export factor 1	Homo sapiens	272-275
6792322-2	1981	Induction of cytochrome P-450 and NADPH-cytochrome P-450 reductase activity in microsomes by phenobarbital pretreatment caused a decrease in the apparent chromate-enzyme dissociation constant, Km, and an increase in the apparent second-order rate constant, kcat/Km, but did not affect the kcat of NADPH-mediated microsomal metabolism of chromate.	Phenobarbital	93-106	cytochrome p450 oxidoreductase	Rattus norvegicus	34-66
7280702-0	1981	Effect of phenobarbital on 99mTc-IDA scintigraphy in the evaluation of neonatal jaundice.	Phenobarbital	10-23	alpha-L-iduronidase	Homo sapiens	33-36
7268211-4	1981	In rats pretreated with phenobarbital or 3-methylcholanthrene, cimetidine caused a 50% and 90% reduction or aryl hydrocarbon hydroxylase activity respectively, compared to 70% inhibition in uninduced animals.	Phenobarbital	24-37	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	108-136
7280702-7	1981	The results of this study show that administration of phenobarbital in a dose of 5 mg/kg/day for at least 5 days prior to the examination enhances and accelerates biliary excretion of IDA compounds and thereby significantly increases the accuracy of 99mTc-IDA scintigraphy in differentiating extrahepatic biliary atresia from neonatal hepatitis.	Phenobarbital	54-67	alpha-L-iduronidase	Homo sapiens	184-187
7280702-7	1981	The results of this study show that administration of phenobarbital in a dose of 5 mg/kg/day for at least 5 days prior to the examination enhances and accelerates biliary excretion of IDA compounds and thereby significantly increases the accuracy of 99mTc-IDA scintigraphy in differentiating extrahepatic biliary atresia from neonatal hepatitis.	Phenobarbital	54-67	alpha-L-iduronidase	Homo sapiens	256-259
6115647-0	1981	Comparison of gamma-glutamyl transferase induction by phenobarbital in the rat, guinea pig and rabbit.	Phenobarbital	54-67	gamma-glutamyltransferase 1	Rattus norvegicus	14-40
7317020-0	1981	Induction by phenobarbital of the mRNA for a specific variant of rat liver microsomal cytochrome P-450.	Phenobarbital	13-26	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	86-102
7317020-1	1981	The treatment of rats for 4 days with phenobarbital causes an apparent 3-fold increase in the amount of total liver cytochrome P-450.	Phenobarbital	38-51	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	116-132
6169709-0	1981	Construction and identification of a hybrid plasmid containing DNA sequence complementary to phenobarbital-inducible cytochrome P-450 messenger RNA from rat liver.	Phenobarbital	93-106	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	117-133
7317020-5	1981	cytochrome P-450 showed that phenobarbital induces the mRNA in polyribosomes for this variant 20-fold.	Phenobarbital	29-42	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
6169709-1	1981	Cytochrome P-450 mRNA has been partially purified from membrane-bound polysomes of the livers of phenobarbital-treated rats by SDS-phenol-chloroform extraction, followed by poly(U)-Sepharose chromatography and by centrifugation through a sucrose density gradient.	Phenobarbital	97-110	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
7250371-0	1981	Effects of dietary lipid and phenobarbitone on the distribution and concentration of cytochrome P-450 in the liver studied by quantitative cytochemistry.	Phenobarbital	29-43	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	85-101
6894616-6	1981	Hepatic microsomal cytochrome P-450 specific contents were similar in control and copper-deficient animals in the uninduced state and following induction of cytochrome P-450 by treatment with phenobarbital.	Phenobarbital	192-205	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	19-35
6894616-6	1981	Hepatic microsomal cytochrome P-450 specific contents were similar in control and copper-deficient animals in the uninduced state and following induction of cytochrome P-450 by treatment with phenobarbital.	Phenobarbital	192-205	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	157-173
7336952-6	1981	Cytochrome P-450LM4 isolated after pretreatment with 3-methylcholanthrene or phenobarbital showed roughly the same characteristics except in the formation of 1-hexanol where cytochrome P-450LM4 isolated after phenobarbital treatment was the most effective.	Phenobarbital	77-90	cytochrome P450 1A2	Oryctolagus cuniculus	0-19
7336952-6	1981	Cytochrome P-450LM4 isolated after pretreatment with 3-methylcholanthrene or phenobarbital showed roughly the same characteristics except in the formation of 1-hexanol where cytochrome P-450LM4 isolated after phenobarbital treatment was the most effective.	Phenobarbital	209-222	cytochrome P450 1A2	Oryctolagus cuniculus	0-19
7336952-6	1981	Cytochrome P-450LM4 isolated after pretreatment with 3-methylcholanthrene or phenobarbital showed roughly the same characteristics except in the formation of 1-hexanol where cytochrome P-450LM4 isolated after phenobarbital treatment was the most effective.	Phenobarbital	209-222	cytochrome P450 1A2	Oryctolagus cuniculus	174-193
7197926-2	1981	Chronic administration of morphine, nicotine or phenobarbitone has previously been shown to inhibit rat liver tryptophan pyrrolase activity by increasing hepatic [NADPH], whereas subsequent withdrawal enhances pyrrolase activity by a hormonal-type mechanism.	Phenobarbital	48-62	tryptophan 2,3-dioxygenase	Rattus norvegicus	110-130
6113928-8	1981	The phenobarbital-dependent increases in 2- and 3-hydroxylation appear due to the induction of two forms of cytochrome P-450, as indicated by different changes in sensitivity to the effects of dimethyl sulfoxide and 7,8-benzoflavone.	Phenobarbital	4-17	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	108-124
6113938-4	1981	Phenobarbital increased AHH in nuclei from immature males and females.	Phenobarbital	0-13	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	24-27
6894731-6	1981	For low dexamethasone concentrations (between 1 nM and 0.1 microM) a cytochrome P-450 is formed displaying biochemical and biophysical properties similar to those induced by phenobarbital in the adult rat liver.	Phenobarbital	174-187	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	69-85
7281573-0	1981	[Effect of the long-term administration of testosterone on induction of cytochrome P-450 in female rat live tissue using phenobarbital].	Phenobarbital	121-134	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	72-88
7281573-1	1981	A preadministration of testosterone propionate into rat females within 8 days caused an increase in the inducing effect of phenobarbital (after its single injection) on the content of cytochrome P-450 in liver tissue.	Phenobarbital	123-136	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	184-200
7306018-0	1981	Newly biosynthesized cytochrome P-450 associated with the golgi apparatus from livers of rats induced with phenobarbital.	Phenobarbital	107-120	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	21-37
7269901-2	1981	These substances, acting as inductors of microsomal oxidases with mixed function (cytochrome P-450 and P-448), are phenobarbital, 3-methylcholanthrene, DDT, diphenin, rifampicin, benzodiazepin derivatives (diazepam and phenazepam).	Phenobarbital	115-128	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	82-108
7306018-2	1981	Cytochrome P-450 has been detected in preparations of golgi apparatus from the livers of phenobarbital-induced rats.	Phenobarbital	89-102	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
7273008-0	1981	Induction by phenobarbital of ornithine decarboxylase activity in rat liver after initiation with diethylnitrosamine.	Phenobarbital	13-26	ornithine decarboxylase 1	Rattus norvegicus	30-53
7273008-1	1981	Dietary administration of 0.1% phenobarbital (PB) for 1-2 weeks increased ornithine decarboxylase (ODC) activity slightly but to a significant extent (P less than 0.05) in livers of rats into which diethylnitrosamine (DEN) (200 mg/kg body wt) had been injected intraperitoneally 2 weeks before phenobarbital feeding.	Phenobarbital	31-44	ornithine decarboxylase 1	Rattus norvegicus	74-97
7273008-1	1981	Dietary administration of 0.1% phenobarbital (PB) for 1-2 weeks increased ornithine decarboxylase (ODC) activity slightly but to a significant extent (P less than 0.05) in livers of rats into which diethylnitrosamine (DEN) (200 mg/kg body wt) had been injected intraperitoneally 2 weeks before phenobarbital feeding.	Phenobarbital	31-44	ornithine decarboxylase 1	Rattus norvegicus	99-102
7273008-1	1981	Dietary administration of 0.1% phenobarbital (PB) for 1-2 weeks increased ornithine decarboxylase (ODC) activity slightly but to a significant extent (P less than 0.05) in livers of rats into which diethylnitrosamine (DEN) (200 mg/kg body wt) had been injected intraperitoneally 2 weeks before phenobarbital feeding.	Phenobarbital	46-48	ornithine decarboxylase 1	Rattus norvegicus	74-97
7273008-1	1981	Dietary administration of 0.1% phenobarbital (PB) for 1-2 weeks increased ornithine decarboxylase (ODC) activity slightly but to a significant extent (P less than 0.05) in livers of rats into which diethylnitrosamine (DEN) (200 mg/kg body wt) had been injected intraperitoneally 2 weeks before phenobarbital feeding.	Phenobarbital	46-48	ornithine decarboxylase 1	Rattus norvegicus	99-102
7326828-0	1981	Induction of rat hepatic ornithine decarboxylase by the tumor promotors 12-O-tetradecanoylphorbol-13-acetate and phenobarbital in vivo; effect of retinyl-acetate.	Phenobarbital	113-126	ornithine decarboxylase 1	Rattus norvegicus	25-48
6782237-5	1981	At all stages of development studied (8-30 days), phenobarbital treatment increased the liver weight, cytochrome P-450 content and and in vitro p-nitroanisole O-demethylase and glucuronyltransferase activities.	Phenobarbital	50-63	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	102-118
6787032-7	1981	These findings and data on the detergent treatment of nuclei suggest that the nuclear cytochrome P-448 system, induced by 3-methylcholanthrene and localized in the outer membrane, catalyzes the aflatoxin M1 formation, and the cytochrome P-450 system induced by phenobarbital biotransforms aflatoxin B1 into aflatoxin Q1.	Phenobarbital	261-274	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	86-102
6787032-7	1981	These findings and data on the detergent treatment of nuclei suggest that the nuclear cytochrome P-448 system, induced by 3-methylcholanthrene and localized in the outer membrane, catalyzes the aflatoxin M1 formation, and the cytochrome P-450 system induced by phenobarbital biotransforms aflatoxin B1 into aflatoxin Q1.	Phenobarbital	261-274	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	226-242
7285278-3	1981	Both NADPH oxidation and metabolite production are inhibited by CO, SKF 525A and/or metyrapone The induction of cytochrome P-450 with phenobarbital enhances the binding and metabolism of the chloroalkanes, while the induction of cytochrome P-448 with beta-naphthoflavone does not.	Phenobarbital	134-147	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	112-128
7313607-5	1981	Xylene was shown to be a phenobarbital-like inducer of rat liver microsomal cytochrome P-450.	Phenobarbital	25-38	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	76-92
7213733-1	1981	We demonstrate the in vitro synthesis of cytochrome P-450-LM2 (phenobarbital-inducible form of liver microsomal cytochrome P-450) from a rabbit liver polysomal mRNA template by specific immunoprecipitation of the product.	Phenobarbital	63-76	cytochrome P450 2B4	Oryctolagus cuniculus	41-61
7213733-3	1981	In addition, we demonstrate that phenobarbital increases the amount of translatable mRNA for cytochrome P-450-LM2 but not for albumin, suggesting that phenobarbital has selective effects on the amount of available translatable mRNA or on mRNA biosynthesis.	Phenobarbital	33-46	cytochrome P450 2B4	Oryctolagus cuniculus	93-113
7213733-3	1981	In addition, we demonstrate that phenobarbital increases the amount of translatable mRNA for cytochrome P-450-LM2 but not for albumin, suggesting that phenobarbital has selective effects on the amount of available translatable mRNA or on mRNA biosynthesis.	Phenobarbital	151-164	cytochrome P450 2B4	Oryctolagus cuniculus	93-113
7326828-2	1981	injection in rats of 20 microgram 12-O-tetradecanoylphorbol-13-acetate (TPA) or 100 mg phenobarbital (PB)/kg body weight resulted in a transient increase in liver ornithine decarboxylase (ODC) activity.	Phenobarbital	87-100	ornithine decarboxylase 1	Rattus norvegicus	163-186
7326828-2	1981	injection in rats of 20 microgram 12-O-tetradecanoylphorbol-13-acetate (TPA) or 100 mg phenobarbital (PB)/kg body weight resulted in a transient increase in liver ornithine decarboxylase (ODC) activity.	Phenobarbital	87-100	ornithine decarboxylase 1	Rattus norvegicus	188-191
7326828-2	1981	injection in rats of 20 microgram 12-O-tetradecanoylphorbol-13-acetate (TPA) or 100 mg phenobarbital (PB)/kg body weight resulted in a transient increase in liver ornithine decarboxylase (ODC) activity.	Phenobarbital	102-104	ornithine decarboxylase 1	Rattus norvegicus	163-186
7326828-2	1981	injection in rats of 20 microgram 12-O-tetradecanoylphorbol-13-acetate (TPA) or 100 mg phenobarbital (PB)/kg body weight resulted in a transient increase in liver ornithine decarboxylase (ODC) activity.	Phenobarbital	102-104	ornithine decarboxylase 1	Rattus norvegicus	188-191
7326828-3	1981	Maximal stimulation of ODC activity was observed approximately 4 h after application of TPA and 4-6 h after treatment of PB.	Phenobarbital	121-123	ornithine decarboxylase 1	Rattus norvegicus	23-26
6111425-1	1981	Cytochrome P-450, NADPH-cytochrome P-450 reductase, and glucuronyltransferase were immobilized simultaneously on cyanogen bromide-activated Sepharose from phenobarbital-induced rabbit liver microsomes.	Phenobarbital	155-168	cytochrome P-450	Oryctolagus cuniculus	0-16
7326828-4	1981	Six hours after TPA injection and greater than 8 h after treatment with PB the ODC activity had returned to control level.	Phenobarbital	72-74	ornithine decarboxylase 1	Rattus norvegicus	79-82
6111425-1	1981	Cytochrome P-450, NADPH-cytochrome P-450 reductase, and glucuronyltransferase were immobilized simultaneously on cyanogen bromide-activated Sepharose from phenobarbital-induced rabbit liver microsomes.	Phenobarbital	155-168	NADPH--cytochrome P450 reductase	Oryctolagus cuniculus	18-77
6935662-5	1980	Proteins collected from the major peaks induced by PB or 3-MC treatment were found to retain spectral characteristics of cytochrome P-450.	Phenobarbital	51-53	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	121-137
7307867-3	1981	Enzymes from control (beta A1DH), pregnant (pi A1DH) and phenobarbital-treated (phi AlDH) were partially purified and compared.	Phenobarbital	57-70	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	84-88
7297580-5	1981	(3) The mechanism of the influence of PB on DNA synthesis is unclear, but present data suggest that in one single dose PB may behave in two different ways: in intact liver it causes the accumulation of cytochrome P-450 and in partially resected liver it enhances the rate of DNA synthesis; mitochondria playing apparently no important role in this interaction.	Phenobarbital	119-121	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	202-218
6112214-5	1981	ATPase activity was increase in about half of spontaneous and carcinogen-induced neoplasms but all induced neoplasms in mice treated with phenobarbitone showed deficient activity.	Phenobarbital	138-152	dynein, axonemal, heavy chain 8	Mus musculus	0-6
6112214-7	1981	However, all induced neoplasms in the mice receiving phenobarbitone showed some degree of gamma-glutamyltransferase activity together with deficient glucose-6-phosphatase and ATPase activities.	Phenobarbital	53-67	glucose-6-phosphatase, catalytic	Mus musculus	149-170
6112214-7	1981	However, all induced neoplasms in the mice receiving phenobarbitone showed some degree of gamma-glutamyltransferase activity together with deficient glucose-6-phosphatase and ATPase activities.	Phenobarbital	53-67	dynein, axonemal, heavy chain 8	Mus musculus	175-181
6783636-0	1981	Selective induction of two different molecular species of cytochrome P-450 by phenobarbital and 3-methylcholanthrene.	Phenobarbital	78-91	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	58-74
6783636-1	1981	Two forms of cytochrome P-450, P-450PB and P-450MC, were purified to homogeneity from the liver microsomes of phenobarbital (PB)-treated and 3-methylcholanthrene (MC)-treated rats, respectively.	Phenobarbital	110-123	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
6783636-1	1981	Two forms of cytochrome P-450, P-450PB and P-450MC, were purified to homogeneity from the liver microsomes of phenobarbital (PB)-treated and 3-methylcholanthrene (MC)-treated rats, respectively.	Phenobarbital	110-123	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	43-50
6783636-1	1981	Two forms of cytochrome P-450, P-450PB and P-450MC, were purified to homogeneity from the liver microsomes of phenobarbital (PB)-treated and 3-methylcholanthrene (MC)-treated rats, respectively.	Phenobarbital	36-38	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
6783636-8	1981	The administration of MC to PB-treated rats induced a drastic decrease in the P-450PB-dependent oxidations of benzo(a)pyrene and 7-ethoxycoumarin, while the corresponding activities of P-450MC increased sharply, and these changes were much more rapid than the change of the amount of each form of cytochrome P-450.	Phenobarbital	28-30	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	185-192
6783636-8	1981	The administration of MC to PB-treated rats induced a drastic decrease in the P-450PB-dependent oxidations of benzo(a)pyrene and 7-ethoxycoumarin, while the corresponding activities of P-450MC increased sharply, and these changes were much more rapid than the change of the amount of each form of cytochrome P-450.	Phenobarbital	28-30	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	297-313
7322218-4	1981	Hepatocytes prepared from rats after daily treatment with phenobarbital during 5 days contained 3-4-fold concentrations of ligandin and bound greater amounts of BSP than controls, Nevertheless the velocity of the uptake both of [3H]-demethylphalloin ([3H]-DMP) and of [35S]-BSP was not augmented.	Phenobarbital	58-71	glutathione S-transferase alpha 2	Rattus norvegicus	123-131
7255876-1	1981	Cytochrome P-450 concentrations in rat liver and kidney were differentially altered by pretreatment with phenobarbital (PB), cadmium or fasting.	Phenobarbital	105-118	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
7255876-1	1981	Cytochrome P-450 concentrations in rat liver and kidney were differentially altered by pretreatment with phenobarbital (PB), cadmium or fasting.	Phenobarbital	120-122	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
7255876-5	1981	PB induction increased and cadmium decreased the liver cytochrome P-450 concentrations and the hepatotoxicity mediated by chloroform.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	55-71
7213402-0	1980	Sex and age dependence of the "selective" induction of rat hepatic microsomal epoxide hydratase following trans-stilbene oxide, l-alpha-acetylmethadol, or phenobarbital treatment.	Phenobarbital	155-168	epoxide hydrolase 2	Rattus norvegicus	78-95
7438078-6	1980	The major phenobarbital-inducible cytochrome P-450, Form 2, exhibited practically no catalytic activity (< 1% of the other forms) with AAF as a substrate.	Phenobarbital	10-23	cytochrome P-450	Oryctolagus cuniculus	34-50
7213485-1	1980	In the livers of rats treated with phenobarbital an increase of glutathione-S-transferase and glutathione is observed.	Phenobarbital	35-48	hematopoietic prostaglandin D synthase	Rattus norvegicus	64-89
6783785-7	1981	With the phenobarbital treatment the induction of hepatic cyt P 450 and UDPGT is higher in the animals fed dietary fats than in animals fed free fat diets.	Phenobarbital	9-22	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	72-77
6783785-11	1981	The inducting effect of phenobarbital on microsomal cyt P 450 is unchanged but significantly enhanced in the case of hepatic UDPGT.	Phenobarbital	24-37	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	125-130
7430117-5	1980	The heme-mediated increase of cytochrome P-450 was most pronounced in phenobarbital-pretreated rats (46%), but was detectable also in 3-methylcholanthrene-pretreated (6%) and in untreated animals (7%).	Phenobarbital	70-83	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	30-46
7430117-6	1980	Restoration of mixed function oxidase activity by heme appeared to depend on reconstitution of cytochrome P-450 and was greatest for oxidases whose activity is stimulated by phenobarbital.	Phenobarbital	174-187	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	95-111
7438682-3	1980	Phenobarbital (PB) and medroxyprogesterone acetate (MPA), both known inducers, improved drug metabolism in patients with normal or decreased serum albumin.	Phenobarbital	0-13	albumin	Homo sapiens	147-154
7438682-3	1980	Phenobarbital (PB) and medroxyprogesterone acetate (MPA), both known inducers, improved drug metabolism in patients with normal or decreased serum albumin.	Phenobarbital	15-17	albumin	Homo sapiens	147-154
7430707-4	1980	Significant inhibition of ornithine decarboxylase induction was found in epidermis from animals receiving diets containing butylated hydroxytoluene, the antioxidant mixture, or disulfiram whereas no significant effects were noted in animals receiving reduced glutathione or phenobarbital.	Phenobarbital	274-287	ornithine decarboxylase, structural 1	Mus musculus	26-49
6935662-7	1980	Purified P-450b obtained from PB-treated rats was found to cochromatograph with one of the peaks selectively induced by PB treatment.	Phenobarbital	30-32	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	9-15
6935662-7	1980	Purified P-450b obtained from PB-treated rats was found to cochromatograph with one of the peaks selectively induced by PB treatment.	Phenobarbital	120-122	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	9-15
6780342-3	1980	Cytochrome P-450, purified from hepatic microsomes of phenobarbital-treated rats, exhibited a high rate of dieldrin formation.	Phenobarbital	54-67	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
6786276-1	1980	Apparent kinetic constant (NADPH) have been calculated for NADPH-cytochrome P450 reductase and parahydroxylase in the presence of aniline with hepatic microsomes from both phenobarbital pre-treated and untreated rats.	Phenobarbital	172-185	cytochrome p450 oxidoreductase	Rattus norvegicus	59-90
6786276-3	1980	It is proposed that the increase in aniline metabolism with NADH is due to an increase in the NADPH-cytochrome P450 reductase activity which is rate limiting in microsomes from both phenobarbital and untreated rats.	Phenobarbital	182-195	cytochrome p450 oxidoreductase	Rattus norvegicus	94-125
7428105-3	1980	Following the pretreatment of rats intraperitoneally with 9-hydroxyellipticine and phenobarbitone, the cytochrome P-448-specific enzyme activity, ethoxyresorufin O-deethylase, was 50% inhibited in vitro but cytochrome P-450, cytochrome P-450 reductase, and other mixed function oxidase activities were unaffected.	Phenobarbital	83-97	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	103-119
7428105-3	1980	Following the pretreatment of rats intraperitoneally with 9-hydroxyellipticine and phenobarbitone, the cytochrome P-448-specific enzyme activity, ethoxyresorufin O-deethylase, was 50% inhibited in vitro but cytochrome P-450, cytochrome P-450 reductase, and other mixed function oxidase activities were unaffected.	Phenobarbital	83-97	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	207-251
7428109-8	1980	PB pretreatment resulted in less than two-fold induction of AHH and alkali-extractable radioactivity.	Phenobarbital	0-2	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	60-63
6780342-14	1980	These results indicate that aldrin is a highly selective substrate for cytochrome P-450 species present in microsomes of phenobarbital-treated animals and is a poor substrate for cytochrome P-448.	Phenobarbital	121-134	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	71-87
16661486-2	1980	Although the microsomal hydroxylating complex is already induced by the slicing and aging process, 25 millimolar MnCl(2), 4 millimolar phenobarbital, and 300 millimolar ethanol caused a marked increase of hydroxylase activity and cytochrome P-450 content and shifted their time course.	Phenobarbital	135-148	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	230-246
16661486-0	1980	Time Course of Induction of Cytochrome P-450, NADPH-Cytochrome c Reductase, and Cinnamic Acid Hydroxylase by Phenobarbital, Ethanol, Herbicides, and Manganese in Higher Plant Microsomes.	Phenobarbital	109-122	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	28-44
6779432-3	1980	In addition the in vitro inhibition of 7-ethoxycoumarin-deethylase by metyrapone (phenobarbital induced cytochrome P-450) or naphthoflavone (benzo[a]pyrene induced cytochrome P-448) was estimated.	Phenobarbital	82-95	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	104-120
16661486-5	1980	NADPH cytochrome c reductase was significantly increased only in phenobarbital-treated slices.	Phenobarbital	65-78	cytochrome c, somatic	Homo sapiens	6-18
16661486-0	1980	Time Course of Induction of Cytochrome P-450, NADPH-Cytochrome c Reductase, and Cinnamic Acid Hydroxylase by Phenobarbital, Ethanol, Herbicides, and Manganese in Higher Plant Microsomes.	Phenobarbital	109-122	cytochrome c, somatic	Homo sapiens	52-64
7417485-1	1980	A procedure is described for the purification of a major form of cytochrome P-450 from the livrs of rabbits treated with phenobarbital and a major form of the cytochrome from the lungs of untreated rabbits.	Phenobarbital	121-134	cytochrome P-450	Oryctolagus cuniculus	65-81
7417485-4	1980	These data are consistent with a major indigenous form of rabbit pulmonary cytochrome P-450 being the same as the major form of hepatic cytochrome induced by phenobarbital.	Phenobarbital	158-171	cytochrome P-450	Oryctolagus cuniculus	75-91
6780329-5	1980	A phenobarbital (PHB) injection (100 mg/kg, sc) at 1900 hr on D1 initiated daily PRL surges, which were similar to those observed following cervical stimulation though of less magnitude, without altering the levels of LH and FSH significantly.	Phenobarbital	2-15	prolactin	Rattus norvegicus	81-84
6780329-5	1980	A phenobarbital (PHB) injection (100 mg/kg, sc) at 1900 hr on D1 initiated daily PRL surges, which were similar to those observed following cervical stimulation though of less magnitude, without altering the levels of LH and FSH significantly.	Phenobarbital	17-20	prolactin	Rattus norvegicus	81-84
7389009-4	1980	The capacity of isosafrole and piperonyl butoxide to induced cytochrome P-450 was evaluated by measurement of biphenyl 2- and 4-hydroxylase, ethoxyresofurin O-deethylase and ethylmorphine N-demethylase and by sodium dodecyl sulphate (SDS) polyacrylamide gel electrophoresis and compared with results obtained for phenobarbitone, 3-methylcholanthrene and pregnenolone-16 alpha-carbonitrile.	Phenobarbital	313-327	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	61-77
7389010-3	1980	PB, Rifa and PCN induced the aryl hydrocarbon hydroxylase (AHH) in the skin though to a lesser extent than MC.	Phenobarbital	0-2	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	29-57
7389010-3	1980	PB, Rifa and PCN induced the aryl hydrocarbon hydroxylase (AHH) in the skin though to a lesser extent than MC.	Phenobarbital	0-2	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	59-62
6780329-9	1980	Therefore, PRL surges induced by PHB administration will be solely responsible for the luteal functionalization in PHB-PSP rats.	Phenobarbital	33-36	prolactin	Rattus norvegicus	11-14
7419508-3	1980	A method is described for the separation and purification of different forms of cytochrome P-450 from liver microsomes of phenobarbital (PB)- and 3-methylcholanthrene (MC)-pretreated rabbits.	Phenobarbital	122-135	cytochrome P-450	Oryctolagus cuniculus	80-96
7419508-3	1980	A method is described for the separation and purification of different forms of cytochrome P-450 from liver microsomes of phenobarbital (PB)- and 3-methylcholanthrene (MC)-pretreated rabbits.	Phenobarbital	137-139	cytochrome P-450	Oryctolagus cuniculus	80-96
6156019-2	1980	The activity of aryl hydrocarbon hydroxylase (AHH) and/or epoxide hydratase (EH) is induced in primary fetal rat liver cell culture by benz-[alpha]anthracene (BA), phenobarbital (PB), cigarette smoke condensate (CSC), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and trans-stilbene oxide (TSO).	Phenobarbital	179-181	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	16-44
6156019-2	1980	The activity of aryl hydrocarbon hydroxylase (AHH) and/or epoxide hydratase (EH) is induced in primary fetal rat liver cell culture by benz-[alpha]anthracene (BA), phenobarbital (PB), cigarette smoke condensate (CSC), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and trans-stilbene oxide (TSO).	Phenobarbital	164-177	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	16-44
6156019-2	1980	The activity of aryl hydrocarbon hydroxylase (AHH) and/or epoxide hydratase (EH) is induced in primary fetal rat liver cell culture by benz-[alpha]anthracene (BA), phenobarbital (PB), cigarette smoke condensate (CSC), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and trans-stilbene oxide (TSO).	Phenobarbital	164-177	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	46-49
6156019-2	1980	The activity of aryl hydrocarbon hydroxylase (AHH) and/or epoxide hydratase (EH) is induced in primary fetal rat liver cell culture by benz-[alpha]anthracene (BA), phenobarbital (PB), cigarette smoke condensate (CSC), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and trans-stilbene oxide (TSO).	Phenobarbital	179-181	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	46-49
6156019-2	1980	The activity of aryl hydrocarbon hydroxylase (AHH) and/or epoxide hydratase (EH) is induced in primary fetal rat liver cell culture by benz-[alpha]anthracene (BA), phenobarbital (PB), cigarette smoke condensate (CSC), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and trans-stilbene oxide (TSO).	Phenobarbital	164-177	epoxide hydrolase 2	Rattus norvegicus	58-75
6156019-2	1980	The activity of aryl hydrocarbon hydroxylase (AHH) and/or epoxide hydratase (EH) is induced in primary fetal rat liver cell culture by benz-[alpha]anthracene (BA), phenobarbital (PB), cigarette smoke condensate (CSC), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and trans-stilbene oxide (TSO).	Phenobarbital	179-181	epoxide hydrolase 2	Rattus norvegicus	58-75
6156019-2	1980	The activity of aryl hydrocarbon hydroxylase (AHH) and/or epoxide hydratase (EH) is induced in primary fetal rat liver cell culture by benz-[alpha]anthracene (BA), phenobarbital (PB), cigarette smoke condensate (CSC), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and trans-stilbene oxide (TSO).	Phenobarbital	164-177	epoxide hydrolase 2	Rattus norvegicus	77-79
6156019-2	1980	The activity of aryl hydrocarbon hydroxylase (AHH) and/or epoxide hydratase (EH) is induced in primary fetal rat liver cell culture by benz-[alpha]anthracene (BA), phenobarbital (PB), cigarette smoke condensate (CSC), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and trans-stilbene oxide (TSO).	Phenobarbital	179-181	epoxide hydrolase 2	Rattus norvegicus	77-79
6156019-7	1980	Added together with PB, BA, CSC or PB plus BA, TSO induces the EH activity in a more than additive manner.	Phenobarbital	35-37	epoxide hydrolase 2	Rattus norvegicus	63-65
6156019-3	1980	The response of the two enzymes to the different chemicals varies as follows: (a) AHH is induced by lower concentrations of BA, PB and CSC than those required to significantly induce EH; (b) AHH is selectively induced by TCDD and by low BA concentrations; (c) the kinetics of AHH induction by BA, PB and CSC is faster than that of EH; (d) TSO is a selective inducer of EH.	Phenobarbital	128-130	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	82-85
6156019-3	1980	The response of the two enzymes to the different chemicals varies as follows: (a) AHH is induced by lower concentrations of BA, PB and CSC than those required to significantly induce EH; (b) AHH is selectively induced by TCDD and by low BA concentrations; (c) the kinetics of AHH induction by BA, PB and CSC is faster than that of EH; (d) TSO is a selective inducer of EH.	Phenobarbital	297-299	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	82-85
6156019-3	1980	The response of the two enzymes to the different chemicals varies as follows: (a) AHH is induced by lower concentrations of BA, PB and CSC than those required to significantly induce EH; (b) AHH is selectively induced by TCDD and by low BA concentrations; (c) the kinetics of AHH induction by BA, PB and CSC is faster than that of EH; (d) TSO is a selective inducer of EH.	Phenobarbital	297-299	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	191-194
6156019-3	1980	The response of the two enzymes to the different chemicals varies as follows: (a) AHH is induced by lower concentrations of BA, PB and CSC than those required to significantly induce EH; (b) AHH is selectively induced by TCDD and by low BA concentrations; (c) the kinetics of AHH induction by BA, PB and CSC is faster than that of EH; (d) TSO is a selective inducer of EH.	Phenobarbital	297-299	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	191-194
6156019-6	1980	The removal of the inducer determines a decay of the EH activity, allowing the estimation of a biological tau 1/2 of about 72 h. TSO prevents the AHH induction by PB, but not that mediated by BA and CSC.	Phenobarbital	163-165	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	146-149
7375915-2	1980	Antibody to the cytochrome P-450 induced by phenobarbital has relatively little or no effect on the aryl hydrocarbon hydroxylase activity of the same human cells.	Phenobarbital	44-57	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	16-32
6105052-4	1980	Microsomal cytochrome P-450 levels were increased 3-fold upon phenobarbital treatment; during incubations of less than 30 min duration, increased N-demethylase activity could be entirely accounted for by this increase in cytochrome P-450.	Phenobarbital	62-75	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	11-27
6105052-4	1980	Microsomal cytochrome P-450 levels were increased 3-fold upon phenobarbital treatment; during incubations of less than 30 min duration, increased N-demethylase activity could be entirely accounted for by this increase in cytochrome P-450.	Phenobarbital	62-75	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	221-237
6770872-0	1980	In vivo administration of hydroxylated phenobarbital metabolites: effect on rat hepatic cytochromes P-450, epoxide hydrolase and UDP-glucuronosyltransferase.	Phenobarbital	39-52	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	129-156
7376887-1	1980	Multiple forms of liver microsomal cytochrome P-450 in rats were identified on SDS-polyacrylamide gels stained for protein and peroxidase activity after induction with phenobarbital, 3-methylcholanthrene, and 16 alpha-cyanopregnenolone.	Phenobarbital	168-181	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	35-51
7396894-0	1980	Purification of cytochrome P-450 from liver microsomes of phenobarbital-treated guinea pigs.	Phenobarbital	58-71	cytochrome P450 3A14	Cavia porcellus	16-32
7388141-0	1980	[Induction of cytochrome P-450 and the immune response by free and covalently bound to albumin phenobarbital].	Phenobarbital	95-108	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	14-30
6252201-4	1980	Both optical absorption and EPR studies have shown that the oxidized forms of P-450(1), P-450(2) (from PB-treated animals), and P-450(3) (from MC-treated animals) are in the low spin state, having a Soret absorption peak at 417-418 nm.	Phenobarbital	103-105	cytochrome P450 2C5	Oryctolagus cuniculus	78-86
7416885-2	1980	Antiserum obtained from a rabbit immunized with CBP-bovine serum albumin conjugates is specific for phenobarbital and does not substantially cross-react with a major metabolite, p-hydroxyphenobarbital.	Phenobarbital	100-113	albumin	Oryctolagus cuniculus	59-72
6103842-5	1980	gamma-Glutamyl transpeptidase activity increased, and serum bilirubin concentration decreased during phenobarbital treatment.	Phenobarbital	101-114	inactive glutathione hydrolase 2	Homo sapiens	0-29
7356631-3	1980	Translation of poly(A)-containing RNA from phenobarbital-treated rats in the wheat germ cell-free system reveals that the cell-free product immunoprecipitated with anti-cytochrome P-450 antibody has a molecular weight close to 47,000.	Phenobarbital	43-56	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	169-185
6771516-0	1980	Identification of the form of cytochrome P-450 induced in neonatal rabbit liver microsomes by phenobarbital.	Phenobarbital	94-107	cytochrome P-450	Oryctolagus cuniculus	30-46
6778467-2	1980	Apparent kinetic constants for NADPH have been calculated for NADPH-cytochrome P450 reductase and demethylase activity in the presence of aminopyrine and ethylmorphine with hepatic microsomal preparations from phenobarbital pre-treated rats.	Phenobarbital	210-223	cytochrome p450 oxidoreductase	Rattus norvegicus	62-93
6767247-1	1980	Treatment of rats with phenobarbital leads to a substantial increase in levels of translatable liver cytochrome P-450 mRNA.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	101-117
6765944-2	1980	Several properties of this cytochrome are contrasted with those of form 2, the major phenobarbital-inducible cytochrome P-450, form 4, the major 2,3,7,8-tetrachlorodibenzo-p-dioxin-inducible cytochrome, and form 6, a cytochrome that is selectively induced in liver microsomes by 2,3,7,8-tetrachlorodibenzo-p-dioxin during the perinatal period.	Phenobarbital	85-98	cytochrome P-450	Oryctolagus cuniculus	109-125
7359190-0	1980	The effect of phenobarbital on the toxicity and tumoricidal activity of CCNU in a murine brain tumor model.	Phenobarbital	14-27	cyclin O	Mus musculus	72-76
7356631-6	1980	Phenobarbital and 3-methylcholanthrene enhance the translatable messenger RNA contents for cytochrome P-450 and cytochrome P-448, respectively.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	91-128
7424729-1	1980	Ethanol induces in rat liver microsomes a form of cytochrome P-450 differing in substrate specificity from cytochrome P-450 species present in controls or in rats treated with phenobarbital or 3-methylcholanthrene.	Phenobarbital	176-189	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	50-66
7424708-2	1980	The involvement of cytochrome P-450 in vivo was shown indirectly by (a) the ability of SKF-525A to block pargyline-induced acetaldehydemia, (b) the prolongation of phenobarbital sleeping time by pargyline, and (c) the enhancement of pargyline-induced acetaldehydemia by phenobarbital pretreatment.	Phenobarbital	164-177	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	19-35
6767337-3	1980	Aryl hydrocarbon hydroxylase activity was decreased in the liver and intestinal mucosa after treatment with CCl4 alone and in combination with phenobarbital.	Phenobarbital	143-156	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-28
6767337-6	1980	In the intestinal mucosa the enhanced UDPglucuronosyltransferase activity was observed only after phenobarbital pretreatment and the activity was decreased by CCl4.	Phenobarbital	98-111	C-C motif chemokine ligand 4	Rattus norvegicus	159-163
7424729-1	1980	Ethanol induces in rat liver microsomes a form of cytochrome P-450 differing in substrate specificity from cytochrome P-450 species present in controls or in rats treated with phenobarbital or 3-methylcholanthrene.	Phenobarbital	176-189	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	107-123
7424708-2	1980	The involvement of cytochrome P-450 in vivo was shown indirectly by (a) the ability of SKF-525A to block pargyline-induced acetaldehydemia, (b) the prolongation of phenobarbital sleeping time by pargyline, and (c) the enhancement of pargyline-induced acetaldehydemia by phenobarbital pretreatment.	Phenobarbital	270-283	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	19-35
7424733-1	1980	Cytosolic aldehyde dehydrogenase (AlDH) activity was increased in DBA and C57Bl mice following phenobarbital (Pb) treatment.	Phenobarbital	95-108	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	34-38
7424733-1	1980	Cytosolic aldehyde dehydrogenase (AlDH) activity was increased in DBA and C57Bl mice following phenobarbital (Pb) treatment.	Phenobarbital	110-112	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	34-38
6259312-5	1980	PB pretreatment produced a significant loss of both enzymes by CHCl3, and enhanced the loss of cytochrome P-450 induced by CCl4, while G-6-Pase activity was little affected by CCl4 in PB-pretreated rats.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	95-111
7348195-5	1980	Phenobarbital enhanced PC synthesis Via N-methylation of PE and depressed via CDP-choline pathway.	Phenobarbital	0-13	cut-like homeobox 1	Rattus norvegicus	78-81
11219852-1	1980	Administration of phenobarbital for 5 to 7.5 weeks to aged C3HfB/HeN mice with spontaneous liver tumors produced an enhancement of gamma glutamyl transpeptidase activity in the tumors and a decrease in glucose-6-phosphatase and adenosine triphosphatase activity.	Phenobarbital	18-31	glucose-6-phosphatase, catalytic	Mus musculus	202-223
7356533-5	1980	Epoxide hydratase activities were stimulated about three fold by pretreating rats with phenobarbitone.	Phenobarbital	87-101	epoxide hydrolase 2	Rattus norvegicus	0-17
6930944-3	1980	Phenobarbital is also able to potentiate the inducing action of low doses of benzo(a)pyrene on the lung AHH activity.	Phenobarbital	0-13	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	104-107
6930944-6	1980	Phenobarbital, which also induces the AHH activity in cell culture, produces a more than additive effect when added to the culture medium in a mixture with benz(a)anthracene.	Phenobarbital	0-13	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	38-41
6930944-7	1980	Trans-stilbene oxide prevents the AHH induction by phenobarbital and not by benz(a)anthracene.	Phenobarbital	51-64	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	34-37
6250870-0	1980	Effects of animal age and phenobarbital on rat liver glucose-6-phosphatase activity.	Phenobarbital	26-39	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	53-74
6259312-5	1980	PB pretreatment produced a significant loss of both enzymes by CHCl3, and enhanced the loss of cytochrome P-450 induced by CCl4, while G-6-Pase activity was little affected by CCl4 in PB-pretreated rats.	Phenobarbital	0-2	C-C motif chemokine ligand 4	Rattus norvegicus	123-127
6113606-6	1980	Phenobarbital administration to rats resulted in an enhancement of GGTP activity in the liver whether given orally or intraperitoneally.	Phenobarbital	0-13	gamma-glutamyltransferase 1	Rattus norvegicus	67-71
6113606-7	1980	In addition, intestinal GGTP activity after oral phenobarbital was also significantly increased, although its activity after intraperitoneal administration was not enhanced.	Phenobarbital	49-62	gamma-glutamyltransferase 1	Rattus norvegicus	24-28
6996219-4	1980	Addition of beta-glucuronidase to the incubation mixtures enhanced the mutagenicity of the urines from both phenobarbital untreated and treated rats and mice injected with acrylonitrile.	Phenobarbital	108-121	glucuronidase, beta	Rattus norvegicus	12-30
43977-0	1979	Phenobarbitone modulation of postsynaptic GABA receptor function on cultured mammalian neurons.	Phenobarbital	0-14	GABA type A receptor-associated protein	Homo sapiens	42-55
44195-6	1979	Glucose 6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, isocitrate dehydrogenase and "malic" enzyme, partially purified from livers of phenobarbital-treated rats, were inhibited by ATP and ADP.	Phenobarbital	148-161	glucose-6-phosphate dehydrogenase	Rattus norvegicus	0-33
116598-0	1979	Studies on the biosynthesis of cytochrome P-450 in rat liver--a probe with phenobarbital.	Phenobarbital	75-88	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	31-47
498713-2	1979	An inverse correlation was observed between phenobarbital levels and renin activity or concentration.	Phenobarbital	44-57	renin	Homo sapiens	69-74
498713-3	1979	There was a positive correlation between phenobarbital and renin substrate.	Phenobarbital	41-54	renin	Homo sapiens	59-64
498713-4	1979	Since elevation of renin substrate should have resulted in increased renin activity, it is possible that phenobarbital exerts 2 effects on the renin system: induction of renin substrate synthesis and suppression of renin release.	Phenobarbital	105-118	renin	Homo sapiens	19-24
498713-4	1979	Since elevation of renin substrate should have resulted in increased renin activity, it is possible that phenobarbital exerts 2 effects on the renin system: induction of renin substrate synthesis and suppression of renin release.	Phenobarbital	105-118	renin	Homo sapiens	69-74
498713-4	1979	Since elevation of renin substrate should have resulted in increased renin activity, it is possible that phenobarbital exerts 2 effects on the renin system: induction of renin substrate synthesis and suppression of renin release.	Phenobarbital	105-118	renin	Homo sapiens	69-74
498713-4	1979	Since elevation of renin substrate should have resulted in increased renin activity, it is possible that phenobarbital exerts 2 effects on the renin system: induction of renin substrate synthesis and suppression of renin release.	Phenobarbital	105-118	renin	Homo sapiens	69-74
498713-4	1979	Since elevation of renin substrate should have resulted in increased renin activity, it is possible that phenobarbital exerts 2 effects on the renin system: induction of renin substrate synthesis and suppression of renin release.	Phenobarbital	105-118	renin	Homo sapiens	69-74
230618-2	1979	The changes induced by phenobarbital in cerebral enzymatic activities of the Krebs" cycle (citrate synthase, malate dehydrogenase) and electron transfer chain (total NADH-cytochrome c reductase and cytochrome oxidase) were studied.	Phenobarbital	23-36	citrate synthase	Rattus norvegicus	91-107
523771-7	1979	Pretreatment of rats with phenobarbital increased the AlDH inhibitor produced by incubation of their microsomes with pargyline.	Phenobarbital	26-39	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	54-58
498354-5	1979	Inducers for microsomal mixed-function oxidases induced activating enzyme(s) for Trp-P-2, 3-methylcholanthrene being most effective, followed by polychlorinated biphenyls and then phenobarbital.	Phenobarbital	180-193	polycystin 2, transient receptor potential cation channel	Rattus norvegicus	81-88
507813-0	1979	Induction by manganese, ethanol, phenobarbital, and herbicides of microsomal cytochrome P-450 in higher plant tissues.	Phenobarbital	33-46	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	77-93
118106-5	1979	Addition of phenobarbital or methylcholanthrene at day 5 in culture caused an increase in cytochromes P-450 and P-448, respectively, only in hepatocytes cultured on collagen membranes and confluent fibroblasts.	Phenobarbital	12-25	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	102-117
521111-0	1979	Effect of acute and chronic treatment of phenobarbital and chloroquin on the turnover of 2- [2-(3-pyridyl)vinyl] -3-o-tolyl-3,4-dihydro quinazoline-4-one (SRC-909).	Phenobarbital	41-54	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	155-158
496999-0	1979	Regulation of rat liver epoxide hydratase activity by phenobarbital and 3-methylcholanthrene.	Phenobarbital	54-67	epoxide hydrolase 2	Rattus norvegicus	24-41
486022-4	1979	Treatment with phenobarb and magnesium chloride enteric tablets ("Slow Mag", 2 x 535 mg/d) reversed the biochemical abnormality.	Phenobarbital	15-24	reticulophagy regulator family member 2	Homo sapiens	71-78
465602-1	1979	A purified low-spin form of cytochrome P-450 was isolated from phenobarbital-induced rabbit liver microsomes.	Phenobarbital	63-76	cytochrome P-450	Oryctolagus cuniculus	28-44
375751-2	1979	Ligandin concentrations, measured immunologically, increased 25% after thyroidectomy and approximately doubled after phenobarbital pretreatment but decreased to normal during perfusion in the thyroidectomized nonpretreated group.	Phenobarbital	117-130	glutathione S-transferase alpha 2	Rattus norvegicus	0-8
375751-5	1979	Efflux coefficients were significantly smaller (P less than 0.001), and hepatic ligandin concentrations were significantly larger (p less than 0.001) in phenobarbital-treated rats than in other groups.	Phenobarbital	153-166	glutathione S-transferase alpha 2	Rattus norvegicus	80-88
375751-7	1979	The increased net uptake of tracer bilirubin by the liver of phenobarbital-pretreated animals is due to decreased tracer efflux secondary to the increase in intracellular binding of bilirubin by ligandin.	Phenobarbital	61-74	glutathione S-transferase alpha 2	Rattus norvegicus	195-203
457773-1	1979	Intracellular sites of synthesis of cytochrome P-450 and the subsequent incorporation of it into membrane structures of the endoplasmic reticulum (ER) in rat hepatocytes have been studied using an antibody monospecific for phenobarbital-inducible cytochrome P-450.	Phenobarbital	223-236	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	36-52
538316-0	1979	[Activity of the pseudocholinesterase in subjects treated with phenobarbital].	Phenobarbital	63-76	butyrylcholinesterase	Homo sapiens	17-37
38935-0	1979	Effect of phenobarbitone on plasma apolipoprotein B and plasma high-density-lipoprotein cholesterol in normal subjects.	Phenobarbital	10-24	apolipoprotein B	Homo sapiens	35-51
461991-2	1979	Subsequent induction of microsomal metabolism by 50 mg phenobarbital/kg.day over 5 days revealed increased microsomal cytochrome P 450 content in Cd+2-pretreated animals as compared to animals treated only with phenobarbital.	Phenobarbital	55-68	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	118-134
38075-4	1979	The hydroxylamine-nitro-oxidation appears to be dependent on cytochrome P-450, as the reaction was induced by phenobarbital pretreatment and inhibited by carbon monoxide and 2,4-dichloro-6-phenylphenoxyethylamine.	Phenobarbital	110-123	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	61-77
457816-1	1979	Specific antibodies to phenobarbital-induced cytochrome P-450 were prepared by affinity chromatography and coupled to ferritin with glutaraldehyde.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	45-61
43909-3	1979	Antiserum to cytochrome P-450 isolated from phenobarbital-treated rat liver microsomes inhibited the NADH-dependent O-demethylation activity as well as the NADPH-dependent O-demethylation activity seen in rat liver microsomes.	Phenobarbital	44-57	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
43909-4	1979	Addition of either purified cytochrome P-450 or cytochrome P-448 to an incubation mixture containing phenobarbital-treated rat liver microsomes enhanced the NADH-dependent p-nitroanisole O-demethylation activity.	Phenobarbital	101-114	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	28-44
43909-4	1979	Addition of either purified cytochrome P-450 or cytochrome P-448 to an incubation mixture containing phenobarbital-treated rat liver microsomes enhanced the NADH-dependent p-nitroanisole O-demethylation activity.	Phenobarbital	101-114	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	48-64
453857-0	1979	A simple and rapid procedure for the purification of phenobarbital-inducible cytochrome P-450 from rat liver microsomes.	Phenobarbital	53-66	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	77-93
427763-5	1979	It was tentatively concluded that some parent urea is formed by a cytochrome P-450 dependent reaction because of a requirement for reduced nicotinamide adenine dinucleotide phosphate and inhibition by CO. Microsomes from rats pretreated with phenobarbital showed about a 3-fold increase in hydroxylation rate while phenobarbital-treated mice microsomes were induced 8-fold.	Phenobarbital	242-255	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	66-82
427763-5	1979	It was tentatively concluded that some parent urea is formed by a cytochrome P-450 dependent reaction because of a requirement for reduced nicotinamide adenine dinucleotide phosphate and inhibition by CO. Microsomes from rats pretreated with phenobarbital showed about a 3-fold increase in hydroxylation rate while phenobarbital-treated mice microsomes were induced 8-fold.	Phenobarbital	315-328	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	66-82
105007-0	1979	Separation and characterization of highly purified forms of liver microsomal cytochrome P-450 from rats treated with polychlorinated biphenyls, phenobarbital, and 3-methylcholanthrene.	Phenobarbital	144-157	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	77-93
449630-2	1979	Phenobarbital enhanced BA and C secretion (BA-636 +/- 166 to 2110 +/- 382 mg/hr, p less than 0.001 and C-42 +/- 5 to 224 +/- 48 mg/hr, p less than 0.001) and BA cycling rate in all subjects studied during stimulated enterohepatic circulation but, during fasting, it only enhanced BA secretion (451 +/- 129 vs. 759 +/- 159 mg/hr, p less than 0.05) in gallstone subjects.	Phenobarbital	0-13	CDK5 regulatory subunit associated protein 1	Homo sapiens	103-107
428009-4	1979	Differences exist between the mechanisms of inhibition according to the form of cytochrome P-450 present in microsomes of differently pretreated rats; whichever the activities studied, one observes: (a) a competitive inhibition towards the activity of non-induced or PB-induced microsomes and (b) a non-competitive inhibition towards the activity of Aroclor or BP-induced microsomes, at variance with 7,8-BF.	Phenobarbital	267-269	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	80-96
437253-0	1979	Phenobarbitone induction of microsomal mono-oxygenase activity in primary cultures of adult rat hepatocytes [proceedings].	Phenobarbital	0-14	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	28-53
35157-9	1979	Phenobarbital is a potent inhibitor of aldehyde reductase, inhibiting both substrate and cofactor non-competitively (Ki = 80.4 +/- 10.5 micrometer and 66.9 +/- 1.6 micrometer respectively).	Phenobarbital	0-13	aldo-keto reductase family 1 member B	Sus scrofa	39-57
33261-8	1979	TRH also caused a significant increase in cerebellar cGMP in rats pretreated with phenobarbital and chlordiazepoxide.	Phenobarbital	82-95	thyrotropin releasing hormone	Rattus norvegicus	0-3
376289-0	1979	Rapid direct effects of castration and androgen treatment on luteinizing hormone-releasing hormone-induced leutinizing hormone release in the phenobarbital-treated male rat: examination of the roles direct and indirect androgen feedback mechanisms might play in the physiological control of luteinizing hormone release.	Phenobarbital	142-155	gonadotropin releasing hormone 1	Rattus norvegicus	61-98
422533-5	1979	Phenobarbital treatment enhanced this demethylation activity more markedly than glucose dehydrogenase activity itself.	Phenobarbital	0-13	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	80-101
117660-1	1979	A reconstituted hydroxylation system consisting of electrophoretically homogeneous phenobarbital-inducible rabbit liver microsomal cytochrome P-450 (P-450 LM2), NADPH-cytochrome P-450 reductase, phospholipid, buffer, NADPH, and O2 was used to oxidize four cyclohexane derivatives: cyclohexene, methylcyclohexane, norcarane and norbornane.	Phenobarbital	83-96	cytochrome P-450	Oryctolagus cuniculus	131-147
103585-1	1979	Cytochrome P-450 and NADPH-cytochrome P-450 REDUctase, both purified from liver microsomes of phenobarbital-pretreated rabbits, have been incorporated into the membrane of phosphoaditylcholine vesicles by the cholate dialysis method.	Phenobarbital	94-107	cytochrome P-450	Oryctolagus cuniculus	0-16
103585-1	1979	Cytochrome P-450 and NADPH-cytochrome P-450 REDUctase, both purified from liver microsomes of phenobarbital-pretreated rabbits, have been incorporated into the membrane of phosphoaditylcholine vesicles by the cholate dialysis method.	Phenobarbital	94-107	NADPH--cytochrome P450 reductase	Oryctolagus cuniculus	21-53
221433-0	1979	Induction of the FAD synthetase system in rat liver by phenobarbital administration.	Phenobarbital	55-68	flavin adenine dinucleotide synthetase 1	Rattus norvegicus	17-31
517011-1	1979	Hydrocarbons of different structures interact with microsomal and solubilized cytochrome P-450 from liver of phenobarbital-pretreated rats forming a high spin enzyme-substrate type complex.	Phenobarbital	109-122	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	78-94
517011-8	1979	The LM2 fraction of cytochrome P-450 from phenobarbital-pretreated rabbits interacts only with aliphatic hydrocarbons with wide variation of the binding capacity.	Phenobarbital	42-55	cytochrome P-450	Oryctolagus cuniculus	20-36
104547-0	1979	Carbon disulphide induced activation of liver UDP glucuronosyltransferase in rats pretreated with phenobarbitone.	Phenobarbital	98-112	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	46-73
104547-1	1979	Carbon disulphide (CS2) exposure has been shown to activate the UDP glucuronosyltransferase of liver microsomes in rats pretreated with phenobarbitone.	Phenobarbital	136-150	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	64-91
583215-0	1979	The effects of pretreatment with phenobarbital (PB) and sulfobromophthalein (BSP) on the metabolism and the biliary excretion of BSP in the rat.	Phenobarbital	33-46	integrin-binding sialoprotein	Rattus norvegicus	129-132
583215-0	1979	The effects of pretreatment with phenobarbital (PB) and sulfobromophthalein (BSP) on the metabolism and the biliary excretion of BSP in the rat.	Phenobarbital	48-50	integrin-binding sialoprotein	Rattus norvegicus	129-132
229673-3	1979	The contribution of the native high spin species to the total cytochrome P-450 content of microsomes was calculated to be between 40% and 65% after induction with phenobarbital and polycyclic hydrocarbons, respectively.	Phenobarbital	163-176	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	62-78
229674-1	1979	The LM2 fraction of cytochrome P-450 from phenobarbital induced rabbit liver microsomes in the presence and in the absence of substrate (benzphetamine) is shown to be a thermal equilibrium of a high spin (S = 5/2) and a low spin (S = 1/2) state each of which exhibiting its individual optical basic spectrum with the Soret maxima at 387 nm and 417 nm for the high spin form and the low spin form, respectively.	Phenobarbital	42-55	cytochrome P-450	Oryctolagus cuniculus	20-36
229678-1	1979	The paper presents results of a comparative study of the haem environment, by proton magnetic relaxation, in P-450 and P-448 monooxygenases from rat and rabbit, induced by phenobarbital and 3-methylcholanthrene, in both species.	Phenobarbital	172-185	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	109-124
506777-0	1979	Effects of whole body X-ray irradiation on induction by phenobarbital of rat liver glucose-6-phosphate dehydrogenase and glutathione reductase.	Phenobarbital	56-69	glucose-6-phosphate dehydrogenase	Rattus norvegicus	83-116
288335-2	1979	Induction of mAHH was obtained after phenobarbitone treatment (180% of control), which increased DNA binding to 210%, but left the nAHH unchanged.	Phenobarbital	37-51	aryl-hydrocarbon receptor	Mus musculus	13-17
399908-2	1979	When the S-9 was derived from Aroclor- or phenobarbital-induced mouse or hamster liver or from uninduced hamster liver, mutagenic activity was observed.	Phenobarbital	42-55	proteasome (prosome, macropain) 26S subunit, non-ATPase, 11	Mus musculus	9-12
716947-1	1978	Cytochrome P-450 in mouse liver microsomes was characterized by SDS-polyacrylamide gel electrophoresis after intraperitoneal injection of 80 mg phenobarbital, 4.5 and 45 mg acrylamide and 60 and 600 mg methylmethacrylate per kg body weight each day for four days.	Phenobarbital	144-157	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	0-16
719999-8	1978	Study in vitro of the kinetics of two reactions, namely aminopyrine N-demethylation and 3,4-benzpyrene hydroxylation, catalysed by the hepatic microsomal cytochrom P-450-dependent enzyme system, suggested that hexachlorobenzene induced a form of cytochrome P-450-dependent enzyme system, suggested that hexachlorobenzene induced a form of cytochrome P-450 with different catalytic properties from those of forms induced by either phenobarbital or 3-methylcholanthrene.	Phenobarbital	430-443	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	246-262
719999-8	1978	Study in vitro of the kinetics of two reactions, namely aminopyrine N-demethylation and 3,4-benzpyrene hydroxylation, catalysed by the hepatic microsomal cytochrom P-450-dependent enzyme system, suggested that hexachlorobenzene induced a form of cytochrome P-450-dependent enzyme system, suggested that hexachlorobenzene induced a form of cytochrome P-450 with different catalytic properties from those of forms induced by either phenobarbital or 3-methylcholanthrene.	Phenobarbital	430-443	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	339-355
719633-2	1978	The increases in epoxide hydratase activities produced by BHA were far greater (11-fold) than were those produced by the administration of well-known enzyme inducers such as 3-methylcholanthrene, phenobarbital, and Aroclor 1254 (2- to 3-fold).	Phenobarbital	196-209	epoxide hydrolase 2, cytoplasmic	Mus musculus	17-34
30521-0	1978	Benzodiasepine and neurotransmitter receptor binding in rat brain after chronic administration of diazepam or phenobarbital.	Phenobarbital	110-123	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	19-44
362104-0	1978	Restoration of the periovulatory follicle-stimulating hormone surges in sera by luteinizing hormone releasing hormone in phenobarbital-blocked rats.	Phenobarbital	121-134	gonadotropin releasing hormone 1	Rattus norvegicus	80-117
716947-3	1978	The amount of cytochrome P-450 with a molecular weight of 47,000 (MLvMcP-450(47) decreased in the phenobarbital group and in both acrylamide groups.	Phenobarbital	98-111	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	14-30
716947-5	1978	The cytochrome P-450 form with a molecular weight of 50,000 (MLvMcP-450(50) was significantly increased only in the phenobarbital group.	Phenobarbital	116-129	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	4-20
716947-6	1978	An increase in the total amount of cytochrome P-450 was only observed following treatment with phenobarbital.	Phenobarbital	95-108	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	35-51
695749-6	1978	The activity of serum GPT when CCl4 and phenobarbitone were administered together showed value of about 1/2 of the value when CCl4 was administered alone, while it remained high when CCl4 administration was combined with propionyl-promazine.	Phenobarbital	40-54	glutamic--pyruvic transaminase	Rattus norvegicus	22-25
688193-0	1978	Liver ornithine decarboxylase during phenobarbital promotion of nitrosamine carcinogenesis.	Phenobarbital	37-50	ornithine decarboxylase 1	Rattus norvegicus	6-29
688194-0	1978	Effects of dietary butylated hydroxytoluene and phenobarbital on the activities of ornithine decarboxylase and thymidine kinase in rat liver and lung.	Phenobarbital	48-61	ornithine decarboxylase 1	Rattus norvegicus	83-106
695749-6	1978	The activity of serum GPT when CCl4 and phenobarbitone were administered together showed value of about 1/2 of the value when CCl4 was administered alone, while it remained high when CCl4 administration was combined with propionyl-promazine.	Phenobarbital	40-54	C-C motif chemokine ligand 4	Rattus norvegicus	126-130
695749-6	1978	The activity of serum GPT when CCl4 and phenobarbitone were administered together showed value of about 1/2 of the value when CCl4 was administered alone, while it remained high when CCl4 administration was combined with propionyl-promazine.	Phenobarbital	40-54	C-C motif chemokine ligand 4	Rattus norvegicus	126-130
695749-9	1978	It is concluded that in the present experimental conditions phenobarbitone protected the liver from the hepatotoxic effect of CCl4, while propionyl-promazine did not.	Phenobarbital	60-74	C-C motif chemokine ligand 4	Rattus norvegicus	126-130
667133-1	1978	Cytochrome P-450 in microsomes from liver of phenobarbital treated and control rats has been studied by light absorption and by magnetic resonance methods (EPR and NMR).	Phenobarbital	45-58	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
32125-1	1978	The effects of acute and chronic administration of D-Galactosamine (GalN), Ethanol and Phenobarbital were investigated on the activities of lysosomal enzymes, i.e.; acid phosphatase, beta-glucuronidase and n-acetyl-beta-glucosaminidase, and others such as gamma-GTP and adenosine triphosphatase.	Phenobarbital	87-100	glucuronidase beta	Homo sapiens	183-201
96118-1	1978	Hepatic microsomal azoreductase activity with amaranth (3-hydroxy-4[(4-sulfo-1-naphthalenyl)azo]-2,7-naphthalenedisulfonic acid trisodium salt) as a substrate is proportional to the levels of microsomal cytochrome P-450 from control or phenobarbital-pretreated rats and mice or cytochrome P-448 from 3-methylchol-anthrene-pretreated animals.	Phenobarbital	236-249	NAD(P)H dehydrogenase, quinone 1	Mus musculus	19-31
96118-2	1978	In the "inducible" C57B/6J strain of mice, 3-methylcholanthrene and phenobarbital pretreatment cause an increase in cytochrome P-448 and P-450 levels, respectively, which is directly proportional to the increase of azoreductase activity.	Phenobarbital	68-81	NAD(P)H dehydrogenase, quinone 1	Mus musculus	215-227
96118-3	1978	However, in the "noninducible" DBA/2J strain of mice, only phenobarbital treatment causes the increase both in cytochrome P-450 levels and azoreductase activity, while 3-methylcholanthrene has no effect.	Phenobarbital	59-72	NAD(P)H dehydrogenase, quinone 1	Mus musculus	111-151
688180-0	1978	Phenobarbital stimulation of cytochrome P-450 and aminopyrine N-demethylase in hyperplastic liver nodules during LD-ethionine carcinogenesis.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	29-75
688180-2	1978	Phenobarbital administration to rats caused an increase of microsomal protein, cytochrome P-450 and aminopyrine N-demethylase in all tissue tested.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	79-125
32125-10	1978	4) It has been shown by histochemical and biochemical techniques that hepatic gamma-GTP activity was increased after phenobarbital administration in rats.	Phenobarbital	117-130	inactive glutathione hydrolase 2	Homo sapiens	78-87
207450-5	1978	In the livers from similar rats, killed at the same time, but which has received 1 mg/ml sodium phenobarbitone in their drinking water for one week, the cells near the central vein contained up to five times as much cytochrome P-450 as those near the portal tract (mean cell concentrations of 77.3 (+/-25.0) mumol/l and 28.3 (+/-9.6) mumol/l respectively).	Phenobarbital	89-110	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	216-232
103104-0	1978	The influence of age and of the inducer phenobarbital on the cytochrome P-450 dependent monooxygenation of drugs in rat liver.	Phenobarbital	40-53	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	61-77
26401-1	1978	Solubilized NADPH-cytochrome P-450 reductase has been purified from liver microsomes of phenobarbital-treated rats.	Phenobarbital	88-101	cytochrome p450 oxidoreductase	Rattus norvegicus	12-44
632295-2	1978	NADPH-cytochrome P-450 reductase was isolated from liver microsomes of phenobarbital-induced rats.	Phenobarbital	71-84	cytochrome p450 oxidoreductase	Rattus norvegicus	0-32
629331-1	1978	The objective of this study was to determine whether the inductive effect of phenobarbital (PB) on liver cytochrome P-450 was the result of the action of this drug on all or some hepatocytes.	Phenobarbital	77-90	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	105-121
629331-1	1978	The objective of this study was to determine whether the inductive effect of phenobarbital (PB) on liver cytochrome P-450 was the result of the action of this drug on all or some hepatocytes.	Phenobarbital	92-94	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	105-121
629331-8	1978	These results indicated that PB induces cytochrome P-450 in a selective subpopulation of hepatocytes, most likely located near the terminal hepatic venule.	Phenobarbital	29-31	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	40-56
27210-5	1978	The reductase reduced cytochrome P-450 (from phenobarbital-treated rabbits) and cytochrome P-448 (from 3-methylcholanthrene-treated rabbits).	Phenobarbital	45-58	cytochrome P-450	Oryctolagus cuniculus	22-38
369828-2	1978	LHRH was infused iv at a constant rate (50 ng/h) into phenobarbital-treated rats at different times during the estrous cycle.	Phenobarbital	54-67	gonadotropin releasing hormone 1	Rattus norvegicus	0-4
207450-6	1978	The results show a selective increase in cytochrome P-450 content by the cells in the centrilobular region after treatment with sodium phenobarbitone and a smaller increase by some of the cells in the periportal region.	Phenobarbital	128-149	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	41-57
627141-7	1978	The elimination of phenobarbital decreased at an exponential rate with a t1/2 of 4.6 days.	Phenobarbital	19-32	interleukin 1 receptor like 1	Homo sapiens	73-84
205535-4	1978	Cytochrome P-450 and NADPH-cytochrome c reductase were increased by PB treatment and cytochrome P-448 was induced by beta-NF treatment both in nuclei and in microsomes.	Phenobarbital	68-70	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
710737-3	1978	These results further support the hypothesis that microsomal cytochrome P-450-dependent enzyme induction and increase in bile flow are two separate effects of phenobarbital.	Phenobarbital	159-172	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	61-77
697926-0	1978	Effect of dietary phenobarbital, 3,4-benzo(alpha)pyrene and 3-methylcholanthrene on hepatic, intestinal and renal glutathione s-transferase activities in the rat.	Phenobarbital	18-31	hematopoietic prostaglandin D synthase	Rattus norvegicus	114-139
728164-0	1978	Time course of the induction of aryl hydrocarbon hydroxylase in rat liver nuclei and microsomes by phenobarbital, 3-methylcholanthrene, 2,3,7,8-tetrachloro-dibenzo-p-dioxin, dieldrin and other inducers.	Phenobarbital	99-112	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	32-60
755667-0	1978	Interaction of parathion and malathion with hepatic cytochrome P-450 from rats treated with phenobarbital and carbon disulfide.	Phenobarbital	92-105	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	52-68
755667-1	1978	Alterations in the activity of drug-metabolizing enzymes and the concentration of cytochrome p-450 from liver microsomes of rats pretreated with phenobarbital for enzyme induction and later given a single oral dose (0.4 ml/kg) of carbon disulfide (CS2) have been examined.	Phenobarbital	145-158	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	82-98
633074-9	1978	Evidence that these polypeptides are cytochrome P-450 was obtained from heme staining with tetramethylbenzidine and from induction studies with phenobarbital and 3-methylcholanthrene.	Phenobarbital	144-157	cytochrome P450 3A14	Cavia porcellus	37-53
318378-10	1978	Induction with alpha-pinene and phenobarbital was expressed by a shift of the maximum absorbance at 452 nm in the CO-difference spectrum to lower wavelengths in the NAIDM strain; whereas, beta-naphthoflavone, although increasing the amount of cytochrome P-450, did not change the wavelength of maximum absorbance.	Phenobarbital	32-45	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	243-259
733893-1	1978	Administration of phenobarbital to rats over a period of 5 days was shown to increase hepatic lipid peroxidation concomitant with induction of cytochrome P-450 and cytochrome c reductase.	Phenobarbital	18-31	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	143-186
597257-2	1977	Hepatic microsomal cytochrome P-450 concentrations are lower in selenium-deficient rats treated with phenobarbital for 4 days than in similarly treated control rats.	Phenobarbital	101-114	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	19-35
909072-5	1977	Phenobarbital pretreatment of the animals resulted ina significant increase in both the formation of TFAA and the cytochrome P-450 content of microsomes.	Phenobarbital	0-13	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	114-130
597257-12	1977	These studies demonstrate that the defective induction of cytochrome P-450 by phenobarbital in selenium-deficient rats is accompanied by increased haem catabolism.	Phenobarbital	78-91	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	58-74
901525-0	1977	Amino-terminal sequence of phenobarbital-inducible cytochrome P-450 from rabbit liver microsomes: similarity to hydrophobic amino-terminal segments of preproteins.	Phenobarbital	27-40	cytochrome P-450	Oryctolagus cuniculus	51-67
411532-3	1977	Phenobarbitone stimulated an increased NADPH-cytochrome c reductase activity and cytochrome P-450 concentration.	Phenobarbital	0-14	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	81-97
23104-9	1977	Activities of both glucose 6-phosphate dehydrogenase and ;malic" enzyme were increased by phenobarbital treatment.	Phenobarbital	90-103	glucose-6-phosphate dehydrogenase	Rattus norvegicus	19-52
901418-8	1977	In microsomal fractions from phenobarbitone-pretreated rats the norethindrone-mediated loss of cytochrome P-450 was increased relative to controls.	Phenobarbital	29-43	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	95-111
889709-5	1977	Phenobarbitone treatment, which produced a marked fall in hepatic ferritin iron concentration but no change in haemoglobin or plasma iron concentrations, promoted a specific enhancement of transferrin synthesis in both control and iron deficient livers.	Phenobarbital	0-14	transferrin	Rattus norvegicus	189-200
578406-3	1977	Daily exposure to 4.0 mg/l CS2 (first exposure 24 h after the first phenobarbitone injection) for 4 h prevented the decline in susceptibility on the 3rd and 4th days after phenobarbitone, when the reaction of unexposed rats to noradrenaline returned to normal.	Phenobarbital	68-82	calsyntenin 2	Rattus norvegicus	27-30
578406-3	1977	Daily exposure to 4.0 mg/l CS2 (first exposure 24 h after the first phenobarbitone injection) for 4 h prevented the decline in susceptibility on the 3rd and 4th days after phenobarbitone, when the reaction of unexposed rats to noradrenaline returned to normal.	Phenobarbital	172-186	calsyntenin 2	Rattus norvegicus	27-30
857345-0	1977	The binding of CS2 in central nervous system of control and phenobarbitone-pretreated rats.	Phenobarbital	60-74	calsyntenin 2	Rattus norvegicus	15-18
20083-0	1977	The involvement of cytochrome P-450 in the NADH-dependent O-demethylation of p-nitroanisole in phenobarbital-treated rabbit liver microsomes.	Phenobarbital	95-108	cytochrome P-450	Oryctolagus cuniculus	19-35
880239-2	1977	Phenobarbital was used to stimulate apo-(cytochrome P-450) synthesis.	Phenobarbital	0-13	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	41-57
880239-7	1977	In animals receiving successive injections of phenobarbital plus 3-amino-1,2,4-triazole, compared with those receiving phenobarbital only, the holo-(cytochrome P-450) content measured spectrally shows a greater decrease than could be accounted for by the decrease in the content of the total apoprotein.	Phenobarbital	46-59	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	149-165
880239-7	1977	In animals receiving successive injections of phenobarbital plus 3-amino-1,2,4-triazole, compared with those receiving phenobarbital only, the holo-(cytochrome P-450) content measured spectrally shows a greater decrease than could be accounted for by the decrease in the content of the total apoprotein.	Phenobarbital	119-132	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	149-165
870682-6	1977	Phenobarbital increased cytosolic ALDH activity 23-fold only in the RR animals, while TCDD increased activity 155-fold in both groups.	Phenobarbital	0-13	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	34-38
870682-13	1977	did not significantly inhibit cytosolic ALDH activity, while total mitochondrial ALDH activity was inhibited by 28 and 57% in RR animals receiving TCDD and phenobarbital, respectively.	Phenobarbital	156-169	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	81-85
872268-1	1977	The effect of acute CS2 exposure on the rat brain protein metabolism was studied with control and phenobarbitone pretreated adult male rats 1, 4 and 46 h after exposure.	Phenobarbital	98-112	calsyntenin 2	Rattus norvegicus	20-23
857582-3	1977	The binding of CS2 sulphur was 31% higher in the control neurofilaments than that in the phenobarbitone pretreated group.	Phenobarbital	89-103	calsyntenin 2	Rattus norvegicus	15-18
413503-0	1977	The effects of phenobarbital and 3,4-benzypyrene on microsomal cytochrome P-450 and NADPH-cytochrome C reductase in regenerating rat liver after partial hepatectomy or chemical injury.	Phenobarbital	15-28	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	63-79
919368-3	1977	All the inductors studied increased the activity of cholesterol 7alpha-hydroxylase: pregnenolone-16alpha-carbonitrile--by 50%, 16-dehydropregnenolone--by 80%, 3-acetate-16alpha-isthiocyanogen pregnenolone--by 110% and phenobarbital--by 200%.	Phenobarbital	218-231	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	52-82
888489-7	1977	After phenobarbital pretreatment liver weight increased and cytochrome P 450 and hexobarbital oxidation rate were distinctly enhanced.	Phenobarbital	6-19	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	60-76
884258-3	1977	There was a distinct difference in the sensitivity of cytochrome P-448 and cytochromes P-450 in rats--intact and those given PB--to desoxycholate-Na treatment in vitro.	Phenobarbital	125-127	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	54-70
857345-1	1977	The binding of 35S- and 14C-labelled CS2 in rat central nervous system (CNS) was studied in control and phenobarbitone-pretreated rats in vivo and in vitro.	Phenobarbital	104-118	calsyntenin 2	Rattus norvegicus	37-40
857345-8	1977	The present findings suggest that a considerable amount of injected CS2 is retained in the nervous system and that phenobarbitone pretreatment of test subjects may also alter brain metabolism of CS2.	Phenobarbital	115-129	calsyntenin 2	Rattus norvegicus	195-198
402793-1	1977	The binding of 35S and 14C labelled CS2 to liver microsomes was studied in control and phenobarbitone pretreated rats 3 and 6 hrs after an intraperitoneal injection.	Phenobarbital	87-101	calsyntenin 2	Rattus norvegicus	36-39
402793-6	1977	The increase was evident 3 hrs after the injection of CS2 in the phenobarbitone pretreated rats.	Phenobarbital	65-79	calsyntenin 2	Rattus norvegicus	54-57
838185-10	1977	The increase of the cytochrome P-450 concentration in the liver after 80 mg phenobarbital sodium/kg was lowered by alcohol.	Phenobarbital	76-96	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	20-36
837930-7	1977	Phenobarbital treatment induced an increase in the cytochrome P-450 content that was different for the various subfractions.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	51-67
187601-3	1976	P-450LM2, which was isolated from phenobarbital-induced animals, has a subunit molecular weight of 48,700.	Phenobarbital	34-47	cytochrome P450 2B4	Oryctolagus cuniculus	0-8
13069-2	1977	NADPH-cytochrome P-450 reductase was purified from hepatic microsomes of phenobarbital and hydrocortisone-treated rats by detergent solubilization and column chromatography.	Phenobarbital	73-86	cytochrome p450 oxidoreductase	Rattus norvegicus	0-32
913919-3	1977	It was found that: (1) phenobarbital, barbital, and thiopental, but not pentobarbital, significantly increased liver weight, cytochrome P-450 concentration in the liver, decreased pentobarbital sleeping time and induced a hypertrophy of the smooth endoplasmic reticulum in the hepatocytes at electron microscopy; (2) in contrast, the four barbiturates, including pentobarbital, significantly increased bile flow; this increase was attributed to an increase in the bile acid independent bile flow.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	125-141
402587-4	1977	Phenobarbital-treated rats were used to enhance the hepatotoxicity of CCl4.	Phenobarbital	0-13	C-C motif chemokine ligand 4	Rattus norvegicus	70-74
833122-1	1977	Solubilized cytochromes P-450 and P-448 have been prepared from liver microsomes of phenobarbital- and 3-methylcholanthrene-pretreated rats, respectively.	Phenobarbital	84-97	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	24-39
13937-7	1977	3-MC and PB specifically act on cytochrome P-450 and do not modify the physico-chemical properties of the microsomal membrane as measured by the non-specific binding of benzpyrene (BP).	Phenobarbital	9-11	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	32-48
187601-5	1976	P-450LM4, which is induced by beta-naphthoflavone but is also present in phenobarbital-induced and untreated animals, was isolated from all three sources and found to have a subunit molecular weight of 55,300.	Phenobarbital	73-86	cytochrome P450 1A2	Oryctolagus cuniculus	0-8
13927-2	1976	The addition of vinyl chloride to microsomes causes a Type 1 spectra shift, similar to that seen for phenobarbital [11[ which indicates the direct involvement of a cytochrome P-450 species; this difference spectrum is characteristic of substrate binding to this type of enzyme.	Phenobarbital	101-114	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	164-180
191326-5	1976	The hyperplastic nodules of the animals treated with phenobarbital showed almost the same amount of cytochrome P-450 as that in the controls.	Phenobarbital	53-66	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	100-116
11634-4	1976	In newborns treated for 3 days following the birth with a combination of phenobarbital and nicethamide an increase of gamma-glutamyl transpeptidase activity occurred from the 4th to the 7th days.	Phenobarbital	73-86	inactive glutathione hydrolase 2	Homo sapiens	118-147
1021219-1	1976	Mephenytoin, diphenylhydantoin, pheneturide, and phenobarbital produced a concentration-dependent inhibition in the binding of hexobarbital to cytochrome P-450 at the type 1 site, while sulthiame slightly potentiated, and ethosuximide did not affect the binding characteristic of hexobarbital.	Phenobarbital	49-62	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	143-159
187352-10	1976	The induction by phenobarbital of cytochrome P-450 and p-nitrosanisole O-demethylase was partially prevented on concomitant treatment with disulfiram and diethyldithiocarbamate.	Phenobarbital	17-30	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	34-84
187353-6	1976	Treatment with phenobarbital (80 mg/kg, i.p., per day, 4 X) enhanced UDP glucuronosyl-transferase, but brought about different effects on the other enzymes.	Phenobarbital	15-28	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	69-97
994730-0	1976	Stimulation of serum lecithin-cholesterol acyltransferase activity by phenobarbital in the rat.	Phenobarbital	70-83	lecithin cholesterol acyltransferase	Rattus norvegicus	21-57
1011793-0	1976	Solubilization and partial purification of cytochrome P-450 from hepatic microsomes of phenobarbital-treated rat.	Phenobarbital	87-100	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	43-59
997586-9	1976	Phenobarbital increased the cytochrome P-450 as expected.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	28-44
789806-1	1976	Continuous infusions of luteinizing hormone releasing hormone (LH-RH) into phenobarbitone-treated long-term ovariectomized rats, resulted in patterns of LH secretion which were determined by the blood LH-RH concentration.	Phenobarbital	75-89	gonadotropin releasing hormone 1	Rattus norvegicus	24-61
789806-1	1976	Continuous infusions of luteinizing hormone releasing hormone (LH-RH) into phenobarbitone-treated long-term ovariectomized rats, resulted in patterns of LH secretion which were determined by the blood LH-RH concentration.	Phenobarbital	75-89	gonadotropin releasing hormone 1	Rattus norvegicus	63-68
789806-1	1976	Continuous infusions of luteinizing hormone releasing hormone (LH-RH) into phenobarbitone-treated long-term ovariectomized rats, resulted in patterns of LH secretion which were determined by the blood LH-RH concentration.	Phenobarbital	75-89	gonadotropin releasing hormone 1	Rattus norvegicus	201-206
184834-2	1976	Cytochrome P-450 was solubilized from phenobarbital induced rabbit liver and purified by affinity chromatography.	Phenobarbital	38-51	cytochrome P-450	Oryctolagus cuniculus	0-16
948753-0	1976	Cytochrome P-450 induction by phenobarbital and 3-methylcholanthrene in primary cultures of hepatocytes.	Phenobarbital	30-43	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-16
971417-0	1976	Influence of tryptophan on the level of hepatic microsomal cytochrome P-450 in well-fed normal, adrenalectomized, and phenobarbital-treated rats.	Phenobarbital	118-131	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	59-75
971417-1	1976	In well-fed normal male rats, either force-feeding of tryptophan or a single injection of phenobarbital produced significant increments in hepatic microsomal cytochrome P-450 and the associated aniline hydroxylase activity.	Phenobarbital	90-103	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	158-174
971417-5	1976	While in cortisol-treated adrenalectomized rats administration of phenobarbital caused a 56% increment in cytochrome P-450 as compared to controls, tryptophan produced only a minor (9%) increase.	Phenobarbital	66-79	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	106-122
971417-8	1976	Further administration of either tryptophan or phenobarbital slightly increased the level of cytochrome P-450, and the two compounds together caused 40 and 21% increments of the same compared to actinomycin-treated and non-treated controls, respectively.	Phenobarbital	47-60	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	93-109
948753-1	1976	The characteristic hepatocellular changes resulting from phenobarbital administration in vivo, namely an increase in the levels of cytochrome P-450 and proliferation of membranes of the smooth endoplasmic reticulum, have been demonstrated in primary cultures of nonreplicating hepatocytes on floating collagen membranes.	Phenobarbital	57-70	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	131-147
821945-4	1976	Highly purified cytochrome P-450 from phenobarbital-treated rats is relatively poor in catalyzing the formation of mutagenic metabolites from benzo (a)pyrene.	Phenobarbital	38-51	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	16-32
956171-5	1976	The amount of CCl4 producing a 50% increase in malondialdehyde formation was about 3-fold less for cells from phenobarbital-treated rats than for those from control rats.	Phenobarbital	110-123	C-C motif chemokine ligand 4	Rattus norvegicus	14-18
822448-5	1976	However, TRH exerted a prolonged antagonism or reversal of the phenobarbital-induced hypothermia.	Phenobarbital	63-76	thyrotropin releasing hormone	Oryctolagus cuniculus	9-12
954149-3	1976	Similarly, the formation is mainly a property of phenobarbital-induced cytochrome P-450 and is inhibited by comparable concentrations of metyrapone and 2-O-iodophenoxymethylimidazole.	Phenobarbital	49-62	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	71-87
956171-4	1976	Phenobarbital pretreatment increased peroxidation due to exposure of the cells to CCl4 but not that associated with NADPH addition.	Phenobarbital	0-13	C-C motif chemokine ligand 4	Rattus norvegicus	82-86
947901-0	1976	Separation, purification, and properties of multiple forms of cytochrome P-450 from the liver microsomes of phenobarbital-treated mice.	Phenobarbital	108-121	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	62-78
947901-4	1976	All four fractions with respect to their spectral and catalytic properties, thereby demonstrating that mouse liver microsomes from phenobarbital-treated hybrid mice contain at least four forms of cytochrome P-450.	Phenobarbital	131-144	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	196-212
182393-8	1976	It was concluded that lipophilic thiols can be bound as ligands by at least two species of oxidized cytochrome P-450 which represent, however, not more than about one fifth of the total cytochrome P-450 content in liver microsomes from phenobarbital-pretreated rats.	Phenobarbital	236-249	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	100-116
967161-7	1976	Induction with either naphthalene or phenobarbital appears to increase cytochrome P-450I preferentially.	Phenobarbital	37-50	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	71-88
931995-10	1976	The stimulatory effect of phenobarbital treatment on 25-hydroxylation and the inhibitory effect of this treatment on 26-hydroxylation were associated with the cytochrome P-450 fraction.	Phenobarbital	26-39	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	159-175
1268849-5	1976	3-Methylcholanthrene, phenobarbital, and 2-acetylaminofluorene had a greater inductive effect and cytochrome P-450 in vitamin A-deficient rats.	Phenobarbital	22-35	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	98-114
1260949-8	1976	However, while both phenobarbital and MC powerfully repress the DMN-demethylase, we have confirmed that they are strong inducers of the synthesis of P-450 and P-448, respectively, as estimated from the difference spectra.	Phenobarbital	20-33	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	149-164
1267808-0	1976	Phenobarbital induction of egasyn: availability of egasyn in vivo determines glucuronidase binding to membrane.	Phenobarbital	0-13	carboxylesterase 1	Homo sapiens	27-33
6182-11	1976	Serum gamma-glutamyl transpeptidase was also increased after phenobarbitone administration, the increase being unrelated to changes in antipyrine clearance or plasma cholesterol.	Phenobarbital	61-75	inactive glutathione hydrolase 2	Homo sapiens	6-35
820452-2	1976	Ellipticine is able to induce cytochrome P448 synthesis in Rat liver microsomes which converts the drug into 9-hydroxy derivative, with a higher rate than microsomal cytochrome P450 of non-treated or phenobarbital induced Rats.	Phenobarbital	200-213	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	30-45
820452-2	1976	Ellipticine is able to induce cytochrome P448 synthesis in Rat liver microsomes which converts the drug into 9-hydroxy derivative, with a higher rate than microsomal cytochrome P450 of non-treated or phenobarbital induced Rats.	Phenobarbital	200-213	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	166-181
1254598-4	1976	In contrast, phenobarbital or pregnenolone-16 alpha-carbonitrile induces in both responsive and nonresponsive strains a different profile of enzyme activities and the appearance of cytochrome P-450 (rather than cytochrome P-448).	Phenobarbital	13-26	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	181-197
1267008-8	1976	Phenobarbital pretreatment of rats increased binding of T3 by ligandin and of T4 by albumin-containing fractions.	Phenobarbital	0-13	glutathione S-transferase alpha 2	Rattus norvegicus	62-70
131362-2	1976	The CCl4 induced polysome breakdown process is more intense in the phenobarbital treated than in control rats while the 3-MC prior treatment does not modify its intensity.	Phenobarbital	67-80	C-C motif chemokine ligand 4	Rattus norvegicus	4-8
815258-4	1976	Purified hepatic cytochrome P-450 from phenobarbital-treated rats cross-reacts poorly with the cytochrome P-448 antibody as do purified rabbit hepatic cytochrome P-448 and P-450.	Phenobarbital	39-52	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	17-33
177981-4	1976	Similarly, after the administration of phenobarbital, there was first an increase in the cAMP concentration and in the activity of cAMP-dependent protein kinase, then the induction of ornithine decarboxylase, and finally, an enhanced activity of ethylmorphine N-demethylase and an increased content of cytochrome P-450.	Phenobarbital	39-52	ornithine decarboxylase 1	Rattus norvegicus	184-207
177981-4	1976	Similarly, after the administration of phenobarbital, there was first an increase in the cAMP concentration and in the activity of cAMP-dependent protein kinase, then the induction of ornithine decarboxylase, and finally, an enhanced activity of ethylmorphine N-demethylase and an increased content of cytochrome P-450.	Phenobarbital	39-52	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	302-318
815258-4	1976	Purified hepatic cytochrome P-450 from phenobarbital-treated rats cross-reacts poorly with the cytochrome P-448 antibody as do purified rabbit hepatic cytochrome P-448 and P-450.	Phenobarbital	39-52	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	106-111
815258-7	1976	In contrast, purified liver cytochrome P-450 from phenobarbital-treated rats gives three precipitin bands, all of which contain hemeprotein as judged by benzidine staining.	Phenobarbital	50-63	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	28-44
815258-11	1976	In addition, the pattern and extent of inhibition of the cytochrome P-450 system depends on the substrate used, suggesting that multiple forms of the hemeprotein are present in the purified preparation from phenobarbital-treated rats.	Phenobarbital	207-220	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	57-73
815258-12	1976	The observed patterns of immunoprecipitation and inhibition of catalytic activity indicate that (a) cytochrome P-448 from 3-methylcholanthrene-treated rats is immunochemically different from cytochrome P-450 from phenobarbital-treated rats, and (b) there appear to be at least three hemeprotein forms in the purified cytochrome P-450 preparation from phenobarbital-treated rats.	Phenobarbital	213-226	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	111-116
815258-12	1976	The observed patterns of immunoprecipitation and inhibition of catalytic activity indicate that (a) cytochrome P-448 from 3-methylcholanthrene-treated rats is immunochemically different from cytochrome P-450 from phenobarbital-treated rats, and (b) there appear to be at least three hemeprotein forms in the purified cytochrome P-450 preparation from phenobarbital-treated rats.	Phenobarbital	351-364	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	111-116
5265-5	1976	In the presence of fixed amounts of lipid and NADPH-cytochrome c reductase, the rate of complex formation with cytochrome P-450 isolated from phenobarbital-treated rats was much greater than that observed with cytochrome P-48 from 3-methylcholanthrene-treated rats or rabbits.	Phenobarbital	142-155	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	111-127
1245792-11	1976	PB reduced the saturation less effectively than CDC; it increased 7alpha-hydroxylase but also increased HMG-CoA reductase.	Phenobarbital	0-2	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	104-121
765123-0	1976	Simulation of the early phase of the proestrous follicle-stimulating hormone rise after infusion of luteinizing hormone-releasing hormone in phenobarbital-blocked rats.	Phenobarbital	141-154	gonadotropin releasing hormone 1	Rattus norvegicus	100-137
1249471-5	1976	However, with dye infusion of 3.6 mumoles per kilogram per minute, phenobarbital significantly enhanced the rate of biliary excretion of BSP but not BSP-GSH and ANIT treatment had a greater inhibitory effect on biliary excretion of BSP-GSH than BSP.	Phenobarbital	67-80	integrin-binding sialoprotein	Rattus norvegicus	137-140
1255670-2	1976	The 8a-aryl-3,4,6,7,8,8a-hexahydro-2H-pyrrolo[2,1-beta][1,3]oxazin-6-ones possessed the best overall spectrum of activity relative to the standard agents glutethimide and phenobarbital.	Phenobarbital	171-184	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	50-59
3152-9	1975	3) Altered microsomal cytochrome P-450 concentrations in newborn animals, or produced by pretreatment of rats with phenobarbital, 3-methylcholanthrene (MC), or CoCl2 effected similar, but not proportional changes in the rates of irreversible protein and lipid binding.	Phenobarbital	115-128	cytochrome P-450	Oryctolagus cuniculus	22-38
1274375-11	1976	Treatment of 7 day-old chicks with exogenous inducers, 3-methylcholanthrene or phenobarbital sodium (100 mg/kg, intraperitoneally) brought about maximal stimulation of microsomal activity as 18-24 h. The time-course of this induction was reflected by changes in microsomal cytochrome P-450 content and NADPH-cytochrome P=450 reductase activities.	Phenobarbital	79-99	cytochrome p450 oxidoreductase	Gallus gallus	302-334
1037202-6	1976	It can be shown that repeated pretreatment of rats with phenobarbital increases the activity of hepatic cholesterol 7alpha-hydroxylase by more than three times over the control values.	Phenobarbital	56-69	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	104-134
820074-2	1976	Phenobarbital and medinal administration resulted in a 2-8 fold increase in cytochrome P-450 amount.	Phenobarbital	0-13	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	76-92
1020568-1	1976	Repeated pretreatment with p-aminohippuric acid (PAH), probenecide, cyclopenthiazide, and phenobarbital stimulates the renal excretion of PAH.	Phenobarbital	90-103	phenylalanine hydroxylase	Rattus norvegicus	138-141
813642-0	1975	Response of NADPH cytochrome c reductase and cytochrome P-450 in hepatic microsomes to treatment with phenobarbital--differences in rat strains.	Phenobarbital	102-115	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	45-61
1204657-1	1975	Octyl methyl-, butyl methyl- and pentamethylene sulfide react with about 50% of oxidized cytochrome P-450 in liver microsomes from phenobarbital-pretreated rats by formation of optical difference spectra with maxima at 435 and 552 nm and concomitant shifts in the electron paramagnetic resonance spectrum.	Phenobarbital	131-144	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	89-105
811776-5	1975	The low doses of PB used in this study caused significant induction of cytochrome P-450 (P less than 0.10), biphenyl 4-hydroxylase, and p-nitrobenzoate reductase (except in LP and NP females).	Phenobarbital	17-19	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	71-87
1185600-6	1975	Treatment of adult rats for 4 days with phenobarbital increased the amount of ligandin by 85%, whereas spironolactone increased it by 35% and 3-methylcholanthrene by 17%.	Phenobarbital	40-53	glutathione S-transferase alpha 2	Rattus norvegicus	78-86
1184723-9	1975	Major increases in urinary metabolites after DPH and PB were in the unconjugated ethyl acetate fraction, and this suggests that MP metabolism is significantly altered by hepatic microsomal hydroxylation enzyme induction by DHP and PB, but not DZP.	Phenobarbital	53-55	dihydropyrimidinase	Homo sapiens	223-226
1233256-4	1975	Assuming that CSF is an ultrafiltrate of plasma, the percentage of phenytoin, phenobarbitone and primidone which was unbound in plasma was 10-14%, 43% and 81% respectively.	Phenobarbital	78-92	colony stimulating factor 2	Homo sapiens	14-17
1182096-1	1975	Magnetic circular dichroism (MCD) spectra have been measured for cytochrome P-450 (P-450) purified from phenobarbital-induced rabbit liver microsomes.	Phenobarbital	104-117	cytochrome P-450	Oryctolagus cuniculus	65-81
1239780-5	1975	Excluding amphetamine, low-dose morphine and phenobarbital groups, substantial extinction of CAR occurred during the drug phase only; these three groups, as well as the high-dose alcohol, barbiturates and medazepam ones, showed extinction during the nondrug phase also.	Phenobarbital	45-58	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	93-96
1208905-3	1975	Phenobarbital was shown to lower the toxicity of DDT, norethandrolone had the opposite effect, and 3-methylcholanthrene was without any significant effect.	Phenobarbital	0-13	D-dopachrome tautomerase	Rattus norvegicus	49-52
1208905-4	1975	After a phenobarbital pretreatment, the cerebral concentration of DDT was lowered, possibly as a result of an increased biotransformation of DDT to DDD in the liver.	Phenobarbital	8-21	D-dopachrome tautomerase	Rattus norvegicus	66-69
1208905-4	1975	After a phenobarbital pretreatment, the cerebral concentration of DDT was lowered, possibly as a result of an increased biotransformation of DDT to DDD in the liver.	Phenobarbital	8-21	D-dopachrome tautomerase	Rattus norvegicus	141-144
167029-1	1975	Daily phenobarbital (PB) injections, on 3-7 consecutive days, induce an intense proliferation of smooth endoplasmic reticulum (ER) associated with a decrease of the glucose-6-phosphatase activity.	Phenobarbital	6-19	glucose-6-phosphatase catalytic subunit 1	Homo sapiens	165-186
241786-3	1975	The latter (phenobarbitone, pentobarbitone and allobarbitone) were shown by spectral technique to interact with cytochrome P-450 suggesting that their mechanism of enzyme induction was "substrate induction" in type.	Phenobarbital	12-26	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	112-128
1172492-4	1975	in a two part study, noticed when phenobarbital was administered to sexually mature male rats, it accelerated the metabolism of androgen as reflected by significant reductions in weight and RNA content of male accessory organs [3]; it was also observed that vitamin B 12 is an enzyme inducer [2].	Phenobarbital	34-47	NADH:ubiquinone oxidoreductase subunit B3	Homo sapiens	266-270
167029-1	1975	Daily phenobarbital (PB) injections, on 3-7 consecutive days, induce an intense proliferation of smooth endoplasmic reticulum (ER) associated with a decrease of the glucose-6-phosphatase activity.	Phenobarbital	21-23	glucose-6-phosphatase catalytic subunit 1	Homo sapiens	165-186
1178765-1	1975	Part 7: Formulation and evaluation of ascorbic acid and phenobarbitone tablets.	Phenobarbital	56-70	poly(ADP-ribose) polymerase family member 15	Homo sapiens	0-6
9297-6	1975	Gamma-glutamyl-transpeptidase activity increased only in the phenobarbital group.	Phenobarbital	61-74	inactive glutathione hydrolase 2	Homo sapiens	0-29
807960-2	1975	Various test compounds: coumarin, 4-methylcoumarin, phenobarbital and CCl4 all elevated serum prolactin level, but only coumarin and 4-methylcoumarin reduced tumor incidence.	Phenobarbital	52-65	prolactin	Rattus norvegicus	94-103
237636-3	1975	The results of these studies also suggest that the decrease in the concentration of cytochrome P-450 and the liver damage seen on in vivo administration of CS2 to phenobarbital pretreated rats, is due to the mixed-function oxidase catalyzed release and binding of the sulfur atoms of CS2.	Phenobarbital	163-176	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	84-100
1123353-5	1975	P-450LM2, which was purified to apparent homogeneity, is induced by phenobarbital and has a subunit molecular weight of 50,000.	Phenobarbital	68-81	cytochrome P450 2B4	Oryctolagus cuniculus	0-8
237636-3	1975	The results of these studies also suggest that the decrease in the concentration of cytochrome P-450 and the liver damage seen on in vivo administration of CS2 to phenobarbital pretreated rats, is due to the mixed-function oxidase catalyzed release and binding of the sulfur atoms of CS2.	Phenobarbital	163-176	calsyntenin 2	Rattus norvegicus	156-159
237636-3	1975	The results of these studies also suggest that the decrease in the concentration of cytochrome P-450 and the liver damage seen on in vivo administration of CS2 to phenobarbital pretreated rats, is due to the mixed-function oxidase catalyzed release and binding of the sulfur atoms of CS2.	Phenobarbital	163-176	calsyntenin 2	Rattus norvegicus	284-287
804493-8	1975	Pretreatment with phenobarbital, DDT, or pregnene-16alpha-carbonitrile did not increase renal ligandin concentration but doubled hepatic ligandin concentration.	Phenobarbital	18-31	glutathione S-transferase alpha 2	Rattus norvegicus	137-145
239443-2	1975	After 5 days of pretreatment, phenobarbital and methyprylon significantly increased aminopyrine demethylation, aniline hydroxylation, and cytochrome P-450 content in hepatic microsomes.	Phenobarbital	30-43	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	138-154
239443-4	1975	After 29 days of pretreatment, phenobarbital significantly increases aminopyrine demethylase, aniline hydroxylase activity, liver weight and cytochrome P-450 content.	Phenobarbital	31-44	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	141-157
173382-3	1975	Prior dosing with phenobarbitone augments CCl4 toxicity only in the adult and the newborn but the foetus continues to be resistant.	Phenobarbital	18-32	C-C motif chemokine ligand 4	Rattus norvegicus	42-46
805836-6	1975	In addition, TRH reduced the sleep and hypothermia produced by thiopental, amobarbital, secobarbital and phenobarbital, and it antagonized the hypothermia and reduced motor activity produced by chloral hydrate, reserpine, chlorpromazine and diazepam.	Phenobarbital	105-118	thyrotropin releasing hormone	Homo sapiens	13-16
1227906-0	1975	[Increasing rat liver glutathione peroxidase and glutathione reductase activity by administering phenobarbital].	Phenobarbital	97-110	glutathione-disulfide reductase	Rattus norvegicus	49-70
164171-4	1975	The protective effect is abolished if the animals are administered phenobarbital prior to the administration of CCl4.	Phenobarbital	67-80	C-C motif chemokine 4	Macaca mulatta	112-116
236156-8	1975	Pretreatment with phenobarbital increased both microsomal cytochrome P-450 levels and the rate of conversion of dibromomethane to carbon monoxide.	Phenobarbital	18-31	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	58-74
1205492-0	1975	Phenobarbital induced variations in hepatic ethyl-morphine n-demethylase and inorganic pyrophosphatase during riboflavin deficiency.	Phenobarbital	0-13	inorganic pyrophosphatase 1	Homo sapiens	77-102
1128171-3	1975	In the Wistar rat, injection of phenobarbital produced a doubling of fecal bile acid output (controls, 5.3 mg/rat/day; treated rats, 10.6 mg/rat/day) and a two-threefold increase in cholesterol 7alpha-hydroxylase.	Phenobarbital	32-45	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	182-212
234439-13	1975	Cytochrome P-450 is fairly stable, whereas cytochrome P-450I can be isolated only when protected by a substrate (phenobarbital).	Phenobarbital	113-126	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	43-60
1182203-0	1975	Induction of UDPglucose dehydrogenase during development, organ culture, and exposure to phenobarbital.	Phenobarbital	89-102	UDP-glucose dehydrogenase	Mus musculus	13-37
1182203-6	1975	UDPglucose dehydrogenase increases in embryo liver, probably by induction, 2-3-fold during culture with phenobarbital and some 5-fold when exposed to the drug in ovo.	Phenobarbital	104-117	UDP-glucose dehydrogenase	Mus musculus	0-24
1182203-8	1975	Differences between induction of UDPglucose dehydrogenase and UDPglucuronyl transferase during development, culture and phenobarbital treatment indicate that control mechanism for these two enzymes are not directly linked.	Phenobarbital	120-133	UDP-glucose dehydrogenase	Mus musculus	33-57
1210995-0	1975	The NADPH-dependent cytochrome P-450 reduction in liver microsomes of rats of different ages with and without phenobarbital pretreatment.	Phenobarbital	110-123	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	20-36
1061478-4	1975	With 50 mg/kg of phenobarbitone, CBF and CMRO2 were reduced by about 20%.	Phenobarbital	17-31	CCAAT/enhancer binding protein zeta	Rattus norvegicus	33-36
1088983-0	1975	[The effect of alpha methyldopa and phenobarbital on angiotensin sensitivity and renin activity in man].	Phenobarbital	36-49	renin	Homo sapiens	81-86
168747-0	1975	Effect of cyclic AMP on the phenobarbital induced increase in cytochrome P-450 and hypertrophy of the endoplasmic reticulum of the rat liver.	Phenobarbital	28-41	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	62-78
168750-1	1975	Cytochrome P-450 has been purified from liver microsomes of phenobarbital-induced rabbits in the presence of ionic and nonionic detergents to concentrations over 17 nmoles per mg of protein.	Phenobarbital	60-73	cytochrome P-450	Oryctolagus cuniculus	0-16
808108-3	1975	Partial purification of liver microsomal cytochrome p-450 results in the separation of two forms of cytochrome p-450 from phenobarbital-treated rats and two forms of cytochrome p-44, from 3-methylcholanthrene-treated rats.	Phenobarbital	122-135	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	41-57
808108-3	1975	Partial purification of liver microsomal cytochrome p-450 results in the separation of two forms of cytochrome p-450 from phenobarbital-treated rats and two forms of cytochrome p-44, from 3-methylcholanthrene-treated rats.	Phenobarbital	122-135	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	100-116
168750-4	1975	NADPH-cytochrome P-450 reductase has been purified from liver microsomes of phenobarbital-induced rats in the presence of ionic and nonionic detergents to a stage where it catalyzes the reduction of 33,000 nmoles of cytochrome c per min per mg of protein.	Phenobarbital	76-89	cytochrome p450 oxidoreductase	Rattus norvegicus	0-32
1116950-8	1975	The content of cytochrome P450 in animals fed with phenobarbitone was 2.4 times greater than in control animals.	Phenobarbital	51-65	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	15-30
1188268-0	1975	Relationships among dose, serum and CSF levels and urinary output in fenobarbital and fenitoin treatment of epileptics.	Phenobarbital	69-81	colony stimulating factor 2	Homo sapiens	36-39
817374-0	1975	Thyrotropin-releasing hormone (TRH) and its beta-alanine analogue: potentiation of the anticonvulsant potency of phenobarbital in mice.	Phenobarbital	113-126	thyrotropin releasing hormone	Mus musculus	0-29
1054513-2	1975	Dissociation of apoprotein and heme synthesis by concomitant treatment of rats with inducers of cytochrome P-450 (i.e., phenobarbital) and inhibitors of heme synthesis (i.e., cobalt) resulted in a relative excess of apocytochrome P-450.	Phenobarbital	120-133	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	96-112
817374-0	1975	Thyrotropin-releasing hormone (TRH) and its beta-alanine analogue: potentiation of the anticonvulsant potency of phenobarbital in mice.	Phenobarbital	113-126	thyrotropin releasing hormone	Mus musculus	31-34
817374-4	1975	None of the peptides studied had any anticonvulsant properties of their own, but TRH and beta-ala TRH, though not pro-leu-gly-NH2, potentiated the anticonvulsant potency of phenobarbital.	Phenobarbital	173-186	thyrotropin releasing hormone	Mus musculus	81-84
817374-4	1975	None of the peptides studied had any anticonvulsant properties of their own, but TRH and beta-ala TRH, though not pro-leu-gly-NH2, potentiated the anticonvulsant potency of phenobarbital.	Phenobarbital	173-186	thyrotropin releasing hormone	Mus musculus	98-101
4153862-0	1974	Highly purified detergent-solubilized NADPH-cytochrome P-450 reductase from phenobarbital-induced rat liver microsomes.	Phenobarbital	76-89	cytochrome p450 oxidoreductase	Rattus norvegicus	38-70
1863-5	1975	We conclude that it is elevated levels of cytochrome P-450 which potentiate the toxicity of fluroxene anaesthesia in phenobarbital treated animals and that cytochrome P-448 does not bind or metabolize fluroxene.	Phenobarbital	117-130	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	42-58
4472879-0	1974	A gel-electrophoretically homogeneous preparation of cytochrome P-450 from liver microsomes of phenobarbital-pretreated rabbits.	Phenobarbital	95-108	cytochrome P-450	Oryctolagus cuniculus	53-69
4418358-0	1974	Cytochrome P-450 purified to apparent homogeneity from phenobarbital-induced rabbit liver microsomes: catalytic activity and other properties.	Phenobarbital	55-68	cytochrome P-450	Oryctolagus cuniculus	0-16
4367881-0	1974	An affinity column method for partial purification of cytochrome P-450 from phenobarbital-induced rabbit liver microsomes.	Phenobarbital	76-89	cytochrome P-450	Oryctolagus cuniculus	54-70
4853617-1	1974	1 A study is reported of the effects of phenytoin and phenobarbitone on bone calcium mobilization by parathyroid hormone in vitro.2 In a therapeutic concentration (15 mug/ml), phenytoin significantly inhibited parathyroid hormone-induced calcium release from bone.3 The inhibitory effect of phenytoin on bone calcium mobilization could play a role in the maintenance of hypocalcaemia in epileptic patients on long-term anticonvulsant drug therapy.	Phenobarbital	54-68	parathyroid hormone	Homo sapiens	101-120
4522784-1	1974	Induction of hepatic microsomal cytochrome P-450 and ethylmorphine N-demethylase activity by phenobarbital requires de novo synthesis of mRNA.	Phenobarbital	93-106	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	32-80
4134563-0	1974	Glucose-6-phosphatase heterogeneity within the hepatic lobule of the phenobarbital-treated rat.	Phenobarbital	69-82	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	0-21
17342914-1	1973	Phenobarbital sodium considerably increases the liver toxicity of CCl4.	Phenobarbital	0-20	C-C motif chemokine ligand 4	Rattus norvegicus	66-70
4377507-0	1974	Changes in pressor activity of angiotensin II induced by pentolinium and phenobarbital in rats.	Phenobarbital	73-86	angiotensinogen	Rattus norvegicus	31-45
4799079-2	1973	Drugs such as phenobarbitone and phenylbutazone, which increase the concentration of microsomal haem and cytochrome P-450, also increase the saturation of rat liver apo-(tryptophan pyrrolase) with its haem activator, as does the haem precursor 5-aminolaevulinate.	Phenobarbital	14-28	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	105-121
4799079-2	1973	Drugs such as phenobarbitone and phenylbutazone, which increase the concentration of microsomal haem and cytochrome P-450, also increase the saturation of rat liver apo-(tryptophan pyrrolase) with its haem activator, as does the haem precursor 5-aminolaevulinate.	Phenobarbital	14-28	tryptophan 2,3-dioxygenase	Rattus norvegicus	170-190
4768733-0	1973	Tryptophan pyrrolase in rat liver after phenobarbital administration.	Phenobarbital	40-53	tryptophan 2,3-dioxygenase	Rattus norvegicus	0-20
4741599-0	1973	Some spectral properties of cytochrome P-450 from microsomes isolated from control, phenobarbital- and naphthalene-treated houseflies.	Phenobarbital	84-97	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	28-44
4198543-0	1973	Production of anti phenobarbital antibody in rabbits by immunization with p-azophenobarbital acetylated bovine serum albumin.	Phenobarbital	19-32	albumin	Oryctolagus cuniculus	111-124
4728068-0	1973	Potentiation of CCl4-induced hepatotoxicity in the dog by chronic exposure  to phenobarbital.	Phenobarbital	79-92	C-C motif chemokine 4	Canis lupus familiaris	16-20
4149893-0	1973	[Hepatic and plasmatic gamma-glutamyl-transpeptidase during induction with phenobarbital: preliminary results].	Phenobarbital	75-88	inactive glutathione hydrolase 2	Homo sapiens	23-52
4197089-3	1973	These findings are similar to those seen in rats treated with the polycyclic hydrocarbon, 3-methylcholanthrene, but differ from those that characterize cytochrome P-450 in control or phenobarbital-treated rats.	Phenobarbital	183-196	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	152-168
4151093-0	1973	Effect of phenobarbital administration on liver and plasma gamma-glutamyl-transpeptidase: clinical and experimental investigations.	Phenobarbital	10-23	inactive glutathione hydrolase 2	Homo sapiens	59-88
4145407-0	1973	Stability of messenger RNA"s for microsomal NADPH-cytochrome c reductase and cytochrome b 5  in the livers of normal and phenobarbital-treated rats.	Phenobarbital	121-134	cytochrome b5 type A	Rattus norvegicus	77-91
4403783-0	1972	Differential acute effects of phenobarbital and 3-methylcholanthrene pretreatment on CCl 4 -induced hepatotoxicity in rats.	Phenobarbital	30-43	C-C motif chemokine ligand 4	Rattus norvegicus	85-90
5033652-1	1972	Oxidation-reduction changes of cytochrome P-450 and oxygen consumption were measured in isolated perfused livers from normal and phenobarbital-treated rats.	Phenobarbital	129-142	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	31-47
5033652-2	1972	Phenobarbital treatment markedly increased the aminopyrine-induced reduction of cytochrome P-450, but ethanol did not cause any redox changes of this cytochrome.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	80-96
5059201-1	1972	The effect of phenobarbital administration on the in vitro activity of cholesterol 7alpha-hydroxylase was investigated in two strains of rats.	Phenobarbital	14-27	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	71-101
5151876-0	1971	[Behavior of prothrombin complex and its factors after phenobarbital and glutethimide administration].	Phenobarbital	55-68	coagulation factor II, thrombin	Homo sapiens	13-24
4261774-0	1972	Albumin synthesis in isolated perfused livers from phenobarbital pretreated rats.	Phenobarbital	51-64	albumin	Rattus norvegicus	0-7
5131732-10	1971	The loss of cytochrome P-450 as well as the loss of microsomal haem and the discoloration of the microsomal fraction were more intense in animals pretreated with phenobarbitone and were much less evident when compound SKF 525-A (2-diethylaminoethyl 3,3-diphenylpropylacetate) was given before 2-allyl-2-isopropylacetamide, suggesting that the activity of the drug-metabolizing enzymes may be involved in these effects.	Phenobarbital	162-176	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	12-28
5117524-0	1971	A comparison of some properties of microsomal cytochrome P-450 from normal, methylcholanthrene-, and phenobarbital-treated rats.	Phenobarbital	101-114	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	46-62
5123890-0	1971	A requirement for dietary lipids for induction of cytochrome P-450 by phenobarbitone in rat liver microsomal fraction.	Phenobarbital	70-84	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	50-66
4322719-10	1971	Cytochrome P 450 was not decreased after a 3 wk exposure to the deficient diet and responded normally to phenobarbital treatment with a fourfold increase in total hepatic content; its concentration was depressed only after 8 wk of exposure to the deficient diet.	Phenobarbital	105-118	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
5547730-1	1971	Aryl hydrocarbon hydroxylase induction by phenobarbital, polycyclic hydrocarbons, and the insecticide, 2.2-bis(p-chlorophenyl)-1,1,1-trichloroethane (p,p"-DDT), occurs in rat fetal liver cell cultures.	Phenobarbital	42-55	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-28
5166400-6	1971	Treatment with phenobarbitone significantly increased the cytochrome P-450 concentration, the activity of NADPH-cytochrome c reductase (EC 1.6.2.3) and the rates of metabolism of aniline, ethylmorphine and [2-(14)C]pentobarbitone.	Phenobarbital	15-29	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	58-74
5542700-5	1971	Specific activity of diglyceride acyltransferase, which catalyzes triglyceride biosynthesis, was increased to a degree comparable to the increase in specific activity found in the phenobarbital-induced drug-metabolizing enzyme which oxidatively demethylates aminopyrine.	Phenobarbital	180-193	diacylglycerol O-acyltransferase 1	Rattus norvegicus	21-48
5497719-1	1970	V. Independent formation of cytochromes P-450 and P1-450 in rats treated with phenobarbital and 3-methylcholanthrene simultaneously.	Phenobarbital	78-91	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	50-56
5552260-0	1971	Effect of methylcholanthrene or phenobarbital pretreatment of rabbits and rats on the extinction coefficient for cytochrome P-450.	Phenobarbital	32-45	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	113-129
5524091-0	1970	Depression of microsomal 5"-nucleotidase and cellular ribonucleases in rat liver after phenobarbital administration.	Phenobarbital	87-100	5' nucleotidase, ecto	Rattus norvegicus	25-40
5412508-0	1970	The influence of phenobarbital on the turnover of hepatic microsomal cytochrome b5 and cytochrome P-450 hemes in the rat.	Phenobarbital	17-30	cytochrome b5 type A	Rattus norvegicus	69-82
4314413-0	1970	Effect of fasting and of phenobarbital on the distribution and latency of glucose-6-phosphatase in microsomal sub-fractions of rat liver.	Phenobarbital	25-38	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	74-95
5414102-6	1970	Treatment with sodium phenobarbitone increased the total liver ATP and the total amount of ATP in the cell sap.	Phenobarbital	15-36	amyloid P component, serum	Rattus norvegicus	107-110
5349284-0	1969	Metyrapone interaction with hepatic microsomal cytochrome P-450 from rats treated with phenobarbital.	Phenobarbital	87-100	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	47-63
5313497-2	1970	Influence of phenobarbital and cholestasis on the activity of glucuronyl transferase and beta-glucuronidase in rat liver.	Phenobarbital	13-26	glucuronidase, beta	Rattus norvegicus	89-107
5345894-0	1969	Repeated derepression cycles of the glucuronolactone dehydrogenase and cytochrome P-450 in the rat liver induced by phenobarbitone administration.	Phenobarbital	116-130	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	71-87
5735794-0	1968	[Influence of pretreatment with phenobarbital on the methemoglobin-inducing activity of phenacetin].	Phenobarbital	32-45	hemoglobin subunit gamma 2	Homo sapiens	53-66
4306789-11	1969	The phenobarbital-induced increase in the phospholipid and cytochrome P-450 content of the microsomes, as well as in the activities of microsomal reduced nicotinamide-adenine dinucleotide phosphate-cytochrome c reductase and N-demethylase, was correlated with the morphometric data on the endoplasmic reticulum.	Phenobarbital	4-17	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	59-75
5637103-0	1968	The stimulation of liver growth and demethylase activity following phenobarbital treatment.	Phenobarbital	67-80	methyl-CpG binding domain protein 2	Homo sapiens	36-47
5688265-0	1968	Effect of partial hepatectomy of the responsiveness of microsomal enzymes and cytochrome P-450 to phenobarbital or 3-methylcholanthrene.	Phenobarbital	98-111	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	78-94
5653209-8	1968	Rats pretreated with phenobarbital at a dose level of 60 mg/kg with induction of cytochrome P-450 synthesis showed a minor increase in early labeling when glycine-2-(14)C but not when delta ALA-4-(14)C was used as precursor.	Phenobarbital	21-34	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	81-97
4296852-0	1967	Ultracytochemical changes of the glucose-6-phosphatase (D-glucose-6-phosphate phosphohydrolase) activity in liver cells of the rat treated with phenobarbital.	Phenobarbital	144-157	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	33-54
6040440-0	1967	Potentiation by phenobarbital of the protection afforded by atropine and 2-PAM against parathion poisoning in rats.	Phenobarbital	16-29	peptidylglycine alpha-amidating monooxygenase	Rattus norvegicus	75-78
19866699-0	1966	On the relationship of liver glucose-6-phosphatase to the proliferation of endoplasmic reticulum in phenobarbital induction.	Phenobarbital	100-113	glucose-6-phosphatase catalytic subunit 1	Homo sapiens	29-50
19866699-3	1966	Biochemically and histochemically demonstrable glucose-6-phosphatase activity was found to be present in all endoplasmic reticulum membranes, including the phenobarbital-induced smooth-surfaced proliferates, even though there was an over-all decrease in activity.	Phenobarbital	156-169	glucose-6-phosphatase catalytic subunit 1	Homo sapiens	47-68
13899140-0	1961	[A study of C-14 labelled phenobarbital in the body of the rat.	Phenobarbital	26-39	anti-Mullerian hormone receptor type 2	Rattus norvegicus	12-16
13526705-0	1958	Effect of phenobarbitone on the requirement of Lactobacillus leichmannil for vitamin B12.	Phenobarbital	10-24	NADH:ubiquinone oxidoreductase subunit B3	Homo sapiens	85-88
20253390-0	1947	The effect of phenobarbital on the action of insulin.	Phenobarbital	14-27	insulin	Homo sapiens	45-52
34007308-9	2021	In addition, luminal A and human epidermal growth factor receptor 2 (HER2)-enriched breast cancer tissues expressed lower levels of ING3 compared with normal breast tissues.	Phenobarbital	13-20	inhibitor of growth family member 3	Homo sapiens	132-136
1133769-5	1975	The incorporation of 14-C(U)-L-leucine into 9000 x g liver supernatant fraction protein was decreased in phenobarbital-pretreated rats when measured immediately following or 24 hours after inhalation of CCl4.	Phenobarbital	105-118	C-C motif chemokine ligand 4	Rattus norvegicus	203-207
1133769-7	1975	The centrolobular hepatocytes of phenobarbital-pretreated rats exposed to CCl4 showed dilation and vesiculation of cisternae of the rough endoplasmic reticulum and striking changes in the nuclear double membrane.	Phenobarbital	33-46	C-C motif chemokine ligand 4	Rattus norvegicus	74-78
33894309-2	2021	We have previously shown that activation and nuclear accumulation of MRTFA mediate endocrine resistance of estrogen receptor alpha (ERalpha) positive breast cancers by initiating a partial transition from luminal to basal-like phenotype and impairing ERalpha cistrome and transcriptome.	Phenobarbital	205-212	myocardin related transcription factor A	Homo sapiens	69-74
33894672-5	2021	This system expresses a chimeric protein containing a synthetic transcription factor followed by the transmembrane domain and C-terminal luminal domain of ATF6beta.	Phenobarbital	137-144	activating transcription factor 6	Homo sapiens	155-163
33894309-2	2021	We have previously shown that activation and nuclear accumulation of MRTFA mediate endocrine resistance of estrogen receptor alpha (ERalpha) positive breast cancers by initiating a partial transition from luminal to basal-like phenotype and impairing ERalpha cistrome and transcriptome.	Phenobarbital	205-212	estrogen receptor 1	Homo sapiens	107-130
33894309-2	2021	We have previously shown that activation and nuclear accumulation of MRTFA mediate endocrine resistance of estrogen receptor alpha (ERalpha) positive breast cancers by initiating a partial transition from luminal to basal-like phenotype and impairing ERalpha cistrome and transcriptome.	Phenobarbital	205-212	estrogen receptor 1	Homo sapiens	132-139
33104865-14	2021	The luminal concentrations reported would allow modulation of the homeostatic control of food intake via activation of GPR119 receptors located on the gastro-intestinal mucosa.	Phenobarbital	4-11	G protein-coupled receptor 119	Homo sapiens	119-125
34056976-6	2021	In 16/50 (32%) primary mammary carcinomas and 6/15 (40%) metastases of mammary carcinomas, cytoplasmic nestin expression was detected in luminal epithelial cells.	Phenobarbital	137-144	nestin	Canis lupus familiaris	103-109
33531207-5	2021	The Hrd1 complex, mediating the retrotranslocation of misfolded proteins from the endoplasmic reticulum (ER) lumen into the cytosol, contains multispanning proteins with aqueous luminal and cytosolic cavities, and lateral gates juxtaposed in a thinned membrane region.	Phenobarbital	178-185	synoviolin 1	Homo sapiens	4-8
33819746-1	2021	In the initial stages of atherosclerosis, vascular adhesion molecule-1 (VCAM-1) is a surface protein that mediates leukocyte adhesion to the endothelium"s luminal surface.	Phenobarbital	155-162	vascular cell adhesion molecule 1	Homo sapiens	42-70
33994513-0	2021	FABP5 Is a Sensitive Marker for Lipid-Rich Macrophages in the Luminal Side of Atherosclerotic Lesions.	Phenobarbital	62-69	fatty acid binding protein 5, epidermal	Mus musculus	0-5
33994513-11	2021	These findings, along with previous reports, suggest a novel notion that FABP5 is a sensitive marker for bone marrow-derived lipid-rich macrophages in the luminal side of atherosclerotic lesions, although its functional significance remains elusive.	Phenobarbital	155-162	fatty acid binding protein 5, epidermal	Mus musculus	73-78
33819746-1	2021	In the initial stages of atherosclerosis, vascular adhesion molecule-1 (VCAM-1) is a surface protein that mediates leukocyte adhesion to the endothelium"s luminal surface.	Phenobarbital	155-162	vascular cell adhesion molecule 1	Homo sapiens	72-78
34043149-7	2021	Upregulation of DUXAP8 and FOXD2-AS1 was significantly associated with progesterone receptor-positive (PR+) and p53 protein expression in luminal BC patients, respectively.	Phenobarbital	138-145	double homeobox A pseudogene 8	Homo sapiens	16-22
34057115-11	2021	GATA-3 positive breast cancer showed luminal differentiation characterized by high ER expression and mainly was classified as luminal A type tumor with a better prognosis.	Phenobarbital	37-44	GATA binding protein 3	Homo sapiens	0-6
34057115-11	2021	GATA-3 positive breast cancer showed luminal differentiation characterized by high ER expression and mainly was classified as luminal A type tumor with a better prognosis.	Phenobarbital	37-44	epiregulin	Homo sapiens	83-85
34043149-7	2021	Upregulation of DUXAP8 and FOXD2-AS1 was significantly associated with progesterone receptor-positive (PR+) and p53 protein expression in luminal BC patients, respectively.	Phenobarbital	138-145	forkhead box D2	Homo sapiens	27-32
34057115-11	2021	GATA-3 positive breast cancer showed luminal differentiation characterized by high ER expression and mainly was classified as luminal A type tumor with a better prognosis.	Phenobarbital	126-133	GATA binding protein 3	Homo sapiens	0-6
34043149-7	2021	Upregulation of DUXAP8 and FOXD2-AS1 was significantly associated with progesterone receptor-positive (PR+) and p53 protein expression in luminal BC patients, respectively.	Phenobarbital	138-145	prostaglandin D2 receptor	Homo sapiens	33-36
34043149-7	2021	Upregulation of DUXAP8 and FOXD2-AS1 was significantly associated with progesterone receptor-positive (PR+) and p53 protein expression in luminal BC patients, respectively.	Phenobarbital	138-145	progesterone receptor	Homo sapiens	71-92
34043149-7	2021	Upregulation of DUXAP8 and FOXD2-AS1 was significantly associated with progesterone receptor-positive (PR+) and p53 protein expression in luminal BC patients, respectively.	Phenobarbital	138-145	transmembrane protein 37	Homo sapiens	103-106
34043149-7	2021	Upregulation of DUXAP8 and FOXD2-AS1 was significantly associated with progesterone receptor-positive (PR+) and p53 protein expression in luminal BC patients, respectively.	Phenobarbital	138-145	tumor protein p53	Homo sapiens	112-115
34043149-8	2021	Based on bioinformatic analyses, DUXAP8 can be considered as a prognostic biomarker for patients with luminal BC.	Phenobarbital	102-109	double homeobox A pseudogene 8	Homo sapiens	33-39
34043149-11	2021	In conclusion, dysregulation of DUXAP8, LINC00963, and FOXD2-AS1 can play roles in the development of luminal BC.	Phenobarbital	102-109	double homeobox A pseudogene 8	Homo sapiens	32-38
34043149-11	2021	In conclusion, dysregulation of DUXAP8, LINC00963, and FOXD2-AS1 can play roles in the development of luminal BC.	Phenobarbital	102-109	long intergenic non-protein coding RNA 963	Homo sapiens	40-49
34043149-11	2021	In conclusion, dysregulation of DUXAP8, LINC00963, and FOXD2-AS1 can play roles in the development of luminal BC.	Phenobarbital	102-109	forkhead box D2	Homo sapiens	55-60
34043149-11	2021	In conclusion, dysregulation of DUXAP8, LINC00963, and FOXD2-AS1 can play roles in the development of luminal BC.	Phenobarbital	102-109	prostaglandin D2 receptor	Homo sapiens	61-64
34036331-12	2021	CONCLUSIONS: Oral administration of omega-3 PUFAs leads to increased luminal omega-3 PUFA concentrations and changes to the microbiome, in the ileum of individuals with a temporary ileostomy.	Phenobarbital	69-76	pumilio RNA binding family member 3	Homo sapiens	44-48
34034728-10	2021	VDR expression was absent in HER2-overexpression tumours and low in luminal A and B molecular subtypes.	Phenobarbital	68-75	vitamin D receptor	Canis lupus familiaris	0-3
34019628-12	2021	CONCLUSION: SATB2 plays a vital role in maintaining intestinal homeostasis and its deficiency promotes the development of colitis and CAC by influencing the intestinal luminal environment and gut flora.	Phenobarbital	168-175	special AT-rich sequence binding protein 2	Mus musculus	12-17
34023861-9	2021	The underlying mechanism of these phenotypes seems to be a specific reduction of the tumor suppressor TAp63 isoform in p63+/- luminal cells, including PIMECs, with concomitant aberrant upregulation of the oncogenic DeltaNp63 isoform, as determined by qRT-PCR and scRNA-seq analyses.	Phenobarbital	126-133	tumor protein p63	Homo sapiens	104-107
34052673-2	2021	Alpha Tubulin Acetyltransferase 1 (ATAT1) is a major enzyme that acetylates "Lys-40" in alpha-tubulin on the luminal side of microtubules and is a drug target that lacks inhibitors.	Phenobarbital	109-116	alpha tubulin acetyltransferase 1	Homo sapiens	0-33
34052673-2	2021	Alpha Tubulin Acetyltransferase 1 (ATAT1) is a major enzyme that acetylates "Lys-40" in alpha-tubulin on the luminal side of microtubules and is a drug target that lacks inhibitors.	Phenobarbital	109-116	alpha tubulin acetyltransferase 1	Homo sapiens	35-40
34006834-6	2021	In this study, we found that Notch3 and PTEN levels correlated with the luminal phenotype in breast cancer cell lines.	Phenobarbital	72-79	notch receptor 3	Homo sapiens	29-35
34052673-2	2021	Alpha Tubulin Acetyltransferase 1 (ATAT1) is a major enzyme that acetylates "Lys-40" in alpha-tubulin on the luminal side of microtubules and is a drug target that lacks inhibitors.	Phenobarbital	109-116	tubulin alpha 1b	Homo sapiens	88-101
34023783-3	2021	Here, we discovered that Par3 down-regulation was associated with shorter relapse-free survival in Luminal A subtype of breast cancer.	Phenobarbital	99-106	par-3 family cell polarity regulator	Homo sapiens	25-29
34006834-6	2021	In this study, we found that Notch3 and PTEN levels correlated with the luminal phenotype in breast cancer cell lines.	Phenobarbital	72-79	phosphatase and tensin homolog	Homo sapiens	40-44
34000298-3	2021	It is known that, upon sensing unfolded proteins via its ER luminal domain, IRE1alpha dimerizes and then oligomerizes (often visualized as clustering).	Phenobarbital	60-67	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	76-85
33727227-5	2021	The aberrant luminal progenitor cells with impaired differentiation were significantly increased in normal breast tissues in BRCA1 mutation carriers compared with non-carriers.	Phenobarbital	13-20	BRCA1 DNA repair associated	Homo sapiens	125-130
33727227-7	2021	These data suggest that the cell of origin of basal-like breast tumors (ERneg) in BRCA1 mutation carriers might be luminal progenitor cells.	Phenobarbital	115-122	BRCA1 DNA repair associated	Homo sapiens	82-87
33727227-8	2021	The expression of TP53 and BRCA1 was decreased in luminal progenitor cells from normal breast tissue in BRCA1 mutation carriers, which might trigger the basal/mesenchymal transition of luminal progenitors and might result in basal-like tumor development.	Phenobarbital	50-57	tumor protein p53	Homo sapiens	18-22
33727227-8	2021	The expression of TP53 and BRCA1 was decreased in luminal progenitor cells from normal breast tissue in BRCA1 mutation carriers, which might trigger the basal/mesenchymal transition of luminal progenitors and might result in basal-like tumor development.	Phenobarbital	50-57	BRCA1 DNA repair associated	Homo sapiens	27-32
33727227-8	2021	The expression of TP53 and BRCA1 was decreased in luminal progenitor cells from normal breast tissue in BRCA1 mutation carriers, which might trigger the basal/mesenchymal transition of luminal progenitors and might result in basal-like tumor development.	Phenobarbital	50-57	BRCA1 DNA repair associated	Homo sapiens	104-109
33727227-8	2021	The expression of TP53 and BRCA1 was decreased in luminal progenitor cells from normal breast tissue in BRCA1 mutation carriers, which might trigger the basal/mesenchymal transition of luminal progenitors and might result in basal-like tumor development.	Phenobarbital	185-192	tumor protein p53	Homo sapiens	18-22
33727227-8	2021	The expression of TP53 and BRCA1 was decreased in luminal progenitor cells from normal breast tissue in BRCA1 mutation carriers, which might trigger the basal/mesenchymal transition of luminal progenitors and might result in basal-like tumor development.	Phenobarbital	185-192	BRCA1 DNA repair associated	Homo sapiens	27-32
33727227-8	2021	The expression of TP53 and BRCA1 was decreased in luminal progenitor cells from normal breast tissue in BRCA1 mutation carriers, which might trigger the basal/mesenchymal transition of luminal progenitors and might result in basal-like tumor development.	Phenobarbital	185-192	BRCA1 DNA repair associated	Homo sapiens	104-109
33985378-5	2021	Grhl2 protein signals were detected in both the mammary luminal epithelial and myoepithelial nuclei.	Phenobarbital	56-63	grainyhead like transcription factor 2	Mus musculus	0-5
33985378-9	2021	These results suggest that Grhl2 expressed in the luminal epithelial and myoepithelial cells from the early phase of ductal development, controlling the expression of cell adhesion molecules to establish functional ducts.	Phenobarbital	50-57	grainyhead like transcription factor 2	Mus musculus	27-32
33693689-12	2021	In anesthetized rats, luminal meal + CaCl2 induced a 4-fold higher increase in plasma PYY than the control treatment did.	Phenobarbital	22-29	peptide YY	Rattus norvegicus	86-89
34055036-10	2021	Furthermore, our analysis demonstrated that CEP55 was remarkably upregulated in the advanced stage of breast cancer compared to the stage I breast cancer sample and was significantly upregulated in triple-negative breast cancers (TNBC) compared to other types of breast cancers, including luminal and HER2-positive cancers, demonstrating CEP55 may have a regulatory role in TNBC.	Phenobarbital	289-296	centrosomal protein 55	Homo sapiens	44-49
33857420-3	2021	Binding of sGAGs promoted STING polymerization through luminal, positively charged, polar residues.	Phenobarbital	55-62	stimulator of interferon response cGAMP interactor 1	Mus musculus	26-31
34054952-10	2021	A significant correlation between high Ki-67 reduction and luminal B HER-2-negative subtype was observed (p = 0,0035).	Phenobarbital	59-66	erb-b2 receptor tyrosine kinase 2	Homo sapiens	69-74
33963374-9	2021	Low PD-L1 expression was associated with human epidermal growth factor receptor 2 (OR 3.98, 1.81 to 8.75; P < 0.001; I2 = 96 per cent) and luminal (OR 14.93, 6.46 to 34.51; P < 0.001; I2 = 99 per cent) breast cancer subtypes.	Phenobarbital	139-146	CD274 molecule	Homo sapiens	4-9
33296665-2	2021	Recently, SLC38A9, a lysosomal amino acid transporter, emerged as a sensor for luminal arginine and as an activator of mTORC1.	Phenobarbital	79-86	solute carrier family 38 member 9	Danio rerio	10-17
33296665-6	2021	We propose a ball-and-chain model for mTORC1 activation, where N-plug insertion and Rag GTPase binding with SLC38A9 is regulated by luminal arginine levels.	Phenobarbital	132-139	CREB regulated transcription coactivator 1	Mus musculus	38-44
33296665-6	2021	We propose a ball-and-chain model for mTORC1 activation, where N-plug insertion and Rag GTPase binding with SLC38A9 is regulated by luminal arginine levels.	Phenobarbital	132-139	solute carrier family 38 member 9	Danio rerio	108-115
33484965-3	2021	We identified two "scaffold" proteins, PTGFRN and BASP1, that are preferentially sorted into EVs and enable high-density surface display and luminal loading of a wide range of molecules including cytokines, antibody fragments, RNA binding proteins, vaccine antigens, Cas9, and members of the TNF superfamily.	Phenobarbital	141-148	prostaglandin F2 receptor inhibitor	Homo sapiens	39-45
33484965-3	2021	We identified two "scaffold" proteins, PTGFRN and BASP1, that are preferentially sorted into EVs and enable high-density surface display and luminal loading of a wide range of molecules including cytokines, antibody fragments, RNA binding proteins, vaccine antigens, Cas9, and members of the TNF superfamily.	Phenobarbital	141-148	brain abundant membrane attached signal protein 1	Homo sapiens	50-55
33903236-3	2021	The loss of Crb3 in adult luminal airway epithelium promotes the uncontrolled activation of the transcriptional regulators YAP and TAZ, which stimulate intrinsic signals that promote epithelial cell plasticity and paracrine signals that induce basal-like cell growth.	Phenobarbital	26-33	crumbs cell polarity complex component 3	Homo sapiens	12-16
33963042-1	2022	OBJECTIVE: Although immunoglobulin A (IgA) is abundantly expressed in the gut and known to be an important component of mucosal barriers against luminal pathogens, its precise function remains unclear.	Phenobarbital	145-152	immunoglobulin heavy constant alpha	Mus musculus	20-36
33963042-1	2022	OBJECTIVE: Although immunoglobulin A (IgA) is abundantly expressed in the gut and known to be an important component of mucosal barriers against luminal pathogens, its precise function remains unclear.	Phenobarbital	145-152	immunoglobulin heavy constant alpha	Mus musculus	38-41
33954907-0	2021	Hyaluronan synthase 2 (HAS2) regulates cell phenotype and invadopodia formation in luminal-like breast cancer cells.	Phenobarbital	83-90	hyaluronan synthase 2	Mus musculus	0-21
33954907-0	2021	Hyaluronan synthase 2 (HAS2) regulates cell phenotype and invadopodia formation in luminal-like breast cancer cells.	Phenobarbital	83-90	hyaluronan synthase 2	Mus musculus	23-27
33616774-9	2021	Copy number increase was found within all molecular subtypes except the 5 negative phenotype and the Luminal B (HER2 +) subtype.	Phenobarbital	101-108	erb-b2 receptor tyrosine kinase 2	Homo sapiens	112-116
33747161-8	2021	It was found that TRPA1 expression was concentrated to the luminal surface of the colon in the heat exposed group compared with that in the control group.	Phenobarbital	59-66	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	18-23
34003256-4	2021	Here, we use a CRE-activated HER2 orthologue to specifically target HER2/ERBB2 oncogenic activity to basal or luminal ER- mammary epithelial cells and perform a detailed analysis of the tumours that develop.	Phenobarbital	110-117	erb-b2 receptor tyrosine kinase 2	Mus musculus	29-33
34003256-4	2021	Here, we use a CRE-activated HER2 orthologue to specifically target HER2/ERBB2 oncogenic activity to basal or luminal ER- mammary epithelial cells and perform a detailed analysis of the tumours that develop.	Phenobarbital	110-117	erb-b2 receptor tyrosine kinase 2	Mus musculus	68-72
34003256-4	2021	Here, we use a CRE-activated HER2 orthologue to specifically target HER2/ERBB2 oncogenic activity to basal or luminal ER- mammary epithelial cells and perform a detailed analysis of the tumours that develop.	Phenobarbital	110-117	erb-b2 receptor tyrosine kinase 2	Mus musculus	73-78
33382535-10	2021	DNA methylation profiling identified aberrant hypermethylation of CpG sites within GATA3, a key transcription factor required for luminal differentiation.	Phenobarbital	130-137	GATA binding protein 3	Homo sapiens	83-88
33465373-6	2021	Lineage tracing revealed that Axin2-expressing periampullary PBG cells are capable of self-renewal and supplying new biliary epithelial cells (BECs) to the luminal surface.	Phenobarbital	156-163	axin 2	Mus musculus	30-35
33846571-0	2021	Aberrant CREB1 activation in prostate cancer disrupts normal prostate luminal cell differentiation.	Phenobarbital	70-77	cAMP responsive element binding protein 1	Homo sapiens	9-14
33846571-2	2021	Using RNA-Seq analysis, we discovered that CREB1 plays a central role in maintaining new luminal cell survival and that oncogenesis dramatically changes the CREB1-induced transcriptome.	Phenobarbital	89-96	cAMP responsive element binding protein 1	Homo sapiens	43-48
33846571-3	2021	CREB1 is active in luminal cells, but not basal cells.	Phenobarbital	19-26	cAMP responsive element binding protein 1	Homo sapiens	0-5
33846571-4	2021	We identified ING4 and its E3 ligase, JFK, as CREB1 transcriptional targets in luminal cells.	Phenobarbital	79-86	inhibitor of growth family member 4	Homo sapiens	14-18
33846571-4	2021	We identified ING4 and its E3 ligase, JFK, as CREB1 transcriptional targets in luminal cells.	Phenobarbital	79-86	F-box protein 42	Homo sapiens	38-41
33846571-4	2021	We identified ING4 and its E3 ligase, JFK, as CREB1 transcriptional targets in luminal cells.	Phenobarbital	79-86	cAMP responsive element binding protein 1	Homo sapiens	46-51
33846571-5	2021	During luminal cell differentiation, transient induction of ING4 expression is followed by a peak in CREB1 activity, while JFK increases concomitantly with CREB1 activation.	Phenobarbital	7-14	inhibitor of growth family member 4	Homo sapiens	60-64
33846571-5	2021	During luminal cell differentiation, transient induction of ING4 expression is followed by a peak in CREB1 activity, while JFK increases concomitantly with CREB1 activation.	Phenobarbital	7-14	cAMP responsive element binding protein 1	Homo sapiens	156-161
33846571-6	2021	Transient expression of ING4 is required for luminal cell induction; however, failure to properly down-regulate ING4 leads to luminal cell death.	Phenobarbital	45-52	inhibitor of growth family member 4	Homo sapiens	24-28
33846571-7	2021	Consequently, blocking CREB1 increased ING4 expression, suppressed JFK, and led to luminal cell death.	Phenobarbital	83-90	cAMP responsive element binding protein 1	Homo sapiens	23-28
33846571-11	2021	Blocking CREB1 in tumorigenic cells suppressed tumor growth in vivo, rescued ING4 expression, and restored luminal cell formation, but ultimately induced luminal cell death.	Phenobarbital	107-114	cAMP responsive element binding protein 1	Homo sapiens	9-14
33846571-11	2021	Blocking CREB1 in tumorigenic cells suppressed tumor growth in vivo, rescued ING4 expression, and restored luminal cell formation, but ultimately induced luminal cell death.	Phenobarbital	154-161	cAMP responsive element binding protein 1	Homo sapiens	9-14
33846571-13	2021	This is the first study to define a molecular mechanism whereby oncogenic loss of PTEN, leading to aberrant CREB1 activation, suppresses ING4 expression causing disruption of luminal cell differentiation.	Phenobarbital	175-182	cAMP responsive element binding protein 1	Homo sapiens	108-113
33846571-13	2021	This is the first study to define a molecular mechanism whereby oncogenic loss of PTEN, leading to aberrant CREB1 activation, suppresses ING4 expression causing disruption of luminal cell differentiation.	Phenobarbital	175-182	inhibitor of growth family member 4	Homo sapiens	137-141
33939141-7	2021	RESULTS: Cytoplasmic CAII expression was predominantly detected in the upper luminal part of the squamous epithelium and was significantly (p < 0.01) increased in GERD.	Phenobarbital	77-84	carbonic anhydrase 2	Homo sapiens	21-25
33911165-11	2021	IM and dDAVP increased the intracellular cAMP levels and caused the AQP2 molecule to localize to the collecting duct cells" luminal side.	Phenobarbital	124-131	aquaporin 2	Rattus norvegicus	68-72
33926547-2	2021	METHODS: In the current study, we investigated TNF-alpha modulated mitochondrial proteome using high-resolution mass spectrometry and identified the differentially expressed proteins in two different breast cancer cell lines, ER/PR positive cell line; luminal, MCF-7 and ER/PR negative cell line; basal-like, MDA-MB-231 and explored its implication in regulating the tumorigenic potential of breast cancer cells.	Phenobarbital	252-259	tumor necrosis factor	Homo sapiens	47-56
33909026-0	2021	Polypeptide N-acetylgalactosaminyltransferase 18 Retains in Endoplasmic Reticulum Depending on its Luminal Regions Interacting with ER resident UGGT1, PLOD3 and LPCAT1.	Phenobarbital	99-106	UDP-glucose glycoprotein glucosyltransferase 1	Homo sapiens	144-149
33909026-0	2021	Polypeptide N-acetylgalactosaminyltransferase 18 Retains in Endoplasmic Reticulum Depending on its Luminal Regions Interacting with ER resident UGGT1, PLOD3 and LPCAT1.	Phenobarbital	99-106	procollagen-lysine,2-oxoglutarate 5-dioxygenase 3	Homo sapiens	151-156
33909026-0	2021	Polypeptide N-acetylgalactosaminyltransferase 18 Retains in Endoplasmic Reticulum Depending on its Luminal Regions Interacting with ER resident UGGT1, PLOD3 and LPCAT1.	Phenobarbital	99-106	lysophosphatidylcholine acyltransferase 1	Homo sapiens	161-167
33909026-6	2021	Results from co-immunoprecipitation assays showed that the luminal region interacts with ER resident proteins UGGT1, PLOD3 and LPCAT1.	Phenobarbital	59-66	UDP-glucose glycoprotein glucosyltransferase 1	Homo sapiens	110-115
33909026-6	2021	Results from co-immunoprecipitation assays showed that the luminal region interacts with ER resident proteins UGGT1, PLOD3 and LPCAT1.	Phenobarbital	59-66	procollagen-lysine,2-oxoglutarate 5-dioxygenase 3	Homo sapiens	117-122
33909026-6	2021	Results from co-immunoprecipitation assays showed that the luminal region interacts with ER resident proteins UGGT1, PLOD3 and LPCAT1.	Phenobarbital	59-66	lysophosphatidylcholine acyltransferase 1	Homo sapiens	127-133
33909826-7	2021	The luminal immunohistochemical subtype (CK5 negative and CK20 positive, or CK5 negative and GATA3 positive) was associated with micropapillary and plasmacytoid variants.	Phenobarbital	4-11	keratin 5	Homo sapiens	41-44
33909826-7	2021	The luminal immunohistochemical subtype (CK5 negative and CK20 positive, or CK5 negative and GATA3 positive) was associated with micropapillary and plasmacytoid variants.	Phenobarbital	4-11	keratin 20	Homo sapiens	58-62
33909826-7	2021	The luminal immunohistochemical subtype (CK5 negative and CK20 positive, or CK5 negative and GATA3 positive) was associated with micropapillary and plasmacytoid variants.	Phenobarbital	4-11	keratin 5	Homo sapiens	76-79
33909826-7	2021	The luminal immunohistochemical subtype (CK5 negative and CK20 positive, or CK5 negative and GATA3 positive) was associated with micropapillary and plasmacytoid variants.	Phenobarbital	4-11	GATA binding protein 3	Homo sapiens	93-98
33903734-12	2021	Luminal A and AVPC-M predicted to be resistant to docetaxel and have high PSA/PAP Ratio.	Phenobarbital	0-7	poly(A) polymerase alpha	Homo sapiens	78-81
33903882-5	2021	The XBP1 protein was mainly detected in the luminal and glandular epithelia on days 1-4 of pregnancy, and was strongly detected in the decidual area on days 5-8 of pregnancy.	Phenobarbital	44-51	X-box binding protein 1	Mus musculus	4-8
33903882-8	2021	In the ovariectomized uterus, the expression of XBP1 in luminal and glandular epithelia was up-regulated after estrogen treatment.	Phenobarbital	56-63	X-box binding protein 1	Mus musculus	48-52
33903882-9	2021	These results suggest that XBP1 is associated with embryo implantation and decidualization during early pregnancy in mice, and the expression of XBP1 in luminal and glandular epithelia may be regulated by estrogen.	Phenobarbital	153-160	X-box binding protein 1	Mus musculus	145-149
33574090-4	2021	Interfering with YAP activity delayed basal-like cancer formation, prevented luminal to basal trans-differentiation, and reduced CSC.	Phenobarbital	77-84	Yes1 associated transcriptional regulator	Homo sapiens	17-20
33913090-8	2021	Moreover, here we present new pseudo-temporal trajectories of MEC populations at two resolution levels, that is either considering all mammary cell subtypes or focusing specifically on the luminal lineages.	Phenobarbital	189-196	chemokine (C-C motif) ligand 28	Mus musculus	62-65
33919281-6	2021	While 64.3% of CHEK2 tumors were luminal A-like, 56.2% of ATM tumors were luminal B-like/HER2-negative.	Phenobarbital	74-81	ATM serine/threonine kinase	Homo sapiens	58-61
33863895-5	2021	The PsbS response mechanism at low pH involves the concerted action of repositioning of a short amphipathic helix containing E176 facing the lumen and folding of the luminal loop fragment adjacent to E71 to a 310-helix, providing clear evidence of a conformational pH switch.	Phenobarbital	166-173	PSBS	Physcomitrella patens	4-8
33434267-11	2021	Last but not least, FoxO1 seems to act like a navigator molecule for embryo homing owing to its notably decreased nuclear expression in endometrial luminal epithelial cells, specifically at the blastocyst attachment region, which results in differentiation, entosis and apoptosis of endometrial epithelial cells during the peri-implantation period.	Phenobarbital	148-155	forkhead box O1	Mus musculus	20-25
33919875-7	2021	The number of CD1a+ DCs in both locations was the highest in luminal B/HER2+ cancers.	Phenobarbital	61-68	CD1a molecule	Homo sapiens	14-18
33858483-2	2021	Transcriptionally, FOXA1, GATA3, and PPARG are shown to be essential for luminal subtype-specific gene regulation and subtype switching, while TP63, STAT3, and TFAP2 family members are critical for regulation of basal subtype-specific genes.	Phenobarbital	73-80	forkhead box A1	Homo sapiens	19-24
33858483-2	2021	Transcriptionally, FOXA1, GATA3, and PPARG are shown to be essential for luminal subtype-specific gene regulation and subtype switching, while TP63, STAT3, and TFAP2 family members are critical for regulation of basal subtype-specific genes.	Phenobarbital	73-80	GATA binding protein 3	Homo sapiens	26-31
33858483-2	2021	Transcriptionally, FOXA1, GATA3, and PPARG are shown to be essential for luminal subtype-specific gene regulation and subtype switching, while TP63, STAT3, and TFAP2 family members are critical for regulation of basal subtype-specific genes.	Phenobarbital	73-80	peroxisome proliferator activated receptor gamma	Homo sapiens	37-42
33858483-4	2021	RESULT: We determine the genome-wide transcriptome, enhancer landscape, and transcription factor binding profiles of FOXA1 and GATA3 in luminal and basal subtypes of bladder cancer.	Phenobarbital	136-143	forkhead box A1	Homo sapiens	117-122
33858483-4	2021	RESULT: We determine the genome-wide transcriptome, enhancer landscape, and transcription factor binding profiles of FOXA1 and GATA3 in luminal and basal subtypes of bladder cancer.	Phenobarbital	136-143	GATA binding protein 3	Homo sapiens	127-132
33858483-8	2021	CONCLUSION: In summary, our work identifies unique epigenomic signatures and 3D genome structures in luminal and basal urinary bladder cancers and suggests a novel link between the circadian transcription factor NPAS2 and a clinical bladder cancer subtype.	Phenobarbital	101-108	neuronal PAS domain protein 2	Homo sapiens	212-217
34007958-6	2021	Consequently, a differentiation bias toward luminal epithelial cell type was detected with loss of mature, alpha-SMA-expressing ME cells and reduced deposition of basement membrane protein laminin-5.	Phenobarbital	44-51	actin alpha 1, skeletal muscle	Homo sapiens	107-116
33919875-7	2021	The number of CD1a+ DCs in both locations was the highest in luminal B/HER2+ cancers.	Phenobarbital	61-68	erb-b2 receptor tyrosine kinase 2	Homo sapiens	71-75
33884288-0	2021	Alternative splicing of CERS2 promotes cell proliferation and migration in luminal B subtype breast cancer cells.	Phenobarbital	75-82	ceramide synthase 2	Homo sapiens	24-29
33869000-11	2021	Survival analysis suggested that CCT2 overexpression was independently associated with worse prognosis of patients with breast cancer, especially in luminal A subtype.	Phenobarbital	149-156	chaperonin containing TCP1 subunit 2	Homo sapiens	33-37
33837914-9	2022	For HER2-positive breast cancer, the copper content in saliva is 51.9% higher than for HER2-negative, a similar pattern was observed for luminal A and B breast cancer subtypes.	Phenobarbital	137-144	erb-b2 receptor tyrosine kinase 2	Homo sapiens	4-8
33920299-5	2021	Drawing attention to these studies, this review discusses the possible negative role of albumin as a drug carrier and the rationale for a new strategy for cancer therapy based on follicle-stimulating hormone receptor (FSHR) expressed on the luminal endothelial cell surface of peritumoral blood vessels associated with the major human cancers.	Phenobarbital	241-248	follicle stimulating hormone receptor	Homo sapiens	179-216
33920299-5	2021	Drawing attention to these studies, this review discusses the possible negative role of albumin as a drug carrier and the rationale for a new strategy for cancer therapy based on follicle-stimulating hormone receptor (FSHR) expressed on the luminal endothelial cell surface of peritumoral blood vessels associated with the major human cancers.	Phenobarbital	241-248	follicle stimulating hormone receptor	Homo sapiens	218-222
33830296-7	2021	PTGS2 immunopositivity was noted in foetal trophoblasts, luminal and superficial glandular epithelial cells, smooth muscle cells of both myometrial layers, and weakly and sporadically in deep uterine glands.	Phenobarbital	57-64	prostaglandin-endoperoxide synthase 2	Canis lupus familiaris	0-5
33830296-8	2021	PGFS was localized in luminal epithelial cells and in the epithelium of superficial uterine glands.	Phenobarbital	22-29	aldo-keto reductase family 1 member C21	Canis lupus familiaris	0-4
33827682-7	2021	In particular, CBP was more expressed in luminal A and B subtypes.	Phenobarbital	41-48	CREB binding protein	Homo sapiens	15-18
33827682-10	2021	Amplification of CREBBP gene was observed in luminal A, luminal B and triple-negative but not in HER2 overexpressing subtypes.	Phenobarbital	45-52	CREB binding protein	Homo sapiens	17-23
33827682-10	2021	Amplification of CREBBP gene was observed in luminal A, luminal B and triple-negative but not in HER2 overexpressing subtypes.	Phenobarbital	56-63	CREB binding protein	Homo sapiens	17-23
33917614-7	2021	The GC rs2282679 minor allele was significantly associated with luminal subtype of the primary tumor compared to Her2+/TN breast cancer (p = 0.007).	Phenobarbital	64-71	erb-b2 receptor tyrosine kinase 2	Homo sapiens	113-117
33656882-4	2021	Differences were observed in terms of the luminal concentration of triglycerides, monoglycerides, and fatty acids in the different TIM-1 compartments, indicating a reduction and delay in the lipolysis of formulation excipients in CD.	Phenobarbital	42-49	Rho guanine nucleotide exchange factor 5	Homo sapiens	131-136
33656882-7	2021	The dynamic luminal environment in CD and healthy conditions after administration of a lipid-based formulation can be simulated using the TIM-1 system.	Phenobarbital	12-19	Rho guanine nucleotide exchange factor 5	Homo sapiens	138-143
33533304-1	2021	Glucagon-like peptide-1 (GLP-1) is an incretin secreted from enteroendocrine preproglucagon-expressing (PPG)-cells (traditionally known as L-cells) in response to luminal nutrients that potentiates insulin secretion.	Phenobarbital	163-170	glucagon	Mus musculus	0-23
33326312-8	2021	Globally, in IBD animal models, apical KCa1.1 channels, responsible for luminal secretion, were upregulated.	Phenobarbital	72-79	potassium calcium-activated channel subfamily M alpha 1	Homo sapiens	39-45
33533304-1	2021	Glucagon-like peptide-1 (GLP-1) is an incretin secreted from enteroendocrine preproglucagon-expressing (PPG)-cells (traditionally known as L-cells) in response to luminal nutrients that potentiates insulin secretion.	Phenobarbital	163-170	glucagon	Mus musculus	25-30
33987436-10	2021	PC was not taken up by the cells but moved paracellularly via TJ to the apical side driven by luminal HCO3- generated by the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) and the anion exchange protein 2 (AE2).	Phenobarbital	94-101	cystic fibrosis transmembrane conductance regulator	Mus musculus	125-176
33987436-10	2021	PC was not taken up by the cells but moved paracellularly via TJ to the apical side driven by luminal HCO3- generated by the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) and the anion exchange protein 2 (AE2).	Phenobarbital	94-101	cystic fibrosis transmembrane conductance regulator	Mus musculus	178-182
33421534-7	2021	The trypanosome IP3R is stimulated by luminal phosphate and pyrophosphate, which are hydrolysis products of polyphosphate (polyP), and inhibited by tripolyphosphate (polyP3), which is the most abundant polyP in acidocalcisomes.	Phenobarbital	38-45	inositol 1,4,5-trisphosphate receptor type 3	Homo sapiens	16-20
33417085-5	2021	FOXA1, together with EP300 and RUNX1, regulates the expression of E-cadherin, and is expressed in luminal, but absent in triple-negative and basal-like breast cancers.	Phenobarbital	98-105	forkhead box A1	Homo sapiens	0-5
33631190-6	2021	Indeed, the SCFA GPCRs FFA2 (previously termed GPR43), FFA3 (previously termed GPR41), and GPR109A are now well established to be expressed within the GI tract, where they modulate a variety of functions in response to luminal SCFA.	Phenobarbital	219-226	free fatty acid receptor 2	Homo sapiens	47-52
33631190-6	2021	Indeed, the SCFA GPCRs FFA2 (previously termed GPR43), FFA3 (previously termed GPR41), and GPR109A are now well established to be expressed within the GI tract, where they modulate a variety of functions in response to luminal SCFA.	Phenobarbital	219-226	hydroxycarboxylic acid receptor 2	Homo sapiens	91-98
33417085-8	2021	RESULTS: Upon FOXA1 knockdown in luminal MCF-7 and T47D cells, we found an increase in doxorubicin and paclitaxel sensitivity as well as a decrease in anchorage independence.	Phenobarbital	33-40	forkhead box A1	Homo sapiens	14-19
33258158-3	2021	In a neonatal hypoxia-only model based on 11-day-old (P11) rats, the NKCC1 inhibitor bumetanide was reported to potentiate the antiseizure activity of phenobarbital, whereas it was ineffective in a human trial in neonates.	Phenobarbital	151-164	solute carrier family 12 member 2	Rattus norvegicus	69-74
33482317-10	2021	The additional utilization of Eudragit EPO for SNEDDS preparations of both complexes successfully maintained the high concentrations of rebamipide in the gastric luminal condition.	Phenobarbital	162-169	erythropoietin	Homo sapiens	39-42
33851617-10	2021	The results also emphasize FGFR1 correlation expression with distant metastasis in luminal B tumors (P = 0.035) but not with luminal A and with overexpressed HER2 protein in both luminal tumors.	Phenobarbital	83-90	fibroblast growth factor receptor 1	Homo sapiens	27-32
33280209-7	2021	We found a relationship between Luminal B with Her2(-) and LVI, basal like and LVI(p=0.00).	Phenobarbital	32-39	erb-b2 receptor tyrosine kinase 2	Homo sapiens	47-51
33851617-11	2021	FGFR1 expression affect luminal B patients survival with poor outcome.	Phenobarbital	24-31	fibroblast growth factor receptor 1	Homo sapiens	0-5
33400051-10	2021	Abundant expression (~ 48%) and luminal localization of ALDH1 precludes its use as a bovine MaSC marker but may include transamplifying progenitor cells.	Phenobarbital	32-39	aldehyde dehydrogenase 1 family member A1	Bos taurus	56-61
33687169-9	2021	Results: Uterine tissue on D4 showed strong expression of Flk-1/KDR in luminal and uterine glandular epithelium.	Phenobarbital	71-78	kinase insert domain protein receptor	Mus musculus	58-63
33687169-9	2021	Results: Uterine tissue on D4 showed strong expression of Flk-1/KDR in luminal and uterine glandular epithelium.	Phenobarbital	71-78	kinase insert domain protein receptor	Mus musculus	64-67
33400051-12	2021	Onset of lumen formation in mammary ducts of prepubertal gland was associated with Notch 3 expression in the apical surface of luminal cells.	Phenobarbital	127-134	notch receptor 3	Bos taurus	83-90
33448622-0	2021	Platelet alpha-Granule Cargo Packaging and Release are Affected by the Luminal Proteoglycan, Serglycin.	Phenobarbital	71-78	serglycin	Mus musculus	93-102
33976641-15	2021	Immunohistochemistry using D2-40 and CD31 antibodies showed irregular luminal proliferation at the anastomosis, infiltration into the surrounding tissue, and massive necrosis, thereby leading to the diagnosis of breast angiosarcoma.	Phenobarbital	70-77	platelet and endothelial cell adhesion molecule 1	Homo sapiens	37-41
34041004-6	2021	Results: Our immunohistochemical findings of fertile and busulfan-treated mice showed expression of DDX4 in the basal and luminal compartment of seminiferous tubules of fertile mice whereas no expression was detected in busulfan-treated mice.	Phenobarbital	122-129	DEAD box helicase 4	Mus musculus	100-104
34041004-7	2021	The immunohistochemical analysis of two human cases with different levels of non-obstructive azoospermia revealed more luminal DDX4 positive cells.	Phenobarbital	119-126	DEAD-box helicase 4	Homo sapiens	127-131
33955429-8	2021	Results: TRPM8 expression marks luminal epithelial cells in benign prostate tissue.	Phenobarbital	32-39	transient receptor potential cation channel subfamily M member 8	Homo sapiens	9-14
33563021-9	2021	CONCLUSIONS: Higher luminal concentrations of lipoprotein(a) in the aneurysm sac were significantly associated with increased wall enhancement of UIAs.	Phenobarbital	20-27	lipoprotein(a)	Homo sapiens	46-60
33011748-5	2021	Moreover, high mRNA level of TRPS1 was found in all four subtypes of breast carcinoma including ER/PR-positive luminal A and B types, HER2-positive type, and basal-type/TNBC.	Phenobarbital	111-118	transcriptional repressor GATA binding 1	Homo sapiens	29-34
33011748-5	2021	Moreover, high mRNA level of TRPS1 was found in all four subtypes of breast carcinoma including ER/PR-positive luminal A and B types, HER2-positive type, and basal-type/TNBC.	Phenobarbital	111-118	estrogen receptor 1	Homo sapiens	96-98
33011748-5	2021	Moreover, high mRNA level of TRPS1 was found in all four subtypes of breast carcinoma including ER/PR-positive luminal A and B types, HER2-positive type, and basal-type/TNBC.	Phenobarbital	111-118	transmembrane protein 37	Homo sapiens	99-101
33647867-7	2021	CD10 highlights the apical-luminal aspect of the cells.	Phenobarbital	27-34	membrane metalloendopeptidase	Homo sapiens	0-4
33841417-4	2021	In contrast, food allergy sensitive Il4ra F709 mice housed under standard temperature conditions translocated the luminal antigens in the SI across the epithelium via secretory antigen passages (SAPs).	Phenobarbital	114-121	interleukin 4 receptor, alpha	Mus musculus	36-41
33753561-3	2021	ZNF703 is located close to FGFR1 at 8p11-12 and is frequently expressed in the luminal B subtype of breast cancer.	Phenobarbital	79-86	zinc finger protein 703	Homo sapiens	0-6
33753865-11	2021	Our findings highlight that TN-ILC is a unique aggressive breast cancer associated with elderly age, which belong to the luminal androgen receptor subtype as determined by immunohistochemistry and transcriptomic profiling.	Phenobarbital	121-128	androgen receptor	Homo sapiens	129-146
33753561-3	2021	ZNF703 is located close to FGFR1 at 8p11-12 and is frequently expressed in the luminal B subtype of breast cancer.	Phenobarbital	79-86	fibroblast growth factor receptor 1	Homo sapiens	27-32
33431704-1	2021	The mucin Muc2 is a major constituent of the mucus layer that covers the intestinal epithelium and creates a barrier between epithelial cells and luminal commensal or pathogenic microorganisms.	Phenobarbital	146-153	mucin 2	Mus musculus	10-14
33739352-8	2021	The biological pathways observed for the HCG11 network are linked to the epithelial-to-mesenchymal transition; while NORAD associated pathways appear to be related to luminal epithelial cell transformation.	Phenobarbital	167-174	HLA complex group 11	Homo sapiens	41-46
33884281-0	2021	The helix-loop-helix transcriptional regulator Id4 is required for terminal differentiation of luminal epithelial cells in the prostate.	Phenobarbital	95-102	inhibitor of DNA binding 4	Mus musculus	47-50
33884281-11	2021	The results suggest that loss of Id4 maintains stem cell phenotype of "luminal committed basal cells", identifying a unique prostate developmental pathway regulated by Id4.	Phenobarbital	71-78	inhibitor of DNA binding 4	Mus musculus	33-36
33118597-6	2021	RESULTS: The phenotype of NVUC was classified as luminal from 60.1% (FOXA1+/CK5/6-) to 100% (GATA3+/CK14-) of cases using composite phenotypes.	Phenobarbital	49-56	forkhead box A1	Homo sapiens	69-74
33712056-9	2021	Immunohistochemically, the luminal epithelial configurations showed strong expression of CK7 along the luminal cell membrane, while the basal myoepithelia displayed strong nuclear p63 expression.	Phenobarbital	27-34	keratin 7	Homo sapiens	89-92
33472889-6	2021	For all tissues combined, hierarchical clustering of subtype gene expression revealed three subtypes: "luminal," "basal," and a "luminal p53-/ extracellular matrix (ECM)-like" phenotype of ECM-related genes enriched in tumor-associated urothelium, non-invasive urothelial lesions, and CIS, but rarely invasive carcinomas.	Phenobarbital	129-136	tumor protein p53	Homo sapiens	137-140
33472889-8	2021	A PanCancer Progression Panel of 681 genes unveiled pathways specific for the luminal p53-/ECM-like cluster, e.g., ECM remodeling, angiogenesis, epithelial to mesenchymal transition (EMT), cellular discohesion, cell motility involved in tumor progression; and cell proliferation and oncogenic ERBB2/ERBB3 signaling for invasive carcinomas.	Phenobarbital	78-85	tumor protein p53	Homo sapiens	86-89
33472889-8	2021	A PanCancer Progression Panel of 681 genes unveiled pathways specific for the luminal p53-/ECM-like cluster, e.g., ECM remodeling, angiogenesis, epithelial to mesenchymal transition (EMT), cellular discohesion, cell motility involved in tumor progression; and cell proliferation and oncogenic ERBB2/ERBB3 signaling for invasive carcinomas.	Phenobarbital	78-85	erb-b2 receptor tyrosine kinase 2	Homo sapiens	293-298
33472889-8	2021	A PanCancer Progression Panel of 681 genes unveiled pathways specific for the luminal p53-/ECM-like cluster, e.g., ECM remodeling, angiogenesis, epithelial to mesenchymal transition (EMT), cellular discohesion, cell motility involved in tumor progression; and cell proliferation and oncogenic ERBB2/ERBB3 signaling for invasive carcinomas.	Phenobarbital	78-85	erb-b2 receptor tyrosine kinase 3	Homo sapiens	299-304
32989468-2	2021	Slc26a3 (DRA), as a key chloride-bicarbonate exchanger protein in the intestinal epithelial luminal membrane, participates in the electroneutral NaCl absorption of intestine, together with Na+/H+ exchangers.	Phenobarbital	92-99	solute carrier family 26 member 3	Homo sapiens	0-7
32989468-2	2021	Slc26a3 (DRA), as a key chloride-bicarbonate exchanger protein in the intestinal epithelial luminal membrane, participates in the electroneutral NaCl absorption of intestine, together with Na+/H+ exchangers.	Phenobarbital	92-99	solute carrier family 26 member 3	Homo sapiens	9-12
33707576-0	2021	MAGI1 inhibits the AMOTL2/p38 stress pathway and prevents luminal breast tumorigenesis.	Phenobarbital	58-65	membrane associated guanylate kinase, WW and PDZ domain containing 1	Homo sapiens	0-5
33721012-7	2021	According to TCGA data, AQP4-AS1 is down-regulated in BC tissue, and the overexpression is associated with better prognoses, including Luminal A, HER2-, stage 1 of disease and smaller tumor.	Phenobarbital	135-142	aquaporin 4	Homo sapiens	24-28
33721012-7	2021	According to TCGA data, AQP4-AS1 is down-regulated in BC tissue, and the overexpression is associated with better prognoses, including Luminal A, HER2-, stage 1 of disease and smaller tumor.	Phenobarbital	135-142	prostaglandin D2 receptor	Homo sapiens	29-32
33707576-2	2021	We show here that the loss of the junctional scaffold protein MAGI1 is associated with bad prognosis in luminal BCa, and promotes tumorigenesis.	Phenobarbital	104-111	membrane associated guanylate kinase, WW and PDZ domain containing 1	Homo sapiens	62-67
33686070-0	2021	Time-resolved single-cell analysis of Brca1 associated mammary tumourigenesis reveals aberrant differentiation of luminal progenitors.	Phenobarbital	114-121	breast cancer 1, early onset	Mus musculus	38-43
33686070-4	2021	We found that perturbing Brca1/p53 in luminal progenitors induces aberrant alveolar differentiation pre-malignancy accompanied by pro-tumourigenic changes in the immune compartment.	Phenobarbital	38-45	breast cancer 1, early onset	Mus musculus	25-30
33674387-5	2021	We find that seipin clusters TG, as well as its precursor diacylglycerol, inside its unconventional ring-like oligomeric structure and that both its luminal and transmembrane regions contribute to this process.	Phenobarbital	149-156	BSCL2 lipid droplet biogenesis associated, seipin	Homo sapiens	13-19
33686070-4	2021	We found that perturbing Brca1/p53 in luminal progenitors induces aberrant alveolar differentiation pre-malignancy accompanied by pro-tumourigenic changes in the immune compartment.	Phenobarbital	38-45	transformation related protein 53, pseudogene	Mus musculus	31-34
33686070-6	2021	Based on our data we propose a model where Brca1/p53 LOF inadvertently promotes a differentiation program hardwired in luminal progenitors, highlighting the deterministic role of the cell-of-origin and offering a potential explanation for the tissue specificity of BRCA1 tumours.	Phenobarbital	119-126	breast cancer 1, early onset	Mus musculus	43-48
33686070-6	2021	Based on our data we propose a model where Brca1/p53 LOF inadvertently promotes a differentiation program hardwired in luminal progenitors, highlighting the deterministic role of the cell-of-origin and offering a potential explanation for the tissue specificity of BRCA1 tumours.	Phenobarbital	119-126	transformation related protein 53, pseudogene	Mus musculus	49-52
33622785-5	2021	Using a combination of quantum dots (QDs) conjugated to antibodies against the luminal domain of the vesicular GABA transporter to selectively label GABAergic (i.e., predominantly inhibitory) vesicles together with dual-focus imaging optics, we tracked the real-time three-dimensional position of single GABAergic vesicles up to the moment of exocytosis (i.e., fusion).	Phenobarbital	79-86	solute carrier family 32 member 1	Homo sapiens	101-127
33446483-6	2021	A 25HC molecule is sandwiched between the S4-S6 segments in Scap and TMs 3/4 in Insig-2 in the luminal leaflet of the membrane.	Phenobarbital	95-102	tropomyosin 3	Homo sapiens	69-76
33446483-6	2021	A 25HC molecule is sandwiched between the S4-S6 segments in Scap and TMs 3/4 in Insig-2 in the luminal leaflet of the membrane.	Phenobarbital	95-102	insulin induced gene 2	Homo sapiens	80-87
33664379-7	2021	In contrast, FAP-hESCs carrying APC truncation mutations (FAP1 and FAP2) generated only few cyst-like structures and cell aggregates of various shape, occasionally with luminal parts, which aligned with their failure to upregulate critical differentiation genes early in the process, as shown by RNA sequencing.	Phenobarbital	169-176	protein tyrosine phosphatase non-receptor type 13	Homo sapiens	58-62
33221433-2	2021	To screen natural inhibitors of breast cancer metastasis, we adopted small interfering RNAs to transiently knock down 591 ERF-coding genes in luminal breast cancer MCF-7 cells and found that depletion of AF9 significantly promoted MCF-7 cell invasion and migration.	Phenobarbital	142-149	MLLT3 super elongation complex subunit	Homo sapiens	204-207
33654150-6	2021	Finally, the luminal presence of amino acids led to important changes in ghrelin, cholecystokinin, peptide YY and proglucagon mRNAs and/or protein levels.	Phenobarbital	13-20	ghrelin	Oncorhynchus mykiss	73-80
33747959-9	2021	We also discovered that stromal score and the level of CXCL12 were higher in luminal subtype, and immune score and the level of CD3E were higher in the basal subtype.	Phenobarbital	77-84	C-X-C motif chemokine ligand 12	Homo sapiens	55-61
33675651-0	2021	Par3/Integrin beta1 regulates embryo adhesion via changing endometrial luminal epithelium polarity.	Phenobarbital	71-78	par-3 family cell polarity regulator	Homo sapiens	0-4
33675651-0	2021	Par3/Integrin beta1 regulates embryo adhesion via changing endometrial luminal epithelium polarity.	Phenobarbital	71-78	integrin subunit beta 1	Homo sapiens	5-19
33263786-6	2021	Furthermore, we showed that CYP1A1 and CYP1B1 were induced by beta-naphtoflavone in all three models, whereas CYP3A4 was induced by phenobarbital and rifampicin in HIOs, in the IEC-based model (although not statistically significant), but not in Caco-2 cells.	Phenobarbital	132-145	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	110-116
33356945-4	2021	Interestingly, several lines of recent evidence have indicated that the enterocytes use CaSR to monitor luminal and extracellular calcium levels, thereby reducing the activity of transient receptor potential channel, subfamily V, member 6, and inducing paracrine and endocrine feedback responses to restrict calcium absorption.	Phenobarbital	104-111	calcium-sensing receptor	Danio rerio	88-92
32830517-3	2021	OBJECTIVE: To describe the use of fixed-dose phenobarbital monotherapy for the management of patients at risk for AWS in the surgical-trauma intensive care unit.	Phenobarbital	45-58	jagged canonical Notch ligand 1	Homo sapiens	114-117
32830517-4	2021	METHODS: Surgical-trauma critically ill patients who received phenobarbital monotherapy, loading dose followed by a taper regimen, for the management of AWS were included in this evaluation.	Phenobarbital	62-75	jagged canonical Notch ligand 1	Homo sapiens	153-156
32830517-5	2021	The effectiveness of phenobarbital monotherapy to treat AWS and prevent development of AWS-related complications were evaluated.	Phenobarbital	21-34	jagged canonical Notch ligand 1	Homo sapiens	56-59
32830517-7	2021	RESULTS: A total of 31 patients received phenobarbital monotherapy; the majority of patients were at moderate risk for developing AWS (n = 20; 65%) versus high risk (n = 11; 35%).	Phenobarbital	41-54	jagged canonical Notch ligand 1	Homo sapiens	130-133
32830517-12	2021	CONCLUSION AND RELEVANCE: Fixed-dose phenobarbital monotherapy appears to be well tolerated and effective in the management of AWS.	Phenobarbital	37-50	jagged canonical Notch ligand 1	Homo sapiens	127-130
32830517-13	2021	Further evaluation is needed to determine the extent of benefit with the use of phenobarbital monotherapy for management of AWS.	Phenobarbital	80-93	jagged canonical Notch ligand 1	Homo sapiens	124-127
33654150-6	2021	Finally, the luminal presence of amino acids led to important changes in ghrelin, cholecystokinin, peptide YY and proglucagon mRNAs and/or protein levels.	Phenobarbital	13-20	glucagon-1	Oncorhynchus mykiss	114-125
33398415-4	2021	After 20 weeks of treatment, preneoplastic lesions detected by immunostaining with an anti-KRT8/18 antibody were observed in PB-treated but not PCN-treated mice, and PCN cotreatment augmented the formation of preneoplastic lesions by PB.	Phenobarbital	125-127	keratin 8	Mus musculus	91-98
33398415-2	2021	While CAR activation by its activators, such as phenobarbital (PB), induces hepatocyte proliferation and liver carcinogenesis in rodents, it remains unclear whether PXR activation drives liver cancer.	Phenobarbital	48-61	nuclear receptor subfamily 1, group I, member 3	Mus musculus	6-9
33398415-2	2021	While CAR activation by its activators, such as phenobarbital (PB), induces hepatocyte proliferation and liver carcinogenesis in rodents, it remains unclear whether PXR activation drives liver cancer.	Phenobarbital	63-65	nuclear receptor subfamily 1, group I, member 3	Mus musculus	6-9
33067762-9	2021	Tumor KRAS expression in the subtypes of basal-like, HER2-enriched, Luminal A and Luminal B were 1.64, 1.67, 1.51 and 1.42 times of normal, respectively.	Phenobarbital	68-75	KRAS proto-oncogene, GTPase	Homo sapiens	6-10
33067762-9	2021	Tumor KRAS expression in the subtypes of basal-like, HER2-enriched, Luminal A and Luminal B were 1.64, 1.67, 1.51 and 1.42 times of normal, respectively.	Phenobarbital	82-89	KRAS proto-oncogene, GTPase	Homo sapiens	6-10
33421842-8	2021	In contrast to HFF-1, T. gondii infected in mouse fibroblast (MF), labelings of both GM1 and GM3 were detected in the IMC luminal leaflet, although GM1"s gold labeling density was very low.	Phenobarbital	122-129	granulocyte macrophage antigen 3	Mus musculus	93-96
33688250-7	2021	Results: Our analyses reveal that FOXQ1 mRNA is differentially expressed between different subtypes of BC and is significantly decreased in luminal BC and HER2 patients when compared to normal breast tissue samples.	Phenobarbital	140-147	forkhead box Q1	Homo sapiens	34-39
32859560-14	2021	CONCLUSION: Women with ER+/HER2- breast cancer >=75 years old had higher rates of the more aggressive luminal B subtype and inferior outcomes.	Phenobarbital	102-109	erb-b2 receptor tyrosine kinase 2	Homo sapiens	27-31
33653085-5	2021	In cells, Hhat promotes the transfer of palmitoyl-CoA from the cytoplasmic to the luminal side of the endoplasmic reticulum membrane, where Shh palmitoylation occurs.	Phenobarbital	82-89	hedgehog acyltransferase	Homo sapiens	10-14
33733541-7	2021	Second, in a reconstituted in vitro blood-brain barrier system, inclusion of the soluble form of RAGE (endogenous secretory RAGE [esRAGE]), an alternative splicing variant, in the luminal (blood) side had no effect on the transport of OT to the abluminal (brain) chamber.	Phenobarbital	180-187	advanced glycosylation end product-specific receptor	Mus musculus	97-101
33733541-7	2021	Second, in a reconstituted in vitro blood-brain barrier system, inclusion of the soluble form of RAGE (endogenous secretory RAGE [esRAGE]), an alternative splicing variant, in the luminal (blood) side had no effect on the transport of OT to the abluminal (brain) chamber.	Phenobarbital	180-187	advanced glycosylation end product-specific receptor	Mus musculus	124-128
33653085-5	2021	In cells, Hhat promotes the transfer of palmitoyl-CoA from the cytoplasmic to the luminal side of the endoplasmic reticulum membrane, where Shh palmitoylation occurs.	Phenobarbital	82-89	sonic hedgehog signaling molecule	Homo sapiens	140-143
33411419-10	2021	In vivo, Runx2 was detected during early prostate development (E16.5) and in adult mice where it was present in basal and luminal cells of ventral and anterior lobes.	Phenobarbital	122-129	runt related transcription factor 2	Mus musculus	9-14
32713353-9	2021	The luminal contents from rats gavaged with whey protein decreased DPP-4 activity in vitro.	Phenobarbital	4-11	dipeptidylpeptidase 4	Rattus norvegicus	67-72
33627709-4	2021	At the beginning of this study, we obtained a luminal-domain mutant of Saccharomyces cerevisiae Ire1, deltaIdeltaIIIdeltaV/Y225H Ire1, which is deduced to be controlled by none of the luminal-side regulatory events.	Phenobarbital	46-53	bifunctional endoribonuclease/protein kinase IRE1	Saccharomyces cerevisiae S288C	96-100
33948296-7	2021	In a univariate analysis, the Luminal-B-human-epidermal-growth-receptor-positive (HER2+) subtype had the longest median OS at 39.1 months (95% CI: 34.1-44.1, p = 0.004).	Phenobarbital	30-37	erb-b2 receptor tyrosine kinase 2	Homo sapiens	82-86
33627709-4	2021	At the beginning of this study, we obtained a luminal-domain mutant of Saccharomyces cerevisiae Ire1, deltaIdeltaIIIdeltaV/Y225H Ire1, which is deduced to be controlled by none of the luminal-side regulatory events.	Phenobarbital	46-53	bifunctional endoribonuclease/protein kinase IRE1	Saccharomyces cerevisiae S288C	129-133
33627709-6	2021	Therefore, in addition to the ER-luminal domain of Ire1, which monitors ER conditions, the kinase region is directly involved in the ER-stress responsiveness of Ire1.	Phenobarbital	33-40	bifunctional endoribonuclease/protein kinase IRE1	Saccharomyces cerevisiae S288C	51-55
33627709-6	2021	Therefore, in addition to the ER-luminal domain of Ire1, which monitors ER conditions, the kinase region is directly involved in the ER-stress responsiveness of Ire1.	Phenobarbital	33-40	bifunctional endoribonuclease/protein kinase IRE1	Saccharomyces cerevisiae S288C	161-165
33591965-6	2021	In human and mouse eccrine sweat glands, corin and ANP are expressed in the luminal epithelial cells.	Phenobarbital	76-83	corin, serine peptidase	Mus musculus	41-46
33594081-3	2021	Here, we show that secretion of luminal glycoprotein 2 (GP2) from pancreatic acinar cells is induced in a TNF-dependent manner in mice with chemically induced colitis.	Phenobarbital	32-39	glycoprotein 2 (zymogen granule membrane)	Mus musculus	40-54
33594081-3	2021	Here, we show that secretion of luminal glycoprotein 2 (GP2) from pancreatic acinar cells is induced in a TNF-dependent manner in mice with chemically induced colitis.	Phenobarbital	32-39	glycoprotein 2 (zymogen granule membrane)	Mus musculus	56-59
33594081-3	2021	Here, we show that secretion of luminal glycoprotein 2 (GP2) from pancreatic acinar cells is induced in a TNF-dependent manner in mice with chemically induced colitis.	Phenobarbital	32-39	tumor necrosis factor	Mus musculus	106-109
33644157-6	2021	CASP3, cleaved-CASP3, and CASP7 proteins were localized to endometrial cells, with increased levels in luminal and glandular epithelial cells during early pregnancy, whereas apoptotic cells in the endometrium were limited to some scattered stromal cells with increased numbers on Day 15 of pregnancy.	Phenobarbital	103-110	caspase 3	Sus scrofa	0-5
33579951-2	2021	We here assess pretreatment gene-expression data from 66 HR+/HER2- early BCs from the LETLOB trial and show that non-luminal tumors (HER2-enriched, Basal-like) present higher tumor-infiltrating lymphocyte levels than luminal tumors.	Phenobarbital	117-124	erb-b2 receptor tyrosine kinase 2	Homo sapiens	133-137
33644151-4	2021	The results showed that the Free Leptin Index is significantly decreased in cats with mammary carcinoma (p = 0.0006), particularly in those with luminal B and HER2-positive tumors, and that these animals also present significantly lower serum leptin levels (p < 0.0001 and p < 0.005, respectively).	Phenobarbital	145-152	leptin	Felis catus	33-39
33399260-7	2021	TNFalpha is expressed in the luminal epithelium and the embryo at the embryo attachment site.	Phenobarbital	29-36	tumor necrosis factor	Mus musculus	0-8
33536395-0	2021	The fission yeast gmn2+ gene encodes an ERD1 homologue of Saccharomyces cerevisiae required for protein glycosylation and retention of luminal endoplasmic reticulum proteins.	Phenobarbital	135-142	Erd1p	Saccharomyces cerevisiae S288C	40-44
33536395-8	2021	The Gmn2 protein shares sequence similarity with Kluyveromyces lactis and Saccharomyces cerevisiae Erd1 proteins, which are required for retention of luminal endoplasmic reticulum (ER) proteins.	Phenobarbital	150-157	Erd1p	Saccharomyces cerevisiae S288C	99-103
33161753-0	2021	Luminal Ca<sup>2+</sup> Regulation of RyR1 Ca<sup>2+</sup> Channel Leak Activation and Inactivation in Sarcoplasmic Reticulum Membrane Vesicles.	Phenobarbital	0-7	ryanodine receptor 1	Homo sapiens	38-42
33599301-4	2021	A covariate analysis for age, sex, race, and co-administration of other antiepileptic drugs identified phenobarbital and felbamate to significantly increase lacosamide clearance (1.71 and 1.46-fold, respectively).	Phenobarbital	103-116	renin binding protein	Homo sapiens	25-28
33571253-10	2021	For example, the Luminal A network includes a single, highly connected cluster of genes, which is enriched in the human diseases category, and in the Her2 subtype network we find a distinct, and highly interconnected cluster which is uniquely enriched in drug metabolism pathways.	Phenobarbital	17-24	erb-b2 receptor tyrosine kinase 2	Homo sapiens	150-154
33568634-3	2021	We show that ceramide synthase 2 (CERS2) undergoes a unique cassette exon event specifically in Luminal B subtype tumors.	Phenobarbital	96-103	ceramide synthase 2	Homo sapiens	13-32
33568634-3	2021	We show that ceramide synthase 2 (CERS2) undergoes a unique cassette exon event specifically in Luminal B subtype tumors.	Phenobarbital	96-103	ceramide synthase 2	Homo sapiens	34-39
33568634-5	2021	Differential AS-based survival analysis shows that this AS event of CERS2 is a poor prognostic factor for Luminal B patients.	Phenobarbital	106-113	ceramide synthase 2	Homo sapiens	68-73
33568634-6	2021	As Exon 8 corresponds to catalytic Lag1p domain, overexpression of AS transcript of CERS2 in Luminal B cancer cells leads to a reduction in the level of very-long-chain ceramides compared to overexpression of protein-coding (PC) transcript of CERS2.	Phenobarbital	93-100	ceramide synthase 2	Homo sapiens	84-89
33568634-6	2021	As Exon 8 corresponds to catalytic Lag1p domain, overexpression of AS transcript of CERS2 in Luminal B cancer cells leads to a reduction in the level of very-long-chain ceramides compared to overexpression of protein-coding (PC) transcript of CERS2.	Phenobarbital	93-100	ceramide synthase 2	Homo sapiens	243-248
33616107-11	2021	This model provides researchers with a new tool to study the impact of both TO and increased luminal pressure on lung development.	Phenobarbital	93-100	ceramide synthase 1	Mus musculus	43-45
33254086-2	2021	The component of early high-grade transformation was characterized by 1) selective expansion of the luminal (CK7+, c-kit+, p63-) cell component with severe cytologic atypia and significantly increased Ki-67 proliferation index, and 2) retained albeit attenuated abluminal (CK7-, c-kit-, p63+) cells, surrounding nests of high-grade luminal cells.	Phenobarbital	100-107	keratin 7	Homo sapiens	109-112
33254086-2	2021	The component of early high-grade transformation was characterized by 1) selective expansion of the luminal (CK7+, c-kit+, p63-) cell component with severe cytologic atypia and significantly increased Ki-67 proliferation index, and 2) retained albeit attenuated abluminal (CK7-, c-kit-, p63+) cells, surrounding nests of high-grade luminal cells.	Phenobarbital	100-107	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	115-120
33517284-0	2021	Chloride Intracellular Channel Protein 1 (CLIC1), E-cadherin and P-cadherin Define Distinct Subclasses of HER2, Luminal B and Triple-negative Breast Cancer.	Phenobarbital	112-119	chloride intracellular channel 1	Homo sapiens	0-40
33161753-7	2021	This, in turn, is influenced by the activity of SERCA1 pumps to both fill luminal pools while synchronously reducing Ca2+ levels on the cytosolic face of RyR1 channels.	Phenobarbital	74-81	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 1	Homo sapiens	48-54
33161753-7	2021	This, in turn, is influenced by the activity of SERCA1 pumps to both fill luminal pools while synchronously reducing Ca2+ levels on the cytosolic face of RyR1 channels.	Phenobarbital	74-81	ryanodine receptor 1	Homo sapiens	154-158
33591965-6	2021	In human and mouse eccrine sweat glands, corin and ANP are expressed in the luminal epithelial cells.	Phenobarbital	76-83	natriuretic peptide type A	Mus musculus	51-54
33167684-12	2021	Therapeutic neutralization of histone H2a by antibodies or by in silico designed cyclical peptides enables us to reduce luminal monocyte adhesion and lesion expansion during endotoxinemia.	Phenobarbital	120-127	H2A.B variant histone 2	Mus musculus	30-41
32980989-10	2021	TPO expression was mainly localized to glandular and luminal epithelial cells in the endometrium.	Phenobarbital	53-60	thyroid peroxidase	Homo sapiens	0-3
32452625-9	2021	Finally, keratin-5-positive basal cells constantly replenished the luminal ciliated cells; the new dynamic ciliated cells were also oriented parallel to the tissue axis.	Phenobarbital	67-74	keratin 5	Homo sapiens	9-18
33398175-5	2021	We further show that the lateral gate of Sec61 must first be partially opened by interactions between Sec61 and Sec63 in cytosolic and luminal domains, a simultaneous disruption of which completely closes the channel.	Phenobarbital	135-142	translocon subunit SEC61	Saccharomyces cerevisiae S288C	41-46
33398175-5	2021	We further show that the lateral gate of Sec61 must first be partially opened by interactions between Sec61 and Sec63 in cytosolic and luminal domains, a simultaneous disruption of which completely closes the channel.	Phenobarbital	135-142	translocon subunit SEC61	Saccharomyces cerevisiae S288C	102-107
33398175-5	2021	We further show that the lateral gate of Sec61 must first be partially opened by interactions between Sec61 and Sec63 in cytosolic and luminal domains, a simultaneous disruption of which completely closes the channel.	Phenobarbital	135-142	protein-transporting protein SEC63	Saccharomyces cerevisiae S288C	112-117
33432245-6	2021	Both TLRs interact with the UNC93B1 amino-terminal six-helix bundle through their transmembrane and luminal juxtamembrane regions, but the complexes of TLR3 and TLR7 with UNC93B1 differ in their oligomerization state.	Phenobarbital	100-107	unc-93 homolog B1, TLR signaling regulator	Homo sapiens	28-35
33432245-6	2021	Both TLRs interact with the UNC93B1 amino-terminal six-helix bundle through their transmembrane and luminal juxtamembrane regions, but the complexes of TLR3 and TLR7 with UNC93B1 differ in their oligomerization state.	Phenobarbital	100-107	toll like receptor 7	Homo sapiens	161-165
33432245-6	2021	Both TLRs interact with the UNC93B1 amino-terminal six-helix bundle through their transmembrane and luminal juxtamembrane regions, but the complexes of TLR3 and TLR7 with UNC93B1 differ in their oligomerization state.	Phenobarbital	100-107	unc-93 homolog B1, TLR signaling regulator	Homo sapiens	171-178
32951906-9	2021	Interestingly, INSM1 expression segregated IBC with neuroendocrine differentiation into different prognostic subgroups, particularly within luminal B subtype.	Phenobarbital	140-147	INSM transcriptional repressor 1	Homo sapiens	15-20
32951906-11	2021	Multivariate analysis showed that synaptophysin/chromogranin+ INSM1- status was an independent adverse factor for DFS (HR=2.282, 95%CI=1.196-4.356, p=0.012) in the luminal B subtype.	Phenobarbital	164-171	synaptophysin	Homo sapiens	34-47
32951906-11	2021	Multivariate analysis showed that synaptophysin/chromogranin+ INSM1- status was an independent adverse factor for DFS (HR=2.282, 95%CI=1.196-4.356, p=0.012) in the luminal B subtype.	Phenobarbital	164-171	INSM transcriptional repressor 1	Homo sapiens	62-67
33172965-5	2021	We find that CIRBP transcript levels correlate with breast cancer subtype and are an indicator of luminal A/B prognosis.	Phenobarbital	98-105	cold inducible RNA binding protein	Homo sapiens	13-18
33514305-5	2021	The luminal-Cl--dependent HCO3- secretions in the cecum and middle-distal colon were abolished in the DRA-KO mice.	Phenobarbital	4-11	solute carrier family 26, member 3	Mus musculus	102-105
33537462-0	2021	Intestinal TMEM16A control luminal chloride secretion in a NHERF1 dependent manner.	Phenobarbital	27-34	anoctamin 1	Homo sapiens	11-18
33537462-0	2021	Intestinal TMEM16A control luminal chloride secretion in a NHERF1 dependent manner.	Phenobarbital	27-34	SLC9A3 regulator 1	Homo sapiens	59-65
33551819-6	2020	As expected, CITCO, the direct activator, and PB, the indirect activator of CAR, induced CYP3A4 (31 and 40-fold), CYP2B6 (24 and 28-fold) and UGT1A1 (2.9 and 4.2-fold), respectively.	Phenobarbital	46-48	nuclear receptor subfamily 1 group I member 3	Homo sapiens	76-79
33551819-6	2020	As expected, CITCO, the direct activator, and PB, the indirect activator of CAR, induced CYP3A4 (31 and 40-fold), CYP2B6 (24 and 28-fold) and UGT1A1 (2.9 and 4.2-fold), respectively.	Phenobarbital	46-48	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	89-95
33551819-6	2020	As expected, CITCO, the direct activator, and PB, the indirect activator of CAR, induced CYP3A4 (31 and 40-fold), CYP2B6 (24 and 28-fold) and UGT1A1 (2.9 and 4.2-fold), respectively.	Phenobarbital	46-48	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	114-120
33551819-6	2020	As expected, CITCO, the direct activator, and PB, the indirect activator of CAR, induced CYP3A4 (31 and 40-fold), CYP2B6 (24 and 28-fold) and UGT1A1 (2.9 and 4.2-fold), respectively.	Phenobarbital	46-48	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	142-148
33389351-0	2021	ZNF703 gene copy number and protein expression in breast cancer; associations with proliferation, prognosis and luminal subtypes.	Phenobarbital	112-119	zinc finger protein 703	Homo sapiens	0-6
33389351-8	2021	RESULTS: We found mean ZNF703 copy number >= 6 in 7% of tumours, most frequently in Luminal B subtypes.	Phenobarbital	84-91	zinc finger protein 703	Homo sapiens	23-29
33389351-13	2021	CONCLUSIONS: In breast cancer, high ZNF703 copy number is associated with increased proliferation, Luminal B subtypes and poor prognosis.	Phenobarbital	99-106	zinc finger protein 703	Homo sapiens	36-42
33140857-5	2021	However, the analysis of copy number variation showed that another fraction of luminal BC displayed loss (8%) or gain (6%) of the CDKN1B gene, further reinforcing the idea that the function of p27kip1 is important in this type of tumor.	Phenobarbital	79-86	cyclin dependent kinase inhibitor 1B	Homo sapiens	130-136
33140857-5	2021	However, the analysis of copy number variation showed that another fraction of luminal BC displayed loss (8%) or gain (6%) of the CDKN1B gene, further reinforcing the idea that the function of p27kip1 is important in this type of tumor.	Phenobarbital	79-86	cyclin dependent kinase inhibitor 1B	Homo sapiens	193-200
33176066-10	2021	In particular, up-regulation of BCAM and CELSR1 differentiates luminal subtypes, while up-regulation of MIEN1 differentiates Her2 subtypes.	Phenobarbital	63-70	basal cell adhesion molecule (Lutheran blood group)	Homo sapiens	32-36
33323967-6	2021	Markedly, early-stage lesions exhibited a decreased expression of AR and its target genes, accompanied by reduced CK18 and E-cadherin expression, suggesting a shift from a luminal to a dedifferentiated epithelial phenotype.	Phenobarbital	172-179	androgen receptor	Mus musculus	66-68
33351196-5	2021	At mucosal sites, FcRn transports IgG across polarized epithelial cells where it retrieves IgG in complex with luminal antigens that is delivered to tissue-localized immune cells.	Phenobarbital	111-118	Fc gamma receptor and transporter	Homo sapiens	18-22
33513818-2	2021	P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) are transport proteins localized at the BBB luminal membrane and play an important role in the clearance of amyloid-beta (Abeta).	Phenobarbital	110-117	phosphoglycolate phosphatase	Mus musculus	0-14
33513818-2	2021	P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) are transport proteins localized at the BBB luminal membrane and play an important role in the clearance of amyloid-beta (Abeta).	Phenobarbital	110-117	phosphoglycolate phosphatase	Mus musculus	16-20
33513818-2	2021	P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) are transport proteins localized at the BBB luminal membrane and play an important role in the clearance of amyloid-beta (Abeta).	Phenobarbital	110-117	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	26-58
33513818-2	2021	P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) are transport proteins localized at the BBB luminal membrane and play an important role in the clearance of amyloid-beta (Abeta).	Phenobarbital	110-117	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	60-64
33513818-2	2021	P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) are transport proteins localized at the BBB luminal membrane and play an important role in the clearance of amyloid-beta (Abeta).	Phenobarbital	110-117	amyloid beta (A4) precursor protein	Mus musculus	188-193
33481779-2	2021	Here we show through biomolecular simulations bridged to experiments that seipin can trap TAGs in the ER bilayer via the luminal hydrophobic helices of the protomers delineating the inner opening of the seipin disk.	Phenobarbital	121-128	BSCL2 lipid droplet biogenesis associated, seipin	Homo sapiens	74-80
33481779-2	2021	Here we show through biomolecular simulations bridged to experiments that seipin can trap TAGs in the ER bilayer via the luminal hydrophobic helices of the protomers delineating the inner opening of the seipin disk.	Phenobarbital	121-128	BSCL2 lipid droplet biogenesis associated, seipin	Homo sapiens	203-209
33481779-6	2021	Together, these results suggest that seipin traps TAGs via its luminal hydrophobic helices, serving as a catalyst for seeding the TAG cluster from dissolved monomers inside the seipin ring, thereby generating a favorable promethin binding interface.	Phenobarbital	63-70	BSCL2 lipid droplet biogenesis associated, seipin	Homo sapiens	37-43
33481779-6	2021	Together, these results suggest that seipin traps TAGs via its luminal hydrophobic helices, serving as a catalyst for seeding the TAG cluster from dissolved monomers inside the seipin ring, thereby generating a favorable promethin binding interface.	Phenobarbital	63-70	BSCL2 lipid droplet biogenesis associated, seipin	Homo sapiens	177-183
33481779-6	2021	Together, these results suggest that seipin traps TAGs via its luminal hydrophobic helices, serving as a catalyst for seeding the TAG cluster from dissolved monomers inside the seipin ring, thereby generating a favorable promethin binding interface.	Phenobarbital	63-70	lipid droplet assembly factor 1	Homo sapiens	221-230
33486192-2	2021	This receptor is also expressed in intestinal enteroendocrine cells and is required for sensing luminal sugars and sweeteners to regulate expression of intestinal Na+-glucose cotransporter 1 (SGLT1).	Phenobarbital	96-103	solute carrier family 5 member 1	Sus scrofa	163-190
33486192-2	2021	This receptor is also expressed in intestinal enteroendocrine cells and is required for sensing luminal sugars and sweeteners to regulate expression of intestinal Na+-glucose cotransporter 1 (SGLT1).	Phenobarbital	96-103	solute carrier family 5 member 1	Sus scrofa	192-197
33431687-2	2021	One of the functions of GCs is to produce and secrete MUC2, the mucin that forms the scaffold of the intestinal mucus layer coating the epithelium and separates the luminal pathogens and commensal microbiota from the host tissues.	Phenobarbital	165-172	mucin 2	Mus musculus	54-58
33458942-6	2021	The helical structure and dynamics are further regulated by glycine and another proline residue in the luminal part of LAT transmembrane domain.	Phenobarbital	103-110	linker for activation of T cells	Homo sapiens	119-122
33166849-7	2021	Cathelicidin protein was mainly localized to luminal epithelial cells and some immune cells in blood vessels and to chorionic epithelial cells of chorioallantoic membranes during mid-to late pregnancy.	Phenobarbital	45-52	antibacterial peptide PMAP-23	Sus scrofa	0-12
33503182-6	2021	This was more pronounced in luminal and triple-negative patients, and patient"s response to NAC was correlated with an increase in miRNA-195 expression.	Phenobarbital	28-35	microRNA 195	Homo sapiens	131-140
33215623-2	2021	Their dysfunction is associated with a number of diseases, which are often related to an altered localization or luminal pH.	Phenobarbital	113-120	phenylalanine hydroxylase	Homo sapiens	121-123
33446633-0	2021	Prolactin receptor-driven combined luminal and epithelial differentiation in breast cancer restricts plasticity, stemness, tumorigenesis and metastasis.	Phenobarbital	35-42	prolactin receptor	Homo sapiens	0-18
33446633-5	2021	Whereas loss of PRLR expression in HER2-E breast cancer cells resulted in loss of their luminal differentiation yet enriched for epithelial ALDH+ BCSC population showing elevated HER2-driven tumorigenic, multi-organ metastatic spread, and resistance to anti-HER2 therapy.	Phenobarbital	88-95	prolactin receptor	Homo sapiens	16-20
33446633-5	2021	Whereas loss of PRLR expression in HER2-E breast cancer cells resulted in loss of their luminal differentiation yet enriched for epithelial ALDH+ BCSC population showing elevated HER2-driven tumorigenic, multi-organ metastatic spread, and resistance to anti-HER2 therapy.	Phenobarbital	88-95	erb-b2 receptor tyrosine kinase 2	Homo sapiens	35-39
33446633-6	2021	Collectively, this study defines PRLR as a driver of precise luminal and epithelial differentiation limiting cellular plasticity, stemness, and tumorigenesis and emphasizing the function of pro/forward-differentiation pathways as a foundation for the discovery of anti-cancer therapeutic targets.	Phenobarbital	61-68	prolactin receptor	Homo sapiens	33-37
33511077-15	2020	Conclusion: A heterogeneous distribution of ER within the tumor in IHC appeared as an EFS-8y prognosticator in luminal non-metastatic breast cancers.	Phenobarbital	111-118	estrogen receptor 1	Homo sapiens	44-46
33382976-4	2021	Loss of AP-2gamma in the basal epithelium profoundly altered the transcriptomes and decreased the number of cells within several clusters of mammary epithelial cells, including adult MaSCs and luminal progenitors.	Phenobarbital	193-200	transcription factor AP-2, gamma	Mus musculus	8-17
33505976-1	2020	The ability of phagosomes to halt microbial growth is intimately linked to their ability to acidify their luminal pH.	Phenobarbital	106-113	phenylalanine hydroxylase	Homo sapiens	114-116
33551819-9	2020	Twenty-four hepatic drug transporter genes were characterized, and of those, SLC51B was induced the most by PB and OP by about 3.3 and 6.5 fold, respectively.	Phenobarbital	108-110	solute carrier family 51 subunit beta	Homo sapiens	77-83
33416944-5	2021	Total CD73 (T +) was calculated as the average of luminal (L +) and basolateral (BL +) percentage membrane expression scores for each LUAD and was used to classify tumors into three groups based on the extent of T CD73 expression (high, low, and negative).	Phenobarbital	50-57	5'-nucleotidase ecto	Homo sapiens	6-10
33262312-7	2021	We also reveal, however, that lactation and involution proceed normally in mice with luminal-specific Piezo1 deletion.	Phenobarbital	85-92	piezo-type mechanosensitive ion channel component 1	Mus musculus	102-108
33407452-14	2021	CTTN overexpression was associated with the increased chance of luminal-A positivity vs. non-luminal-A (ORadj.	Phenobarbital	64-71	cortactin	Homo sapiens	0-4
33407452-14	2021	CTTN overexpression was associated with the increased chance of luminal-A positivity vs. non-luminal-A (ORadj.	Phenobarbital	93-100	cortactin	Homo sapiens	0-4
33397968-5	2021	Second, within HR-positive disease, ERBB2 and luminal-related genes were more expressed in HER2-low than HER2 0.	Phenobarbital	46-53	erb-b2 receptor tyrosine kinase 2	Homo sapiens	91-95
33469513-10	2020	In HER2 positive-type and triple-negative breast cancer (TNBC) patients, it had the lower rate of nuclear ING3 with high expression than that in luminal-type.	Phenobarbital	145-152	erb-b2 receptor tyrosine kinase 2	Homo sapiens	3-7
33397968-5	2021	Second, within HR-positive disease, ERBB2 and luminal-related genes were more expressed in HER2-low than HER2 0.	Phenobarbital	46-53	erb-b2 receptor tyrosine kinase 2	Homo sapiens	105-109
33128919-13	2021	We also detected leptin receptor protein in late pregnant mouse uterus located in endometrial luminal epithelium and myometrial layers.	Phenobarbital	94-101	leptin receptor	Mus musculus	17-32
33444922-8	2021	The majority of luminal A cases (67/78; 85.9%) had low ROR score whereas ODX classified almost two-thirds (50/78~ 64%) as low RS.	Phenobarbital	16-23	long intergenic non-protein coding RNA, regulator of reprogramming	Homo sapiens	55-58
33517235-6	2021	RESULTS: There is minimal expression of ACE2 in the luminal classes, but significantly higher levels in the Basal-like and HER2-enriched subclasses.	Phenobarbital	52-59	angiotensin converting enzyme 2	Homo sapiens	40-44
33186222-1	2021	PURPOSE OF REVIEW: Pendrin resides on the luminal membrane of type B intercalated cells in the renal collecting tubule system mediating the absorption of chloride in exchange for bicarbonate.	Phenobarbital	42-49	solute carrier family 26, member 4	Mus musculus	19-26
33130103-2	2021	Recently, ACE2 was identified as a primary receptor for SARS coronaviruses, SARS-CoV and SARS-CoV-2, being expressed in multiple tissues including the luminal surface of the gut.	Phenobarbital	151-158	angiotensin converting enzyme 2	Homo sapiens	10-14
32951290-6	2021	Immunohistochemistry demonstrated diffuse staining for CK7, SOX10, and p16; the abluminal layer was highlighted by CK5 and p63, while the luminal cells expressed CD117.	Phenobarbital	82-89	keratin 5	Homo sapiens	115-118
32951290-6	2021	Immunohistochemistry demonstrated diffuse staining for CK7, SOX10, and p16; the abluminal layer was highlighted by CK5 and p63, while the luminal cells expressed CD117.	Phenobarbital	82-89	tumor protein p63	Homo sapiens	123-126
33633982-7	2021	BRCA1 carriers tended to exhibit the triple-negative phenotype with a more benign shape and margin (P=0.006 and 0.019), whereas BRCA2 mutations were associated with the luminal phenotype and more malignant features.	Phenobarbital	169-176	BRCA2 DNA repair associated	Homo sapiens	128-133
33391379-6	2021	Results: There was a significant correlation between the luminal intensity of CD133 and neural invasion (P=0.05) and between the cytoplasmic intensity of CD133 and metastasis (P=0.05).	Phenobarbital	57-64	prominin 1	Homo sapiens	78-83
33105993-7	2021	Proteomics analysis showed that numerous DE proteins were enriched after phenobarbital administration, among which CALM1, ARAF, and Cbl proteins (related to the insulin signaling pathway) were significantly downregulated on day 60 but not day 90.	Phenobarbital	73-86	calmodulin 1	Rattus norvegicus	115-120
33105993-7	2021	Proteomics analysis showed that numerous DE proteins were enriched after phenobarbital administration, among which CALM1, ARAF, and Cbl proteins (related to the insulin signaling pathway) were significantly downregulated on day 60 but not day 90.	Phenobarbital	73-86	A-Raf proto-oncogene, serine/threonine kinase	Rattus norvegicus	122-126
33105993-7	2021	Proteomics analysis showed that numerous DE proteins were enriched after phenobarbital administration, among which CALM1, ARAF, and Cbl proteins (related to the insulin signaling pathway) were significantly downregulated on day 60 but not day 90.	Phenobarbital	73-86	Cbl proto-oncogene	Rattus norvegicus	132-135
32949575-8	2021	Scanning electron microscopy showed the attachment of endothelial cells to the luminal surface of the PU/PCL scaffold.	Phenobarbital	79-86	PHD finger protein 1	Homo sapiens	105-108
33626315-8	2021	The intestinal ACE2 receptor is associated with the neutral amino acid transporter B0AT1 and ACE2 is necessary for the expression of this transporter on the luminal surface of intestinal epithelial cells.	Phenobarbital	157-164	angiotensin converting enzyme 2	Homo sapiens	15-19
33626315-8	2021	The intestinal ACE2 receptor is associated with the neutral amino acid transporter B0AT1 and ACE2 is necessary for the expression of this transporter on the luminal surface of intestinal epithelial cells.	Phenobarbital	157-164	solute carrier family 6 member 19	Homo sapiens	83-88
33626315-8	2021	The intestinal ACE2 receptor is associated with the neutral amino acid transporter B0AT1 and ACE2 is necessary for the expression of this transporter on the luminal surface of intestinal epithelial cells.	Phenobarbital	157-164	angiotensin converting enzyme 2	Homo sapiens	93-97
33780963-6	2021	The increase in luminal area preceded the increase in AAA diameter and was characterized by an overall deceleration in recirculation flow velocity with a coinciding increase in flow velocity penetrating the ILT.	Phenobarbital	16-23	AAA1	Homo sapiens	54-57
33334698-17	2021	Furthermore, the expression of ING4 in BC cell lines was significantly greater in luminal A and basal-like cells compared with human epidermal growth factor receptor 2-positive cells, which was also observed in the clinical samples.	Phenobarbital	82-89	inhibitor of growth family member 4	Homo sapiens	31-35
33110232-4	2021	The adult mouse prostate luminal cells contain both castration-resistant Sox2-expressing Sca-1+ cells and castration-responsive Sca-1- cells.	Phenobarbital	25-32	SRY (sex determining region Y)-box 2	Mus musculus	73-77
33110232-4	2021	The adult mouse prostate luminal cells contain both castration-resistant Sox2-expressing Sca-1+ cells and castration-responsive Sca-1- cells.	Phenobarbital	25-32	ataxin 1	Mus musculus	89-94
33110232-4	2021	The adult mouse prostate luminal cells contain both castration-resistant Sox2-expressing Sca-1+ cells and castration-responsive Sca-1- cells.	Phenobarbital	25-32	ataxin 1	Mus musculus	128-133
33110232-5	2021	We show that both types of the luminal cell are susceptible to oncogenic transformation induced by loss of function of the tumor suppressor Pten.	Phenobarbital	31-38	phosphatase and tensin homolog	Mus musculus	140-144
32779157-11	2021	On immunocytochemistry, the luminal cells showed positivity for CK7 (epithelial marker) and the abluminal cells showed positivity for p63 (myoepithelial marker).	Phenobarbital	28-35	keratin 7	Homo sapiens	64-67
33511376-6	2021	The luminal surface was partly covered by a single layer of CD31, von Willebrand factor, and partly CD144 positive cells.	Phenobarbital	4-11	platelet and endothelial cell adhesion molecule 1	Homo sapiens	60-64
33511376-6	2021	The luminal surface was partly covered by a single layer of CD31, von Willebrand factor, and partly CD144 positive cells.	Phenobarbital	4-11	cadherin 5	Homo sapiens	100-105
33473352-0	2021	Species differences in phenobarbital-mediated UGT gene induction in rat and human liver microtissues.	Phenobarbital	23-36	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	46-49
33473352-2	2021	To investigate this hypothesis we examined profiles of hepatic UGT induction by the prototypical CAR activator phenobarbital (PB) in rat and human liver 3D microtissues.	Phenobarbital	111-124	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	63-66
33473352-2	2021	To investigate this hypothesis we examined profiles of hepatic UGT induction by the prototypical CAR activator phenobarbital (PB) in rat and human liver 3D microtissues.	Phenobarbital	111-124	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	97-100
33473352-2	2021	To investigate this hypothesis we examined profiles of hepatic UGT induction by the prototypical CAR activator phenobarbital (PB) in rat and human liver 3D microtissues.	Phenobarbital	126-128	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	63-66
33371217-1	2020	Lymphocyte transendothelial migration (TEM) relies on ICAM-1 engagement on the luminal surface of the endothelial cells (ECs).	Phenobarbital	79-86	intercellular adhesion molecule 1	Homo sapiens	54-60
33437389-8	2020	Subgroup analysis revealed that luminal and HER2 patients with positive SOX12 expression had a shorter OS period than those with negative SOX12 expression.	Phenobarbital	32-39	SRY-box transcription factor 12	Homo sapiens	72-77
33437389-8	2020	Subgroup analysis revealed that luminal and HER2 patients with positive SOX12 expression had a shorter OS period than those with negative SOX12 expression.	Phenobarbital	32-39	SRY-box transcription factor 12	Homo sapiens	138-143
33335078-9	2020	These findings might provide new PR-B/FASN-centered predictive and therapeutic modalities in luminal intrinsic BC subtypes.	Phenobarbital	93-100	RB transcriptional corepressor 1	Homo sapiens	33-37
33335078-9	2020	These findings might provide new PR-B/FASN-centered predictive and therapeutic modalities in luminal intrinsic BC subtypes.	Phenobarbital	93-100	fatty acid synthase	Homo sapiens	38-42
33296646-4	2020	Opening of MCU requires hydrophobic interactions mediated by MCU residues near the pore"s luminal end.	Phenobarbital	90-97	mitochondrial calcium uniporter	Homo sapiens	11-14
33296646-4	2020	Opening of MCU requires hydrophobic interactions mediated by MCU residues near the pore"s luminal end.	Phenobarbital	90-97	mitochondrial calcium uniporter	Homo sapiens	61-64
33363504-9	2020	The luminal (endothelial) compartment was stimulated with t-PA or TNK-tPA together with plasminogen, in the presence of PMX205 (a non-competitive C5aR1 antagonist), Avacopan (a competitive C5aR1 antagonist) or Eculizumab (a humanized monoclonal inhibitor of human C5).	Phenobarbital	4-11	plasminogen activator, tissue type	Homo sapiens	58-62
33273625-3	2020	In this study, using a mouse model of acute bacterial cystitis, we demonstrate that the bladder urothelium senses luminal extracellular bacterial lipopolysaccharide (LPS) through Toll-like receptor 4 and releases the transmitter ATP.	Phenobarbital	114-121	toll-like receptor 4	Mus musculus	179-199
33276477-9	2020	HER-2+ (non-luminal) tumours displayed higher ANXA1 expression than luminal B-like (HER-2+) tumours.	Phenobarbital	12-19	annexin A1	Homo sapiens	46-51
32476256-2	2020	The aims of this work were: i) to evaluate whether a short-term regulation of intestinal MRP2 barrier function takes place in vivo after luminal incorporation of nutrients and ii) to explore the underlying mechanism.	Phenobarbital	137-144	ATP binding cassette subfamily C member 2	Rattus norvegicus	89-93
32888142-0	2020	Luminal subtypes and response to neoadjuvant chemotherapy for hormone receptor-positive HER2-negative patients.	Phenobarbital	0-7	nuclear receptor subfamily 4 group A member 1	Homo sapiens	62-78
32888142-0	2020	Luminal subtypes and response to neoadjuvant chemotherapy for hormone receptor-positive HER2-negative patients.	Phenobarbital	0-7	erb-b2 receptor tyrosine kinase 2	Homo sapiens	88-92
32508251-5	2020	We found that SOD3 expression was significantly reduced in breast carcinoma samples compared to normal tissues with the lowest levels observed in Luminal B subtype.	Phenobarbital	146-153	superoxide dismutase 3	Homo sapiens	14-18
33412751-3	2020	Luminal breast cancer is characterized by a relatively high expression of estrogen receptor (ER) and progesterone receptor (PR) genes, which are expressed in breast luminal cells.	Phenobarbital	165-172	estrogen receptor 1	Homo sapiens	74-91
33412751-3	2020	Luminal breast cancer is characterized by a relatively high expression of estrogen receptor (ER) and progesterone receptor (PR) genes, which are expressed in breast luminal cells.	Phenobarbital	165-172	estrogen receptor 1	Homo sapiens	93-95
33412751-3	2020	Luminal breast cancer is characterized by a relatively high expression of estrogen receptor (ER) and progesterone receptor (PR) genes, which are expressed in breast luminal cells.	Phenobarbital	165-172	progesterone receptor	Homo sapiens	101-122
33412751-3	2020	Luminal breast cancer is characterized by a relatively high expression of estrogen receptor (ER) and progesterone receptor (PR) genes, which are expressed in breast luminal cells.	Phenobarbital	165-172	progesterone receptor	Homo sapiens	124-126
33127441-7	2020	Collectively, our results indicate that hippocampal arterioles in CADASIL mice display a blunted contractile response to luminal pressure, similar to the defect we previously reported in cortical arterioles and pial arteries, that is rescued by HB-EGF.	Phenobarbital	121-128	heparin-binding EGF-like growth factor	Mus musculus	245-251
33106658-6	2020	These results suggest that phospholipids delivered by Atg2 are translocated from the cytoplasmic to the luminal leaflet by Atg9, thereby driving autophagosomal membrane expansion.	Phenobarbital	104-111	Atg2p	Saccharomyces cerevisiae S288C	54-58
33106658-6	2020	These results suggest that phospholipids delivered by Atg2 are translocated from the cytoplasmic to the luminal leaflet by Atg9, thereby driving autophagosomal membrane expansion.	Phenobarbital	104-111	autophagy protein ATG9	Saccharomyces cerevisiae S288C	123-127
32829006-5	2020	LIMK1 and PAK4 pharmacological inhibition synergistically reduced the survival of various cancer cell lines, exhibiting specific efficacy in luminal and HER2-enriched models, and suppressed development and ERalpha-driven signals in a BT474 xenograft model.	Phenobarbital	141-148	LIM domain kinase 1	Homo sapiens	0-5
32829006-5	2020	LIMK1 and PAK4 pharmacological inhibition synergistically reduced the survival of various cancer cell lines, exhibiting specific efficacy in luminal and HER2-enriched models, and suppressed development and ERalpha-driven signals in a BT474 xenograft model.	Phenobarbital	141-148	p21 (RAC1) activated kinase 4	Homo sapiens	10-14
32829006-7	2020	Double LIMK1 and PAK4 targeting therapy can be a successful therapeutic strategy for breast cancer, with a unique efficiency in the subtypes of luminal and HER2-enriched tumors.	Phenobarbital	144-151	LIM domain kinase 1	Homo sapiens	7-12
32829006-7	2020	Double LIMK1 and PAK4 targeting therapy can be a successful therapeutic strategy for breast cancer, with a unique efficiency in the subtypes of luminal and HER2-enriched tumors.	Phenobarbital	144-151	p21 (RAC1) activated kinase 4	Homo sapiens	17-21
33238591-3	2020	In this study we evaluated association of PD-L1 expression with other prognostic biomarkers, such as expression of miRNA-145 and miRNA-200a, FGFR3 gene expression, and mutation status in tissue specimens of the luminal subtype of newly diagnosed high and low grade NMIBC.	Phenobarbital	211-218	CD274 molecule	Homo sapiens	42-47
33292460-0	2020	Secretory phospholipase A2-X (Pla2g10) is a novel progesterone receptor target gene exclusively induced in uterine luminal epithelium for uterine receptivity in mice.	Phenobarbital	115-122	phospholipase A2, group X	Mus musculus	30-37
33248414-9	2021	There was a statistically significant difference in the number of CTCs between luminal A (ER+/PR+/HER2-) and HER-2+ (ER-/PR-/HER2+) (P < 0.05).	Phenobarbital	79-86	epiregulin	Homo sapiens	90-92
33248414-9	2021	There was a statistically significant difference in the number of CTCs between luminal A (ER+/PR+/HER2-) and HER-2+ (ER-/PR-/HER2+) (P < 0.05).	Phenobarbital	79-86	transmembrane protein 37	Homo sapiens	94-96
33380394-7	2020	In breast cancer tissues of different molecular types, ZNF652 was down-regulated in TNBC breast cancer tissues but increased in HER2+, Luminal A and Luminal B breast cancer tissues (P < 0.01 or 0.001).	Phenobarbital	135-142	zinc finger protein 652	Homo sapiens	55-61
33378667-5	2020	We find that Sec63 recruits and activates BiP ATPase through its luminal J-domain to bind onto IRE1alpha.	Phenobarbital	65-72	SEC63 homolog, protein translocation regulator	Homo sapiens	13-18
33378667-5	2020	We find that Sec63 recruits and activates BiP ATPase through its luminal J-domain to bind onto IRE1alpha.	Phenobarbital	65-72	growth differentiation factor 10	Homo sapiens	42-45
33378667-5	2020	We find that Sec63 recruits and activates BiP ATPase through its luminal J-domain to bind onto IRE1alpha.	Phenobarbital	65-72	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	95-104
33317560-8	2020	Staining of mid-secretory endometrial tissues of women with normal fertility and primary unexplained infertility showed reduced immunostaining intensity of TPP1 in luminal epithelial cells of infertile tissues compared to fertile tissues.	Phenobarbital	164-171	tripeptidyl peptidase 1	Homo sapiens	156-160
33322603-5	2020	Whole-mount in situ hybridization revealed cyp2y3, 2r1, and 3a65 transcripts in larvae at 55 hpf after exposure to rifampicin, phenobarbital, or 2,3,7,8-tetrachlorodibenzo-p-dioxin from 30 hpf onward.	Phenobarbital	127-140	cytochrome P450, family 2, subfamily Y, polypeptide 3	Danio rerio	43-49
33299040-6	2020	In the validation cohort, the radiomics signature yielded an AUC of 0.838, 0.556, and 0.645 for the TN, HER2 and luminal subtypes, respectively.	Phenobarbital	113-120	C-type lectin domain family 3 member B	Homo sapiens	100-102
33344592-6	2020	RESULTS: The proportion of patients with CD155 expression was higher in triple negative breast cancer (72.7%) than in Luminal A patients (22.2%, P < 0.05).	Phenobarbital	118-125	PVR cell adhesion molecule	Homo sapiens	41-46
33217309-3	2020	Endolysosomal CLC Cl-/H+ exchangers function as electric shunts for proton pumping and in luminal Cl- accumulation.	Phenobarbital	90-97	Charcot-Leyden crystal galectin	Homo sapiens	14-17
33299353-8	2020	Results: Both bioinformatics analysis and experimental verification confirmed that the FAM234B expression was significantly higher at the mRNA and protein levels in luminal BC tissues than in adjacent normal tissues.	Phenobarbital	165-172	family with sequence similarity 234 member B	Homo sapiens	87-94
33299353-12	2020	Besides, mechanism exploration indicated that pseudogene HTR7P1 might act as endogenous RNA to compete with has-miR-1271-5p or has-miR-381-3p for binding to FAM234B, thereby upregulating the expression of FAM234B in luminal BC.	Phenobarbital	216-223	5-hydroxytryptamine receptor 7 pseudogene 1	Homo sapiens	57-63
33299353-12	2020	Besides, mechanism exploration indicated that pseudogene HTR7P1 might act as endogenous RNA to compete with has-miR-1271-5p or has-miR-381-3p for binding to FAM234B, thereby upregulating the expression of FAM234B in luminal BC.	Phenobarbital	216-223	microRNA 1271	Homo sapiens	112-120
33299353-12	2020	Besides, mechanism exploration indicated that pseudogene HTR7P1 might act as endogenous RNA to compete with has-miR-1271-5p or has-miR-381-3p for binding to FAM234B, thereby upregulating the expression of FAM234B in luminal BC.	Phenobarbital	216-223	family with sequence similarity 234 member B	Homo sapiens	157-164
33299353-12	2020	Besides, mechanism exploration indicated that pseudogene HTR7P1 might act as endogenous RNA to compete with has-miR-1271-5p or has-miR-381-3p for binding to FAM234B, thereby upregulating the expression of FAM234B in luminal BC.	Phenobarbital	216-223	family with sequence similarity 234 member B	Homo sapiens	205-212
33273511-7	2020	Unlike the ePTFE graft, CD31-positive endothelial cells covered the whole luminal surface of the SF vascular graft at 4 weeks, indicating better endothelialization.	Phenobarbital	74-81	platelet and endothelial cell adhesion molecule 1	Rattus norvegicus	24-28
33129080-5	2020	DKK1 protein was detected in the luminal intimal area and in the necrotic core of plaques.	Phenobarbital	33-40	dickkopf WNT signaling pathway inhibitor 1	Homo sapiens	0-4
32915211-5	2020	During pregnancy, PGRMC1 was expressed within both the luminal and basal epithelium and gradually increased with gestation and decreased rapidly after parturition.	Phenobarbital	55-62	progesterone receptor membrane component 1	Mus musculus	18-24
33078616-2	2020	The role of endocrine therapy (ET), due to its favorable toxicity profile and first-line indication in luminal ABC, appears promising in the setting of LMD, where symptom stabilization and quality-of-life preservation are the main goals; however, evidenced-based data are lacking.	Phenobarbital	103-110	major facilitator superfamily domain containing 11	Homo sapiens	31-33
33078616-3	2020	We conducted a thorough review of published evidence, aiming to investigate the role of ET in LMD treatment in luminal ABC.	Phenobarbital	111-118	major facilitator superfamily domain containing 11	Homo sapiens	88-90
32436169-7	2020	CK7 expression was limited to a few luminal ductal cells.	Phenobarbital	36-43	keratin 7	Homo sapiens	0-3
33087404-9	2020	IL-1alpha is expressed predominantly by luminal cells of the genital tract in response to infection, and low levels of expression persisted after the infection cleared.	Phenobarbital	40-47	interleukin 1 alpha	Mus musculus	0-9
32656959-7	2020	Luminal TDCA crossed the epithelial lining via the apical sodium-dependent BA transporter (ASBT) and its inhibitor, GSK2330672 significantly reduced luminal, but not basolateral TDCA activity.	Phenobarbital	0-7	solute carrier family 10 member 2	Homo sapiens	51-89
32656959-7	2020	Luminal TDCA crossed the epithelial lining via the apical sodium-dependent BA transporter (ASBT) and its inhibitor, GSK2330672 significantly reduced luminal, but not basolateral TDCA activity.	Phenobarbital	0-7	solute carrier family 10 member 2	Homo sapiens	91-95
32656959-7	2020	Luminal TDCA crossed the epithelial lining via the apical sodium-dependent BA transporter (ASBT) and its inhibitor, GSK2330672 significantly reduced luminal, but not basolateral TDCA activity.	Phenobarbital	149-156	solute carrier family 10 member 2	Homo sapiens	51-89
32656959-7	2020	Luminal TDCA crossed the epithelial lining via the apical sodium-dependent BA transporter (ASBT) and its inhibitor, GSK2330672 significantly reduced luminal, but not basolateral TDCA activity.	Phenobarbital	149-156	solute carrier family 10 member 2	Homo sapiens	91-95
32656959-11	2020	Furthermore, luminal-conjugated BAs require transport across the epithelium via ASBT in order to activate basolateral GPBA.	Phenobarbital	13-20	solute carrier family 10 member 2	Homo sapiens	80-84
32986296-4	2020	Ubiquitin-fold modifier conjugating enzyme 1 (UFM1) and DDRGK domain containing 1 (DDRGK1) were mainly localized in the luminal epithelium and glandular epithelium of mouse and goat endometrial tissues.	Phenobarbital	120-127	ubiquitin-fold modifier conjugating enzyme 1	Mus musculus	0-44
32986296-4	2020	Ubiquitin-fold modifier conjugating enzyme 1 (UFM1) and DDRGK domain containing 1 (DDRGK1) were mainly localized in the luminal epithelium and glandular epithelium of mouse and goat endometrial tissues.	Phenobarbital	120-127	ubiquitin-fold modifier conjugating enzyme 1	Mus musculus	46-50
32986296-4	2020	Ubiquitin-fold modifier conjugating enzyme 1 (UFM1) and DDRGK domain containing 1 (DDRGK1) were mainly localized in the luminal epithelium and glandular epithelium of mouse and goat endometrial tissues.	Phenobarbital	120-127	DDRGK domain containing 1	Mus musculus	56-81
32986296-4	2020	Ubiquitin-fold modifier conjugating enzyme 1 (UFM1) and DDRGK domain containing 1 (DDRGK1) were mainly localized in the luminal epithelium and glandular epithelium of mouse and goat endometrial tissues.	Phenobarbital	120-127	DDRGK domain containing 1	Mus musculus	83-89
33325322-10	2020	We showed also that tumorspheres were enriched in differentiated luminal cells (EpCAM+/CD49f-).	Phenobarbital	65-72	epithelial cell adhesion molecule	Homo sapiens	80-85
33325322-10	2020	We showed also that tumorspheres were enriched in differentiated luminal cells (EpCAM+/CD49f-).	Phenobarbital	65-72	integrin subunit alpha 6	Homo sapiens	87-92
33274346-4	2020	Adenosine triphosphate (ATP)-binding cassette (ABC) transporters, such as P-glycoprotein (Pgp), line the luminal membrane of the brain capillary endothelium facing the vascular space.	Phenobarbital	105-112	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	47-50
33164044-11	2020	Our results identify clear differences in the response of ECs to TNF-alpha originating from the abluminal versus luminal side of a monolayer for the first time and may provide novel insight into future inflammatory disease intervention strategies.	Phenobarbital	98-105	eiger	Drosophila melanogaster	65-74
33274346-4	2020	Adenosine triphosphate (ATP)-binding cassette (ABC) transporters, such as P-glycoprotein (Pgp), line the luminal membrane of the brain capillary endothelium facing the vascular space.	Phenobarbital	105-112	ATP binding cassette subfamily B member 1	Homo sapiens	74-88
33274346-4	2020	Adenosine triphosphate (ATP)-binding cassette (ABC) transporters, such as P-glycoprotein (Pgp), line the luminal membrane of the brain capillary endothelium facing the vascular space.	Phenobarbital	105-112	ATP binding cassette subfamily B member 1	Homo sapiens	90-93
32816853-4	2020	In normal breast tissue, parity has been associated with hypermethylation of FOXA1, a pioneer transcription factor which promotes the luminal phenotype in luminal progenitors, while repressing the basal phenotype.	Phenobarbital	134-141	forkhead box A1	Homo sapiens	77-82
32816853-4	2020	In normal breast tissue, parity has been associated with hypermethylation of FOXA1, a pioneer transcription factor which promotes the luminal phenotype in luminal progenitors, while repressing the basal phenotype.	Phenobarbital	155-162	forkhead box A1	Homo sapiens	77-82
33176121-5	2020	Furthermore, molecular analyses of AR-deleted luminal cells isolated from developing prostates indicate their similarity to wild-type cells.	Phenobarbital	46-53	androgen receptor	Mus musculus	35-37
32758578-5	2020	Immunofluorescence results revealed that in the testes, a positive reaction for HSP70 protein was mainly seen in round spermatids and luminal sperms from the groups aged 1 year and 3 years.	Phenobarbital	134-141	heat shock 70 kDa protein 1A/1B	Ovis aries	80-85
33294786-5	2020	These findings suggest that various host- and/or microbiota-derived luminal factors region-specifically and synergistically stabilize the intestinal epithelial barrier following RYGB through FXR signaling, which could potentially be leveraged to better treat endotoxemia-induced insulin resistance in obesity in a non-invasive and more targeted manner.	Phenobarbital	68-75	nuclear receptor subfamily 1 group H member 4	Homo sapiens	191-194
32788213-2	2020	An anti-epileptic drug, phenobarbital (PB), activates CAR and its target CYP2B genes, while PXR is activated by drugs such as rifampicin and statins for the CYP3A genes.	Phenobarbital	24-37	nuclear receptor subfamily 1 group I member 3	Homo sapiens	54-57
32788213-2	2020	An anti-epileptic drug, phenobarbital (PB), activates CAR and its target CYP2B genes, while PXR is activated by drugs such as rifampicin and statins for the CYP3A genes.	Phenobarbital	24-37	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	73-78
32788213-2	2020	An anti-epileptic drug, phenobarbital (PB), activates CAR and its target CYP2B genes, while PXR is activated by drugs such as rifampicin and statins for the CYP3A genes.	Phenobarbital	24-37	nuclear receptor subfamily 1 group I member 2	Homo sapiens	92-95
32788213-2	2020	An anti-epileptic drug, phenobarbital (PB), activates CAR and its target CYP2B genes, while PXR is activated by drugs such as rifampicin and statins for the CYP3A genes.	Phenobarbital	24-37	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	157-162
32788213-2	2020	An anti-epileptic drug, phenobarbital (PB), activates CAR and its target CYP2B genes, while PXR is activated by drugs such as rifampicin and statins for the CYP3A genes.	Phenobarbital	39-41	nuclear receptor subfamily 1 group I member 3	Homo sapiens	54-57
32788213-2	2020	An anti-epileptic drug, phenobarbital (PB), activates CAR and its target CYP2B genes, while PXR is activated by drugs such as rifampicin and statins for the CYP3A genes.	Phenobarbital	39-41	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	73-78
32788213-2	2020	An anti-epileptic drug, phenobarbital (PB), activates CAR and its target CYP2B genes, while PXR is activated by drugs such as rifampicin and statins for the CYP3A genes.	Phenobarbital	39-41	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	157-162
32788213-4	2020	However, PB, which does not bind CAR directly, presented an alternative research avenue for an indirect ligand-mediated nuclear receptor activation mechanism: phosphorylation-mediated signal regulation.	Phenobarbital	9-11	nuclear receptor subfamily 1 group I member 3	Homo sapiens	33-36
32788213-6	2020	First, the review presents how PB activates CAR (and other nuclear receptors) through a conserved phosphorylation motif located between two zinc fingers within its DNA binding domain (DBD).	Phenobarbital	31-33	nuclear receptor subfamily 1 group I member 3	Homo sapiens	44-47
33224932-9	2020	Detection of the luminal membrane protein TSG101 with antibodies depended on membrane permeabilization, consistent with the presence of vesicles on the chip.	Phenobarbital	17-24	tumor susceptibility 101	Homo sapiens	42-48
33195960-5	2020	Luminal flow (in contrast to static culture) decreases the activity of cathepsins in microvessel systems, despite a total protein increase, due to a concurrent increase in the endogenous inhibitor cystatin C.	Phenobarbital	0-7	cystatin C	Homo sapiens	197-207
32839004-6	2020	The Luminal, HER2-enriched, and Basal-like intrinsic subtypes are generally characterized by the presence or absence of ER and HER2.	Phenobarbital	4-11	erb-b2 receptor tyrosine kinase 2	Homo sapiens	127-131
32701507-3	2020	Through integrating analysis of the transcription factors (TFs) from 806 human prostate cancers, we found that ERG was highly correlated with prostate cancer luminal subtyping.	Phenobarbital	158-165	ETS transcription factor ERG	Homo sapiens	111-114
32701507-4	2020	ERG overexpression in luminal epithelial cells inhibited those cells" normal plasticity to transdifferentiate into a basal lineage, and ERG superseded PTEN loss, which favored basal differentiation.	Phenobarbital	22-29	ETS transcription factor ERG	Homo sapiens	0-3
32701507-4	2020	ERG overexpression in luminal epithelial cells inhibited those cells" normal plasticity to transdifferentiate into a basal lineage, and ERG superseded PTEN loss, which favored basal differentiation.	Phenobarbital	22-29	phosphatase and tensin homolog	Homo sapiens	151-155
32701507-5	2020	ERG KO disrupted prostate cell luminal differentiation, whereas AR KO had no such effects.	Phenobarbital	31-38	ETS transcription factor ERG	Homo sapiens	0-3
32805234-1	2020	The prostate epithelium consists of predominantly luminal cells that express androgen receptor and require androgens for growth.	Phenobarbital	50-57	androgen receptor	Mus musculus	77-94
32682817-8	2020	CRISPR/Cas9 or siRNA-mediated SIK3 knockout/knockdown showed an opposite trend in both the luminal and basal-like breast cancer.	Phenobarbital	91-98	SIK family kinase 3	Homo sapiens	30-34
32270769-3	2020	In mice, the risk of oxidative damage to spermatozoa is mitigated through the expression and secretion of glutathione peroxidase 5 (GPX5) as a major luminal scavenger in the proximal caput epididymidal segment.	Phenobarbital	149-156	glutathione peroxidase 5	Mus musculus	106-130
32270769-3	2020	In mice, the risk of oxidative damage to spermatozoa is mitigated through the expression and secretion of glutathione peroxidase 5 (GPX5) as a major luminal scavenger in the proximal caput epididymidal segment.	Phenobarbital	149-156	glutathione peroxidase 5	Mus musculus	132-136
33179538-2	2020	Results & methodology: Using in silico analysis, we found that Luminal A and B patients" short relapse-free survival was associated with low PHLDA1 or PHLDA3 and high PHLDA2 expression.	Phenobarbital	63-70	pleckstrin homology like domain family A member 1	Homo sapiens	141-147
33179538-2	2020	Results & methodology: Using in silico analysis, we found that Luminal A and B patients" short relapse-free survival was associated with low PHLDA1 or PHLDA3 and high PHLDA2 expression.	Phenobarbital	63-70	pleckstrin homology like domain family A member 3	Homo sapiens	151-157
33179538-2	2020	Results & methodology: Using in silico analysis, we found that Luminal A and B patients" short relapse-free survival was associated with low PHLDA1 or PHLDA3 and high PHLDA2 expression.	Phenobarbital	63-70	pleckstrin homology like domain family A member 2	Homo sapiens	167-173
32911258-13	2020	Phenobarbital inhibited hGluA2(R) at an IC50 value of 730,000 nM.	Phenobarbital	0-13	glutamate ionotropic receptor AMPA type subunit 2	Homo sapiens	24-30
32737714-11	2020	CONCLUSIONS: HER2 positivity is related to the longer OS after SRS; however, we should pay attention to preventing recurrence in Luminal-HER2 patients.	Phenobarbital	129-136	erb-b2 receptor tyrosine kinase 2	Homo sapiens	13-17
32737714-11	2020	CONCLUSIONS: HER2 positivity is related to the longer OS after SRS; however, we should pay attention to preventing recurrence in Luminal-HER2 patients.	Phenobarbital	129-136	erb-b2 receptor tyrosine kinase 2	Homo sapiens	137-141
32546648-4	2020	The luminal B/HER2-positive subtype displayed 3+ HER2-IHC or amplification by ISH.	Phenobarbital	4-11	erb-b2 receptor tyrosine kinase 2	Homo sapiens	14-18
32546648-4	2020	The luminal B/HER2-positive subtype displayed 3+ HER2-IHC or amplification by ISH.	Phenobarbital	4-11	erb-b2 receptor tyrosine kinase 2	Homo sapiens	49-53
32911258-16	2020	Perampanel is the only ASM that had a potent inhibitory effect on all AMPA receptor subtypes, but did not inhibit NMDA or kainate receptor subunits; while phenobarbital inhibited GluA2(R), and carbamazepine and lamotrigine inhibited the NMDA receptor at high concentration ranges.	Phenobarbital	155-168	glutamate ionotropic receptor AMPA type subunit 2	Homo sapiens	179-184
32842790-12	2020	By IHC, SAA3 protein was highly expressed in the luminal side of the bronchial epithelium, while SAA1/2 was not expressed.	Phenobarbital	49-56	serum amyloid A 3	Mus musculus	8-12
32870507-0	2020	CrossTalk opposing view: NKCC1 in the luminal membrane of choroid plexus is outwardly directed under basal conditions and contributes directly to cerebrospinal fluid secretion.	Phenobarbital	38-45	solute carrier family 12 member 2	Homo sapiens	25-30
32959924-2	2020	We here refined the molecular interaction of the two proteins and found that the luminal domain of GLMP alone, but not its transmembrane domain or its short cytosolic tail, conveys protection and mediates the interaction with MFSD1.	Phenobarbital	81-88	glycosylated lysosomal membrane protein	Homo sapiens	99-103
32959924-2	2020	We here refined the molecular interaction of the two proteins and found that the luminal domain of GLMP alone, but not its transmembrane domain or its short cytosolic tail, conveys protection and mediates the interaction with MFSD1.	Phenobarbital	81-88	major facilitator superfamily domain containing 1	Homo sapiens	226-231
32687927-14	2020	Exogenous luminal GDNF penetrated aganglionic colon epithelium of HolTg/Tg mice, inducing production of endogenous GDNF, and new enteric neurons and glia appeared to arise from Schwann cells within extrinsic nerves.	Phenobarbital	10-17	glial cell line derived neurotrophic factor	Mus musculus	18-22
32687927-14	2020	Exogenous luminal GDNF penetrated aganglionic colon epithelium of HolTg/Tg mice, inducing production of endogenous GDNF, and new enteric neurons and glia appeared to arise from Schwann cells within extrinsic nerves.	Phenobarbital	10-17	glial cell line derived neurotrophic factor	Mus musculus	115-119
32705365-4	2020	RESULTS: We are the first to report increased NRF1 activity based on its differential effects on genome-wide transcription associated with luminal A and B, HER2+ and triple-negative (TN) molecular subtypes of breast cancer in women of different race/ethnicity.	Phenobarbital	139-146	nuclear respiratory factor 1	Homo sapiens	46-50
32705365-11	2020	CONCLUSION: Our findings showed how sensitivity to high NRF1 transcriptional activity coupled with its target gene signatures contribute to racial differences in luminal A and TN breast cancer subtypes.	Phenobarbital	162-169	nuclear respiratory factor 1	Homo sapiens	56-60
32719544-11	2020	In conclusion, these data suggest that loss of CFTR-mediated anion transport and fluid secretion contribute to microgallbladder development and luminal mucus accumulation in CF.	Phenobarbital	144-151	CF transmembrane conductance regulator	Sus scrofa	47-51
32562180-6	2020	RESULTS: The predictive factors of the luminal B(HER2-) subtype (n = 51) were the mass with microcalcifications, irregular shape, spiculated margins, and shadowing posterior features (all P < 0.01).	Phenobarbital	39-46	erb-b2 receptor tyrosine kinase 2	Homo sapiens	49-53
32562180-7	2020	The predictive factors of the luminal B(HER2+) subtype (n = 26) were the spiculated margins (DBT + DM), angular margins (US), shadowing posterior features, and high vascularity (all P < 0.05).	Phenobarbital	30-37	erb-b2 receptor tyrosine kinase 2	Homo sapiens	40-44
32892155-3	2020	Treatment of mice with the CAR activator phenobarbital, an antiepileptic drug, increased plasma triglyceride levels and decreased the hepatic expression of PPARalpha target genes related to lipid metabolism.	Phenobarbital	41-54	nuclear receptor subfamily 1, group I, member 3	Mus musculus	27-30
32788342-8	2020	Notably, the SEC62 interactome is enriched in redox-linked proteins and ER luminal chaperones, with the latter likely representing proximity to an ER luminal chaperone reflux pathway.	Phenobarbital	75-82	SEC62 homolog, preprotein translocation factor	Homo sapiens	13-18
32788342-8	2020	Notably, the SEC62 interactome is enriched in redox-linked proteins and ER luminal chaperones, with the latter likely representing proximity to an ER luminal chaperone reflux pathway.	Phenobarbital	150-157	SEC62 homolog, preprotein translocation factor	Homo sapiens	13-18
32892155-3	2020	Treatment of mice with the CAR activator phenobarbital, an antiepileptic drug, increased plasma triglyceride levels and decreased the hepatic expression of PPARalpha target genes related to lipid metabolism.	Phenobarbital	41-54	peroxisome proliferator activated receptor alpha	Mus musculus	156-165
32892155-8	2020	In mammalian two-hybrid assays, CAR attenuated the interaction between PGC1alpha and PPARalpha Chemical inhibition of PGC1alpha prevented phenobarbital-dependent increases in plasma triglyceride levels and the inhibition of PPARalpha target gene expression.	Phenobarbital	138-151	PPARG coactivator 1 alpha	Homo sapiens	118-127
32892155-4	2020	The increase in PPARalpha target gene expression induced by fenofibrate, a PPARalpha ligand, was inhibited by cotreatment with phenobarbital.	Phenobarbital	127-140	peroxisome proliferator activated receptor alpha	Mus musculus	16-25
32892155-4	2020	The increase in PPARalpha target gene expression induced by fenofibrate, a PPARalpha ligand, was inhibited by cotreatment with phenobarbital.	Phenobarbital	127-140	peroxisome proliferator activated receptor alpha	Mus musculus	75-84
32892155-8	2020	In mammalian two-hybrid assays, CAR attenuated the interaction between PGC1alpha and PPARalpha Chemical inhibition of PGC1alpha prevented phenobarbital-dependent increases in plasma triglyceride levels and the inhibition of PPARalpha target gene expression.	Phenobarbital	138-151	nuclear receptor subfamily 1 group I member 3	Homo sapiens	32-35
32892155-8	2020	In mammalian two-hybrid assays, CAR attenuated the interaction between PGC1alpha and PPARalpha Chemical inhibition of PGC1alpha prevented phenobarbital-dependent increases in plasma triglyceride levels and the inhibition of PPARalpha target gene expression.	Phenobarbital	138-151	peroxisome proliferator activated receptor alpha	Homo sapiens	224-233
32892155-8	2020	In mammalian two-hybrid assays, CAR attenuated the interaction between PGC1alpha and PPARalpha Chemical inhibition of PGC1alpha prevented phenobarbital-dependent increases in plasma triglyceride levels and the inhibition of PPARalpha target gene expression.	Phenobarbital	138-151	PPARG coactivator 1 alpha	Homo sapiens	71-80
32892155-8	2020	In mammalian two-hybrid assays, CAR attenuated the interaction between PGC1alpha and PPARalpha Chemical inhibition of PGC1alpha prevented phenobarbital-dependent increases in plasma triglyceride levels and the inhibition of PPARalpha target gene expression.	Phenobarbital	138-151	peroxisome proliferator activated receptor alpha	Homo sapiens	85-94
32949181-4	2020	Wnt7a immunostaining was not limited only to the luminal epithelial cells, but also to strong stainings in the stromal and endothelial cells.	Phenobarbital	49-56	Wnt family member 7A	Rattus norvegicus	0-5
33010173-1	2020	We previously showed that annexin A2 was transiently expressed at the embryo-uterine luminal epithelium interface during the window of implantation, and was involved in mouse embryo implantation.	Phenobarbital	85-92	annexin A2	Mus musculus	26-36
32952662-4	2020	Mesothelin expression was detected in 77 (16.0%) cases and was the highest in triple-negative breast cancer (31/75; 41.3%), followed by human epithelial growth factor receptor type 2 type (6/33, 18.2%) and luminal type (36/374; 9.6%).	Phenobarbital	206-213	mesothelin	Homo sapiens	0-10
32952662-7	2020	In the 343 cases of luminal type, the membrane mesothelin expression-positive group had significantly worse prognosis than the membrane mesothelin-expression-negative group (P=0.042).	Phenobarbital	20-27	mesothelin	Homo sapiens	47-57
32826754-8	2020	ACE2 mRNA is expressed by a subset of nociceptors that express MRGPRD mRNA, suggesting that SARS-CoV-2 may gain access to the nervous system through entry into neurons that form free nerve endings at the outermost layers of skin and luminal organs.	Phenobarbital	233-240	angiotensin converting enzyme 2	Homo sapiens	0-4
33000282-3	2020	In the present study, it was revealed that E2F5 gene silencing caused a significant reduction in the proliferation rate of breast cancer MCF7 (ER-positive luminal-type) and MDA-MB-231 (TNBC-type) cells.	Phenobarbital	155-162	E2F transcription factor 5	Homo sapiens	43-47
33000282-3	2020	In the present study, it was revealed that E2F5 gene silencing caused a significant reduction in the proliferation rate of breast cancer MCF7 (ER-positive luminal-type) and MDA-MB-231 (TNBC-type) cells.	Phenobarbital	155-162	estrogen receptor 1	Homo sapiens	143-145
33009488-0	2020	De novo induction of lineage plasticity from human prostate luminal epithelial cells by activated AKT1 and c-Myc.	Phenobarbital	60-67	AKT serine/threonine kinase 1	Homo sapiens	98-102
32627901-2	2020	We show that the Sca-1+ luminal cells at the mouse proximal prostate express Sox2.	Phenobarbital	24-31	ataxin 1	Mus musculus	17-22
33009488-0	2020	De novo induction of lineage plasticity from human prostate luminal epithelial cells by activated AKT1 and c-Myc.	Phenobarbital	60-67	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	107-112
33068730-4	2020	LINC01087 appeared significantly downregulated in triple-negative BCs (TNBCs) and upregulated in the luminal BC subtypes in comparison to mammary samples from cancer-free women and matched normal cancer pairs.	Phenobarbital	101-108	long intergenic non-protein coding RNA 1087	Homo sapiens	0-9
33068730-5	2020	Interestingly, deregulation of LINC01087 allowed to accurately distinguish between luminal and TNBC specimens, independently of the clinicopathological parameters, and of the histological and TP53 or BRCA1/2 mutational status.	Phenobarbital	83-90	long intergenic non-protein coding RNA 1087	Homo sapiens	31-40
32985412-8	2020	The levels of MUC5B, ORM1, RTBDN, and TENP mRNA were significantly high in the oviduct, and the genes were repressed in the regression phase, whereas these were expressed in the recrudescence phase, particularly in the luminal epithelium and glandular epithelium of the oviduct, during molting.	Phenobarbital	219-226	ovomucin, alpha subunit	Gallus gallus	14-19
32985412-8	2020	The levels of MUC5B, ORM1, RTBDN, and TENP mRNA were significantly high in the oviduct, and the genes were repressed in the regression phase, whereas these were expressed in the recrudescence phase, particularly in the luminal epithelium and glandular epithelium of the oviduct, during molting.	Phenobarbital	219-226	BPI fold containing family B member 2	Gallus gallus	38-42
32627901-2	2020	We show that the Sca-1+ luminal cells at the mouse proximal prostate express Sox2.	Phenobarbital	24-31	SRY (sex determining region Y)-box 2	Mus musculus	77-81
32627901-6	2020	Sox2 is dispensable for the maintenance of the Sca-1+ luminal cells but is essential for their facultative bipotent differentiation capacity.	Phenobarbital	54-61	SRY (sex determining region Y)-box 2	Mus musculus	0-4
32627901-7	2020	The Sca-1+ luminal cells share molecular features with the human TACSTD2+ luminal cells.	Phenobarbital	11-18	ataxin 1	Homo sapiens	4-9
32627901-7	2020	The Sca-1+ luminal cells share molecular features with the human TACSTD2+ luminal cells.	Phenobarbital	11-18	tumor associated calcium signal transducer 2	Homo sapiens	65-72
32861000-4	2020	In situ hybridization results revealed that miR-192-5p was primarily expressed in the endometrial epithelium, and dysregulation of miR-192-5p interfered with the performance of the luminal epithelium, resulting in inadequate receptivity.	Phenobarbital	181-188	microRNA 192	Mus musculus	131-138
32627901-7	2020	The Sca-1+ luminal cells share molecular features with the human TACSTD2+ luminal cells.	Phenobarbital	74-81	ataxin 1	Homo sapiens	4-9
32627901-7	2020	The Sca-1+ luminal cells share molecular features with the human TACSTD2+ luminal cells.	Phenobarbital	74-81	tumor associated calcium signal transducer 2	Homo sapiens	65-72
32627901-9	2020	AlphaMed Press 2020 SIGNIFICANCE STATEMENT: This study characterizes the phenotypic and functional heterogeneity of the mouse prostate luminal epithelial cells and demonstrates a critical role of Sox2 in maintaining the facultative bipotent differentiation capacity of the Sca-1+ luminal cells.	Phenobarbital	135-142	SRY (sex determining region Y)-box 2	Mus musculus	196-200
32627901-9	2020	AlphaMed Press 2020 SIGNIFICANCE STATEMENT: This study characterizes the phenotypic and functional heterogeneity of the mouse prostate luminal epithelial cells and demonstrates a critical role of Sox2 in maintaining the facultative bipotent differentiation capacity of the Sca-1+ luminal cells.	Phenobarbital	280-287	SRY (sex determining region Y)-box 2	Mus musculus	196-200
32828539-6	2020	Immunofluorescence analysis illustrated that PGN completely suppressed the IFNT-triggered OAS1 protein expression in the luminal epithelium of explants.	Phenobarbital	121-128	interferon tau-2	Bos taurus	75-79
32451148-7	2020	The method is applied to multi echo spin echo MRI scans and computes myelin water maps of the whole brain in under 2min, and luminal water maps of the prostate in under 1min.	Phenobarbital	125-132	spindlin 1	Homo sapiens	36-40
32998907-7	2020	According to lineage tracing, PAX8 positive (PAX8+) epithelial cells are responsible for long-term maintenance of both luminal and glandular epithelium.	Phenobarbital	119-126	paired box 8	Mus musculus	30-34
32998907-7	2020	According to lineage tracing, PAX8 positive (PAX8+) epithelial cells are responsible for long-term maintenance of both luminal and glandular epithelium.	Phenobarbital	119-126	paired box 8	Mus musculus	45-49
32828539-6	2020	Immunofluorescence analysis illustrated that PGN completely suppressed the IFNT-triggered OAS1 protein expression in the luminal epithelium of explants.	Phenobarbital	121-128	2',5'-oligoadenylate synthetase 1	Bos taurus	90-94
33115736-1	2020	Extended-release gastrointestinal (GI) luminal delivery substantially increases the ease of administration of drugs and consequently the adherence to therapeutic regimens.	Phenobarbital	39-46	G protein subunit alpha i1	Homo sapiens	35-37
33119552-6	2020	High CEP78 expression was found to be correlated with non-papillary histological type, luminal, basal-squamous and neuronal molecular subtypes, TP53 mutation, RB1 mutation, wild-type FGFR3, PPARG fusion and amplification, high total number of single-nucleotide variants, and high neoantigen load, but it was not associated with tumor stages or overall survival.	Phenobarbital	87-94	centrosomal protein 78	Homo sapiens	5-10
32807494-5	2020	CLIC4 expression was significantly reduced in the luminal and glandular epithelium and remained unchanged in the stromal region of mid-secretory infertile endometrium compared to fertile endometrium.	Phenobarbital	50-57	chloride intracellular channel 4	Homo sapiens	0-5
33086071-1	2020	The mammary epithelial cell (MEC) system is a bilayered ductal epithelium of luminal and basal cells, maintained by a lineage of stem and progenitor populations.	Phenobarbital	77-84	chemokine (C-C motif) ligand 28	Mus musculus	29-32
33091174-11	2021	These have potentially detrimental effects on predicted luminal release patterns of pH-dependent 5-aminosalicylic acid release systems.	Phenobarbital	56-63	phenylalanine hydroxylase	Homo sapiens	84-86
33050377-5	2020	Our results of network and pathway analysis of the 12 samples highlighted the importance of VEGFR and CDKs in promoting luminal-A breast cancer.	Phenobarbital	120-127	kinase insert domain receptor	Homo sapiens	92-97
33134390-5	2020	High METTL14 expression was more common in luminal A and luminal B tissue (75.9% and 60.8%, respectively), compared with human epidermal growth factor receptor 2- (HER2-) enriched and triple-negative breast cancer (TNBC) samples (38.2% and 18.6%, respectively).	Phenobarbital	43-50	methyltransferase 14, N6-adenosine-methyltransferase subunit	Homo sapiens	5-12
33066779-11	2020	Analysis of the gene expression data in the context of the survival data revealed that high expression of NMUR1 and NCAM1 in luminal A breast cancer statistically correlated with poor prognosis, whereas the low expression levels of CDC7, KIF18A, STIL, and CKS2 in basal-like breast cancer statistically correlated with poor prognosis.	Phenobarbital	125-132	neuromedin U receptor 1	Homo sapiens	106-111
33066779-11	2020	Analysis of the gene expression data in the context of the survival data revealed that high expression of NMUR1 and NCAM1 in luminal A breast cancer statistically correlated with poor prognosis, whereas the low expression levels of CDC7, KIF18A, STIL, and CKS2 in basal-like breast cancer statistically correlated with poor prognosis.	Phenobarbital	125-132	neural cell adhesion molecule 1	Homo sapiens	116-121
33059724-10	2020	TP53, PIK3R1, and NF1 somatic alterations were more frequently detected in triple negative tumors (p value < 0.05); CCND1, FGF3, and FGFR1 copy number gains were recurrently identified in luminal cases (p value < 0.05).	Phenobarbital	188-195	fibroblast growth factor 3	Homo sapiens	123-127
33059724-10	2020	TP53, PIK3R1, and NF1 somatic alterations were more frequently detected in triple negative tumors (p value < 0.05); CCND1, FGF3, and FGFR1 copy number gains were recurrently identified in luminal cases (p value < 0.05).	Phenobarbital	188-195	fibroblast growth factor receptor 1	Homo sapiens	133-138
32989154-5	2020	We show that UTX loss and FGFR3 activation cooperate to disrupt the balance of luminal and basal gene expression in bladder cells.	Phenobarbital	79-86	lysine demethylase 6A	Homo sapiens	13-16
32989154-5	2020	We show that UTX loss and FGFR3 activation cooperate to disrupt the balance of luminal and basal gene expression in bladder cells.	Phenobarbital	79-86	fibroblast growth factor receptor 3	Homo sapiens	26-31
32989154-6	2020	UTX localized to enhancers surrounding many genes that are important for luminal cell fate, and supported the transcription of these genes in a catalytic-independent manner.	Phenobarbital	73-80	lysine demethylase 6A	Homo sapiens	0-3
32989154-7	2020	In contrast to UTX, FGFR3 activation was associated with lower expression of luminal genes in tumors and FGFR inhibition increased transcription of these same genes in cell culture models.	Phenobarbital	77-84	fibroblast growth factor receptor 3	Homo sapiens	20-25
33123289-1	2020	Breast cancer is one of the most common malignancies worldwide, while the luminal types (ERalpha positive) accounts for two third of all breast cancer cases.	Phenobarbital	74-81	estrogen receptor 1	Homo sapiens	89-96
33050406-10	2020	The results imply that the uptake of exogenous CoQ10 into the brain might be improved by the administration of LDLR inhibitors, or by interventions to stimulate luminal activity of SR-B1 transporters.	Phenobarbital	161-168	scavenger receptor class B member 1	Homo sapiens	181-186
33050377-5	2020	Our results of network and pathway analysis of the 12 samples highlighted the importance of VEGFR and CDKs in promoting luminal-A breast cancer.	Phenobarbital	120-127	cyclin dependent kinase 2	Homo sapiens	102-106
33025905-0	2020	RUNX1 marks a luminal castration resistant lineage established at the onset of prostate development.	Phenobarbital	14-21	runt related transcription factor 1	Mus musculus	0-5
33025905-2	2020	Here, we report that the transcription factor RUNX1 marks a specific subpopulation of proximal luminal cells (PLCs), enriched in the periurethral region of the developing and adult mouse prostate, and distinct from the previously identified NKX3.1+ luminal castration resistant cells.	Phenobarbital	95-102	runt related transcription factor 1	Mus musculus	46-51
33025905-2	2020	Here, we report that the transcription factor RUNX1 marks a specific subpopulation of proximal luminal cells (PLCs), enriched in the periurethral region of the developing and adult mouse prostate, and distinct from the previously identified NKX3.1+ luminal castration resistant cells.	Phenobarbital	249-256	runt related transcription factor 1	Mus musculus	46-51
33342810-10	2020	Moreover, mean transcript levels of TNF-alpha and NF-kappaB1 were significantly elevated in Luminal A and Luminal B subtypes of breast cancer patients, respectively.	Phenobarbital	92-99	tumor necrosis factor	Homo sapiens	36-45
32958677-5	2020	As expected, the conventional catalytic system requires an intact active site in the Man1b1 luminal domain.	Phenobarbital	92-99	mannosidase alpha class 1B member 1	Homo sapiens	85-91
33021976-3	2020	Using atomistic simulations, we show that in the absence of cholesterol in the SSD, the luminal domains of NPC1 are highly dynamic, resulting in the disengagement of the NTD from the rest of the protein.	Phenobarbital	88-95	NPC intracellular cholesterol transporter 1	Homo sapiens	107-111
33021976-5	2020	The binding of cholesterol to the SSD of NPC1 allosterically suppresses the conformational dynamics of the luminal domains resulting in an upright NTD conformation.	Phenobarbital	107-114	NPC intracellular cholesterol transporter 1	Homo sapiens	41-45
33024416-19	2020	Moreover, bioinformatics analysis provided a basis for better identification of the potential role of LINC00961 in luminal subtype of BC.	Phenobarbital	115-122	small regulatory polypeptide of amino acid response	Homo sapiens	102-111
32415725-1	2020	AIM: SLC26A3 (DRA) mediates the absorption of luminal Cl- in exchange for HCO3 - in the distal intestine.	Phenobarbital	46-53	solute carrier family 26, member 3	Mus musculus	5-12
32415725-1	2020	AIM: SLC26A3 (DRA) mediates the absorption of luminal Cl- in exchange for HCO3 - in the distal intestine.	Phenobarbital	46-53	solute carrier family 26, member 3	Mus musculus	14-17
32415725-9	2020	Slc26a3-/- colonic luminal microbiome displayed strong decrease in diversity.	Phenobarbital	19-26	solute carrier family 26, member 3	Mus musculus	0-7
32845431-1	2020	Mesencephalic astrocyte-derived neurotrophic factor (MANF) and cerebral dopamine neurotrophic factor (CDNF) are endoplasmic reticulum (ER) luminal proteins that confer trophic activities in a wide range of tissues under diverse pathological conditions.	Phenobarbital	139-146	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	0-51
32845431-1	2020	Mesencephalic astrocyte-derived neurotrophic factor (MANF) and cerebral dopamine neurotrophic factor (CDNF) are endoplasmic reticulum (ER) luminal proteins that confer trophic activities in a wide range of tissues under diverse pathological conditions.	Phenobarbital	139-146	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	53-57
32845431-1	2020	Mesencephalic astrocyte-derived neurotrophic factor (MANF) and cerebral dopamine neurotrophic factor (CDNF) are endoplasmic reticulum (ER) luminal proteins that confer trophic activities in a wide range of tissues under diverse pathological conditions.	Phenobarbital	139-146	cerebral dopamine neurotrophic factor	Homo sapiens	63-100
32845431-1	2020	Mesencephalic astrocyte-derived neurotrophic factor (MANF) and cerebral dopamine neurotrophic factor (CDNF) are endoplasmic reticulum (ER) luminal proteins that confer trophic activities in a wide range of tissues under diverse pathological conditions.	Phenobarbital	139-146	cerebral dopamine neurotrophic factor	Homo sapiens	102-106
33342796-5	2020	Materials and Methods: EpCAM expression was assessed by immunohistochemical studies on 200 breast carcinoma tissue samples of different molecular subtypes, including luminal A, luminal B, Her2Neu, and triple-negative breast cancer (TNBC).	Phenobarbital	166-173	epithelial cell adhesion molecule	Homo sapiens	23-28
33342796-5	2020	Materials and Methods: EpCAM expression was assessed by immunohistochemical studies on 200 breast carcinoma tissue samples of different molecular subtypes, including luminal A, luminal B, Her2Neu, and triple-negative breast cancer (TNBC).	Phenobarbital	177-184	epithelial cell adhesion molecule	Homo sapiens	23-28
33024416-5	2020	The purpose of the present study was to investigate the possible role of LINC00961 in luminal A and B subtypes of BC.	Phenobarbital	86-93	small regulatory polypeptide of amino acid response	Homo sapiens	73-82
33024416-7	2020	After performing literature review, the expression level of the selected lncRNA (LINC00961) was evaluated in 79 luminal A and B BC specimens and adjacent non-cancerous tissues by Quantitative Reverse Transcription PCR (qRT-PCR).	Phenobarbital	112-119	small regulatory polypeptide of amino acid response	Homo sapiens	81-90
33024416-13	2020	According to q-RT PCR assay, LINC00961 was downregulated in luminal BC tissues and cell lines.	Phenobarbital	60-67	small regulatory polypeptide of amino acid response	Homo sapiens	29-38
33024416-16	2020	The final results indicated that LINC00961 might be involved in multiple cancer-associated pathways such as chemokine, Ras and PI3K-Akt signaling pathways, GPCR ligand binding, and signal transduction in luminal subtypes of BC.	Phenobarbital	204-211	small regulatory polypeptide of amino acid response	Homo sapiens	33-42
33024416-16	2020	The final results indicated that LINC00961 might be involved in multiple cancer-associated pathways such as chemokine, Ras and PI3K-Akt signaling pathways, GPCR ligand binding, and signal transduction in luminal subtypes of BC.	Phenobarbital	204-211	AKT serine/threonine kinase 1	Homo sapiens	132-135
33024416-17	2020	CDH5, GNG11, GNG8, SELL, S1PR1, CCL19, FYN, ACAN, CD3E, ACVRL1, CAV1, and PPARGC1A were identified as the top hub genes of the PPI networks across luminal subgroup.	Phenobarbital	147-154	cadherin 5	Homo sapiens	0-4
33024416-18	2020	Conclusion: Our findings suggested that LINC00961 was significantly downregulated in luminal A and B subtypes of BC.	Phenobarbital	85-92	small regulatory polypeptide of amino acid response	Homo sapiens	40-49
32988879-9	2020	Progesterone receptor (PR) expression influenced E-cadh M pattern in the Luminal B/HER2 subtype (p=0.042).	Phenobarbital	73-80	progesterone receptor	Homo sapiens	0-21
32988879-9	2020	Progesterone receptor (PR) expression influenced E-cadh M pattern in the Luminal B/HER2 subtype (p=0.042).	Phenobarbital	73-80	progesterone receptor	Homo sapiens	23-25
32988879-9	2020	Progesterone receptor (PR) expression influenced E-cadh M pattern in the Luminal B/HER2 subtype (p=0.042).	Phenobarbital	73-80	erb-b2 receptor tyrosine kinase 2	Homo sapiens	83-87
32685993-5	2020	RESULTS: We found subtype-specific expression differences for ATG4B, with its expression lowest in basal-like breast cancer and highest in Luminal A, but there were no significant associations with patient prognosis.	Phenobarbital	139-146	autophagy related 4B cysteine peptidase	Homo sapiens	62-67
32467058-10	2020	Younger patients (<= 50 years), grade 3 tumors, positive axillary nodes, recurrence, and distant metastasis had a positive statistical correlation with luminal B-like (HER2-) subtype.	Phenobarbital	152-159	erb-b2 receptor tyrosine kinase 2	Homo sapiens	168-172
33122354-11	2020	Finally, a miR-100-based signature developed in patients enrolled in the prospective study outperformed Ki67 alone in predicting the luminal A phenotype.	Phenobarbital	133-140	microRNA 100	Homo sapiens	11-18
32707133-0	2020	Notch activation in the mouse mammary luminal lineage leads to ductal hyperplasia and altered partitioning of luminal cell subtypes.	Phenobarbital	38-45	notch 1	Mus musculus	0-5
32707133-0	2020	Notch activation in the mouse mammary luminal lineage leads to ductal hyperplasia and altered partitioning of luminal cell subtypes.	Phenobarbital	110-117	notch 1	Mus musculus	0-5
32707133-2	2020	In this study, we express an activated form of Notch1 in the mouse mammary luminal lineage and analyse the consequences for tumour formation and the transcriptomic landscape in the luminal lineage.	Phenobarbital	75-82	notch 1	Mus musculus	47-53
32707133-3	2020	Simultaneous conditional activation of a Notch1 intracellular domain (Notch1 ICD) and EGFP in the luminal lineage was achieved by removal of a stop cassette by CRE-recombinase expression from the whey acidic protein (WAP) promoter.	Phenobarbital	98-105	notch 1	Mus musculus	41-47
32707133-3	2020	Simultaneous conditional activation of a Notch1 intracellular domain (Notch1 ICD) and EGFP in the luminal lineage was achieved by removal of a stop cassette by CRE-recombinase expression from the whey acidic protein (WAP) promoter.	Phenobarbital	98-105	whey acidic protein	Mus musculus	217-220
32707133-4	2020	Mice in which Notch1 ICD was activated in the luminal lineage (WAP-CRE;R26-N1ICD mice) exhibit ductal hyperplasia after lactation with an increase in branching frequency and in the number of side-branch ends in the ductal tree.	Phenobarbital	46-53	notch 1	Mus musculus	14-20
32707133-4	2020	Mice in which Notch1 ICD was activated in the luminal lineage (WAP-CRE;R26-N1ICD mice) exhibit ductal hyperplasia after lactation with an increase in branching frequency and in the number of side-branch ends in the ductal tree.	Phenobarbital	46-53	whey acidic protein	Mus musculus	63-66
32707133-8	2020	In conclusion, we show that Notch1 ICD expression in the luminal lineage produces a ductal hyperplasia and branching phenotype accompanied by altered luminal cell subtype partitioning.	Phenobarbital	57-64	notch 1	Mus musculus	28-34
32707133-8	2020	In conclusion, we show that Notch1 ICD expression in the luminal lineage produces a ductal hyperplasia and branching phenotype accompanied by altered luminal cell subtype partitioning.	Phenobarbital	150-157	notch 1	Mus musculus	28-34
32479949-9	2020	Luminal subtype has shown to follow Wnt/beta-catenin whereas in the basal subtype localization of CD44 from surface to cytosol was observed in response to HA.	Phenobarbital	0-7	catenin beta 1	Homo sapiens	40-52
33098391-4	2020	Results: IHC analysis showed that there were two groups of GFRa1 positive cells in the seminiferous tubules based on their location and expression shape - a small round punctuated shape on the basal compartment donut shape and a C-shaped expression located between the basal and the luminal compartments of the seminiferous tubules.	Phenobarbital	283-290	glial cell line derived neurotrophic factor family receptor alpha 1	Mus musculus	59-64
33342810-10	2020	Moreover, mean transcript levels of TNF-alpha and NF-kappaB1 were significantly elevated in Luminal A and Luminal B subtypes of breast cancer patients, respectively.	Phenobarbital	106-113	tumor necrosis factor	Homo sapiens	36-45
32374509-12	2020	Increased expression of the luminal markers FOXA1 and SCUBE2, were found to be significantly associated with better DFS.	Phenobarbital	28-35	forkhead box A1	Homo sapiens	44-49
32374509-12	2020	Increased expression of the luminal markers FOXA1 and SCUBE2, were found to be significantly associated with better DFS.	Phenobarbital	28-35	signal peptide, CUB domain and EGF like domain containing 2	Homo sapiens	54-60
32417325-1	2020	P-glycoprotein (P-gp) is located on the luminal surface of brain vascular endothelium and its status may determine the delivery of the agents into the brain tissues.	Phenobarbital	40-47	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-14
32954424-7	2020	The OA treatment also elicited the highest (P < 0.05) concentrations of circulating tumor necrosis factor-alpha and volatile fatty acid concentrations in luminal contents at various postinoculation time-points, compared with other treatments.	Phenobarbital	154-161	tumor necrosis factor	Sus scrofa	84-111
32754922-5	2020	Complementing our published findings in basal-like subtype, immunohistochemistry revealed upregulation of FoxQ1 protein in luminal-type human breast cancer tissue microarrays when compared with normal mammary tissues.	Phenobarbital	123-130	forkhead box Q1	Homo sapiens	106-111
32706432-11	2020	Immunohistochemical analysis revealed intense immunostaining of HIF-1alpha proteins in the follicular granulosa cells, granular luteal cells, villous epithelial cells of the oviduct, endometrial glandular epithelium and luminal epithelium, foetal villous trophoblast, and epithelia of caruncular crypts.	Phenobarbital	220-227	hypoxia inducible factor 1 subunit alpha	Homo sapiens	64-74
32735318-4	2020	Treatment of humanized CAR and pregnane X receptor (PXR) mice (hCAR/hPXR mice) with 1000 ppm PB for 7 days significantly increased hepatocyte RDS together with increases in several mitogenic genes.	Phenobarbital	93-95	nuclear receptor subfamily 1, group I, member 3	Mus musculus	23-26
32735318-4	2020	Treatment of humanized CAR and pregnane X receptor (PXR) mice (hCAR/hPXR mice) with 1000 ppm PB for 7 days significantly increased hepatocyte RDS together with increases in several mitogenic genes.	Phenobarbital	93-95	nuclear receptor subfamily 1, group I, member 2	Mus musculus	31-50
32735318-4	2020	Treatment of humanized CAR and pregnane X receptor (PXR) mice (hCAR/hPXR mice) with 1000 ppm PB for 7 days significantly increased hepatocyte RDS together with increases in several mitogenic genes.	Phenobarbital	93-95	nuclear receptor subfamily 1, group I, member 2	Mus musculus	52-55
32735318-4	2020	Treatment of humanized CAR and pregnane X receptor (PXR) mice (hCAR/hPXR mice) with 1000 ppm PB for 7 days significantly increased hepatocyte RDS together with increases in several mitogenic genes.	Phenobarbital	93-95	CXADR Ig-like cell adhesion molecule	Homo sapiens	63-67
32735318-4	2020	Treatment of humanized CAR and pregnane X receptor (PXR) mice (hCAR/hPXR mice) with 1000 ppm PB for 7 days significantly increased hepatocyte RDS together with increases in several mitogenic genes.	Phenobarbital	93-95	nuclear receptor subfamily 1 group I member 2	Homo sapiens	68-72
32735318-5	2020	Global gene expression analysis was performed with liver samples from this and from previous studies focusing on PB-induced Wnt/beta-catenin signaling, and showed that altered genes in hCAR/hPXR mice clustered most closely with liver tumor samples from a diethylnitrosamine/PB initiation/promotion study than with wild type mice.	Phenobarbital	113-115	catenin (cadherin associated protein), beta 1	Mus musculus	128-140
32735318-5	2020	Global gene expression analysis was performed with liver samples from this and from previous studies focusing on PB-induced Wnt/beta-catenin signaling, and showed that altered genes in hCAR/hPXR mice clustered most closely with liver tumor samples from a diethylnitrosamine/PB initiation/promotion study than with wild type mice.	Phenobarbital	113-115	CXADR Ig-like cell adhesion molecule	Homo sapiens	185-189
32735318-5	2020	Global gene expression analysis was performed with liver samples from this and from previous studies focusing on PB-induced Wnt/beta-catenin signaling, and showed that altered genes in hCAR/hPXR mice clustered most closely with liver tumor samples from a diethylnitrosamine/PB initiation/promotion study than with wild type mice.	Phenobarbital	113-115	nuclear receptor subfamily 1 group I member 2	Homo sapiens	190-194
32735318-5	2020	Global gene expression analysis was performed with liver samples from this and from previous studies focusing on PB-induced Wnt/beta-catenin signaling, and showed that altered genes in hCAR/hPXR mice clustered most closely with liver tumor samples from a diethylnitrosamine/PB initiation/promotion study than with wild type mice.	Phenobarbital	274-276	CXADR Ig-like cell adhesion molecule	Homo sapiens	185-189
32735318-5	2020	Global gene expression analysis was performed with liver samples from this and from previous studies focusing on PB-induced Wnt/beta-catenin signaling, and showed that altered genes in hCAR/hPXR mice clustered most closely with liver tumor samples from a diethylnitrosamine/PB initiation/promotion study than with wild type mice.	Phenobarbital	274-276	nuclear receptor subfamily 1 group I member 2	Homo sapiens	190-194
33072131-0	2020	The Involvement of the Chemokine RANTES in Regulating Luminal Acidification in Rat Epididymis.	Phenobarbital	54-61	C-C motif chemokine ligand 5	Rattus norvegicus	33-39
33072131-2	2020	Basal cells sense the luminal angiotensin II (ANG II) and stimulate proton secretion in clear cells through nitric oxide (NO).	Phenobarbital	22-29	angiotensinogen	Rattus norvegicus	30-44
33072131-4	2020	The objective of this study was to explore the involvement of RANTES in regulating the luminal acidification in the rat epididymis.	Phenobarbital	87-94	C-C motif chemokine ligand 5	Rattus norvegicus	62-68
33072131-15	2020	Thus, RANTES is possible to participate in the crosstalk among basal cells, macrophages and clear cells for the fine control of an optimum acidic luminal environment that is critical for male fertility.	Phenobarbital	146-153	C-C motif chemokine ligand 5	Rattus norvegicus	6-12
32934200-0	2020	TET2 directs mammary luminal cell differentiation and endocrine response.	Phenobarbital	21-28	tet methylcytosine dioxygenase 2	Mus musculus	0-4
32934200-3	2020	Here, using our recently established mammary specific Tet2 deletion mouse model, the data reveals that TET2 plays a pivotal role in mammary gland development and luminal lineage commitment.	Phenobarbital	162-169	tet methylcytosine dioxygenase 2	Mus musculus	54-58
32934200-3	2020	Here, using our recently established mammary specific Tet2 deletion mouse model, the data reveals that TET2 plays a pivotal role in mammary gland development and luminal lineage commitment.	Phenobarbital	162-169	tet methylcytosine dioxygenase 2	Mus musculus	103-107
32934200-4	2020	We show that TET2 and FOXP1 form a chromatin complex that mediates demethylation of ESR1, GATA3, and FOXA1, three key genes that are known to coordinately orchestrate mammary luminal lineage specification and endocrine response, and also are often silenced by DNA methylation in aggressive breast cancers.	Phenobarbital	175-182	tet methylcytosine dioxygenase 2	Mus musculus	13-17
32934200-4	2020	We show that TET2 and FOXP1 form a chromatin complex that mediates demethylation of ESR1, GATA3, and FOXA1, three key genes that are known to coordinately orchestrate mammary luminal lineage specification and endocrine response, and also are often silenced by DNA methylation in aggressive breast cancers.	Phenobarbital	175-182	forkhead box P1	Mus musculus	22-27
32934200-4	2020	We show that TET2 and FOXP1 form a chromatin complex that mediates demethylation of ESR1, GATA3, and FOXA1, three key genes that are known to coordinately orchestrate mammary luminal lineage specification and endocrine response, and also are often silenced by DNA methylation in aggressive breast cancers.	Phenobarbital	175-182	estrogen receptor 1 (alpha)	Mus musculus	84-88
32934200-4	2020	We show that TET2 and FOXP1 form a chromatin complex that mediates demethylation of ESR1, GATA3, and FOXA1, three key genes that are known to coordinately orchestrate mammary luminal lineage specification and endocrine response, and also are often silenced by DNA methylation in aggressive breast cancers.	Phenobarbital	175-182	GATA binding protein 3	Mus musculus	90-95
32934200-4	2020	We show that TET2 and FOXP1 form a chromatin complex that mediates demethylation of ESR1, GATA3, and FOXA1, three key genes that are known to coordinately orchestrate mammary luminal lineage specification and endocrine response, and also are often silenced by DNA methylation in aggressive breast cancers.	Phenobarbital	175-182	forkhead box A1	Mus musculus	101-106
32934200-6	2020	As a result, this study elucidates a role for TET2 in governing luminal cell differentiation and endocrine response that underlies breast cancer resistance to anti-estrogen treatments.	Phenobarbital	64-71	tet methylcytosine dioxygenase 2	Mus musculus	46-50
32586983-6	2020	Increased differentiation correlated with a luminal cell fate that could be reversed by inhibition of PDGFR activity.	Phenobarbital	44-51	platelet derived growth factor receptor, beta polypeptide	Mus musculus	102-107
32829466-3	2020	SGLT1 and GLUT5 are constantly localized in the brush border membrane (BBM) of enterocytes, whereas GLUT2 is localized in the basolateral membrane (BLM) or the BBM plus BLM at low and high luminal D-glucose concentrations, respectively.	Phenobarbital	189-196	solute carrier family 2 member 2	Homo sapiens	100-105
32829466-4	2020	At high luminal D-glucose, the abundance SGLT1 in the BBM is increased.	Phenobarbital	8-15	solute carrier family 5 member 1	Homo sapiens	41-46
32531861-4	2020	ESR1 is involved in the reabsorption of luminal fluid during the transit of spermatozoa from the testis to the head of the epididymis which is important for their survival and maturation during epididymal storage.	Phenobarbital	40-47	estrogen receptor 1	Homo sapiens	0-4
32446131-5	2020	CCN2 was not detected by in situ hybridization at ED0 (Day 0 of the estrous cycle), but at ED6 (metestrus), ED12 (dioestrus), and ED16 (proestrus), with high signals in luminal epithelium, superficial glands, and caruncula matrix.	Phenobarbital	169-176	cellular communication network factor 2	Homo sapiens	0-4
32446131-10	2020	In conclusion, CCN2 expression may be induced by 17beta-estradiol, progesterone, and IFNtau in the luminal epithelium of goat receptive uterus, suggesting that CCN2 is involved in goat embryo adhesion during early pregnancy.	Phenobarbital	99-106	cellular communication network factor 2	Homo sapiens	15-19
32446131-10	2020	In conclusion, CCN2 expression may be induced by 17beta-estradiol, progesterone, and IFNtau in the luminal epithelium of goat receptive uterus, suggesting that CCN2 is involved in goat embryo adhesion during early pregnancy.	Phenobarbital	99-106	cellular communication network factor 2	Homo sapiens	160-164
32616332-2	2020	The Hrd1 complex represents the main gate mediating retrotranslocation of ER luminal misfolded (ERAD-L) substrates to the cytosol.	Phenobarbital	77-84	synoviolin 1	Homo sapiens	4-8
32911332-5	2020	Inhibition of IRE1 endoribonuclease activity with the pharmacological compound 4mu8C or genetic approaches effectively suppresses luminal breast cancer cell proliferation and aggressive cancer phenotypes.	Phenobarbital	130-137	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	14-18
32846884-7	2020	Particularly, cathepsin D was highly expressed in the luminal B subtype.	Phenobarbital	54-61	cathepsin D	Homo sapiens	14-25
32355954-6	2020	PROK1 protein was detected mainly in luminal epithelial cells, glandular epithelial cells and blood vessels in the endometrium.	Phenobarbital	37-44	prokineticin 1	Sus scrofa	0-5
32891886-3	2020	Recently, it has been shown that the Hrd1 E3 ligase forms a retrotranslocation channel for luminal (ERAD-L) substrates.	Phenobarbital	91-98	synoviolin 1	Homo sapiens	37-41
32822399-4	2020	The luminal subtype is less aggressive and is predominately characterized by elevated gene expression of peroxisome proliferator-activated receptor- gamma (PPARgamma) and forkhead box protein A1 (FOXA1).	Phenobarbital	4-11	peroxisome proliferator activated receptor gamma	Homo sapiens	105-154
32822399-4	2020	The luminal subtype is less aggressive and is predominately characterized by elevated gene expression of peroxisome proliferator-activated receptor- gamma (PPARgamma) and forkhead box protein A1 (FOXA1).	Phenobarbital	4-11	peroxisome proliferator activated receptor gamma	Homo sapiens	156-165
32822399-4	2020	The luminal subtype is less aggressive and is predominately characterized by elevated gene expression of peroxisome proliferator-activated receptor- gamma (PPARgamma) and forkhead box protein A1 (FOXA1).	Phenobarbital	4-11	forkhead box A1	Homo sapiens	171-194
32822399-4	2020	The luminal subtype is less aggressive and is predominately characterized by elevated gene expression of peroxisome proliferator-activated receptor- gamma (PPARgamma) and forkhead box protein A1 (FOXA1).	Phenobarbital	4-11	forkhead box A1	Homo sapiens	196-201
32822399-10	2020	Our data suggests that activation of PPARgamma while inhibiting cell proliferation facilitates the regulation of genes involved in maintaining the luminal subtype of UC.	Phenobarbital	147-154	peroxisome proliferator activated receptor gamma	Homo sapiens	37-46
32801338-0	2020	Triggering a switch from basal- to luminal-like breast cancer subtype by the small-molecule diptoindonesin G via induction of GABARAPL1.	Phenobarbital	35-42	GABA type A receptor associated protein like 1	Homo sapiens	126-135
32923400-0	2020	High Parity Predicts Poor Outcomes in Patients With Luminal B-Like (HER2 Negative) Early Breast Cancer: A Prospective Finnish Single-Center Study.	Phenobarbital	52-59	erb-b2 receptor tyrosine kinase 2	Homo sapiens	68-72
32923400-8	2020	However, when the subtypes were assessed separately in a multivariate analysis that included tumor size and nodal status, high parity remained significant only in luminal B-like (HER2 negative) cancers (HR = 2.63; 95% confidence interval = 1.04-6.62; P = 0.040).	Phenobarbital	163-170	erb-b2 receptor tyrosine kinase 2	Homo sapiens	179-183
32923400-9	2020	Our results suggest excellent overall 10-year BCSS but indicate that high parity is an adverse prognostic factor in luminal B-like (HER2 negative) breast cancers.	Phenobarbital	116-123	erb-b2 receptor tyrosine kinase 2	Homo sapiens	132-136
32776921-7	2020	TM6SF2 bound and stabilized APOB via two luminal loops.	Phenobarbital	41-48	transmembrane 6 superfamily member 2	Homo sapiens	0-6
32776921-7	2020	TM6SF2 bound and stabilized APOB via two luminal loops.	Phenobarbital	41-48	apolipoprotein B	Homo sapiens	28-32
32929335-6	2020	Among them, ST3GAL6, a glycotransferase to transfer sialic acid to 3"-hydroxyl group of a galactose residue, showed a significant negative association with the subtype with luminal feature in UBC patients (n=2,130 in total).	Phenobarbital	173-180	ST3 beta-galactoside alpha-2,3-sialyltransferase 6	Homo sapiens	12-19
32960142-5	2020	RNA and protein expressions of TIP60 were shown to decrease in some breast cancer subtypes, particularly in triple-negative breast cancer (TNBC), where a low expression of TIP60 was exhibited compared with luminal subtypes.	Phenobarbital	206-213	lysine acetyltransferase 5	Homo sapiens	31-36
32619596-8	2020	Luminal subtype was found to have much higher PSMA expression when compared to basal (1.01 vs. 0.68, p<0.001).	Phenobarbital	0-7	folate hydrolase 1	Homo sapiens	46-50
32619596-9	2020	The androgen receptor activity signature demonstrated a dramatic difference between basal (0.19) and luminal (0.62) subtypes (p<0.001).	Phenobarbital	101-108	androgen receptor	Homo sapiens	4-21
32619596-11	2020	CONCLUSIONS: High PSMA expression (FOLH1) was associated with high androgen receptor activity and luminal subtype.	Phenobarbital	98-105	folate hydrolase 1	Homo sapiens	18-22
32619596-11	2020	CONCLUSIONS: High PSMA expression (FOLH1) was associated with high androgen receptor activity and luminal subtype.	Phenobarbital	98-105	folate hydrolase 1	Homo sapiens	35-40
33003293-5	2020	In contrast, the IFN-gamma-associated gene signature was an independent prognostic factor in the whole cohort (HR 2.287, 95% CI 1.410-3.633, p < 0.001) as well as in the basal-like (HR 3.458, 95% CI 1.154-10.359, p = 0.027) and luminal B (HR 2.690, 95% CI 1.416-5.112, p = 0.003) molecular subtypes.	Phenobarbital	228-235	interferon gamma	Homo sapiens	17-26
32682203-7	2020	Co-immunolabeling of p62 or light chain 3 (LC3) with vimentin showed increasing expression from the basal to the luminal compartment of the seminiferous tubule and stronger expression during active than inactive spermatogenesis in the testis of goat.	Phenobarbital	113-120	vimentin	Capra hircus	53-61
32678576-4	2020	Herein, an electrospun tubular fibrous (eTF) scaffold was biofunctionalized with tropoelastin at the luminal surface.	Phenobarbital	101-108	elastin	Homo sapiens	81-93
32932770-2	2020	Flow cytometry and mammosphere assays revealed that in murine breast, overexpression of PRB leads to an increase in luminal and basal progenitor/stem cells.	Phenobarbital	116-123	progesterone receptor	Mus musculus	88-91
33013490-1	2020	The luminal endoplasmic reticulum (ER) protein of 29 kDa (ERp29) is a ubiquitously expressed cellular agent with multiple critical roles.	Phenobarbital	4-11	endoplasmic reticulum protein 29	Homo sapiens	58-63
32891135-8	2020	The HER2-amplified (pooled OR, 3.14; 95% CI, 1.95-5.06) and TN (pooled OR, 4.09; 95% CI, 2.71-6.19) phenotypes of breast cancers expressed significantly more high-level TILs than the luminal tumor subtype, although the presentation of those between the former two subsets was not significantly different (pooled OR, 1.30; 95%CI, 0.83-2.04).	Phenobarbital	183-190	erb-b2 receptor tyrosine kinase 2	Homo sapiens	4-8
32668368-3	2020	We highlight a recent paper that demonstrates that luminal [Ca2+] potently inhibits IP3R activity.	Phenobarbital	51-58	inositol 1,4,5-trisphosphate receptor type 3	Homo sapiens	84-88
32826063-10	2020	On the basis of the Accelerate Pheno AST results, antibiotic spectrum was increased in 10 of 11 instances to correct organism-drug mismatch and narrowed in 16 of 33 instances.	Phenobarbital	31-36	solute carrier family 17 member 5	Homo sapiens	37-40
32717131-6	2020	Thus, the membrane organization of endolysosomal CD38, a signal-mediated transport system for NADP+ and luminal NAD+ biosynthetic enzymes integrate signals from a chemokine and cAMP to specify the spatiotemporal mobilization of Ca2+ to drive cell migration.	Phenobarbital	104-111	CD38 molecule	Homo sapiens	49-53
32369651-9	2020	The high immunoexpression of ALDH1A1 was significantly associated with poor BC-specific survival (P<0.001), and specifically in the luminal B and TNBC subtypes (P=0.042 and P=0.003, respectively).	Phenobarbital	132-139	aldehyde dehydrogenase 1 family member A1	Homo sapiens	29-36
32764142-7	2020	RESULTS: Both endogenous podocyte and transfected APOL1 isoforms vA and vB1 (and a little of isoform vC) localize to the luminal face of the endoplasmic reticulum (ER) and to the cell surface, but not to mitochondria, endosomes, or lipid droplets.	Phenobarbital	121-128	apolipoprotein L1	Homo sapiens	50-55
32573490-8	2020	Supervised analysis of 77 primary tumors with paired metastases revealed that the FGFR4-induced signature was significantly higher in luminal/ER+ tumor metastases compared with their primaries.	Phenobarbital	134-141	fibroblast growth factor receptor 4	Homo sapiens	82-87
32367506-5	2020	We observed the distribution of staining of P78 protein was concentrated on the cell membranes of the luminal epithelial cells, not cytoplasm.	Phenobarbital	102-109	microspherule protein 1	Homo sapiens	44-47
32807988-5	2020	Deletion of Pten in Dist-Luminal-C cells resulted in prostatic intraepithelial neoplasia.	Phenobarbital	25-32	phosphatase and tensin homolog	Homo sapiens	12-16
32817544-0	2020	Selenoprotein N is an endoplasmic reticulum calcium sensor that links luminal calcium levels to a redox activity.	Phenobarbital	70-77	selenoprotein N	Homo sapiens	0-15
32817544-3	2020	Here we report that Selenoprotein N (SEPN1) is a type II transmembrane protein that senses ER calcium fluctuations by binding this ion through a luminal EF-hand domain.	Phenobarbital	145-152	selenoprotein N	Homo sapiens	20-35
32817544-3	2020	Here we report that Selenoprotein N (SEPN1) is a type II transmembrane protein that senses ER calcium fluctuations by binding this ion through a luminal EF-hand domain.	Phenobarbital	145-152	selenoprotein N	Homo sapiens	37-42
32817544-4	2020	In vitro and in vivo experiments show that via this domain, SEPN1 responds to diminished luminal calcium levels, dynamically changing its oligomeric state and enhancing its redox-dependent interaction with cellular partners, including the ER calcium pump sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA).	Phenobarbital	89-96	selenoprotein N	Homo sapiens	60-65
32668157-2	2020	SLN has a conserved luminal C-terminal domain that contributes to the its functional divergence among homologous SERCA regulators, but the precise mechanistic role of this domain remains poorly understood.	Phenobarbital	20-27	sarcolipin	Homo sapiens	0-3
32820719-4	2020	Similar to protein-conducting channels that facilitate movement of transmembrane segments, cytosolic and luminal funnels in TMCO1 and TMEM147, respectively, suggest routes into the central membrane cavity.	Phenobarbital	105-112	transmembrane and coiled-coil domains 1	Homo sapiens	124-129
32820719-4	2020	Similar to protein-conducting channels that facilitate movement of transmembrane segments, cytosolic and luminal funnels in TMCO1 and TMEM147, respectively, suggest routes into the central membrane cavity.	Phenobarbital	105-112	transmembrane protein 147	Homo sapiens	134-141
32467227-4	2020	We found that MEOX1 is expressed only in TNBC deficient in P53 or PTEN and that its expression is undetectable in luminal A, luminal B, and HER2+ subtypes as well as in normal breast cells with wild type P53/PTEN.	Phenobarbital	114-121	mesenchyme homeobox 1	Homo sapiens	14-19
32467227-4	2020	We found that MEOX1 is expressed only in TNBC deficient in P53 or PTEN and that its expression is undetectable in luminal A, luminal B, and HER2+ subtypes as well as in normal breast cells with wild type P53/PTEN.	Phenobarbital	125-132	mesenchyme homeobox 1	Homo sapiens	14-19
32703414-2	2020	Expression of colonic MCT1 transporters, localized in surface epithelial cells, is regulated by luminal butyrate levels.	Phenobarbital	96-103	solute carrier family 16 member 1	Homo sapiens	22-26
32929410-3	2020	We previously reported age-related changes within the inflammatory and luminal compartments of the mouse prostate.	Phenobarbital	71-78	renin binding protein	Mus musculus	23-26
32851169-3	2020	The structures revealed that the luminal extension tail (LE) characteristic of SERCA2b runs parallel to the lipid-water boundary near the luminal ends of transmembrane (TM) helices TM10 and TM7 and approaches the luminal loop flanked by TM7 and TM8.	Phenobarbital	33-40	tetraspanin 16	Homo sapiens	245-248
32771039-3	2020	Previously, we reported a recurrent ESR1 fusion called ESR1-CCDC170 in 6-8% of the luminal B breast cancers that has a worse clinical outcome after endocrine therapy.	Phenobarbital	83-90	estrogen receptor 1	Homo sapiens	36-40
32771039-3	2020	Previously, we reported a recurrent ESR1 fusion called ESR1-CCDC170 in 6-8% of the luminal B breast cancers that has a worse clinical outcome after endocrine therapy.	Phenobarbital	83-90	estrogen receptor 1	Homo sapiens	55-59
32771039-3	2020	Previously, we reported a recurrent ESR1 fusion called ESR1-CCDC170 in 6-8% of the luminal B breast cancers that has a worse clinical outcome after endocrine therapy.	Phenobarbital	83-90	coiled-coil domain containing 170	Homo sapiens	60-67
32693087-4	2020	In normal mouse epithelium, LEFTY1 expression in a subset of luminal cells and rare basal cells opposes BMP7 to promote ductal branching.	Phenobarbital	61-68	left right determination factor 1	Mus musculus	28-34
32764411-7	2020	Intravenous administration of DNase I, an enzyme that dissolves the web-like DNA filaments of NETs, during colitis restored the mucosal barrier integrity which reduced the dissemination of luminal bacteria and attenuated intestinal inflammation in both DSS and TNBS models.	Phenobarbital	189-196	deoxyribonuclease I	Mus musculus	30-37
32417325-1	2020	P-glycoprotein (P-gp) is located on the luminal surface of brain vascular endothelium and its status may determine the delivery of the agents into the brain tissues.	Phenobarbital	40-47	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	16-20
32749217-4	2020	In the complex, the luminal surface of CLC-7 is entirely covered by a dimer of the heavily glycosylated and disulfide-bonded OSTM1, which serves to protect CLC-7 from the degradative environment of the lysosomal lumen.	Phenobarbital	20-27	chloride voltage-gated channel 7	Homo sapiens	39-44
32749217-4	2020	In the complex, the luminal surface of CLC-7 is entirely covered by a dimer of the heavily glycosylated and disulfide-bonded OSTM1, which serves to protect CLC-7 from the degradative environment of the lysosomal lumen.	Phenobarbital	20-27	osteoclastogenesis associated transmembrane protein 1	Homo sapiens	125-130
32749217-4	2020	In the complex, the luminal surface of CLC-7 is entirely covered by a dimer of the heavily glycosylated and disulfide-bonded OSTM1, which serves to protect CLC-7 from the degradative environment of the lysosomal lumen.	Phenobarbital	20-27	chloride voltage-gated channel 7	Homo sapiens	156-161
32749219-5	2020	Luminal cells-specific knockout of Rspo1 results in decreased Esr1 expression and reduced mammary side branches.	Phenobarbital	0-7	R-spondin 1	Mus musculus	35-40
32749219-5	2020	Luminal cells-specific knockout of Rspo1 results in decreased Esr1 expression and reduced mammary side branches.	Phenobarbital	0-7	estrogen receptor 1 (alpha)	Mus musculus	62-66
32832803-4	2020	Additionally, GMF administration increased luminal acetate and propionate levels, upregulated the gene expressions of intestinal tight junctions (Occludin, Claudins, and ZO-1), mucins (Mucin-1, Mucin-2, Mucin-4, and Mucin-20), and cytokines (TNF-alpha, IL-1beta, and IL-22) while decreased the plasma diamine oxidase (DAO) level on day 21.	Phenobarbital	43-50	glia maturation factor beta	Homo sapiens	14-17
32749219-6	2020	In contrast, luminal cells-specific knockout of Wnt4, while attenuating basal cell Wnt/beta-catenin signaling activities, enhances Esr1 expression.	Phenobarbital	13-20	wingless-type MMTV integration site family, member 4	Mus musculus	48-52
32749219-6	2020	In contrast, luminal cells-specific knockout of Wnt4, while attenuating basal cell Wnt/beta-catenin signaling activities, enhances Esr1 expression.	Phenobarbital	13-20	wingless-type MMTV integration site family, member 4	Mus musculus	48-51
32749219-6	2020	In contrast, luminal cells-specific knockout of Wnt4, while attenuating basal cell Wnt/beta-catenin signaling activities, enhances Esr1 expression.	Phenobarbital	13-20	catenin (cadherin associated protein), beta 1	Mus musculus	87-99
32749219-6	2020	In contrast, luminal cells-specific knockout of Wnt4, while attenuating basal cell Wnt/beta-catenin signaling activities, enhances Esr1 expression.	Phenobarbital	13-20	estrogen receptor 1 (alpha)	Mus musculus	131-135
32982642-4	2020	Classical invasive lobular breast cancer, typically clustering into luminal subgroup, is characterized by discohesive growth and loss of E-cadherin expression.	Phenobarbital	68-75	cadherin 1	Homo sapiens	137-147
32597833-4	2020	Mutagenesis experiments showed that the second luminal loop of CLN6 is required for the interaction of CLN6 with the enzymes but dispensable for interaction with CLN8.	Phenobarbital	47-54	ceroid-lipofuscinosis, neuronal 6	Mus musculus	63-67
32597833-4	2020	Mutagenesis experiments showed that the second luminal loop of CLN6 is required for the interaction of CLN6 with the enzymes but dispensable for interaction with CLN8.	Phenobarbital	47-54	ceroid-lipofuscinosis, neuronal 6	Mus musculus	103-107
32389638-14	2020	Extracellular conversion of NMN to NR by CD73 localized in the luminal surface of endothelial cells represent important vasoprotective mechanisms to maintain intracellular NAD.	Phenobarbital	63-70	5' nucleotidase, ecto	Mus musculus	41-45
32562116-1	2020	PURPOSE: The ETS transcription factor ESE-1 has been shown to be important in HER2+ breast cancer and ESE-1 mRNA expression has been shown to associate with prognostic outcomes in the HER2+ subtype, as well as in ER+, HER2+ luminal B patients.	Phenobarbital	224-231	E74 like ETS transcription factor 3	Homo sapiens	102-107
32601970-6	2020	RESULTS: We found an increase in the performance of mitochondrial polyubiquitinated proteins in breast cancer tissues of luminal A, luminal B, Her2-overexpression, and TNBC.	Phenobarbital	121-128	erb-b2 receptor tyrosine kinase 2	Homo sapiens	143-147
32982642-6	2020	Breast carcinoma with apocrine differentiation, with characteristic expression of androgen receptor (AR), often clusters into the luminal AR category.	Phenobarbital	130-137	androgen receptor	Homo sapiens	82-99
32982642-6	2020	Breast carcinoma with apocrine differentiation, with characteristic expression of androgen receptor (AR), often clusters into the luminal AR category.	Phenobarbital	130-137	androgen receptor	Homo sapiens	101-103
32982642-6	2020	Breast carcinoma with apocrine differentiation, with characteristic expression of androgen receptor (AR), often clusters into the luminal AR category.	Phenobarbital	130-137	androgen receptor	Homo sapiens	138-140
32543775-4	2020	miR-18a was overexpressed in MCF7 and ZR-75-1 and this led to an increase in the proliferative ability of the cells and concurrently resulted in decreased expression of luminal markers and higher expression of the basal marker, cytokeratin 14.	Phenobarbital	169-176	microRNA 18a	Homo sapiens	0-7
32503880-5	2020	Further, the blood pentobarbital concentration was higher in Nrf2-/- mice than in WT mice at 30-60 min, and the phenobarbital-induced enhancement of its clearance was attenuated in Nrf2-/- mice compared to WT mice.	Phenobarbital	112-125	nuclear factor, erythroid derived 2, like 2	Mus musculus	61-65
32503880-5	2020	Further, the blood pentobarbital concentration was higher in Nrf2-/- mice than in WT mice at 30-60 min, and the phenobarbital-induced enhancement of its clearance was attenuated in Nrf2-/- mice compared to WT mice.	Phenobarbital	112-125	nuclear factor, erythroid derived 2, like 2	Mus musculus	181-185
32503880-6	2020	Total P450 content was decreased in Nrf2-/- mouse livers, and the phenobarbital-induced increase in P450 content was lower in Nrf2-/- mice than WT mice.	Phenobarbital	66-79	nuclear factor, erythroid derived 2, like 2	Mus musculus	36-40
32503880-6	2020	Total P450 content was decreased in Nrf2-/- mouse livers, and the phenobarbital-induced increase in P450 content was lower in Nrf2-/- mice than WT mice.	Phenobarbital	66-79	nuclear factor, erythroid derived 2, like 2	Mus musculus	126-130
32503880-7	2020	Cyp1a2, Cyp2a5, Cyp2c29, and Cyp2e1 gene expression levels under physiological conditions and Cyp1a2, Cyp2a5, and Cyp2b10 gene expression levels under phenobarbital-treated conditions were lower in Nrf2-/- mice compared to WT mice.	Phenobarbital	151-164	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	0-6
32503880-7	2020	Cyp1a2, Cyp2a5, Cyp2c29, and Cyp2e1 gene expression levels under physiological conditions and Cyp1a2, Cyp2a5, and Cyp2b10 gene expression levels under phenobarbital-treated conditions were lower in Nrf2-/- mice compared to WT mice.	Phenobarbital	151-164	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	94-100
32503880-7	2020	Cyp1a2, Cyp2a5, Cyp2c29, and Cyp2e1 gene expression levels under physiological conditions and Cyp1a2, Cyp2a5, and Cyp2b10 gene expression levels under phenobarbital-treated conditions were lower in Nrf2-/- mice compared to WT mice.	Phenobarbital	151-164	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	102-108
32503880-7	2020	Cyp1a2, Cyp2a5, Cyp2c29, and Cyp2e1 gene expression levels under physiological conditions and Cyp1a2, Cyp2a5, and Cyp2b10 gene expression levels under phenobarbital-treated conditions were lower in Nrf2-/- mice compared to WT mice.	Phenobarbital	151-164	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	114-121
32503880-7	2020	Cyp1a2, Cyp2a5, Cyp2c29, and Cyp2e1 gene expression levels under physiological conditions and Cyp1a2, Cyp2a5, and Cyp2b10 gene expression levels under phenobarbital-treated conditions were lower in Nrf2-/- mice compared to WT mice.	Phenobarbital	151-164	nuclear factor, erythroid derived 2, like 2	Mus musculus	198-202
32449190-2	2020	Among the many proteins involved in this process, Arv1 is a candidate, functioning as a flippase that translocates GPI intermediates from the cytoplasmic side into the luminal side of the ER membranes.	Phenobarbital	168-175	sterol homeostasis protein ARV1	Saccharomyces cerevisiae S288C	50-54
32556218-5	2020	SLC2A1 messenger RNA (mRNA) and protein, and SLC2A4 mRNA were abundant in the uterine luminal epithelium of pregnant compared to cycling gilts, and increased in response to progesterone and conceptus-secreted estrogen.	Phenobarbital	86-93	glucose transport protein	Sus scrofa	0-6
32626998-1	2020	Endoplasmic reticulum (ER) oxidase 1alpha (ERO1alpha) is a glycosylated flavoenzyme that is located on the luminal side of the ER membrane, which serves an important role in catalyzing the formation of protein disulfide bonds and ER redox homeostasis.	Phenobarbital	107-114	endoplasmic reticulum oxidoreductase 1 alpha	Homo sapiens	43-52
32497356-6	2020	RESULTS: Our data reveal that previously identified facultative progenitors marked by Trop2, Sca-1, KRT4, and PSCA are actually luminal epithelial cells of the urethra that extend into the proximal region of the prostate, and are resistant to castration-induced androgen deprivation.	Phenobarbital	128-135	ataxin 1	Homo sapiens	93-98
32385899-6	2020	We refined the RRM2 signature by integrating it with two molecular classification systems (PCS and PAM50 subtypes) that define aggressive PC subtypes (PCS1 and luminal B) and correlated signatures with clinical outcomes in six published cohorts comprising 4,000 cases of PC.	Phenobarbital	160-167	ribonucleotide reductase regulatory subunit M2	Homo sapiens	15-19
32497356-6	2020	RESULTS: Our data reveal that previously identified facultative progenitors marked by Trop2, Sca-1, KRT4, and PSCA are actually luminal epithelial cells of the urethra that extend into the proximal region of the prostate, and are resistant to castration-induced androgen deprivation.	Phenobarbital	128-135	tumor associated calcium signal transducer 2	Homo sapiens	86-91
32497356-6	2020	RESULTS: Our data reveal that previously identified facultative progenitors marked by Trop2, Sca-1, KRT4, and PSCA are actually luminal epithelial cells of the urethra that extend into the proximal region of the prostate, and are resistant to castration-induced androgen deprivation.	Phenobarbital	128-135	keratin 4	Homo sapiens	100-104
32497356-6	2020	RESULTS: Our data reveal that previously identified facultative progenitors marked by Trop2, Sca-1, KRT4, and PSCA are actually luminal epithelial cells of the urethra that extend into the proximal region of the prostate, and are resistant to castration-induced androgen deprivation.	Phenobarbital	128-135	prostate stem cell antigen	Homo sapiens	110-114
32944524-6	2020	The luminal/basilar layer of ITGAV expression was striking in cribriform carcinomas, suggestive of a role in molecular pathogenesis.	Phenobarbital	4-11	integrin subunit alpha V	Homo sapiens	29-34
32602545-7	2020	High expression of B7-H3 mRNA was significantly associated with worse overall survival, especially in patients with luminal A and luminal B breast cancer.	Phenobarbital	116-123	CD276 molecule	Homo sapiens	19-24
32647060-5	2020	Lymphoid-restricted membrane protein (LRMP, Jaw1) and inositol trisphosphate receptor-associated guanylate kinase substrate (IRAG, Mrvi1, and Jaw1L) are homologous proteins with small ER luminal domains and large cytoplasmic domains.	Phenobarbital	187-194	inositol 1,4,5-triphosphate receptor associated 2	Mus musculus	0-36
32647060-5	2020	Lymphoid-restricted membrane protein (LRMP, Jaw1) and inositol trisphosphate receptor-associated guanylate kinase substrate (IRAG, Mrvi1, and Jaw1L) are homologous proteins with small ER luminal domains and large cytoplasmic domains.	Phenobarbital	187-194	inositol 1,4,5-triphosphate receptor associated 2	Mus musculus	38-42
32647060-5	2020	Lymphoid-restricted membrane protein (LRMP, Jaw1) and inositol trisphosphate receptor-associated guanylate kinase substrate (IRAG, Mrvi1, and Jaw1L) are homologous proteins with small ER luminal domains and large cytoplasmic domains.	Phenobarbital	187-194	inositol 1,4,5-triphosphate receptor associated 2	Mus musculus	44-48
32647060-5	2020	Lymphoid-restricted membrane protein (LRMP, Jaw1) and inositol trisphosphate receptor-associated guanylate kinase substrate (IRAG, Mrvi1, and Jaw1L) are homologous proteins with small ER luminal domains and large cytoplasmic domains.	Phenobarbital	187-194	inositol 1,4,5-triphosphate receptor associated 1	Mus musculus	125-129
32647060-5	2020	Lymphoid-restricted membrane protein (LRMP, Jaw1) and inositol trisphosphate receptor-associated guanylate kinase substrate (IRAG, Mrvi1, and Jaw1L) are homologous proteins with small ER luminal domains and large cytoplasmic domains.	Phenobarbital	187-194	inositol 1,4,5-triphosphate receptor associated 1	Mus musculus	131-136
32699247-8	2020	Using an open access repository; BreastMark, we found a correlation between high NPNT mRNA levels and poor prognosis for patients with the luminal B subtype.	Phenobarbital	139-146	nephronectin	Homo sapiens	81-85
32719318-7	2020	Besides, BRCA1/2 mutations were dominantly observed in basal and luminal subtypes, respectively.	Phenobarbital	65-72	BRCA1 DNA repair associated	Homo sapiens	9-16
32697770-10	2020	The observed molecular apocrine differentiation implicates that triple-negative PLC can be categorized into the luminal AR subtype.	Phenobarbital	112-119	androgen receptor	Homo sapiens	120-122
32667911-1	2020	In the mammalian gut CD103+ve myeloid DCs are known to suppress inflammation threatened by luminal bacteria, but stimuli driving DC precursor maturation towards this beneficial phenotype are incompletely understood.	Phenobarbital	91-98	integrin subunit alpha E	Homo sapiens	21-26
32692762-0	2020	The mevalonate precursor enzyme HMGCS1 is a novel marker and key mediator of cancer stem cell enrichment in luminal and basal models of breast cancer.	Phenobarbital	108-115	3-hydroxy-3-methylglutaryl-CoA synthase 1	Homo sapiens	32-38
32692762-10	2020	Taken together, this study highlights HMGCS1 as a potential gatekeeper for dysregulated mevalonate metabolism important for CSC-features in both luminal and basal breast cancer subtypes.	Phenobarbital	145-152	3-hydroxy-3-methylglutaryl-CoA synthase 1	Homo sapiens	38-44
32540993-2	2020	The MUC2 mucin is the primary constituent of intestinal mucus and plays critical protective roles against luminal microbes and other noxious agents.	Phenobarbital	106-113	mucin 2	Mus musculus	4-8
32668254-7	2020	Our work explains how antagonistic activities by Vegfr3/Flt4 on the abluminal side and by Notch on the luminal side shape cardiac valve leaflets by triggering unique differences in the fates of endocardial cells.	Phenobarbital	70-77	fms related receptor tyrosine kinase 4	Danio rerio	49-55
32668254-7	2020	Our work explains how antagonistic activities by Vegfr3/Flt4 on the abluminal side and by Notch on the luminal side shape cardiac valve leaflets by triggering unique differences in the fates of endocardial cells.	Phenobarbital	70-77	fms related receptor tyrosine kinase 4	Danio rerio	56-60
32401606-8	2020	On cessation of luminal flow, benzamil-inhibitable cell doming is observed within these 3D CCDs consistent with the presence of ENaC-mediated Na+ absorption.	Phenobarbital	16-23	sodium channel, nonvoltage-gated 1 alpha	Mus musculus	128-132
32760666-6	2020	Also, we modified the MCF-7-derived exosomes loaded with siRNA against CD44 to observe the effects of targeting reduced CD44 expression in luminal A breast cancer cells.	Phenobarbital	139-146	CD44 molecule (Indian blood group)	Homo sapiens	120-124
32665580-6	2020	Thus, IRSp53 acts as a membrane curvature-sensing platform for the assembly of multi-protein complexes that control the trafficking of apical determinants and the integrity of the luminal plasma membrane.	Phenobarbital	180-187	BAR/IMD domain containing adaptor protein 2	Homo sapiens	6-12
32764967-0	2020	MORC4 Promotes Chemoresistance of Luminal A/B Breast Cancer via STAT3-Mediated MID2 Upregulation.	Phenobarbital	34-41	MORC family CW-type zinc finger 4	Homo sapiens	0-5
32764967-0	2020	MORC4 Promotes Chemoresistance of Luminal A/B Breast Cancer via STAT3-Mediated MID2 Upregulation.	Phenobarbital	34-41	signal transducer and activator of transcription 3	Homo sapiens	64-69
32646883-5	2020	Its ECDs reveal an open state, in contrast to its structural homologues PTCH1 and NPC1, whose extracellular/luminal domains adopt a closed state.	Phenobarbital	108-115	patched 1	Homo sapiens	72-77
32646883-5	2020	Its ECDs reveal an open state, in contrast to its structural homologues PTCH1 and NPC1, whose extracellular/luminal domains adopt a closed state.	Phenobarbital	108-115	NPC intracellular cholesterol transporter 1	Homo sapiens	82-86
32460580-5	2020	Manipulation of TAK1 in vivo altered AVF wall thickening and luminal diameter; reduced TAK1 function was associated with reduced thickness and smaller diameter, whereas activation of TAK1 function was associated with increased thickness and larger diameter.	Phenobarbital	61-68	mitogen-activated protein kinase kinase kinase 7	Mus musculus	16-20
32415497-15	2020	In luminal A and luminal B patients, those with high TRPC1 expression had a better prognosis.	Phenobarbital	3-10	transient receptor potential cation channel subfamily C member 1	Homo sapiens	53-58
32742928-10	2020	Furthermore, AR is enriched in the luminal papillary mRNA subtype of urothelial carcinoma and also mediates resistance to cisplatin-based chemotherapy.	Phenobarbital	35-42	androgen receptor	Homo sapiens	13-15
32415497-15	2020	In luminal A and luminal B patients, those with high TRPC1 expression had a better prognosis.	Phenobarbital	17-24	transient receptor potential cation channel subfamily C member 1	Homo sapiens	53-58
32376245-0	2020	IGF1R constitutive activation expands luminal progenitors and influences lineage differentiation during breast tumorigenesis.	Phenobarbital	38-45	insulin like growth factor 1 receptor	Homo sapiens	0-5
32376245-6	2020	In these tumors, IGF1R expands the luminal-progenitor population while influencing myoepithelial differentiation.	Phenobarbital	35-42	insulin like growth factor 1 receptor	Homo sapiens	17-22
32376245-10	2020	These results suggest that IGF1R expands luminal progenitor populations while also stimulating myoepithelial cell differentiation.	Phenobarbital	41-48	insulin like growth factor 1 receptor	Homo sapiens	27-32
32565927-9	2020	Subtype analysis indicated that PBX1 overexpression was associated with luminal-like and hormone receptor-sensitive subtypes.	Phenobarbital	72-79	PBX homeobox 1	Homo sapiens	32-36
32565927-10	2020	In the survival analysis, a high expression level of PBX1 was associated with poor prognosis of patients with estrogen receptor (ER)-positive, luminal A and luminal B subtypes of BC.	Phenobarbital	143-150	PBX homeobox 1	Homo sapiens	53-57
32565927-10	2020	In the survival analysis, a high expression level of PBX1 was associated with poor prognosis of patients with estrogen receptor (ER)-positive, luminal A and luminal B subtypes of BC.	Phenobarbital	157-164	PBX homeobox 1	Homo sapiens	53-57
32565927-11	2020	The results of the present study indicate that PBX1 may serve as a specific biomarker and essential prognostic factor for ER-positive, luminal A and luminal B subtypes of BC.	Phenobarbital	135-142	PBX homeobox 1	Homo sapiens	47-51
32565927-11	2020	The results of the present study indicate that PBX1 may serve as a specific biomarker and essential prognostic factor for ER-positive, luminal A and luminal B subtypes of BC.	Phenobarbital	149-156	PBX homeobox 1	Homo sapiens	47-51
32377705-3	2020	Accumulating preclinical evidence is supporting the efficacy of cyclin-dependent kinase (CDK) 4/6 inhibitors against the luminal androgen receptor sub-type of triple-negative breast cancer (TNBC).	Phenobarbital	121-128	cyclin dependent kinase 4	Homo sapiens	64-97
32616232-7	2020	We conclude that the expression of innate immune molecules, including TLR, inflammation-related cytokines, and antimicrobial peptides, in the cecum are altered in association with changes in the density or composition of the luminal microbiota during the early phase of life in chicks.	Phenobarbital	225-232	toll-like receptor 2 type-1	Gallus gallus	70-73
32323562-5	2020	Treatment with the PKM2 activator TEPP-46 markedly attenuated the progression of TAAD in the mouse model as demonstrated by decreased morbidity and luminal diameter of the aorta.	Phenobarbital	148-155	pyruvate kinase, muscle	Mus musculus	19-23
32493616-9	2020	RESULTS: Arterial microvessels showed responsiveness to the neuropeptide Y agonist (10-9 to 4 x 10-7 mol/L) both before and after cardiopulmonary bypass, reaching a 12.5% vasoconstriction from the baseline luminal diameter.	Phenobarbital	206-213	neuropeptide Y	Homo sapiens	60-74
32600462-12	2020	RESULTS: A significant reduction of CDH6 immunolocalization was recorded in the luminal and glandular epithelium of endometrium from women with infertility (P < 0.05) compared to fertile group respective cellular compartments in the mid-secretory phase.	Phenobarbital	80-87	cadherin 6	Homo sapiens	36-40
32510949-2	2020	Demonstrate Selective Antiproliferative Effects in Cells Representing the Luminal Androgen Receptor Subtype of Triple Negative Breast Cancer.	Phenobarbital	74-81	androgen receptor	Homo sapiens	82-99
32588820-7	2020	Their unfolding occurs on the luminal side of the membrane by cytoplasmic Cdc48 action.	Phenobarbital	30-37	AAA family ATPase CDC48	Saccharomyces cerevisiae S288C	74-79
32513733-9	2020	These granules are involved in trafficking MMP-9 from the stroma to the epithelium to promote luminal epithelial remodeling during embryo invasion.	Phenobarbital	94-101	matrix metallopeptidase 9	Homo sapiens	43-48
32576932-5	2020	We uncovered a remarkable synergism in this stabilization involving the three luminal Cys of STIM2, which is unique to this paralog.	Phenobarbital	78-85	stromal interaction molecule 2	Homo sapiens	93-98
32576932-0	2020	Synergistic stabilization by nitrosoglutathione-induced thiol modifications in the stromal interaction molecule-2 luminal domain suppresses basal and store operated calcium entry.	Phenobarbital	114-121	stromal interaction molecule 2	Homo sapiens	83-113
32576932-7	2020	In HEK293T cells, enhanced free basal cytosolic Ca2+ and SOCE mediated by STIM2 overexpression could be attenuated by GSNO or mutation of the modifiable Cys located in the luminal domain.	Phenobarbital	172-179	stromal interaction molecule 2	Homo sapiens	74-79
32569321-6	2020	Confocal microscopy and real-time videos reveal that caveolin-1 strongly labels intracellular vacuoles and localizes to the EC apical surface as they fuse to form the luminal membrane.	Phenobarbital	167-174	caveolin 1	Homo sapiens	53-63
32585920-7	2020	Immunohistochemistry further revealed that PODXL is localized at the luminal side of human brain microvessels, supporting its potential suitability for translational applications.	Phenobarbital	69-76	podocalyxin like	Homo sapiens	43-48
32580398-4	2020	The proportion of highly expressed STAT6, FOXP3, CD8, CD68, and CD163 proteins was found to be lowest in luminal A type but highest in the HER-2 type.	Phenobarbital	105-112	signal transducer and activator of transcription 6	Homo sapiens	35-40
32580398-4	2020	The proportion of highly expressed STAT6, FOXP3, CD8, CD68, and CD163 proteins was found to be lowest in luminal A type but highest in the HER-2 type.	Phenobarbital	105-112	forkhead box P3	Homo sapiens	42-47
32580398-4	2020	The proportion of highly expressed STAT6, FOXP3, CD8, CD68, and CD163 proteins was found to be lowest in luminal A type but highest in the HER-2 type.	Phenobarbital	105-112	CD8a molecule	Homo sapiens	49-52
32580398-4	2020	The proportion of highly expressed STAT6, FOXP3, CD8, CD68, and CD163 proteins was found to be lowest in luminal A type but highest in the HER-2 type.	Phenobarbital	105-112	CD68 molecule	Homo sapiens	54-58
32580398-4	2020	The proportion of highly expressed STAT6, FOXP3, CD8, CD68, and CD163 proteins was found to be lowest in luminal A type but highest in the HER-2 type.	Phenobarbital	105-112	CD163 molecule	Homo sapiens	64-69
32569321-6	2020	Confocal microscopy and real-time videos reveal that caveolin-1 strongly labels intracellular vacuoles and localizes to the EC apical surface as they fuse to form the luminal membrane.	Phenobarbital	167-174	Polykaryocytosis inducer	Homo sapiens	150-154
32575830-0	2020	Luminal STIM1 Mutants that Cause Tubular Aggregate Myopathy Promote Autophagic Processes.	Phenobarbital	0-7	stromal interaction molecule 1	Homo sapiens	8-13
32427585-4	2020	Here, the anti-seizure efficacy of TrkB agonists LM22A-4, HIOC, and Deoxygedunin (DG), on PB-refractory seizures, and post-ischemic TrkB-pathway activation was investigated in a mouse model (CD-1, P7) of refractory neonatal seizures.	Phenobarbital	90-92	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	35-39
32416067-5	2020	Although deletion of BRD2 enhances sensitivity to BBDIs, BRD7 loss leads to gain of TEAD-YAP chromatin binding and luminal features associated with BBDI resistance.	Phenobarbital	115-122	bromodomain containing 7	Homo sapiens	57-61
32546765-4	2020	In order to facilitate molecular subtyping of bladder cancer in primary care centers, we analyzed the protein expressions of signature luminal (GATA3) and basal (KRT5/6) markers by immunohistochemistry, which identified molecular subtypes in over 80% of the cases.	Phenobarbital	135-142	GATA binding protein 3	Homo sapiens	144-149
32549380-6	2020	This lower prevalence of HER2-positive in-screen-detected breast carcinomas was observed in both hormone receptor positive (luminal HER2) and hormone-receptor-negative (HER2 enriched) tumors.	Phenobarbital	124-131	erb-b2 receptor tyrosine kinase 2	Homo sapiens	25-29
32549380-6	2020	This lower prevalence of HER2-positive in-screen-detected breast carcinomas was observed in both hormone receptor positive (luminal HER2) and hormone-receptor-negative (HER2 enriched) tumors.	Phenobarbital	124-131	nuclear receptor subfamily 4 group A member 1	Homo sapiens	97-113
32606753-0	2020	MCTS1 Directly Binds to TWF1 and Synergistically Modulate Cyclin D1 and C-Myc Translation in Luminal A/B Breast Cancer Cells.	Phenobarbital	93-100	MCTS1 re-initiation and release factor	Homo sapiens	0-5
32606753-9	2020	Conclusion: MCTS1 expression might serve as a potential prognostic biomarker of unfavorable OS in luminal A and luminal B cases.	Phenobarbital	98-105	MCTS1 re-initiation and release factor	Homo sapiens	12-17
32606753-9	2020	Conclusion: MCTS1 expression might serve as a potential prognostic biomarker of unfavorable OS in luminal A and luminal B cases.	Phenobarbital	112-119	MCTS1 re-initiation and release factor	Homo sapiens	12-17
32606753-10	2020	The novel direct interaction between MCTS1 and TWF1 might be necessary for the translation of some downstream genes in common in luminal A/B breast cancer cells.	Phenobarbital	129-136	MCTS1 re-initiation and release factor	Homo sapiens	37-42
32606753-10	2020	The novel direct interaction between MCTS1 and TWF1 might be necessary for the translation of some downstream genes in common in luminal A/B breast cancer cells.	Phenobarbital	129-136	twinfilin actin binding protein 1	Homo sapiens	47-51
32350116-3	2020	At the luminal side and uncommon for Golgi proteins, FUT8 has an Src homology 3 (SH3) domain, which is usually found in cytosolic signal transduction molecules and generally mediates protein-protein interactions in the cytosol.	Phenobarbital	7-14	fucosyltransferase 8	Homo sapiens	53-57
32548262-9	2020	We propose RING1B as a key regulator of the dynamic, liganded-ERalpha transcriptional regulatory circuit in luminal BC.	Phenobarbital	108-115	ring finger protein 2	Homo sapiens	11-17
32548262-9	2020	We propose RING1B as a key regulator of the dynamic, liganded-ERalpha transcriptional regulatory circuit in luminal BC.	Phenobarbital	108-115	estrogen receptor 1	Homo sapiens	62-69
32612999-0	2020	Self-Association of Purified Reconstituted ER Luminal Spacer Climp63.	Phenobarbital	46-53	cytoskeleton associated protein 4	Homo sapiens	61-68
32612999-4	2020	The luminal domain (LD) of Climp63 is predicted to be highly helical, and it may form bridges between parallel membranes, regulating the abundance and width of ER sheets.	Phenobarbital	4-11	cytoskeleton associated protein 4	Homo sapiens	27-34
32612999-9	2020	These results demonstrate a direct self-association of Climp63, supporting its role as an ER luminal spacer.	Phenobarbital	93-100	cytoskeleton associated protein 4	Homo sapiens	55-62
32545448-10	2020	Its association with the response to endocrine therapy and outcome provides evidence for DBN1 as a potential biomarker in luminal breast cancer, particularly for the benefit of endocrine treatment.	Phenobarbital	122-129	drebrin 1	Homo sapiens	89-93
32521267-4	2020	Here, we show that the transcription factor SOX9 acts as a determinant for estrogen-receptor-negative (ER-) luminal stem/progenitor cells (LSPCs).	Phenobarbital	108-115	SRY (sex determining region Y)-box 9	Mus musculus	44-48
32521267-4	2020	Here, we show that the transcription factor SOX9 acts as a determinant for estrogen-receptor-negative (ER-) luminal stem/progenitor cells (LSPCs).	Phenobarbital	108-115	estrogen receptor 1 (alpha)	Mus musculus	75-92
32521267-6	2020	Inactivation of TP53 and RB via expression of SV40 TAg in a BLBC mouse tumor model leads to upregulation of SOX9, which drives luminal-to-basal reprogramming in vivo.	Phenobarbital	127-134	transformation related protein 53	Mus musculus	16-20
32521267-6	2020	Inactivation of TP53 and RB via expression of SV40 TAg in a BLBC mouse tumor model leads to upregulation of SOX9, which drives luminal-to-basal reprogramming in vivo.	Phenobarbital	127-134	SRY (sex determining region Y)-box 9	Mus musculus	108-112
32427585-8	2020	Full TrkB agonists HIOC and DG similarly rescued PB-refractoriness.	Phenobarbital	49-51	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	5-9
32342107-3	2020	We employ a proteomics-based approach to identify myeloid leukemia factor 2 (MLF2) as a luminal component of the bleb.	Phenobarbital	88-95	myeloid leukemia factor 2	Homo sapiens	50-75
32303457-3	2020	Omeprazole and rifampicin respectively induced CYP1A1 and CYP3A8 mRNAs, while phenobarbital induced CYP2C43, CYP2C75, and CYP3A8, and slightly induced CYP2B6.	Phenobarbital	78-91	cytochrome P450 family 2 subfamily C member 9	Macaca fascicularis	100-107
32303457-3	2020	Omeprazole and rifampicin respectively induced CYP1A1 and CYP3A8 mRNAs, while phenobarbital induced CYP2C43, CYP2C75, and CYP3A8, and slightly induced CYP2B6.	Phenobarbital	78-91	cytochrome P450 family 2 subfamily C member 19	Macaca fascicularis	109-116
32303457-3	2020	Omeprazole and rifampicin respectively induced CYP1A1 and CYP3A8 mRNAs, while phenobarbital induced CYP2C43, CYP2C75, and CYP3A8, and slightly induced CYP2B6.	Phenobarbital	78-91	cytochrome P450 family 3 subfamily A member 4	Macaca fascicularis	122-128
32303457-3	2020	Omeprazole and rifampicin respectively induced CYP1A1 and CYP3A8 mRNAs, while phenobarbital induced CYP2C43, CYP2C75, and CYP3A8, and slightly induced CYP2B6.	Phenobarbital	78-91	cytochrome P450 family 2 subfamily B member 6	Macaca fascicularis	151-157
32303457-4	2020	The nuclear receptors AHR, PXR, and CAR mRNA levels, which were activated by omeprazole, rifampicin, and phenobarbital, respectively, tended to decrease via exposure to inducers despite the increase in CYP mRNA levels.	Phenobarbital	105-118	aryl hydrocarbon receptor	Macaca fascicularis	22-25
32303457-4	2020	The nuclear receptors AHR, PXR, and CAR mRNA levels, which were activated by omeprazole, rifampicin, and phenobarbital, respectively, tended to decrease via exposure to inducers despite the increase in CYP mRNA levels.	Phenobarbital	105-118	nuclear receptor subfamily 1 group I member 3	Macaca fascicularis	36-39
32394766-6	2020	The protective effect of cytoplasmic HMGA2 persisted in the Luminal A and triple negative breast cancer subgroups.	Phenobarbital	60-67	high mobility group AT-hook 2	Homo sapiens	37-42
32342107-3	2020	We employ a proteomics-based approach to identify myeloid leukemia factor 2 (MLF2) as a luminal component of the bleb.	Phenobarbital	88-95	myeloid leukemia factor 2	Homo sapiens	77-81
32436776-5	2020	The highest level of mRNA expression of DMBT1 was found in the small intestine, and the expression level was high throughout the luminal digestive tract.	Phenobarbital	129-136	deleted in malignant brain tumors 1	Homo sapiens	40-45
32540859-10	2020	Besides, LAG-3 mRNA level was linked to luminal and basal subtypes of MIBC.	Phenobarbital	40-47	lymphocyte activating 3	Homo sapiens	9-14
32145074-7	2020	There were statistically significant linear correlations between luminal worm burdens and MUC2 (r = -.2358) and RELM-beta (r = -.2261).	Phenobarbital	65-72	MUC2	Equus caballus	90-94
32320717-3	2020	Male CD-1 mice were fed diets to provide intakes of 0 (control), 30, 100 and 300 mg/kg/day PBO and for purposes of comparison 500 ppm sodium phenobarbital (NaPB), a known constitutive androstane receptor (CAR) activator, for 7 and 14 days.	Phenobarbital	134-154	N-ethylmaleimide sensitive fusion protein attachment protein beta	Mus musculus	156-160
32473643-6	2020	Nodal involvement was also significantly associated with the risk of distant metastasis (OR 1.855, 95% CI 1.319-2.611), and the risk was higher in the Luminal A-like subtype (OR 2.572, 95% CI 1.547-4.278).	Phenobarbital	151-158	nodal growth differentiation factor	Homo sapiens	0-5
32460723-11	2020	However, in women with recurrence, there was increased expression of CYP19A1 mRNA in those who had the luminal hybrid subtype and locoregional relapse and decreased expression in those negative for HER2.	Phenobarbital	103-110	cytochrome P450 family 19 subfamily A member 1	Homo sapiens	69-76
32304637-11	2020	After testing both methods using simple model systems, we apply the two assays to investigate a previously proposed model of membrane association for the luminal domain of SUN2, a constituent protein of the linker of nucleoskeleton and cytoskeleton complex.	Phenobarbital	154-161	Sad1 and UNC84 domain containing 2	Homo sapiens	172-176
32420875-4	2020	The widely-expressed Ca2+-binding protein annexin A1 (ANXA1) is present in the nuclear envelope lumen and, through interaction with a luminal region of the channel, can modify high-[Ca2+]ER inhibition of InsP3R activity.	Phenobarbital	134-141	annexin A1	Homo sapiens	54-59
32429297-10	2020	In luminal-like early-onset BC, a lower BRCA detection rate was observed, suggesting a role for other predisposing genes along with BRCA genetic testing.	Phenobarbital	3-10	BRCA1 DNA repair associated	Homo sapiens	40-44
32429297-10	2020	In luminal-like early-onset BC, a lower BRCA detection rate was observed, suggesting a role for other predisposing genes along with BRCA genetic testing.	Phenobarbital	3-10	BRCA1 DNA repair associated	Homo sapiens	132-136
32413024-3	2020	ERbeta is expressed in both basal and luminal cells in the prostate while AR is expressed in luminal but not in the basal cell layer which harbors the prostate stem cells.	Phenobarbital	38-45	estrogen receptor 1 (alpha)	Mus musculus	0-6
32413024-3	2020	ERbeta is expressed in both basal and luminal cells in the prostate while AR is expressed in luminal but not in the basal cell layer which harbors the prostate stem cells.	Phenobarbital	93-100	androgen receptor	Mus musculus	74-76
32332171-3	2020	Polycystin-2 is found in organelle membranes, including the primary cilium-an antennae-like structure on the luminal side of the collecting duct.	Phenobarbital	109-116	polycystin 2, transient receptor potential cation channel	Homo sapiens	0-12
32461977-10	2020	The luminal B/HER2+ subtypes had prolonged DFS when compared with nonluminal B/HER2+ subtypes (P = 0.010).	Phenobarbital	4-11	erb-b2 receptor tyrosine kinase 2	Homo sapiens	14-18
32461977-11	2020	The luminal B/HER2+ subgroup also showed improved DFS in non-pCR patients (P = 0.010).	Phenobarbital	4-11	erb-b2 receptor tyrosine kinase 2	Homo sapiens	14-18
32458655-5	2020	RESULTS: Positive LAT1 expression was found in 27 (84.4%) luminal A subtype, 27 (64.3%) luminal B/triple positive subtype, 29 (82.9%) triple negative subtype, and 24 (66.7%) HER2-only positive subtype (p=0.1).	Phenobarbital	58-65	solute carrier family 7 member 5	Homo sapiens	18-22
32458655-5	2020	RESULTS: Positive LAT1 expression was found in 27 (84.4%) luminal A subtype, 27 (64.3%) luminal B/triple positive subtype, 29 (82.9%) triple negative subtype, and 24 (66.7%) HER2-only positive subtype (p=0.1).	Phenobarbital	88-95	solute carrier family 7 member 5	Homo sapiens	18-22
32113984-6	2020	We show through gene expression microarray analysis that the nuclear accumulation of MKL1 induces dedifferentiation leading to a mixed luminal/basal phenotype and suppresses estrogen-mediated control of gene expression.	Phenobarbital	135-142	myocardin related transcription factor A	Homo sapiens	85-89
32200487-9	2020	High expression of SLC7A8 mRNA and SLC7A8 protein was associated with good patient outcome (P <= 0.001) but only in the low proliferative ER+/luminal A tumours (P = 0.01).	Phenobarbital	142-149	solute carrier family 7 member 8	Homo sapiens	19-25
32181676-4	2020	The low expression level of AR is strongly associated with poor recurrence-free survival, especially with poor distance metastasis-free survival in luminal A patients, but inverse in HER2 (human epidermal growth factor receptor-2) enriched patients.	Phenobarbital	148-155	androgen receptor	Homo sapiens	28-30
32410843-6	2020	PIK3CA mutation and expression were significantly associated with Luminal A type (p = 0.017 and p = 0.011, respectively).	Phenobarbital	66-73	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	0-6
32355025-4	2020	Using single-cell RNA sequencing, we identified a rare luminal population in the mouse prostate that expresses stemlike genes (Sca1 + and Psca +) and a large population of differentiated cells (Nkx3.1 +, Pbsn +).	Phenobarbital	55-62	caspase 3	Mus musculus	127-131
32355025-4	2020	Using single-cell RNA sequencing, we identified a rare luminal population in the mouse prostate that expresses stemlike genes (Sca1 + and Psca +) and a large population of differentiated cells (Nkx3.1 +, Pbsn +).	Phenobarbital	55-62	prostate stem cell antigen	Mus musculus	138-142
32171971-13	2020	Basal SCs in SCT still showed a CLDN11/SOX9 co-localisation, suggesting that luminal neoplastic SCs undergo de-differentiation during tumour progression.	Phenobarbital	77-84	claudin 11	Canis lupus familiaris	32-38
32492958-7	2020	In the duodenum, luminal stimulation with procyanidin dimer B2 increased PYY secretion, but not CCK secretion, while catechin monomers (catechin/epicatechin) significantly increased CCK release, but not PYY release.	Phenobarbital	17-24	peptide YY	Sus scrofa	73-76
32362572-8	2020	Both proteins, CAPS and MSX1, showed a high specificity for endometrium and are both localized in the luminal cells and epithelial cells of the glandular and adenomyotic glands.	Phenobarbital	102-109	calcyphosine	Homo sapiens	15-19
32362572-8	2020	Both proteins, CAPS and MSX1, showed a high specificity for endometrium and are both localized in the luminal cells and epithelial cells of the glandular and adenomyotic glands.	Phenobarbital	102-109	msh homeobox 1	Homo sapiens	24-28
32481300-8	2020	Only tumor differentiation (P = .031) and tumor size (P = .022) were different between IMPCs-L and IMPCs-H. EMA/MUC1 enhanced the characteristic inside-out staining pattern of IMPCs, whereas non-IMPCs showed luminal staining patterns.	Phenobarbital	208-215	mucin 1, cell surface associated	Homo sapiens	112-116
32455829-0	2020	Relapse-Free Survival and PD-L1 Expression in First High- and Low-Grade Relapsed Luminal, Basal and Double-Negative P53-Mutant Non-Muscular Invasive Bladder Cancer Depending on Previous Chemo- and Immunotherapy.	Phenobarbital	81-88	CD274 molecule	Homo sapiens	26-31
32455829-1	2020	The goal of this study was to assess how PD-L1 expression in tissue specimens of patients with main molecular subtypes of NMIBC (luminal, basal and double-negative p53-mutant) associates with relapsed-free survival in dependence on the tumor grade and prior treatment of primary bladder cancer.	Phenobarbital	129-136	CD274 molecule	Homo sapiens	41-46
32455829-2	2020	PD-L1 expressions on the membrane of neoplastic and CD8+ immune cells were assessed in tumor specimens (n = 240) of primary and relapsed luminal, basal and double-negative p53-mutant NMIBC.	Phenobarbital	137-144	CD274 molecule	Homo sapiens	0-5
32499907-6	2020	Results: The results of the pilot study showed expression of AT1-R and AT2-R in all endometrial compartments (luminal epithelium, glandular epithelium, stroma cells, and blood vessels), and altered expression was witnessed in women with recurrent miscarriage when compared with fertile control women from our preliminary result.	Phenobarbital	110-117	angiotensin II receptor type 1	Homo sapiens	61-64
32423137-0	2020	Tumorigenic and Metastatic Role of CD44-/low/CD24-/low Cells in Luminal Breast Cancer.	Phenobarbital	64-71	CD44 molecule (Indian blood group)	Homo sapiens	35-39
32423137-0	2020	Tumorigenic and Metastatic Role of CD44-/low/CD24-/low Cells in Luminal Breast Cancer.	Phenobarbital	64-71	CD24 molecule	Homo sapiens	45-49
32423137-5	2020	Our results demonstrate that the CD44-/low/CD24-/low cell population, which is enriched in luminal cell lines (T47D, MCF-7 and BT-474), possesses metastatic and tumorigenic properties.	Phenobarbital	91-98	CD44 molecule (Indian blood group)	Homo sapiens	33-37
32423137-5	2020	Our results demonstrate that the CD44-/low/CD24-/low cell population, which is enriched in luminal cell lines (T47D, MCF-7 and BT-474), possesses metastatic and tumorigenic properties.	Phenobarbital	91-98	CD24 molecule	Homo sapiens	43-47
32414208-4	2020	We found that the expression levels of miR-200a and the ELK3 mRNA were negatively correlated in the luminal and TNBC subtypes of breast cancer cells.	Phenobarbital	100-107	microRNA 200a	Homo sapiens	39-47
32414208-4	2020	We found that the expression levels of miR-200a and the ELK3 mRNA were negatively correlated in the luminal and TNBC subtypes of breast cancer cells.	Phenobarbital	100-107	ETS transcription factor ELK3	Homo sapiens	56-60
32375698-8	2020	The ALDH1A3 knockout cells gradually acquired resistance to androgen deprivation therapy, a few cells have been found in knockout group showing as that the spindle-like luminal cells in charcoal stripped medium.	Phenobarbital	169-176	aldehyde dehydrogenase family 1, subfamily A3	Mus musculus	4-11
32086991-5	2020	CLDN4 expression in human IDC cell lines MCF-7 (luminal subtype) and MDA-468 (TNBC) was at the same level.	Phenobarbital	48-55	claudin 4	Homo sapiens	0-5
32361918-5	2020	The H-score (median, range) of MUC16 in the luminal epithelium and glandular epithelium was determined by using immunohistochemistry.	Phenobarbital	44-51	mucin 16, cell surface associated	Homo sapiens	31-36
31971917-5	2020	Mechanistically, elevated vascular leakage promoted movement of interstitial chemokines into the bloodstream, a response that supported abluminal-to-luminal neutrophil TEM.	Phenobarbital	138-145	tenomodulin	Rattus norvegicus	168-171
32436776-6	2020	The expression of DMBT1 was especially high in the luminal digestive tract and salivary glands.	Phenobarbital	51-58	deleted in malignant brain tumors 1	Homo sapiens	18-23
31942831-6	2020	In particular, basal cancers are composed of squamous and sarcomatoid pathological findings, while luminal cancers are composed of papillary finding features and genetic mutations (FGFR3).	Phenobarbital	99-106	fibroblast growth factor receptor 3	Homo sapiens	181-186
32353937-7	2020	CD24/49f-based FACS analysis showed that in utero exposure to 500 ng/kg BPA induced expansion of luminal and basal/myoepithelial cell subpopulations at PND 35.	Phenobarbital	97-104	CD24a antigen	Mus musculus	0-4
32426275-0	2020	Dysregulation of TLR2 Serves as a Prognostic Biomarker in Breast Cancer and Predicts Resistance to Endocrine Therapy in the Luminal B Subtype.	Phenobarbital	124-131	toll like receptor 2	Homo sapiens	17-21
32352034-6	2020	Analyses of publicly available databases showed significantly improved overall and relapse-free survival in patients with high Gas6 mRNA, particularly in luminal A breast cancers.	Phenobarbital	154-161	growth arrest specific 6	Homo sapiens	127-131
32395574-2	2020	Previous reports have shown that F11R/JAM-A plays a critical role in the adhesion of platelets to an inflamed endothelium due to its" pathological expression on the luminal surface of the cytokine-inflamed endothelium.	Phenobarbital	165-172	F11 receptor	Mus musculus	38-43
32327568-5	2020	Hrd1 and the rhomboid-like Der1 protein form two "half-channels" with cytosolic and luminal cavities, respectively, and lateral gates facing one another in a thinned membrane region.	Phenobarbital	84-91	synoviolin 1	Homo sapiens	0-4
32327568-5	2020	Hrd1 and the rhomboid-like Der1 protein form two "half-channels" with cytosolic and luminal cavities, respectively, and lateral gates facing one another in a thinned membrane region.	Phenobarbital	84-91	derlin 1	Homo sapiens	27-31
32373367-10	2020	Thus, the expression levels of AR, miR-185, miR-205, and miR-21 can serve as markers to predict cancer spread to the lymph node in luminal B- and HER2-positive subtypes of breast cancer.	Phenobarbital	131-138	androgen receptor	Homo sapiens	31-33
32211762-10	2020	GABAA receptor agonist phenobarbital could rectify the decrease of BrdU+/NeuN+ cells in PRS mice.	Phenobarbital	23-36	RNA binding protein, fox-1 homolog (C. elegans) 3	Mus musculus	73-77
32373367-10	2020	Thus, the expression levels of AR, miR-185, miR-205, and miR-21 can serve as markers to predict cancer spread to the lymph node in luminal B- and HER2-positive subtypes of breast cancer.	Phenobarbital	131-138	microRNA 21	Homo sapiens	57-63
32377198-12	2020	MUC1 expressions among the molecular classes were luminal A (60.7%), luminal B (68.8%), HER2 overexpression (87.5%), and triple negative (56.6%).	Phenobarbital	50-57	mucin 1, cell surface associated	Homo sapiens	0-4
32377198-12	2020	MUC1 expressions among the molecular classes were luminal A (60.7%), luminal B (68.8%), HER2 overexpression (87.5%), and triple negative (56.6%).	Phenobarbital	69-76	mucin 1, cell surface associated	Homo sapiens	0-4
32295249-5	2020	Using digital pathology, ASPH was scored in the luminal area (LM), center tumor (CT) and invasive margin (IM) of 100 human CRCs.	Phenobarbital	48-55	aspartate beta-hydroxylase	Homo sapiens	25-29
32346580-5	2020	We showed that HOXB7 is upregulated in all breast cancer cells analyzed, while HOXB8 and HOXB9 are significantly upregulated in MCF7 (Luminal A), BT474 (Luminal B) and MDA231 cells (Triple-negative Claudin-low).	Phenobarbital	134-141	homeobox B8	Homo sapiens	79-84
32346580-5	2020	We showed that HOXB7 is upregulated in all breast cancer cells analyzed, while HOXB8 and HOXB9 are significantly upregulated in MCF7 (Luminal A), BT474 (Luminal B) and MDA231 cells (Triple-negative Claudin-low).	Phenobarbital	134-141	homeobox B9	Homo sapiens	89-94
32346580-5	2020	We showed that HOXB7 is upregulated in all breast cancer cells analyzed, while HOXB8 and HOXB9 are significantly upregulated in MCF7 (Luminal A), BT474 (Luminal B) and MDA231 cells (Triple-negative Claudin-low).	Phenobarbital	153-160	homeobox B8	Homo sapiens	79-84
32346580-5	2020	We showed that HOXB7 is upregulated in all breast cancer cells analyzed, while HOXB8 and HOXB9 are significantly upregulated in MCF7 (Luminal A), BT474 (Luminal B) and MDA231 cells (Triple-negative Claudin-low).	Phenobarbital	153-160	homeobox B9	Homo sapiens	89-94
32363111-5	2020	Higher expression of B7-H4 was associated with worse survival in muscle-invasive bladder cancer in humans, and increased B7-H4 expression was identified in luminal and luminal-papillary subtypes of bladder cancer.	Phenobarbital	156-163	V-set domain containing T cell activation inhibitor 1	Homo sapiens	121-126
32363111-5	2020	Higher expression of B7-H4 was associated with worse survival in muscle-invasive bladder cancer in humans, and increased B7-H4 expression was identified in luminal and luminal-papillary subtypes of bladder cancer.	Phenobarbital	168-175	V-set domain containing T cell activation inhibitor 1	Homo sapiens	121-126
32548572-5	2020	In vitro REEP5 depletion in mouse cardiac myocytes resulted in SR/ER membrane destabilization and luminal vacuolization along with decreased myocyte contractility and disrupted Ca2+ cycling.	Phenobarbital	98-105	receptor accessory protein 5	Mus musculus	9-14
32249764-3	2020	Basal/stem and luminal progenitor cells can differentiate in culture to generate mature basal and luminal cell types, including ER+ cells that have been challenging to maintain in culture.	Phenobarbital	15-22	epiregulin	Homo sapiens	128-130
32015100-3	2020	In the present report, we present clear evidence that these senescence-related active fibroblasts can dedifferentiate proliferating primary human luminal cells to multipotent stem cells in an interleukin-8 (IL-8)-dependent manner.	Phenobarbital	146-153	C-X-C motif chemokine ligand 8	Homo sapiens	192-205
32015100-3	2020	In the present report, we present clear evidence that these senescence-related active fibroblasts can dedifferentiate proliferating primary human luminal cells to multipotent stem cells in an interleukin-8 (IL-8)-dependent manner.	Phenobarbital	146-153	C-X-C motif chemokine ligand 8	Homo sapiens	207-211
32015100-5	2020	This IL-8-related dedifferentiation of luminal cells was mediated through the STAT3-dependent downregulation of p16INK4A and the microRNA miR-141.	Phenobarbital	39-46	C-X-C motif chemokine ligand 8	Homo sapiens	5-9
32015100-5	2020	This IL-8-related dedifferentiation of luminal cells was mediated through the STAT3-dependent downregulation of p16INK4A and the microRNA miR-141.	Phenobarbital	39-46	signal transducer and activator of transcription 3	Homo sapiens	78-83
32015100-5	2020	This IL-8-related dedifferentiation of luminal cells was mediated through the STAT3-dependent downregulation of p16INK4A and the microRNA miR-141.	Phenobarbital	39-46	cyclin dependent kinase inhibitor 2A	Homo sapiens	112-120
32146834-14	2020	Our results demonstrate that altered beta-glucuronidase activity has implications for the bioavailability of luminal serotonin.	Phenobarbital	109-116	glucuronidase, beta	Mus musculus	37-55
32328632-4	2020	One of these mutants, affecting the vacuolar H+-ATPase gene atp6ap1b, revealed specific requirements for luminal acidification in apical, but not basolateral, membrane protein sorting and transport.	Phenobarbital	105-112	ATPase H+ transporting accessory protein 1b	Danio rerio	60-68
33457092-8	2020	Tumors with high PDPN mRNA expression mainly presented luminal-infiltrated and basal-squamous subtypes (2017 TCGA classification) or stroma-rich and Ba/Sq subtypes (consensus classification).	Phenobarbital	55-62	podoplanin	Homo sapiens	17-21
31991499-9	2020	c-Met protein overexpression was also noted in the Luminal B subtype though no amplification was noted.	Phenobarbital	51-58	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
32216937-4	2020	The YAP1 protein was primarily localized in the endometrial luminal and glandular epithelial cells of the uterine horn of ewes on day 2 of the estrous cycle.	Phenobarbital	60-67	transcriptional coactivator YAP1	Ovis aries	4-8
31991499-11	2020	c-Met downstream pathway genes (RAS-MAPK, PI3K-AKT and angiogenesis pathway) showed significant upregulation in Luminal B molecular subtype, lymph node-positive cases and cases with high MVD.	Phenobarbital	112-119	MET proto-oncogene, receptor tyrosine kinase	Homo sapiens	0-5
31991499-11	2020	c-Met downstream pathway genes (RAS-MAPK, PI3K-AKT and angiogenesis pathway) showed significant upregulation in Luminal B molecular subtype, lymph node-positive cases and cases with high MVD.	Phenobarbital	112-119	AKT serine/threonine kinase 1	Homo sapiens	47-50
32193417-2	2020	Whereas SULT1E1 is expressed low in the liver of adult mice, it is induced by phenobarbital (PB) treatment or spontaneously in diabetic livers via nuclear receptors.	Phenobarbital	78-91	sulfotransferase family 1E, member 1	Mus musculus	8-15
32202166-2	2020	Phenobarbital, a well-known liver cancer promoter, has been found to promote hepatocyte proliferation via CAR activation.	Phenobarbital	0-13	CXADR pseudogene 1	Homo sapiens	106-109
32202166-4	2020	In addition, it is believed that CAR-mediated liver carcinogenesis shows a species difference; phenobarbital treatment induces hepatocyte proliferation and liver cancer in rodents but not in humans.	Phenobarbital	95-108	CXADR pseudogene 1	Homo sapiens	33-36
32193417-2	2020	Whereas SULT1E1 is expressed low in the liver of adult mice, it is induced by phenobarbital (PB) treatment or spontaneously in diabetic livers via nuclear receptors.	Phenobarbital	93-95	sulfotransferase family 1E, member 1	Mus musculus	8-15
32193417-5	2020	Hepatic SULT1E1 mRNA levels are constitutively up-regulated in type 1 diabetic Akita mice; CAR spontaneously accumulates in the nucleus and activates the Sult1e1 promoter by recruiting phosphorylated ERalpha in the liver as observed with PB-induced livers.	Phenobarbital	238-240	sulfotransferase family 1E, member 1	Mus musculus	8-15
32193417-5	2020	Hepatic SULT1E1 mRNA levels are constitutively up-regulated in type 1 diabetic Akita mice; CAR spontaneously accumulates in the nucleus and activates the Sult1e1 promoter by recruiting phosphorylated ERalpha in the liver as observed with PB-induced livers.	Phenobarbital	238-240	nuclear receptor subfamily 1, group I, member 3	Mus musculus	91-94
32193417-5	2020	Hepatic SULT1E1 mRNA levels are constitutively up-regulated in type 1 diabetic Akita mice; CAR spontaneously accumulates in the nucleus and activates the Sult1e1 promoter by recruiting phosphorylated ERalpha in the liver as observed with PB-induced livers.	Phenobarbital	238-240	sulfotransferase family 1E, member 1	Mus musculus	154-161
32193417-6	2020	Thus, this CAR-phosphorylated ERalpha signaling enables these two nuclear receptors to communicate, activating the Sult1e1 gene in response to either PB or diabetes in mice.	Phenobarbital	150-152	nuclear receptor subfamily 1, group I, member 3	Mus musculus	11-14
32193417-6	2020	Thus, this CAR-phosphorylated ERalpha signaling enables these two nuclear receptors to communicate, activating the Sult1e1 gene in response to either PB or diabetes in mice.	Phenobarbital	150-152	estrogen receptor 1 (alpha)	Mus musculus	30-37
32193417-6	2020	Thus, this CAR-phosphorylated ERalpha signaling enables these two nuclear receptors to communicate, activating the Sult1e1 gene in response to either PB or diabetes in mice.	Phenobarbital	150-152	sulfotransferase family 1E, member 1	Mus musculus	115-122
31776133-8	2020	Staining of p53 and PARP1 in breast cancer TMAs and comparison with the TCGA database indicated a higher double-positive signal in basal-like breast cancer than in luminal A or luminal B subtypes.	Phenobarbital	164-171	tumor protein p53	Homo sapiens	12-15
32191225-5	2020	Using high-throughput transcriptional data available from the METABRIC dataset, high expression of SOX2 was significantly more common in luminal-B and HER2-enriched subtypes according to PAM50 classifier and in IntClust1 (high proliferating luminal-B) and IntClust 5 (luminal-B and HER2-amplified) according to integrative clustering.	Phenobarbital	137-144	SRY-box transcription factor 2	Homo sapiens	99-103
32191225-5	2020	Using high-throughput transcriptional data available from the METABRIC dataset, high expression of SOX2 was significantly more common in luminal-B and HER2-enriched subtypes according to PAM50 classifier and in IntClust1 (high proliferating luminal-B) and IntClust 5 (luminal-B and HER2-amplified) according to integrative clustering.	Phenobarbital	241-248	SRY-box transcription factor 2	Homo sapiens	99-103
32191225-5	2020	Using high-throughput transcriptional data available from the METABRIC dataset, high expression of SOX2 was significantly more common in luminal-B and HER2-enriched subtypes according to PAM50 classifier and in IntClust1 (high proliferating luminal-B) and IntClust 5 (luminal-B and HER2-amplified) according to integrative clustering.	Phenobarbital	241-248	erb-b2 receptor tyrosine kinase 2	Homo sapiens	151-155
32191225-7	2020	Iadademstat reduced the expression of SOX2 in luminal-B but not in luminal-A mammospheres, likely indicating a selective targeting of SOX2-driven CSC.	Phenobarbital	46-53	SRY-box transcription factor 2	Homo sapiens	38-42
32098763-7	2020	More importantly, C451A-ERalpha basal cells recovered in vivo repopulating ability when co-transplanted with wild-type luminal cells and specifically with ERalpha-positive luminal cells.	Phenobarbital	119-126	estrogen receptor 1 (alpha)	Mus musculus	24-31
32098763-7	2020	More importantly, C451A-ERalpha basal cells recovered in vivo repopulating ability when co-transplanted with wild-type luminal cells and specifically with ERalpha-positive luminal cells.	Phenobarbital	172-179	estrogen receptor 1 (alpha)	Mus musculus	24-31
32098763-7	2020	More importantly, C451A-ERalpha basal cells recovered in vivo repopulating ability when co-transplanted with wild-type luminal cells and specifically with ERalpha-positive luminal cells.	Phenobarbital	172-179	estrogen receptor 1 (alpha)	Mus musculus	155-162
32132057-9	2020	CONCLUSION: These luminal subtypes may benefit from targeted IGFR therapy in the future.	Phenobarbital	18-25	insulin like growth factor 1 receptor	Homo sapiens	61-65
31879282-12	2020	Although disparate sets of tissue biopsy (atorvastatin and carbamazepine) and in vitro hepatocyte (phenobarbital, chenodeoxycholate, and amprenavir) data present OATP messenger RNA induction (>=2-fold) by agents beyond RIF, the clinical relevance of such data needs to be determined.	Phenobarbital	99-112	solute carrier organic anion transporter family member 1A2	Homo sapiens	162-166
31924695-0	2020	Ser100-Phosphorylated RORalpha Orchestrates CAR and HNF4alpha to Form Active Chromatin Complex in Response to Phenobarbital to Regulate Induction of CYP2B6.	Phenobarbital	110-123	RAR related orphan receptor A	Homo sapiens	22-30
31924695-0	2020	Ser100-Phosphorylated RORalpha Orchestrates CAR and HNF4alpha to Form Active Chromatin Complex in Response to Phenobarbital to Regulate Induction of CYP2B6.	Phenobarbital	110-123	nuclear receptor subfamily 1 group I member 3	Homo sapiens	44-47
31924695-0	2020	Ser100-Phosphorylated RORalpha Orchestrates CAR and HNF4alpha to Form Active Chromatin Complex in Response to Phenobarbital to Regulate Induction of CYP2B6.	Phenobarbital	110-123	hepatocyte nuclear factor 4 alpha	Homo sapiens	52-61
31924695-0	2020	Ser100-Phosphorylated RORalpha Orchestrates CAR and HNF4alpha to Form Active Chromatin Complex in Response to Phenobarbital to Regulate Induction of CYP2B6.	Phenobarbital	110-123	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	149-155
32171971-13	2020	Basal SCs in SCT still showed a CLDN11/SOX9 co-localisation, suggesting that luminal neoplastic SCs undergo de-differentiation during tumour progression.	Phenobarbital	77-84	SRY-box transcription factor 9	Canis lupus familiaris	39-43
31924695-2	2020	Here, we found serine 100-phosphorylated RORalpha orchestrates constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha) to induce CYP2B6 by phenobarbital (PB) in human primary hepatocytes (HPHs).	Phenobarbital	172-185	nuclear receptor subfamily 1 group I member 3	Homo sapiens	63-95
31924695-2	2020	Here, we found serine 100-phosphorylated RORalpha orchestrates constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha) to induce CYP2B6 by phenobarbital (PB) in human primary hepatocytes (HPHs).	Phenobarbital	172-185	nuclear receptor subfamily 1 group I member 3	Homo sapiens	97-100
31924695-2	2020	Here, we found serine 100-phosphorylated RORalpha orchestrates constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha) to induce CYP2B6 by phenobarbital (PB) in human primary hepatocytes (HPHs).	Phenobarbital	172-185	hepatocyte nuclear factor 4 alpha	Homo sapiens	106-139
31924695-2	2020	Here, we found serine 100-phosphorylated RORalpha orchestrates constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha) to induce CYP2B6 by phenobarbital (PB) in human primary hepatocytes (HPHs).	Phenobarbital	172-185	hepatocyte nuclear factor 4 alpha	Homo sapiens	141-150
31924695-2	2020	Here, we found serine 100-phosphorylated RORalpha orchestrates constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha) to induce CYP2B6 by phenobarbital (PB) in human primary hepatocytes (HPHs).	Phenobarbital	172-185	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	162-168
31924695-2	2020	Here, we found serine 100-phosphorylated RORalpha orchestrates constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha) to induce CYP2B6 by phenobarbital (PB) in human primary hepatocytes (HPHs).	Phenobarbital	187-189	nuclear receptor subfamily 1 group I member 3	Homo sapiens	63-95
31924695-2	2020	Here, we found serine 100-phosphorylated RORalpha orchestrates constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha) to induce CYP2B6 by phenobarbital (PB) in human primary hepatocytes (HPHs).	Phenobarbital	187-189	nuclear receptor subfamily 1 group I member 3	Homo sapiens	97-100
31924695-2	2020	Here, we found serine 100-phosphorylated RORalpha orchestrates constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha) to induce CYP2B6 by phenobarbital (PB) in human primary hepatocytes (HPHs).	Phenobarbital	187-189	hepatocyte nuclear factor 4 alpha	Homo sapiens	106-139
31924695-2	2020	Here, we found serine 100-phosphorylated RORalpha orchestrates constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha) to induce CYP2B6 by phenobarbital (PB) in human primary hepatocytes (HPHs).	Phenobarbital	187-189	hepatocyte nuclear factor 4 alpha	Homo sapiens	141-150
31924695-2	2020	Here, we found serine 100-phosphorylated RORalpha orchestrates constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha) to induce CYP2B6 by phenobarbital (PB) in human primary hepatocytes (HPHs).	Phenobarbital	187-189	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	162-168
31924695-5	2020	In PB-treated HPH, p-Ser100 RORalpha was both enriched in the distal phenobarbital response element module (PBREM) and the proximal okadaic acid response element (OARE), a known HNF4alpha binding site.	Phenobarbital	3-5	RAR related orphan receptor A	Homo sapiens	28-36
31924695-5	2020	In PB-treated HPH, p-Ser100 RORalpha was both enriched in the distal phenobarbital response element module (PBREM) and the proximal okadaic acid response element (OARE), a known HNF4alpha binding site.	Phenobarbital	3-5	hepatocyte nuclear factor 4 alpha	Homo sapiens	178-187
31924695-5	2020	In PB-treated HPH, p-Ser100 RORalpha was both enriched in the distal phenobarbital response element module (PBREM) and the proximal okadaic acid response element (OARE), a known HNF4alpha binding site.	Phenobarbital	69-82	RAR related orphan receptor A	Homo sapiens	28-36
31924695-8	2020	A gel shift assay with a radiolabeled OARE module and nuclear extracts prepared from PB-treated mouse liver confirmed that HNF4alpha formed a complex with Ser 100-phosphorylated RORalpha, as shown by supershifted complexes with anti-p-Ser100 RORalpha and anti-HNF4alpha antibodies.	Phenobarbital	85-87	hepatic nuclear factor 4, alpha	Mus musculus	123-132
31924695-8	2020	A gel shift assay with a radiolabeled OARE module and nuclear extracts prepared from PB-treated mouse liver confirmed that HNF4alpha formed a complex with Ser 100-phosphorylated RORalpha, as shown by supershifted complexes with anti-p-Ser100 RORalpha and anti-HNF4alpha antibodies.	Phenobarbital	85-87	RAR-related orphan receptor alpha	Mus musculus	178-186
31924695-8	2020	A gel shift assay with a radiolabeled OARE module and nuclear extracts prepared from PB-treated mouse liver confirmed that HNF4alpha formed a complex with Ser 100-phosphorylated RORalpha, as shown by supershifted complexes with anti-p-Ser100 RORalpha and anti-HNF4alpha antibodies.	Phenobarbital	85-87	hepatic nuclear factor 4, alpha	Mus musculus	260-269
31924695-9	2020	Altogether, the results established that p-Ser100 RORalpha bridging the PBREM and OARE orchestrates CAR and HNF4alpha to form active chromatin complex during PB-induced CYP2B6 expression in human primary hepatocytes.	Phenobarbital	72-74	RAR related orphan receptor A	Homo sapiens	50-58
31924695-9	2020	Altogether, the results established that p-Ser100 RORalpha bridging the PBREM and OARE orchestrates CAR and HNF4alpha to form active chromatin complex during PB-induced CYP2B6 expression in human primary hepatocytes.	Phenobarbital	72-74	nuclear receptor subfamily 1 group I member 3	Homo sapiens	100-103
31924695-9	2020	Altogether, the results established that p-Ser100 RORalpha bridging the PBREM and OARE orchestrates CAR and HNF4alpha to form active chromatin complex during PB-induced CYP2B6 expression in human primary hepatocytes.	Phenobarbital	72-74	hepatocyte nuclear factor 4 alpha	Homo sapiens	108-117
31924695-9	2020	Altogether, the results established that p-Ser100 RORalpha bridging the PBREM and OARE orchestrates CAR and HNF4alpha to form active chromatin complex during PB-induced CYP2B6 expression in human primary hepatocytes.	Phenobarbital	72-74	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	169-175
31924695-10	2020	SIGNIFICANCE STATEMENT: CYP2B6 is a vital enzyme for the metabolic elimination of xenobiotics, and it is prone to induction by xenobiotics, including phenobarbital via constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha).	Phenobarbital	150-163	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	24-30
31924695-10	2020	SIGNIFICANCE STATEMENT: CYP2B6 is a vital enzyme for the metabolic elimination of xenobiotics, and it is prone to induction by xenobiotics, including phenobarbital via constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha).	Phenobarbital	150-163	nuclear receptor subfamily 1 group I member 3	Homo sapiens	168-200
31924695-10	2020	SIGNIFICANCE STATEMENT: CYP2B6 is a vital enzyme for the metabolic elimination of xenobiotics, and it is prone to induction by xenobiotics, including phenobarbital via constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha).	Phenobarbital	150-163	nuclear receptor subfamily 1 group I member 3	Homo sapiens	202-205
31924695-10	2020	SIGNIFICANCE STATEMENT: CYP2B6 is a vital enzyme for the metabolic elimination of xenobiotics, and it is prone to induction by xenobiotics, including phenobarbital via constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha).	Phenobarbital	150-163	hepatocyte nuclear factor 4 alpha	Homo sapiens	211-244
31924695-10	2020	SIGNIFICANCE STATEMENT: CYP2B6 is a vital enzyme for the metabolic elimination of xenobiotics, and it is prone to induction by xenobiotics, including phenobarbital via constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha).	Phenobarbital	150-163	hepatocyte nuclear factor 4 alpha	Homo sapiens	246-255
32094691-7	2020	We identify two binding sites for misfolded proteins in Hrd1, a low-affinity luminal site and a high-affinity cytoplasmic site formed following auto-ubiquitination of specific lysine residues in Hrd1"s RING domain.	Phenobarbital	77-84	synoviolin 1	Homo sapiens	56-60
32094691-7	2020	We identify two binding sites for misfolded proteins in Hrd1, a low-affinity luminal site and a high-affinity cytoplasmic site formed following auto-ubiquitination of specific lysine residues in Hrd1"s RING domain.	Phenobarbital	77-84	synoviolin 1	Homo sapiens	195-199
32094691-8	2020	We propose that the affinity difference between the luminal and cytoplasmic binding sites provides the initial driving force for substrate movement through Hrd1.	Phenobarbital	52-59	synoviolin 1	Homo sapiens	156-160
32075961-4	2020	In vitro REEP5 depletion in mouse cardiac myocytes results in SR/ER membrane destabilization and luminal vacuolization along with decreased myocyte contractility and disrupted Ca2+ cycling.	Phenobarbital	97-104	receptor accessory protein 5	Mus musculus	9-14
32296579-11	2020	Conclusions: This study has proven the ability of miR-6744-5p to increase anoikis sensitivity in both luminal A and triple negative breast cancer cell lines, highlighting its therapeutic potential in treating breast cancer.	Phenobarbital	102-109	microRNA 6744	Homo sapiens	50-58
32296584-7	2020	Among stage 0-III breast cancers, the HER2 subtype included a significantly higher percentage of mesenchymal and biphenotypic (epithelial and mesenchymal) CTCs than the luminal A or B subtypes.	Phenobarbital	169-176	erb-b2 receptor tyrosine kinase 2	Homo sapiens	38-42
31871111-1	2020	BACKGROUND: Forkhead box protein A1 (FOXA1) promotes luminal differentiation, and hypermethylation of the gene can be a mechanism of developing estrogen receptor-negative (ER-) breast cancer.	Phenobarbital	53-60	forkhead box A1	Homo sapiens	12-35
31871111-1	2020	BACKGROUND: Forkhead box protein A1 (FOXA1) promotes luminal differentiation, and hypermethylation of the gene can be a mechanism of developing estrogen receptor-negative (ER-) breast cancer.	Phenobarbital	53-60	forkhead box A1	Homo sapiens	37-42
31610144-5	2020	In response to hormonal signaling, Areg emanating from estrogen receptor (ER)-positive luminal cells, induce the expression of Rspo1 in ER-negative luminal cells.	Phenobarbital	87-94	amphiregulin	Homo sapiens	35-39
31610144-5	2020	In response to hormonal signaling, Areg emanating from estrogen receptor (ER)-positive luminal cells, induce the expression of Rspo1 in ER-negative luminal cells.	Phenobarbital	87-94	estrogen receptor 1	Homo sapiens	55-72
31610144-5	2020	In response to hormonal signaling, Areg emanating from estrogen receptor (ER)-positive luminal cells, induce the expression of Rspo1 in ER-negative luminal cells.	Phenobarbital	87-94	estrogen receptor 1	Homo sapiens	74-76
31610144-5	2020	In response to hormonal signaling, Areg emanating from estrogen receptor (ER)-positive luminal cells, induce the expression of Rspo1 in ER-negative luminal cells.	Phenobarbital	87-94	R-spondin 1	Homo sapiens	127-132
31610144-5	2020	In response to hormonal signaling, Areg emanating from estrogen receptor (ER)-positive luminal cells, induce the expression of Rspo1 in ER-negative luminal cells.	Phenobarbital	87-94	estrogen receptor 1	Homo sapiens	136-138
31610144-5	2020	In response to hormonal signaling, Areg emanating from estrogen receptor (ER)-positive luminal cells, induce the expression of Rspo1 in ER-negative luminal cells.	Phenobarbital	148-155	amphiregulin	Homo sapiens	35-39
31610144-5	2020	In response to hormonal signaling, Areg emanating from estrogen receptor (ER)-positive luminal cells, induce the expression of Rspo1 in ER-negative luminal cells.	Phenobarbital	148-155	estrogen receptor 1	Homo sapiens	55-72
31610144-5	2020	In response to hormonal signaling, Areg emanating from estrogen receptor (ER)-positive luminal cells, induce the expression of Rspo1 in ER-negative luminal cells.	Phenobarbital	148-155	estrogen receptor 1	Homo sapiens	74-76
31610144-5	2020	In response to hormonal signaling, Areg emanating from estrogen receptor (ER)-positive luminal cells, induce the expression of Rspo1 in ER-negative luminal cells.	Phenobarbital	148-155	R-spondin 1	Homo sapiens	127-132
31610144-5	2020	In response to hormonal signaling, Areg emanating from estrogen receptor (ER)-positive luminal cells, induce the expression of Rspo1 in ER-negative luminal cells.	Phenobarbital	148-155	estrogen receptor 1	Homo sapiens	136-138
31932695-0	2020	ARID1A determines luminal identity and therapeutic response in estrogen-receptor-positive breast cancer.	Phenobarbital	18-25	AT-rich interaction domain 1A	Homo sapiens	0-6
31932695-0	2020	ARID1A determines luminal identity and therapeutic response in estrogen-receptor-positive breast cancer.	Phenobarbital	18-25	estrogen receptor 1	Homo sapiens	63-80
31932695-4	2020	ARID1A inactivation in cells and in patients leads to resistance to ER degraders by facilitating a switch from ER-dependent luminal cells to ER-independent basal-like cells.	Phenobarbital	124-131	AT-rich interaction domain 1A	Homo sapiens	0-6
31932695-4	2020	ARID1A inactivation in cells and in patients leads to resistance to ER degraders by facilitating a switch from ER-dependent luminal cells to ER-independent basal-like cells.	Phenobarbital	124-131	epiregulin	Homo sapiens	68-70
31932695-4	2020	ARID1A inactivation in cells and in patients leads to resistance to ER degraders by facilitating a switch from ER-dependent luminal cells to ER-independent basal-like cells.	Phenobarbital	124-131	epiregulin	Homo sapiens	111-113
31932695-4	2020	ARID1A inactivation in cells and in patients leads to resistance to ER degraders by facilitating a switch from ER-dependent luminal cells to ER-independent basal-like cells.	Phenobarbital	124-131	epiregulin	Homo sapiens	111-113
31932695-5	2020	Cellular plasticity is mediated by loss of ARID1A-dependent SWI/SNF complex targeting to genomic sites of the luminal lineage-determining transcription factors including ER, forkhead box protein A1 (FOXA1) and GATA-binding factor 3 (GATA3).	Phenobarbital	110-117	AT-rich interaction domain 1A	Homo sapiens	43-49
31932695-5	2020	Cellular plasticity is mediated by loss of ARID1A-dependent SWI/SNF complex targeting to genomic sites of the luminal lineage-determining transcription factors including ER, forkhead box protein A1 (FOXA1) and GATA-binding factor 3 (GATA3).	Phenobarbital	110-117	epiregulin	Homo sapiens	170-172
31932695-7	2020	Altogether, we uncover a critical role for ARID1A in maintaining luminal cell identity and endocrine therapeutic response in ER+ breast cancer.	Phenobarbital	65-72	AT-rich interaction domain 1A	Homo sapiens	43-49
31852864-2	2020	We previously suggested that ATF6alpha occurs as a monomer, dimer and oligomer in the unstressed ER of Chinese hamster ovary cells due to the presence of two evolutionarily conserved cysteine residues in its luminal region (C467 and C618), and showed that ATF6alpha is reduced upon ER stress, such that only reduced monomer ATF6alpha is translocated to the Golgi apparatus for activation by proteolysis.	Phenobarbital	208-215	activating transcription factor 6	Homo sapiens	29-38
31636386-6	2020	Our results highlight the essential role of AP-2gamma in maintaining the luminal breast cancer phenotype and provide evidence that epigenetic mechanisms silence luminal gene expression in the basal phenotype.	Phenobarbital	73-80	transcription factor AP-2 gamma	Homo sapiens	44-53
31841397-3	2020	Deletion of uterine EZH2 increased proliferation of luminal and glandular epithelial cells.	Phenobarbital	52-59	enhancer of zeste 2 polycomb repressive complex 2 subunit	Mus musculus	20-24
31783045-3	2020	Currently, five crystal structures of the receptor-binding domain (Hc) of BoNT subtypes A1 and A2 complexed to the large luminal domain (LD4) of SV2C have been determined.	Phenobarbital	121-128	synaptic vesicle glycoprotein 2C	Homo sapiens	145-149
31836555-1	2020	In this study liver tumours produced in male and female mice of the low spontaneous liver tumour incidence C57BL/10J strain treated for 99 weeks with 1000 ppm in the diet with the model constitutive androstane receptor (CAR) activator sodium phenobarbital (NaPB) were analysed for beta-catenin mutations by Western immunoblotting and DNA/RNA analysis.	Phenobarbital	235-255	nuclear receptor subfamily 1, group I, member 3	Mus musculus	220-223
31959756-6	2020	Interestingly, increasing the luminal phenotype with anti-HER2 therapy increased sensitivity to CDK4/6 inhibition.	Phenobarbital	30-37	erb-b2 receptor tyrosine kinase 2	Homo sapiens	58-62
31836555-0	2020	Analysis of beta-catenin gene mutations and gene expression in liver tumours of C57BL/10J mice produced by chronic administration of sodium phenobarbital.	Phenobarbital	133-153	catenin (cadherin associated protein), beta 1	Mus musculus	12-24
31836555-1	2020	In this study liver tumours produced in male and female mice of the low spontaneous liver tumour incidence C57BL/10J strain treated for 99 weeks with 1000 ppm in the diet with the model constitutive androstane receptor (CAR) activator sodium phenobarbital (NaPB) were analysed for beta-catenin mutations by Western immunoblotting and DNA/RNA analysis.	Phenobarbital	235-255	nuclear receptor subfamily 1, group I, member 3	Mus musculus	186-218
31959756-6	2020	Interestingly, increasing the luminal phenotype with anti-HER2 therapy increased sensitivity to CDK4/6 inhibition.	Phenobarbital	30-37	cyclin dependent kinase 4	Homo sapiens	96-102
31945100-11	2020	Furthermore, colocalization of CTRP9 and AdipoR1 was noted in the luminal side of intra-renal arterial intima.	Phenobarbital	66-73	C1q and TNF related 9	Homo sapiens	31-36
31945100-11	2020	Furthermore, colocalization of CTRP9 and AdipoR1 was noted in the luminal side of intra-renal arterial intima.	Phenobarbital	66-73	adiponectin receptor 1	Homo sapiens	41-48
31952188-8	2020	The VEGFA protein was localised in intercaruncular luminal, glandular epithelium and in tunica muscularis of blood vessels.	Phenobarbital	51-58	vascular endothelial growth factor A	Bos taurus	4-9
31649042-3	2020	RESULTS: We developed a 109 immune-gene signature that captures abundance of CD8 TILs and is prognostic in basal-like, her2 and luminal-B BC, but not in luminal-A nor normal-like BC.	Phenobarbital	128-137	CD8a molecule	Homo sapiens	77-80
31668924-5	2020	This straightforward method, validated on two well-known protein"s topologies (IL1RI and Nox2), allowed us to discriminate rapidly the topological orientation of protein"s domains facing either the nucleocytosolic or the exterior/luminal compartments.	Phenobarbital	230-237	interleukin 1 receptor type 1	Homo sapiens	79-84
32411795-6	2020	Results: 38.1% patients had an overexpression of CD155, and the proportion of tumor cells with CD155 overexpression was 17%, 39%, 37%, and 62% among Luminal A, Luminal B, HER2-positive, and triple negative breast cancer cases, respectively (p < 0.05).	Phenobarbital	149-156	PVR cell adhesion molecule	Homo sapiens	95-100
32411795-6	2020	Results: 38.1% patients had an overexpression of CD155, and the proportion of tumor cells with CD155 overexpression was 17%, 39%, 37%, and 62% among Luminal A, Luminal B, HER2-positive, and triple negative breast cancer cases, respectively (p < 0.05).	Phenobarbital	160-167	PVR cell adhesion molecule	Homo sapiens	95-100
31923400-5	2020	MMs responded to luminal infection by upregulating a neuroprotective program via beta2-adrenergic receptor (beta2-AR) signaling and mediated neuronal protection through an arginase 1-polyamine axis.	Phenobarbital	17-24	adrenergic receptor, beta 2	Mus musculus	81-106
31923400-5	2020	MMs responded to luminal infection by upregulating a neuroprotective program via beta2-adrenergic receptor (beta2-AR) signaling and mediated neuronal protection through an arginase 1-polyamine axis.	Phenobarbital	17-24	adenosine A2a receptor	Mus musculus	108-116
31668924-5	2020	This straightforward method, validated on two well-known protein"s topologies (IL1RI and Nox2), allowed us to discriminate rapidly the topological orientation of protein"s domains facing either the nucleocytosolic or the exterior/luminal compartments.	Phenobarbital	230-237	cytochrome b-245 beta chain	Homo sapiens	89-93
31568599-3	2020	Leptin expression of moderate intensity was observed in the basal and parabasal epithelial cells of the luminal epithelium, and leptin was strongly expressed in the taste buds of the circumvallate and fungiform papillae and in von Ebner"s glands.	Phenobarbital	104-111	leptin	Ovis aries	0-6
32468659-4	2020	FST was mainly expressed in the luminal and glandular epithelium of the uterine tissues, and their expression intensity was highest in laying hens during the eggshell mineralization.	Phenobarbital	32-39	follistatin	Gallus gallus	0-3
32468659-9	2020	These results indicate that follistatin may regulate the differentiation of uterine luminal and glandular epithelium during eggshell biomineralization.	Phenobarbital	84-91	follistatin	Gallus gallus	28-39
32432166-3	2020	During the first week of AngII infusion, mice fed normal diet had less luminal expansion of the suprarenal aorta compared to those initiated Western diet after the first week of AngII infusion.	Phenobarbital	71-78	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	25-30
32957100-6	2020	The same trend was found in the luminal subgroup analysis (TCs PD-L1: p = 0.02, OR 23.43, 95% CI 1.66-331.58; PTLCs PD-L1: p = 0.01, OR 47.89, 95% CI 2.47-927.41).	Phenobarbital	32-39	CD274 molecule	Homo sapiens	63-68
31864171-0	2020	Rescue of PB-resistant neonatal seizures with single-dose of small-molecule TrkB antagonist show long-term benefits.	Phenobarbital	10-12	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	76-80
31864171-1	2020	A recently characterized CD-1 mouse model of phenobarbital (PB)-resistant neonatal ischemic-seizures (i.e.; unilateral carotid ligation) was shown to be associated with age-dependent (P7 vs. P10) acute seizure severity and PB-efficacy (i.e.; PB-resistant vs. PB-responsive).	Phenobarbital	45-58	S100 calcium binding protein A10 (calpactin)	Mus musculus	191-194
31864171-1	2020	A recently characterized CD-1 mouse model of phenobarbital (PB)-resistant neonatal ischemic-seizures (i.e.; unilateral carotid ligation) was shown to be associated with age-dependent (P7 vs. P10) acute seizure severity and PB-efficacy (i.e.; PB-resistant vs. PB-responsive).	Phenobarbital	60-62	S100 calcium binding protein A10 (calpactin)	Mus musculus	191-194
31864171-2	2020	ANA12, a novel small-molecule TrkB antagonist, rescued the PB-resistance at P7 in a dose-dependent manner and prevented the post-ischemic downregulation of KCC2, the chief Cl- extruder in neurons.	Phenobarbital	59-61	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	30-34
31864171-8	2020	ANA12 + PB treatment, but not PB-alone, rescued the loss of gamma power homeostasis present in P7 ligate-control but absent in P10 ligate group, highlighting the age-dependence.	Phenobarbital	8-10	S100 calcium binding protein A10 (calpactin)	Mus musculus	127-130
31864171-9	2020	In contrast, PB-alone treatment, but not ANA12+PB, significantly reduced the elevated delta-AUC observed in P10 ligate-controls, when PB is efficacious by itself.	Phenobarbital	13-15	S100 calcium binding protein A10 (calpactin)	Mus musculus	108-111
31432507-3	2020	Most importantly, we found that YPAC allows PHHs to retain enzymatic activities of CYP1A2, CYP2B6, and CYP3A4 even after 40 days of culture, and that inducibility of CYP3A4 activity in response to the prototypical inducers rifampicin and phenobarbital is also maintained.	Phenobarbital	238-251	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	166-172
31914618-11	2020	Furthermore, we demonstrate that Cav-a vesicles show polarized trafficking and localize at the luminal membrane during notochord lumenogenesis.	Phenobarbital	95-102	carbonic anhydrase 5A	Homo sapiens	33-36
31179826-8	2020	In contrast, distinct luminal community assembly was observed with dietary iron supplementation in WT versus Il10-/- mice, suggesting that the effects of increased iron on the microbiota differ with host inflammation status.	Phenobarbital	22-29	interleukin 10	Mus musculus	109-113
31722089-6	2020	Phenobarbital (PB) also increased expression levels of CYP2B6, CYP2C18, and CYP3A4 in BH4 and BH, but at a lower level than 3-MC.	Phenobarbital	0-13	cytochrome P450 subfamily 2B	Bos taurus	55-61
32863306-9	2020	Rats consumed 5% apple pectin diet showed significant increases of luminal mucin contents and Muc2 expression in the small intestine, while the luminal mucin contents in rats consumed 1.5% HRC diet were increased by 24% compared to those in rats consumed control diet, but the difference did not reach significant.	Phenobarbital	144-151	solute carrier family 13 member 2	Rattus norvegicus	152-157
33554153-3	2020	We hypothesized that TRPC6 was essential in the maintenance or reexpression of a differentiated SMC phenotype and minimized luminal stenosis following arterial injury.	Phenobarbital	124-131	transient receptor potential cation channel, subfamily C, member 6	Mus musculus	21-26
33554153-5	2020	At baseline, CCA of TRPC6-/- mice had reduced staining of MYH11 and SM22, fewer elastin lamina, luminal dilation, and wall thinning.	Phenobarbital	96-103	transient receptor potential cation channel, subfamily C, member 6	Mus musculus	20-25
33554153-6	2020	After carotid wire injury, TRPC6-/- mice developed significantly more pronounced luminal stenosis compared with WT mice.	Phenobarbital	81-88	transient receptor potential cation channel, subfamily C, member 6	Mus musculus	27-32
32512573-10	2020	The luminal B-like/HER2-negative subtype was significantly associated with worse BCRS (adjusted hazard ratio [HR] = 1.86; 95% CI 1.09-3.16).	Phenobarbital	4-11	erb-b2 receptor tyrosine kinase 2	Homo sapiens	19-23
31879152-5	2020	RESULTS: We found that baseline platelet count directly correlated with peripheral blood CD34+ (PB-CD34+) count after plerixafor treatment (r = 0.36, P &lt; 0.0001) and the number of PB-CD34+ cells collected on the first day of apheresis and inversely correlated with the number of apheresis sessions needed to collect the target number of PB-CD34+ cells (P = 0.0015).	Phenobarbital	96-98	CD34 molecule	Homo sapiens	89-93
31879152-5	2020	RESULTS: We found that baseline platelet count directly correlated with peripheral blood CD34+ (PB-CD34+) count after plerixafor treatment (r = 0.36, P &lt; 0.0001) and the number of PB-CD34+ cells collected on the first day of apheresis and inversely correlated with the number of apheresis sessions needed to collect the target number of PB-CD34+ cells (P = 0.0015).	Phenobarbital	96-98	CD34 molecule	Homo sapiens	99-103
31879152-5	2020	RESULTS: We found that baseline platelet count directly correlated with peripheral blood CD34+ (PB-CD34+) count after plerixafor treatment (r = 0.36, P &lt; 0.0001) and the number of PB-CD34+ cells collected on the first day of apheresis and inversely correlated with the number of apheresis sessions needed to collect the target number of PB-CD34+ cells (P = 0.0015).	Phenobarbital	96-98	CD34 molecule	Homo sapiens	99-103
31879152-5	2020	RESULTS: We found that baseline platelet count directly correlated with peripheral blood CD34+ (PB-CD34+) count after plerixafor treatment (r = 0.36, P &lt; 0.0001) and the number of PB-CD34+ cells collected on the first day of apheresis and inversely correlated with the number of apheresis sessions needed to collect the target number of PB-CD34+ cells (P = 0.0015).	Phenobarbital	96-98	CD34 molecule	Homo sapiens	99-103
31691481-3	2020	These luminal alveolar cells undergo Stat3-mediated programmed cell death following the cessation of lactation.	Phenobarbital	6-13	signal transducer and activator of transcription 3	Homo sapiens	37-42
32495928-7	2020	RESULTS: The results of this study demonstrated that the CD63 immunoreactivity was higher in both luminal and glandular epithelium of infertile patients when compared with fertile patients during the proliferative phase (p = 0.009, p = 0.008).	Phenobarbital	98-105	CD63 molecule	Homo sapiens	57-61
32495928-8	2020	In the infertile proliferation phase, endometrium CD9 immunoreactivity was rarely detected in both the luminal and glandular epithelium.	Phenobarbital	103-110	CD9 molecule	Homo sapiens	50-53
32495928-9	2020	In the secretion phase of endometrium, CD9 immunoreactivity was mild in fertile patients, the increased immunoreactivity of CD9 was observed in both luminal and glandular epithelium of infertile patients (p = 0.037, p = 0.037).	Phenobarbital	149-156	CD9 molecule	Homo sapiens	124-127
32429656-7	2020	GATA3 expression was positively correlated with low histological grades (G1/G2) vs. G3: p = 0.001) with most of G3 (57.89%) cases being negative and with luminal A (72.22%) and B (84.62%) subtypes (p = 0.00001) while most of the triple negative (87.5%) and HER2-overexpressed (66.67%) being negative.	Phenobarbital	154-161	GATA binding protein 3	Homo sapiens	0-5
33456078-9	2020	There were differences in the sites and intensity of membrane protectin expression exclusively on the luminal surfaces in pSS; on the luminal and, partially, antiluminal surface in non-specific inflammation, and on the entire cell surface in unaffected salivary glands.	Phenobarbital	102-109	CD59 molecule (CD59 blood group)	Homo sapiens	62-71
32508292-6	2020	Comparing with luminal A and luminal B subtypes, the ERBB2+ and basal-like subtypes have better complete response and response rate rates.	Phenobarbital	15-22	erb-b2 receptor tyrosine kinase 2	Homo sapiens	53-58
32508292-6	2020	Comparing with luminal A and luminal B subtypes, the ERBB2+ and basal-like subtypes have better complete response and response rate rates.	Phenobarbital	29-36	erb-b2 receptor tyrosine kinase 2	Homo sapiens	53-58
32378658-8	2020	This review article summarizes our data showing that luminal water volume is influenced by the osmolality of the applied solution, and illustrates how this effect may contribute to changes in GI drug concentration, resulting in altered drug absorption.	Phenobarbital	53-60	G protein subunit alpha i1	Homo sapiens	192-194
31888566-0	2019	Androgen receptor and FOXA1 coexpression define a "luminal-AR" subtype of feline mammary carcinomas, spontaneous models of breast cancer.	Phenobarbital	51-58	androgen receptor	Felis catus	0-17
31888566-0	2019	Androgen receptor and FOXA1 coexpression define a "luminal-AR" subtype of feline mammary carcinomas, spontaneous models of breast cancer.	Phenobarbital	51-58	forkhead box A1	Felis catus	22-27
31888566-0	2019	Androgen receptor and FOXA1 coexpression define a "luminal-AR" subtype of feline mammary carcinomas, spontaneous models of breast cancer.	Phenobarbital	51-58	androgen receptor	Felis catus	59-61
31888566-2	2019	Transcriptome studies showed that TNBCs are a heterogeneous group that includes a potentially hormone-dependent subtype named luminal-AR.	Phenobarbital	126-133	androgen receptor	Homo sapiens	134-136
31888566-10	2019	CONCLUSIONS: We identified an AR+ FOXA1+ CK14- subgroup of triple-negative FMCs that might correspond to the luminal-AR subgroup of human triple-negative breast cancers.	Phenobarbital	109-116	androgen receptor	Homo sapiens	30-32
31888566-10	2019	CONCLUSIONS: We identified an AR+ FOXA1+ CK14- subgroup of triple-negative FMCs that might correspond to the luminal-AR subgroup of human triple-negative breast cancers.	Phenobarbital	109-116	forkhead box A1	Homo sapiens	34-39
31888566-10	2019	CONCLUSIONS: We identified an AR+ FOXA1+ CK14- subgroup of triple-negative FMCs that might correspond to the luminal-AR subgroup of human triple-negative breast cancers.	Phenobarbital	109-116	keratin 14	Homo sapiens	41-45
31888566-10	2019	CONCLUSIONS: We identified an AR+ FOXA1+ CK14- subgroup of triple-negative FMCs that might correspond to the luminal-AR subgroup of human triple-negative breast cancers.	Phenobarbital	109-116	androgen receptor	Homo sapiens	117-119
31847122-7	2019	A fusion of the nascent Golgi membranes after BFA washout is forced by giantin re-dimerization via disulfide bond in its luminal domain and assisted by Rab6a GTPase.	Phenobarbital	121-128	golgin B1	Homo sapiens	71-78
31722089-6	2020	Phenobarbital (PB) also increased expression levels of CYP2B6, CYP2C18, and CYP3A4 in BH4 and BH, but at a lower level than 3-MC.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily C, polypeptide 18	Bos taurus	63-70
31722089-6	2020	Phenobarbital (PB) also increased expression levels of CYP2B6, CYP2C18, and CYP3A4 in BH4 and BH, but at a lower level than 3-MC.	Phenobarbital	0-13	cytochrome P450, subfamily IIIA, polypeptide 4	Bos taurus	76-82
31722089-6	2020	Phenobarbital (PB) also increased expression levels of CYP2B6, CYP2C18, and CYP3A4 in BH4 and BH, but at a lower level than 3-MC.	Phenobarbital	15-17	cytochrome P450 subfamily 2B	Bos taurus	55-61
31722089-6	2020	Phenobarbital (PB) also increased expression levels of CYP2B6, CYP2C18, and CYP3A4 in BH4 and BH, but at a lower level than 3-MC.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily C, polypeptide 18	Bos taurus	63-70
31722089-6	2020	Phenobarbital (PB) also increased expression levels of CYP2B6, CYP2C18, and CYP3A4 in BH4 and BH, but at a lower level than 3-MC.	Phenobarbital	15-17	cytochrome P450, subfamily IIIA, polypeptide 4	Bos taurus	76-82
31722089-8	2020	PB-treated co-cultures of BH4 or BH5 cells and liver sinusoidal cell lines also showed synergistic increases in CYP2B6 and CYP2C18 expression.	Phenobarbital	0-2	cytochrome P450 subfamily 2B	Bos taurus	112-118
31722089-8	2020	PB-treated co-cultures of BH4 or BH5 cells and liver sinusoidal cell lines also showed synergistic increases in CYP2B6 and CYP2C18 expression.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily C, polypeptide 18	Bos taurus	123-130
31875564-2	2019	Shh palmitoylation is catalyzed on the luminal side of the endoplasmic reticulum (ER) by Hedgehog acyltransferase (Hhat), an ER-resident enzyme.	Phenobarbital	39-46	sonic hedgehog signaling molecule	Homo sapiens	0-3
31875564-2	2019	Shh palmitoylation is catalyzed on the luminal side of the endoplasmic reticulum (ER) by Hedgehog acyltransferase (Hhat), an ER-resident enzyme.	Phenobarbital	39-46	hedgehog acyltransferase	Homo sapiens	89-113
31875564-2	2019	Shh palmitoylation is catalyzed on the luminal side of the endoplasmic reticulum (ER) by Hedgehog acyltransferase (Hhat), an ER-resident enzyme.	Phenobarbital	39-46	hedgehog acyltransferase	Homo sapiens	115-119
31875564-7	2019	Palmitoyl-CoA uptake was regulated by and could be uncoupled from Hhat enzymatic activity, implying that Hhat serves a dual function as a palmitoyl acyltransferase and a conduit to supply palmitoyl-CoA to the luminal side of the ER.	Phenobarbital	209-216	hedgehog acyltransferase	Homo sapiens	105-109
31735667-6	2019	Luminal deposition of FGF4 expedites fate specification and partially rescues the reduced specification in blastocysts with smaller cavities.	Phenobarbital	0-7	fibroblast growth factor 4	Mus musculus	22-26
31639536-1	2019	Investigations of the luminal immunophilin AtCYP38 (cyclophilin 38) in Arabidopsis thaliana (At), the orthologue of the complex immunophilin TLP40 from Spinacia oleracea, revealed its involvement in photosystem II (PSII) repair and assembly, biogenesis of PSII complex, and cellular signalling.	Phenobarbital	22-29	cyclophilin 38	Arabidopsis thaliana	43-50
31810962-4	2019	RESULTS: HOXB2 mRNA was significantly upregulated in luminal infiltrated and luminal papillary subtypes of BC.	Phenobarbital	53-60	homeobox B2	Homo sapiens	9-14
31810962-4	2019	RESULTS: HOXB2 mRNA was significantly upregulated in luminal infiltrated and luminal papillary subtypes of BC.	Phenobarbital	77-84	homeobox B2	Homo sapiens	9-14
31410629-2	2019	Luminal L-amino acids (L-AA) are detected by several receptors including metabotropic glutamate receptors 1 and 4 (mGluR1 and mGluR4), calcium-sensing receptor (CaSR), GPRC family C group 6 subtype A receptor (GPRC6A) and umami taste receptor heterodimer T1R1/T1R3.	Phenobarbital	0-7	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	86-113
31410629-2	2019	Luminal L-amino acids (L-AA) are detected by several receptors including metabotropic glutamate receptors 1 and 4 (mGluR1 and mGluR4), calcium-sensing receptor (CaSR), GPRC family C group 6 subtype A receptor (GPRC6A) and umami taste receptor heterodimer T1R1/T1R3.	Phenobarbital	0-7	glutamate receptor, metabotropic 1	Mus musculus	115-121
31410629-2	2019	Luminal L-amino acids (L-AA) are detected by several receptors including metabotropic glutamate receptors 1 and 4 (mGluR1 and mGluR4), calcium-sensing receptor (CaSR), GPRC family C group 6 subtype A receptor (GPRC6A) and umami taste receptor heterodimer T1R1/T1R3.	Phenobarbital	0-7	glutamate receptor, ionotropic, AMPA4 (alpha 4)	Mus musculus	126-132
31410629-2	2019	Luminal L-amino acids (L-AA) are detected by several receptors including metabotropic glutamate receptors 1 and 4 (mGluR1 and mGluR4), calcium-sensing receptor (CaSR), GPRC family C group 6 subtype A receptor (GPRC6A) and umami taste receptor heterodimer T1R1/T1R3.	Phenobarbital	0-7	calcium-sensing receptor	Mus musculus	135-159
31410629-2	2019	Luminal L-amino acids (L-AA) are detected by several receptors including metabotropic glutamate receptors 1 and 4 (mGluR1 and mGluR4), calcium-sensing receptor (CaSR), GPRC family C group 6 subtype A receptor (GPRC6A) and umami taste receptor heterodimer T1R1/T1R3.	Phenobarbital	0-7	calcium-sensing receptor	Mus musculus	161-165
31410629-2	2019	Luminal L-amino acids (L-AA) are detected by several receptors including metabotropic glutamate receptors 1 and 4 (mGluR1 and mGluR4), calcium-sensing receptor (CaSR), GPRC family C group 6 subtype A receptor (GPRC6A) and umami taste receptor heterodimer T1R1/T1R3.	Phenobarbital	0-7	G protein-coupled receptor, family C, group 6, member A	Mus musculus	168-208
31410629-2	2019	Luminal L-amino acids (L-AA) are detected by several receptors including metabotropic glutamate receptors 1 and 4 (mGluR1 and mGluR4), calcium-sensing receptor (CaSR), GPRC family C group 6 subtype A receptor (GPRC6A) and umami taste receptor heterodimer T1R1/T1R3.	Phenobarbital	0-7	G protein-coupled receptor, family C, group 6, member A	Mus musculus	210-216
31410629-2	2019	Luminal L-amino acids (L-AA) are detected by several receptors including metabotropic glutamate receptors 1 and 4 (mGluR1 and mGluR4), calcium-sensing receptor (CaSR), GPRC family C group 6 subtype A receptor (GPRC6A) and umami taste receptor heterodimer T1R1/T1R3.	Phenobarbital	0-7	taste receptor, type 1, member 1	Mus musculus	255-259
31410629-2	2019	Luminal L-amino acids (L-AA) are detected by several receptors including metabotropic glutamate receptors 1 and 4 (mGluR1 and mGluR4), calcium-sensing receptor (CaSR), GPRC family C group 6 subtype A receptor (GPRC6A) and umami taste receptor heterodimer T1R1/T1R3.	Phenobarbital	0-7	taste receptor, type 1, member 3	Mus musculus	260-264
31801883-5	2019	CXCR2-driven NE cells were critical for the tumor microenvironment by providing a survival niche for the AR+ luminal cells.	Phenobarbital	109-116	C-X-C motif chemokine receptor 2	Homo sapiens	0-5
31801883-5	2019	CXCR2-driven NE cells were critical for the tumor microenvironment by providing a survival niche for the AR+ luminal cells.	Phenobarbital	109-116	androgen receptor	Homo sapiens	105-107
31168770-12	2019	Coadministration of the known CYP3A4/5 inducers fosphenytoin and/or phenobarbital was associated with significantly increased fentanyl clearance.	Phenobarbital	68-81	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	30-36
31639536-1	2019	Investigations of the luminal immunophilin AtCYP38 (cyclophilin 38) in Arabidopsis thaliana (At), the orthologue of the complex immunophilin TLP40 from Spinacia oleracea, revealed its involvement in photosystem II (PSII) repair and assembly, biogenesis of PSII complex, and cellular signalling.	Phenobarbital	22-29	cyclophilin 38	Arabidopsis thaliana	52-66
31634957-6	2019	Blockage of either P-selectin or PSGL-1 reduced platelet adhesion and leukocyte recruitment on the luminal surface of vein grafts.	Phenobarbital	99-106	selectin, platelet	Mus musculus	19-29
31783316-7	2019	Collectively, this data implies that CD151 suppresses the Wnt1-driven tumorigenesis, at least in part, via counteracting the epithelial-mesenchymal transition (EMT)-like program in luminal epithelial cells.	Phenobarbital	181-188	CD151 antigen	Mus musculus	37-42
31783316-7	2019	Collectively, this data implies that CD151 suppresses the Wnt1-driven tumorigenesis, at least in part, via counteracting the epithelial-mesenchymal transition (EMT)-like program in luminal epithelial cells.	Phenobarbital	181-188	wingless-type MMTV integration site family, member 1	Mus musculus	58-62
31682957-8	2019	GABAAR agonist phenobarbital could rectify the decrease of BrdU+/NeuN+ cells in LPS mice.	Phenobarbital	15-28	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 2	Mus musculus	0-6
31682957-8	2019	GABAAR agonist phenobarbital could rectify the decrease of BrdU+/NeuN+ cells in LPS mice.	Phenobarbital	15-28	RNA binding protein, fox-1 homolog (C. elegans) 3	Mus musculus	65-69
31634957-6	2019	Blockage of either P-selectin or PSGL-1 reduced platelet adhesion and leukocyte recruitment on the luminal surface of vein grafts.	Phenobarbital	99-106	selectin, platelet (p-selectin) ligand	Mus musculus	33-39
31783818-9	2019	In cell lines derived from Luminal and HER2 subtypes, we observed a correlation between TOP1 gene copy number, TOP1 activity, and CPT response, although the data were too limited for statistical analyses.	Phenobarbital	27-34	DNA topoisomerase I	Homo sapiens	88-92
31783818-10	2019	In cell lines representing Luminal and TNBC subtypes, we observed a direct correlation between TOP1 protein abundancy and levels of enzymatic activity.	Phenobarbital	27-34	DNA topoisomerase I	Homo sapiens	95-99
31783818-11	2019	In all three subtypes (Luminal, HER2, and TNBC), TOP1 exhibits approximately the same susceptibility to CPT.	Phenobarbital	23-30	DNA topoisomerase I	Homo sapiens	49-53
31824855-8	2019	in vitro experiment, ectopic expression of FRY could alter the morphology and significantly suppress the growth and proliferation of the breast cancer cell lines, MDA-MB-231 (ER-/PR-/HER2-, Basal-like) and BT474 (ER+/PR+/HER2+, Luminal B).	Phenobarbital	228-237	FRY microtubule binding protein	Mus musculus	43-46
31597813-1	2019	Phenobarbital (PB) decreases the cyclosporine (CsA) blood level in humans.	Phenobarbital	0-13	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	47-50
31597813-1	2019	Phenobarbital (PB) decreases the cyclosporine (CsA) blood level in humans.	Phenobarbital	15-17	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	47-50
31597813-2	2019	However, the interaction of PB with CsA has not been reported in cats.	Phenobarbital	28-30	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	36-39
31597813-3	2019	This study investigated the effects of multiple doses of PB on the pharmacokinetics of CsA in three healthy cats.	Phenobarbital	57-59	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	87-90
31597813-5	2019	Co-administration of PB with CsA resulted in significant decreases in the oral bioavailability of CsA though both the first pass and elimination phases.	Phenobarbital	21-23	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	98-101
31597813-6	2019	These preliminary results suggest that oral administration of multiple doses of PB increases the required CsA dosage in CsA-based immunosuppressive therapy in cats.	Phenobarbital	80-82	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	106-109
31597813-6	2019	These preliminary results suggest that oral administration of multiple doses of PB increases the required CsA dosage in CsA-based immunosuppressive therapy in cats.	Phenobarbital	80-82	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	120-123
31752957-6	2019	In particular, WDR5 loss reduces the metastatic properties of the cells by reverting the mesenchymal phenotype of triple negative- and luminal B-derived cells, thus inducing an epithelial trait.	Phenobarbital	135-142	WD repeat domain 5	Homo sapiens	15-19
31519689-5	2019	MUC1-C/MYC complexes selectively activated the MTA1 and MBD3 genes and posttranscriptionally induced CHD4 expression in basal- but not luminal-type BC cells.	Phenobarbital	135-142	mucin 1, cell surface associated	Homo sapiens	0-4
31519689-5	2019	MUC1-C/MYC complexes selectively activated the MTA1 and MBD3 genes and posttranscriptionally induced CHD4 expression in basal- but not luminal-type BC cells.	Phenobarbital	135-142	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	5-10
31701034-6	2019	Through single-cell RNA sequencing (scRNAseq) analysis, E2 was found to induce Pgr expression in both Esr1 + and Esr1 - luminal epithelial cells and Ccl2 expression in Esr1 + fibroblasts.	Phenobarbital	120-127	progesterone receptor	Mus musculus	79-82
31701034-6	2019	Through single-cell RNA sequencing (scRNAseq) analysis, E2 was found to induce Pgr expression in both Esr1 + and Esr1 - luminal epithelial cells and Ccl2 expression in Esr1 + fibroblasts.	Phenobarbital	120-127	estrogen receptor 1 (alpha)	Mus musculus	113-117
31701034-6	2019	Through single-cell RNA sequencing (scRNAseq) analysis, E2 was found to induce Pgr expression in both Esr1 + and Esr1 - luminal epithelial cells and Ccl2 expression in Esr1 + fibroblasts.	Phenobarbital	120-127	estrogen receptor 1 (alpha)	Mus musculus	113-117
31422497-1	2019	INTRODUCTION: Ki-67 labeling index assessed by immunohistochemical assays has been shown useful in assessing the risk of recurrence for estrogen receptor (ER)-positive HER2-negative breast cancers (BC) and distinguishing Luminal A-like from Luminal B-like tumors.	Phenobarbital	221-228	estrogen receptor 1	Homo sapiens	155-157
31432367-1	2019	PURPOSE: Oestrogen receptor-positive (ER+) and human epidermal receptor 2-negative (HER2-) breast cancers are classified as Luminal A or B based on gene expression, but immunohistochemical markers are used for surrogate subtyping.	Phenobarbital	124-131	epiregulin	Homo sapiens	38-40
31432367-1	2019	PURPOSE: Oestrogen receptor-positive (ER+) and human epidermal receptor 2-negative (HER2-) breast cancers are classified as Luminal A or B based on gene expression, but immunohistochemical markers are used for surrogate subtyping.	Phenobarbital	124-131	erb-b2 receptor tyrosine kinase 2	Homo sapiens	84-88
31340938-7	2019	Enriched proliferation metagene and luminal B features were noticed in node-positive ER+HER2- and HER2+ tumors, while upregulated basal-like features were observed in node-negative TNBC tumors.	Phenobarbital	36-43	erb-b2 receptor tyrosine kinase 2	Homo sapiens	88-92
31340938-7	2019	Enriched proliferation metagene and luminal B features were noticed in node-positive ER+HER2- and HER2+ tumors, while upregulated basal-like features were observed in node-negative TNBC tumors.	Phenobarbital	36-43	erb-b2 receptor tyrosine kinase 2	Homo sapiens	98-102
31372832-3	2019	In this study, the results from noncoding RNA microarray analysis indicated that the miR-375 expression level is significantly decreased in malignant basal-like breast cancer compared with luminal-like breast cancer.	Phenobarbital	189-196	microRNA 375	Homo sapiens	85-92
31983107-4	2019	RESULTS: P53 expression was the lowest in Luminal A subtype and similar in human epidermal growth factor receptor 2 (HER-2)-overexpression subtype and triple-negative subtype, with higher expression rates than those in other molecular subtypes.	Phenobarbital	42-49	tumor protein p53	Homo sapiens	9-12
31983107-6	2019	BRCA1 exhibited the lowest expression in Luminal B-like subtype but the highest expression in Luminal A subtype.	Phenobarbital	41-48	BRCA1 DNA repair associated	Homo sapiens	0-5
31983107-6	2019	BRCA1 exhibited the lowest expression in Luminal B-like subtype but the highest expression in Luminal A subtype.	Phenobarbital	94-101	BRCA1 DNA repair associated	Homo sapiens	0-5
31253864-7	2019	We found that deletion of ANXA2 impeded rickettsial attachment to the ECs in vitro and blocked rickettsial adherence to the blood vessel luminal surface in vivo.	Phenobarbital	137-144	annexin A2	Homo sapiens	26-31
31253864-10	2019	We conclude that the endothelial surface ANXA2 plays an important role in initiating pathogen-host interactions, ultimately leading to bacterial anchoring on the vascular luminal surface.	Phenobarbital	171-178	annexin A2	Homo sapiens	41-46
31395667-4	2019	Here we found that in primary, treatment-naive prostate cancers, ADRB2 mRNA was positively correlated with expression of luminal differentiation markers, and ADRB2 protein levels were inversely correlated with Gleason grade.	Phenobarbital	121-128	adrenoceptor beta 2	Homo sapiens	65-70
31575620-2	2019	Among ALDHs, the rat ALDH1A7 gene displays a curious strain dependence in phenobarbital (PB)-induced hepatic expression: the responsive RR strains exhibit induction of both ALDH1A7 and CYP2B mRNAs and activities, whereas the nonresponsive rr strains show induction of CYP2B only.	Phenobarbital	74-87	aldehyde dehydrogenase family 1, subfamily A7	Rattus norvegicus	21-28
31575620-2	2019	Among ALDHs, the rat ALDH1A7 gene displays a curious strain dependence in phenobarbital (PB)-induced hepatic expression: the responsive RR strains exhibit induction of both ALDH1A7 and CYP2B mRNAs and activities, whereas the nonresponsive rr strains show induction of CYP2B only.	Phenobarbital	74-87	aldehyde dehydrogenase family 1, subfamily A7	Rattus norvegicus	173-180
31575620-2	2019	Among ALDHs, the rat ALDH1A7 gene displays a curious strain dependence in phenobarbital (PB)-induced hepatic expression: the responsive RR strains exhibit induction of both ALDH1A7 and CYP2B mRNAs and activities, whereas the nonresponsive rr strains show induction of CYP2B only.	Phenobarbital	89-91	aldehyde dehydrogenase family 1, subfamily A7	Rattus norvegicus	21-28
31575620-2	2019	Among ALDHs, the rat ALDH1A7 gene displays a curious strain dependence in phenobarbital (PB)-induced hepatic expression: the responsive RR strains exhibit induction of both ALDH1A7 and CYP2B mRNAs and activities, whereas the nonresponsive rr strains show induction of CYP2B only.	Phenobarbital	89-91	aldehyde dehydrogenase family 1, subfamily A7	Rattus norvegicus	173-180
31575620-4	2019	ALDH1A7 mRNA, associated protein and activity were strongly induced by PB and modestly induced by pregnenolone 16alpha-carbonitrile in the RR strain but negligibly in the rr strain, whereas induction of ALDH1A1 and P450 mRNAs was similar between the strains.	Phenobarbital	71-73	aldehyde dehydrogenase family 1, subfamily A7	Rattus norvegicus	0-7
31575620-6	2019	SIGNIFICANCE STATEMENT: Genetic variation in rat ALDH1A7 promoter sequences underlie the large strain-dependent differences in expression and inducibility by phenobarbital of the aldehyde dehydrogenase activity.	Phenobarbital	158-171	aldehyde dehydrogenase family 1, subfamily A7	Rattus norvegicus	49-56
31519689-8	2019	Targeting MUC1-C and these NuRD components also induced expression of FOXA1, GATA3, and other markers associated with the luminal phenotype.	Phenobarbital	122-129	mucin 1, cell surface associated	Homo sapiens	10-14
31685133-5	2019	An association between a single nucleotide variation of the ABCB1 gene (c.-6-180T>G) and phenobarbital resistance has previously been reported in a Border collie population with idiopathic epilepsy.	Phenobarbital	89-102	ATP binding cassette subfamily B member 1	Canis lupus familiaris	60-65
31519689-8	2019	Targeting MUC1-C and these NuRD components also induced expression of FOXA1, GATA3, and other markers associated with the luminal phenotype.	Phenobarbital	122-129	forkhead box A1	Homo sapiens	70-75
31639146-6	2019	The mean luminal area was 333,185.7+-112,665.9 mum2 in the eyes with OIS, 313,983.3+-132,032.1 mum2 in the ipsilateral eyes with symptomatic CAS, and 480,325.0+-185,112.6 mum2 in the control group eyes (P = 0.046).	Phenobarbital	9-16	trafficking protein particle complex subunit 1	Homo sapiens	47-51
31827586-11	2019	The recognition precision for the four molecular subtypes of luminal A, luminal B, HER-2, and basal-like are 0.91, 0.89, 0.83, and 0.87, respectively.	Phenobarbital	61-68	erb-b2 receptor tyrosine kinase 2	Homo sapiens	83-88
31717704-4	2019	The A2A adenosine receptor colocalized with ezrin, an A-kinase anchoring protein, in the luminal membrane of duct cells in the mouse and guinea pig pancreas.	Phenobarbital	89-96	ezrin	Mus musculus	44-49
31352175-6	2019	Furthermore, ERalpha/beta and PGR were mainly detected in the endometrial luminal epithelium and glandular epithelium.	Phenobarbital	74-81	estrogen receptor beta	Ovis aries	13-25
31619022-5	2019	The luminal EC population was significantly greater in fat-1 mice (p <= 0.05), while the total number of mammary ECs were similar between groups (p = 0.79).	Phenobarbital	4-11	FAT atypical cadherin 1	Mus musculus	55-60
31932263-2	2019	The aim: To study the quantitative characteristic and localization of CD68+ and CD163+ M2-like TAM that infiltrate non-luminal HER2-enriched carcinomas of BC in the primary focus without metastases and in paired specimens with metastases in the lymph nodes, as well as the pathomorphological characteristics of this type of BC.	Phenobarbital	119-126	CD163 molecule	Homo sapiens	80-85
31615920-3	2019	Here, using DNase I hypersensitivity mapping coupled with transcriptomic profiling, we investigate perturbations in cis-acting gene regulatory elements associated with the early stages of phenobarbital (PB)-mediated liver tumor promotion in susceptible versus resistant mouse strains (B6C3F1 versus C57BL/6J).	Phenobarbital	188-201	deoxyribonuclease I	Mus musculus	12-19
31615920-3	2019	Here, using DNase I hypersensitivity mapping coupled with transcriptomic profiling, we investigate perturbations in cis-acting gene regulatory elements associated with the early stages of phenobarbital (PB)-mediated liver tumor promotion in susceptible versus resistant mouse strains (B6C3F1 versus C57BL/6J).	Phenobarbital	203-205	deoxyribonuclease I	Mus musculus	12-19
31615920-4	2019	Integrated computational analyses of strain-selective changes in liver chromatin accessibility underlying PB response reveal differential epigenetic regulation of molecular pathways associated with PB-mediated tumor promotion, including Wnt/beta-catenin signaling.	Phenobarbital	106-108	catenin (cadherin associated protein), beta 1	Mus musculus	241-253
31352175-6	2019	Furthermore, ERalpha/beta and PGR were mainly detected in the endometrial luminal epithelium and glandular epithelium.	Phenobarbital	74-81	progesterone receptor	Ovis aries	30-33
31369292-9	2019	Overall, these findings support our conclusion that the biotin transport pathway plays an important role in the maintenance of intestinal homeostasis, and that NF-kappaB and the NLRP3 inflammasome, as well as gut microbiota, drive the development of intestinal inflammation when SMVT is absent.NEW & NOTEWORTHY This study demonstrates that deletion of the intestinal biotin uptake system in adult mice leads to the development of spontaneous gut inflammation and that luminal microbiota plays a role in its development.	Phenobarbital	468-475	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	160-169
31543266-4	2019	NCR1 has its N-terminal domain (NTD) positioned to deliver a sterol to a tunnel connecting NTD to the luminal membrane leaflet 50 A away.	Phenobarbital	102-109	sphingolipid transporter	Saccharomyces cerevisiae S288C	0-4
31364376-0	2019	Mal protein stabilizes luminal membrane PLC-beta3 and negatively regulates ENaC in mouse cortical collecting duct cells.	Phenobarbital	23-30	myelin and lymphocyte protein, T cell differentiation protein	Mus musculus	0-3
31737064-16	2019	Compared with the CUMS+PB group, the expression of ZO-1 in the CUMS+EA group was significantly enhanced.	Phenobarbital	23-25	tight junction protein 1	Rattus norvegicus	51-55
31369292-9	2019	Overall, these findings support our conclusion that the biotin transport pathway plays an important role in the maintenance of intestinal homeostasis, and that NF-kappaB and the NLRP3 inflammasome, as well as gut microbiota, drive the development of intestinal inflammation when SMVT is absent.NEW & NOTEWORTHY This study demonstrates that deletion of the intestinal biotin uptake system in adult mice leads to the development of spontaneous gut inflammation and that luminal microbiota plays a role in its development.	Phenobarbital	468-475	NLR family, pyrin domain containing 3	Mus musculus	178-183
31364376-5	2019	Our hypothesis was that Mal protein negatively regulates renal ENaC activity by stabilizing PLC protein expression at the luminal plasma membrane.	Phenobarbital	122-129	myelin and lymphocyte protein, T cell differentiation protein	Mus musculus	24-27
31364376-5	2019	Our hypothesis was that Mal protein negatively regulates renal ENaC activity by stabilizing PLC protein expression at the luminal plasma membrane.	Phenobarbital	122-129	sodium channel, nonvoltage-gated 1 alpha	Mus musculus	63-67
31364377-9	2019	Knockdown of NHE2 specifically to the stellate cells also increased renal uric acid stone formation, and so a model was developed in which SIP1 normally regulates NHE2 activity and luminal pH, ultimately leading to uric acid stone formation.	Phenobarbital	181-188	Na[+]/H[+] hydrogen exchanger 2	Drosophila melanogaster	13-17
31591601-6	2019	Using insulin as a model drug, we showed that, when actuated, the luminal unfolding microneedle injector provided a faster pharmacokinetic uptake profile and a systemic uptake >10% of that of a subcutaneous injection over a 4-h sampling period.	Phenobarbital	66-73	insulin	Sus scrofa	6-13
31364377-9	2019	Knockdown of NHE2 specifically to the stellate cells also increased renal uric acid stone formation, and so a model was developed in which SIP1 normally regulates NHE2 activity and luminal pH, ultimately leading to uric acid stone formation.	Phenobarbital	181-188	SLC9A3 regulator 2	Homo sapiens	139-143
28647282-2	2019	Recently we showed that CXCR6+ platelets from flowing blood attach to CXCL16 expressed by activated endothelium on the luminal side of the blood vessel.	Phenobarbital	119-126	C-X-C motif chemokine receptor 6	Homo sapiens	24-29
28647282-2	2019	Recently we showed that CXCR6+ platelets from flowing blood attach to CXCL16 expressed by activated endothelium on the luminal side of the blood vessel.	Phenobarbital	119-126	C-X-C motif chemokine ligand 16	Homo sapiens	70-76
31268738-6	2019	In closed colonic loops in vivo, luminal CDCA produced a robust secretory response, which was reduced by ~70% by (R)-BPO-27 or in CFTR-deficient mice.	Phenobarbital	33-40	cystic fibrosis transmembrane conductance regulator	Mus musculus	130-134
31208268-0	2019	Two Patients With KCNT1-Related Epilepsy Responding to Phenobarbital and Potassium Bromide.	Phenobarbital	55-68	potassium sodium-activated channel subfamily T member 1	Homo sapiens	18-23
31202736-5	2019	In this study, we showed that treatment with the indirect CAR activator phenobarbital activated transcription of the CYP3A4 gene in three-dimensionally (3D)-cultured HepG2 cells.	Phenobarbital	72-85	nuclear receptor subfamily 1 group I member 3	Homo sapiens	58-61
31202736-5	2019	In this study, we showed that treatment with the indirect CAR activator phenobarbital activated transcription of the CYP3A4 gene in three-dimensionally (3D)-cultured HepG2 cells.	Phenobarbital	72-85	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	117-123
31202736-6	2019	CAR was retained as its phosphorylated form in the cytoplasm and was translocated to the nucleus in 3D-cultured HepG2 cells in response to treatment with phenobarbital.	Phenobarbital	154-167	nuclear receptor subfamily 1 group I member 3	Homo sapiens	0-3
31202736-7	2019	Moreover, okadaic acid and epidermal growth factor, were found to repress phenobarbital-induced CAR nuclear translocation and subsequent activation of the CYP3A4 gene promoter.	Phenobarbital	74-87	epidermal growth factor	Homo sapiens	27-50
31202736-7	2019	Moreover, okadaic acid and epidermal growth factor, were found to repress phenobarbital-induced CAR nuclear translocation and subsequent activation of the CYP3A4 gene promoter.	Phenobarbital	74-87	nuclear receptor subfamily 1 group I member 3	Homo sapiens	96-99
31202736-7	2019	Moreover, okadaic acid and epidermal growth factor, were found to repress phenobarbital-induced CAR nuclear translocation and subsequent activation of the CYP3A4 gene promoter.	Phenobarbital	74-87	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	155-161
31312932-5	2019	For the luminal A subtype, the CA15-3- and CEA-elevated group had a hazard ratio (HR) of 2.14 (95% CI 1.01-4.55).	Phenobarbital	8-15	mucin 1, cell surface associated	Homo sapiens	31-37
31312932-5	2019	For the luminal A subtype, the CA15-3- and CEA-elevated group had a hazard ratio (HR) of 2.14 (95% CI 1.01-4.55).	Phenobarbital	8-15	CEA cell adhesion molecule 3	Homo sapiens	43-46
31357909-8	2019	In contrast to previous studies, where no oscillations were apparent in any breast cancer cell line, our luminometry data reveal that circadian oscillations of BMAL1 and PER2 in fact exist in the low-grade, luminal A MCF7 cells but are not present in high-grade, basal MDA-MB-231 cells.	Phenobarbital	207-214	aryl hydrocarbon receptor nuclear translocator like	Homo sapiens	160-165
31357909-8	2019	In contrast to previous studies, where no oscillations were apparent in any breast cancer cell line, our luminometry data reveal that circadian oscillations of BMAL1 and PER2 in fact exist in the low-grade, luminal A MCF7 cells but are not present in high-grade, basal MDA-MB-231 cells.	Phenobarbital	207-214	period circadian regulator 2	Homo sapiens	170-174
31271664-5	2019	The results indicated greater DLG3 expression in cancerous breast tissues than normal breast tissues and in luminal and Her2+ subtypes than in the triple-negative subtype.	Phenobarbital	108-115	discs large MAGUK scaffold protein 3	Homo sapiens	30-34
31270009-4	2019	During the follicular phase, in both the cervix and vagina, ErbB1, ErbB2, ErbB3, ErbB4 and EGF expression was higher in the luminal epithelium (LE) than in stromal and smooth muscle (SM) cells (P<0.05).	Phenobarbital	124-131	erb-b2 receptor tyrosine kinase 3	Bos taurus	74-79
31409898-3	2019	By characterizing its role in luminal breast epithelial cells, here we show that inhibition of LSD1 by both genetic and pharmacological approaches increases their invasion and migration, whereas its inhibition by genetic approach, but not by pharmacological approach, impairs their proliferation/survival.	Phenobarbital	30-37	lysine (K)-specific demethylase 1A	Mus musculus	95-99
31409898-4	2019	Induced loss of LSD1 in luminal cells in a mouse model of luminal breast cancer, MMTV-PyMT, leads to a profound increase in lung metastasis.	Phenobarbital	24-31	lysine (K)-specific demethylase 1A	Mus musculus	16-20
31270009-4	2019	During the follicular phase, in both the cervix and vagina, ErbB1, ErbB2, ErbB3, ErbB4 and EGF expression was higher in the luminal epithelium (LE) than in stromal and smooth muscle (SM) cells (P<0.05).	Phenobarbital	124-131	erb-b2 receptor tyrosine kinase 4	Bos taurus	81-86
31270009-4	2019	During the follicular phase, in both the cervix and vagina, ErbB1, ErbB2, ErbB3, ErbB4 and EGF expression was higher in the luminal epithelium (LE) than in stromal and smooth muscle (SM) cells (P<0.05).	Phenobarbital	124-131	LOC521832	Bos taurus	91-94
31465819-6	2019	Significant increases in relative liver weight, centrilobular hepatocyte hypertrophy and hepatocyte RDS were also observed in male and female Wistar rats given and 500 ppm sodium phenobarbital (NaPB) for 3-28 days.	Phenobarbital	172-192	NSF attachment protein beta	Rattus norvegicus	194-198
31170421-3	2019	Recently, trans-3,4,5,4 -tetramethoxystilbene(TMS), a potential anticancer drug (DMU-212), have been shown to alleviate N-nitrosodiethylamine/phenobarbital-induced liver carcinogenesis.	Phenobarbital	142-155	thermosensitivity	Mus musculus	46-49
31170421-2	2019	CAR activators, including phenobarbital, are considered rodent non-genotoxic carcinogens.	Phenobarbital	26-39	nuclear receptor subfamily 1, group I, member 3	Mus musculus	0-3
31673501-9	2019	Ingenuity pathways analysis (IPA) indicated that there was a significant (Z score >2.0;-log p value >) activation of CAR by PB in both human and rat LiMTs.	Phenobarbital	124-126	nuclear receptor subfamily 1 group I member 3	Homo sapiens	117-120
31611907-9	2019	Culture of primary cells from resected tumors revealed a luminal B (ER+/PR-/HER2-) phenotype in response to glyphosate-miR182-5p exposure with sensitivity to tamoxifen and invasive and migratory potentials.	Phenobarbital	57-66	erb-b2 receptor tyrosine kinase 2	Homo sapiens	76-80
31551495-7	2019	OR2W3 was correlated with invasion genes and basal-like subtype whereas OR2B6 was correlated with proliferation genes and luminal A subtype.	Phenobarbital	122-129	olfactory receptor family 2 subfamily B member 6	Homo sapiens	72-77
30720863-5	2019	The BRCA1 gene had the highest mutation frequency in patients with triple-negative breast cancer (TNBC), which was 9.6% (n = 42), while the BRCA2 gene had the highest mutation frequency in patients with Luminal, which was 3.2% (n = 58).	Phenobarbital	203-210	BRCA2 DNA repair associated	Homo sapiens	140-145
31529336-7	2019	In addition, Muc5ac protein was detected only in the luminal fluids from the proximal small intestine after DTT treatment.	Phenobarbital	53-60	mucin 5AC, oligomeric mucus/gel-forming	Rattus norvegicus	13-19
31387993-5	2019	We show that the cavity in the luminal domain of LIMP-2 can bind and deliver exogenous cholesterol to the lysosomal membrane and later to lipid droplets.	Phenobarbital	31-38	scavenger receptor class B, member 2	Mus musculus	49-55
31552024-8	2019	IKKbeta-deficient mice also had distinct differences in colonic tissue-associated and luminal microbiome that may confer protection against C. rodentium.	Phenobarbital	86-93	conserved helix-loop-helix ubiquitous kinase	Mus musculus	0-7
31484062-6	2019	Moreover, blood flow favors luminal deposition of fibronectin on endothelial cells, an integrin alpha5beta1 ligand.	Phenobarbital	28-35	fibronectin 1	Homo sapiens	50-61
31301485-9	2019	Enteroendocrine responses were assessed of the satiety hormones GLP-1 and PYY after stimulation with rebaudioside A and casein, resulting in significantly increased secretion to the luminal side as well as to the basolateral side.	Phenobarbital	182-189	glucagon like peptide 1 receptor	Homo sapiens	64-69
31301485-9	2019	Enteroendocrine responses were assessed of the satiety hormones GLP-1 and PYY after stimulation with rebaudioside A and casein, resulting in significantly increased secretion to the luminal side as well as to the basolateral side.	Phenobarbital	182-189	peptide YY	Homo sapiens	74-77
31436536-0	2019	Mechanistic Insights of Phenobarbital-Mediated Activation of Human but Not Mouse Pregnane X Receptor.	Phenobarbital	24-37	nuclear receptor subfamily 1, group I, member 2	Mus musculus	81-100
31436536-1	2019	Phenobarbital (PB), a broadly used antiseizure drug, was the first to be characterized as an inducer of cytochrome P450 by activation of the constitutive androstane receptor (CAR).	Phenobarbital	0-13	nuclear receptor subfamily 1 group I member 3	Homo sapiens	141-173
31436536-1	2019	Phenobarbital (PB), a broadly used antiseizure drug, was the first to be characterized as an inducer of cytochrome P450 by activation of the constitutive androstane receptor (CAR).	Phenobarbital	0-13	nuclear receptor subfamily 1 group I member 3	Homo sapiens	175-178
31436536-1	2019	Phenobarbital (PB), a broadly used antiseizure drug, was the first to be characterized as an inducer of cytochrome P450 by activation of the constitutive androstane receptor (CAR).	Phenobarbital	15-17	nuclear receptor subfamily 1 group I member 3	Homo sapiens	141-173
31436536-1	2019	Phenobarbital (PB), a broadly used antiseizure drug, was the first to be characterized as an inducer of cytochrome P450 by activation of the constitutive androstane receptor (CAR).	Phenobarbital	15-17	nuclear receptor subfamily 1 group I member 3	Homo sapiens	175-178
31436536-2	2019	Although PB is recognized as a conserved CAR activator among species via a well-documented indirect activation mechanism, conflicting results have been reported regarding PB regulation of the pregnane X receptor (PXR), a sister receptor of CAR, and the underlying mechanisms remain elusive.	Phenobarbital	9-11	nuclear receptor subfamily 1 group I member 3	Homo sapiens	41-44
31436536-3	2019	Here, we show that in a human CAR (hCAR)-knockout (KO) HepaRG cell line, PB significantly induces the expression of CYP2B6 and CYP3A4, two shared target genes of hCAR and human PXR (hPXR).	Phenobarbital	73-75	nuclear receptor subfamily 1 group I member 3	Homo sapiens	30-33
31436536-3	2019	Here, we show that in a human CAR (hCAR)-knockout (KO) HepaRG cell line, PB significantly induces the expression of CYP2B6 and CYP3A4, two shared target genes of hCAR and human PXR (hPXR).	Phenobarbital	73-75	CXADR Ig-like cell adhesion molecule	Homo sapiens	35-39
31436536-3	2019	Here, we show that in a human CAR (hCAR)-knockout (KO) HepaRG cell line, PB significantly induces the expression of CYP2B6 and CYP3A4, two shared target genes of hCAR and human PXR (hPXR).	Phenobarbital	73-75	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	116-122
31436536-3	2019	Here, we show that in a human CAR (hCAR)-knockout (KO) HepaRG cell line, PB significantly induces the expression of CYP2B6 and CYP3A4, two shared target genes of hCAR and human PXR (hPXR).	Phenobarbital	73-75	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	127-133
31436536-3	2019	Here, we show that in a human CAR (hCAR)-knockout (KO) HepaRG cell line, PB significantly induces the expression of CYP2B6 and CYP3A4, two shared target genes of hCAR and human PXR (hPXR).	Phenobarbital	73-75	CXADR Ig-like cell adhesion molecule	Homo sapiens	162-166
31436536-3	2019	Here, we show that in a human CAR (hCAR)-knockout (KO) HepaRG cell line, PB significantly induces the expression of CYP2B6 and CYP3A4, two shared target genes of hCAR and human PXR (hPXR).	Phenobarbital	73-75	nuclear receptor subfamily 1 group I member 2	Homo sapiens	177-180
31436536-3	2019	Here, we show that in a human CAR (hCAR)-knockout (KO) HepaRG cell line, PB significantly induces the expression of CYP2B6 and CYP3A4, two shared target genes of hCAR and human PXR (hPXR).	Phenobarbital	73-75	nuclear receptor subfamily 1 group I member 2	Homo sapiens	182-186
31436536-4	2019	In human primary hepatocytes and hCAR-KO HepaRG cells, PB-induced expression of CYP3A4 was markedly repressed by genetic knockdown or pharmacological inhibition of hPXR.	Phenobarbital	55-57	CXADR Ig-like cell adhesion molecule	Homo sapiens	33-37
31436536-4	2019	In human primary hepatocytes and hCAR-KO HepaRG cells, PB-induced expression of CYP3A4 was markedly repressed by genetic knockdown or pharmacological inhibition of hPXR.	Phenobarbital	55-57	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	80-86
31436536-4	2019	In human primary hepatocytes and hCAR-KO HepaRG cells, PB-induced expression of CYP3A4 was markedly repressed by genetic knockdown or pharmacological inhibition of hPXR.	Phenobarbital	55-57	nuclear receptor subfamily 1 group I member 2	Homo sapiens	164-168
31436536-5	2019	Mechanistically, PB concentration dependently activates hPXR but not its mouse counterpart in cell-based luciferase assays.	Phenobarbital	17-19	nuclear receptor subfamily 1 group I member 2	Homo sapiens	56-60
31436536-6	2019	Mammalian two-hybrid assays demonstrated that PB selectively increases the functional interaction between the steroid receptor coactivator-1 and hPXR but not mouse PXR.	Phenobarbital	46-48	nuclear receptor coactivator 1	Homo sapiens	110-140
31436536-6	2019	Mammalian two-hybrid assays demonstrated that PB selectively increases the functional interaction between the steroid receptor coactivator-1 and hPXR but not mouse PXR.	Phenobarbital	46-48	nuclear receptor subfamily 1 group I member 2	Homo sapiens	145-149
31436536-6	2019	Mammalian two-hybrid assays demonstrated that PB selectively increases the functional interaction between the steroid receptor coactivator-1 and hPXR but not mouse PXR.	Phenobarbital	46-48	nuclear receptor subfamily 1, group I, member 2	Mus musculus	146-149
31436536-7	2019	Moreover, surface plasmon resonance binding affinity assay showed that PB directly binds to the ligand binding domain of hPXR (KD = 1.42 x 10-05).	Phenobarbital	71-73	nuclear receptor subfamily 1 group I member 2	Homo sapiens	121-125
31436536-8	2019	Structure-activity analysis further revealed that the amino acid tryptophan-299 within the ligand binding pocket of hPXR plays a key role in the agonistic binding of PB and mutation of tryptophan-299 disrupts PB activation of hPXR.	Phenobarbital	166-168	nuclear receptor subfamily 1 group I member 2	Homo sapiens	116-120
31436536-8	2019	Structure-activity analysis further revealed that the amino acid tryptophan-299 within the ligand binding pocket of hPXR plays a key role in the agonistic binding of PB and mutation of tryptophan-299 disrupts PB activation of hPXR.	Phenobarbital	166-168	nuclear receptor subfamily 1 group I member 2	Homo sapiens	226-230
31436536-8	2019	Structure-activity analysis further revealed that the amino acid tryptophan-299 within the ligand binding pocket of hPXR plays a key role in the agonistic binding of PB and mutation of tryptophan-299 disrupts PB activation of hPXR.	Phenobarbital	209-211	nuclear receptor subfamily 1 group I member 2	Homo sapiens	116-120
31436536-9	2019	Collectively, these data reveal that PB, a selective mouse CAR activator, activates both hCAR and hPXR, and provide novel mechanistic insights for PB-mediated activation of hPXR.	Phenobarbital	37-39	nuclear receptor subfamily 1, group I, member 3	Mus musculus	59-62
31436536-9	2019	Collectively, these data reveal that PB, a selective mouse CAR activator, activates both hCAR and hPXR, and provide novel mechanistic insights for PB-mediated activation of hPXR.	Phenobarbital	37-39	CXADR Ig-like cell adhesion molecule	Homo sapiens	89-93
31436536-9	2019	Collectively, these data reveal that PB, a selective mouse CAR activator, activates both hCAR and hPXR, and provide novel mechanistic insights for PB-mediated activation of hPXR.	Phenobarbital	37-39	nuclear receptor subfamily 1 group I member 2	Homo sapiens	98-102
31436536-9	2019	Collectively, these data reveal that PB, a selective mouse CAR activator, activates both hCAR and hPXR, and provide novel mechanistic insights for PB-mediated activation of hPXR.	Phenobarbital	37-39	nuclear receptor subfamily 1 group I member 2	Homo sapiens	173-177
31436536-9	2019	Collectively, these data reveal that PB, a selective mouse CAR activator, activates both hCAR and hPXR, and provide novel mechanistic insights for PB-mediated activation of hPXR.	Phenobarbital	147-149	nuclear receptor subfamily 1 group I member 2	Homo sapiens	173-177
31376015-0	2019	C1orf106, an innate immunity activator, is amplified in breast cancer and is required for basal-like/luminal progenitor fate decision.	Phenobarbital	101-108	innate immunity activator	Homo sapiens	0-8
31376015-3	2019	Here, we report that a novel gene C1orf106 plays an important role in maintaining the feature of basal-like/luminal progenitors.	Phenobarbital	108-115	innate immunity activator	Homo sapiens	34-42
31376015-7	2019	These findings suggest that C1orf106 maintains the basal-like/luminal progenitor character through balancing the expression of ELF5 and GATA3.	Phenobarbital	62-69	innate immunity activator	Homo sapiens	28-36
31376015-7	2019	These findings suggest that C1orf106 maintains the basal-like/luminal progenitor character through balancing the expression of ELF5 and GATA3.	Phenobarbital	62-69	E74 like ETS transcription factor 5	Homo sapiens	127-131
31376015-7	2019	These findings suggest that C1orf106 maintains the basal-like/luminal progenitor character through balancing the expression of ELF5 and GATA3.	Phenobarbital	62-69	GATA binding protein 3	Homo sapiens	136-141
31376015-8	2019	Taken together, we demonstrated that C1orf106 is an important regulator for basal-like/luminal progenitors and targeting C1orf106 is of therapeutic value for breast cancer.	Phenobarbital	87-94	innate immunity activator	Homo sapiens	37-45
31443683-4	2019	In this study, we report the presence of a basal-like luminal progenitor (BLP) in human breast epithelial cells.	Phenobarbital	54-61	dynein light chain roadblock-type 1	Homo sapiens	74-77
31443683-6	2019	Loss of function and gain of function studies were employed to demonstrate the role of NOTCH3 (NR3)-FRIZZLED7 (FZD7) signaling in luminal cell fate commitment.	Phenobarbital	130-137	notch receptor 3	Homo sapiens	87-93
31443683-6	2019	Loss of function and gain of function studies were employed to demonstrate the role of NOTCH3 (NR3)-FRIZZLED7 (FZD7) signaling in luminal cell fate commitment.	Phenobarbital	130-137	frizzled class receptor 7	Homo sapiens	100-109
31443683-6	2019	Loss of function and gain of function studies were employed to demonstrate the role of NOTCH3 (NR3)-FRIZZLED7 (FZD7) signaling in luminal cell fate commitment.	Phenobarbital	130-137	frizzled class receptor 7	Homo sapiens	111-115
31443683-7	2019	RESULTS: Our results suggest that, NR3-FZD7 signaling axis was necessary for luminal cell fate commitment.	Phenobarbital	77-84	frizzled class receptor 7	Homo sapiens	39-43
31443683-8	2019	Similar to LRPs, BLPs (NR3highFZD7highCD90+MUC1-ER-) differentiate to generate NR3medFZD7medCD90-MUC1+ER+ luminal cells.	Phenobarbital	106-113	mucin 1, transmembrane	Mus musculus	43-47
31506588-4	2019	We show that STIM1 expression is regulated post-transcriptionally by the miRNA machinery and identify miR-223 and miR-150 as regulators of STIM1 expression in the luminal non-aggressive MCF7 breast cancer cell line.	Phenobarbital	163-170	stromal interaction molecule 1	Homo sapiens	13-18
31506588-4	2019	We show that STIM1 expression is regulated post-transcriptionally by the miRNA machinery and identify miR-223 and miR-150 as regulators of STIM1 expression in the luminal non-aggressive MCF7 breast cancer cell line.	Phenobarbital	163-170	microRNA 223	Homo sapiens	102-109
31506588-4	2019	We show that STIM1 expression is regulated post-transcriptionally by the miRNA machinery and identify miR-223 and miR-150 as regulators of STIM1 expression in the luminal non-aggressive MCF7 breast cancer cell line.	Phenobarbital	163-170	microRNA 150	Homo sapiens	114-121
31506588-4	2019	We show that STIM1 expression is regulated post-transcriptionally by the miRNA machinery and identify miR-223 and miR-150 as regulators of STIM1 expression in the luminal non-aggressive MCF7 breast cancer cell line.	Phenobarbital	163-170	stromal interaction molecule 1	Homo sapiens	139-144
31285043-15	2019	Myoepithelial cells were immunoreactive for smooth muscle actin and p63, while luminal cells were immunoreactive for CK7, CK8, EMA, and, in a more focused and less consistent manner, for Ber-EP4, CD117, PHLDA1 and androgen receptors.	Phenobarbital	79-86	keratin 7	Homo sapiens	117-120
31285043-15	2019	Myoepithelial cells were immunoreactive for smooth muscle actin and p63, while luminal cells were immunoreactive for CK7, CK8, EMA, and, in a more focused and less consistent manner, for Ber-EP4, CD117, PHLDA1 and androgen receptors.	Phenobarbital	79-86	keratin 8	Homo sapiens	122-125
31285043-15	2019	Myoepithelial cells were immunoreactive for smooth muscle actin and p63, while luminal cells were immunoreactive for CK7, CK8, EMA, and, in a more focused and less consistent manner, for Ber-EP4, CD117, PHLDA1 and androgen receptors.	Phenobarbital	79-86	prostaglandin E receptor 4	Homo sapiens	191-194
31285043-15	2019	Myoepithelial cells were immunoreactive for smooth muscle actin and p63, while luminal cells were immunoreactive for CK7, CK8, EMA, and, in a more focused and less consistent manner, for Ber-EP4, CD117, PHLDA1 and androgen receptors.	Phenobarbital	79-86	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	196-201
31285043-15	2019	Myoepithelial cells were immunoreactive for smooth muscle actin and p63, while luminal cells were immunoreactive for CK7, CK8, EMA, and, in a more focused and less consistent manner, for Ber-EP4, CD117, PHLDA1 and androgen receptors.	Phenobarbital	79-86	pleckstrin homology like domain family A member 1	Homo sapiens	203-209
31292943-0	2019	FGF12p.Gly112Ser variant as a cause of phenytoin/phenobarbital responsive epilepsy.	Phenobarbital	49-62	fibroblast growth factor 12	Homo sapiens	0-6
31292943-1	2019	A patient harboring a novel p.Gly112Ser variant in FGF12 gene had a positive response to phenytoin/phenobarbital treatment.	Phenobarbital	99-112	fibroblast growth factor 12	Homo sapiens	51-56
31270214-4	2019	Increased luciferase activity of a reporter plasmid containing the CYP3A4 promoter region by phenobarbital was augmented by transfection of siRNA for ADAR1 (siADAR1) but not by siADAR2.	Phenobarbital	93-106	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	67-73
31270214-4	2019	Increased luciferase activity of a reporter plasmid containing the CYP3A4 promoter region by phenobarbital was augmented by transfection of siRNA for ADAR1 (siADAR1) but not by siADAR2.	Phenobarbital	93-106	adenosine deaminase RNA specific	Homo sapiens	150-155
31270214-5	2019	In addition, the knockdown of ADAR1 resulted in the enhanced induction of CYP2B6 and CYP3A4 mRNA by 6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime and phenobarbital, respectively.	Phenobarbital	193-206	adenosine deaminase RNA specific	Homo sapiens	30-35
31270214-5	2019	In addition, the knockdown of ADAR1 resulted in the enhanced induction of CYP2B6 and CYP3A4 mRNA by 6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime and phenobarbital, respectively.	Phenobarbital	193-206	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	74-80
31270214-5	2019	In addition, the knockdown of ADAR1 resulted in the enhanced induction of CYP2B6 and CYP3A4 mRNA by 6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime and phenobarbital, respectively.	Phenobarbital	193-206	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	85-91
31444332-3	2019	Here we show that E-cadherin loss induces extrusion of luminal MMECs to the basal lamina.	Phenobarbital	55-62	cadherin 1	Mus musculus	18-28
30224344-8	2019	The CC1-Basal and CC2-Luminal subtypes expressed genes consistent with a basal and a luminal phenotype, respectively, and were similar to the corresponding established pretreatment molecular subtypes.	Phenobarbital	22-29	C-C motif chemokine ligand 14	Homo sapiens	4-7
30224344-8	2019	The CC1-Basal and CC2-Luminal subtypes expressed genes consistent with a basal and a luminal phenotype, respectively, and were similar to the corresponding established pretreatment molecular subtypes.	Phenobarbital	85-92	C-C motif chemokine ligand 14	Homo sapiens	4-7
31222103-3	2019	Further, as luminal cells of normal breast epithelial cells are enriched in SOD1, whether SOD1 is essential for normal mammary gland development has never been determined.	Phenobarbital	12-19	superoxide dismutase 1, soluble	Mus musculus	76-80
31087002-5	2019	Our results demonstrate that NHERF1 expression is upregulated during lactation and that it interacts with PMCA2 at the apical membrane of secretory luminal epithelial cells.	Phenobarbital	148-155	solute carrier family 9 (sodium/hydrogen exchanger), member 3 regulator 1	Mus musculus	29-35
31087002-5	2019	Our results demonstrate that NHERF1 expression is upregulated during lactation and that it interacts with PMCA2 at the apical membrane of secretory luminal epithelial cells.	Phenobarbital	148-155	ATPase, Ca++ transporting, plasma membrane 2	Mus musculus	106-111
31087002-7	2019	Examining lactating NHERF1 knockout (KO) mice showed that NHERF1 contributes to the proper apical location of PMCA2, for proper apical-basal polarity in luminal epithelial cells, and that it participates in the suppression of Stat3 activation and the prevention of premature mammary gland involution.	Phenobarbital	153-160	solute carrier family 9 (sodium/hydrogen exchanger), member 3 regulator 1	Mus musculus	58-64
31091422-6	2019	Aquaporin (Aqp) 11 was also potently down-regulated, whereas Aqp5/AQP5 expression persisted, resulting in the inhibition of luminal closure.	Phenobarbital	124-131	aquaporin 5	Mus musculus	61-65
31091422-6	2019	Aquaporin (Aqp) 11 was also potently down-regulated, whereas Aqp5/AQP5 expression persisted, resulting in the inhibition of luminal closure.	Phenobarbital	124-131	aquaporin 5	Mus musculus	66-70
31145039-8	2019	In the luminal epithelium, DROSHA staining intensity was reduced in early and mid-secretory-infertile while DICER staining was reduced in the early secretory-infertile compared with their respective fertile groups.	Phenobarbital	7-14	drosha ribonuclease III	Homo sapiens	27-33
31127007-1	2019	P-glycoprotein (P-gp) is a multidrug transporter that is expressed on the luminal surface of epithelial cells in the kidney, intestine, bile-canalicular membrane in the liver, blood-brain barrier, and adrenal gland.	Phenobarbital	74-81	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
31127007-1	2019	P-glycoprotein (P-gp) is a multidrug transporter that is expressed on the luminal surface of epithelial cells in the kidney, intestine, bile-canalicular membrane in the liver, blood-brain barrier, and adrenal gland.	Phenobarbital	74-81	ATP binding cassette subfamily B member 1	Homo sapiens	16-20
31196969-4	2019	Among the 91 kinases with auto-phosphorylation, elevated EGFR, ERBB2, PRKG1, and WNK1 phosphosignaling were enriched in basal, HER2-E, Luminal A, and Luminal B breast cancers, respectively, revealing subtype-specific regulation.	Phenobarbital	135-142	epidermal growth factor receptor	Homo sapiens	57-61
31196969-4	2019	Among the 91 kinases with auto-phosphorylation, elevated EGFR, ERBB2, PRKG1, and WNK1 phosphosignaling were enriched in basal, HER2-E, Luminal A, and Luminal B breast cancers, respectively, revealing subtype-specific regulation.	Phenobarbital	135-142	erb-b2 receptor tyrosine kinase 2	Homo sapiens	63-68
31196969-4	2019	Among the 91 kinases with auto-phosphorylation, elevated EGFR, ERBB2, PRKG1, and WNK1 phosphosignaling were enriched in basal, HER2-E, Luminal A, and Luminal B breast cancers, respectively, revealing subtype-specific regulation.	Phenobarbital	135-142	protein kinase cGMP-dependent 1	Homo sapiens	70-75
31196969-4	2019	Among the 91 kinases with auto-phosphorylation, elevated EGFR, ERBB2, PRKG1, and WNK1 phosphosignaling were enriched in basal, HER2-E, Luminal A, and Luminal B breast cancers, respectively, revealing subtype-specific regulation.	Phenobarbital	135-142	WNK lysine deficient protein kinase 1	Homo sapiens	81-85
31358837-12	2019	Our study identified, for the first time, that MLH1 V384D germline variant is frequently detected in HER2-positive luminal B BC.	Phenobarbital	115-122	mutL homolog 1	Homo sapiens	47-51
31358837-12	2019	Our study identified, for the first time, that MLH1 V384D germline variant is frequently detected in HER2-positive luminal B BC.	Phenobarbital	115-122	erb-b2 receptor tyrosine kinase 2	Homo sapiens	101-105
31324782-4	2019	Specific inhibition of luminal thrombin activity causes macroscopic and microscopic damage as well as transcriptomic alterations of genes involved in host-microbiota interactions.	Phenobarbital	23-30	coagulation factor II	Mus musculus	31-39
31082439-0	2019	SARAF Luminal Domain Structure Reveals a Novel Domain-Swapped beta-Sandwich Fold Important for SOCE Modulation.	Phenobarbital	6-13	store-operated calcium entry associated regulatory factor	Homo sapiens	0-5
31082439-4	2019	Here, we describe the X-ray crystal structure of the SARAF luminal domain, SARAFL.	Phenobarbital	59-66	store-operated calcium entry associated regulatory factor	Homo sapiens	53-58
31082439-6	2019	The structure reveals a domain-swapped dimer in which the last two beta-strands (beta9 and beta10) are exchanged forming a region denoted the "SARAF luminal switch" that is essential for dimerization.	Phenobarbital	149-156	store-operated calcium entry associated regulatory factor	Homo sapiens	143-148
31289927-3	2019	RECENT FINDINGS: Luminal SCFAs augment the duodenal mucosal defenses via release of serotonin (5-HT) and glucagon-like peptide-2 (GLP-2) from enteroendocrine cells.	Phenobarbital	17-24	glucagon	Homo sapiens	105-128
31289927-3	2019	RECENT FINDINGS: Luminal SCFAs augment the duodenal mucosal defenses via release of serotonin (5-HT) and glucagon-like peptide-2 (GLP-2) from enteroendocrine cells.	Phenobarbital	17-24	glucagon	Homo sapiens	130-135
31015574-6	2019	DDX5 protein level was higher in triple-negative basal-like tumors than in non-basal-like tumors, including luminal A, luminal B, and HER2-enriched subtypes.	Phenobarbital	108-115	DEAD-box helicase 5	Homo sapiens	0-4
31015574-6	2019	DDX5 protein level was higher in triple-negative basal-like tumors than in non-basal-like tumors, including luminal A, luminal B, and HER2-enriched subtypes.	Phenobarbital	119-126	DEAD-box helicase 5	Homo sapiens	0-4
30086993-12	2019	Esophageal wall thickness and SI were reduced, and luminal diameter was increased in Group PRP compared to Group Burn (p < 0.05).	Phenobarbital	51-58	proline rich protein 2-like 1	Rattus norvegicus	91-94
31243370-8	2019	Thus, FOXA1 mutations alter its pioneering function and perturb normal luminal epithelial differentiation programs, providing further support for the role of lineage plasticity in cancer progression.	Phenobarbital	71-78	forkhead box A1	Mus musculus	6-11
31010817-6	2019	Furthermore, when LGG was cultured with the colonic luminal contents from healthy mice, p40 production was upregulated but was attenuated with luminal contents from mice with intestinal inflammation.	Phenobarbital	52-59	interleukin 9	Mus musculus	88-91
31181734-6	2019	This paper will review the GI sensing of meal-related stimuli and the relationship with appetite and energy intake, and examine changes in GI responses to luminal stimuli in obesity, functional dyspepsia and anorexia of ageing, as examples of eating-related disorders.	Phenobarbital	155-162	G protein subunit alpha i1	Homo sapiens	139-141
31244859-7	2019	The intraperitoneal administration of RANKL in mice effectively induced M cells, which have a high capacity to take up luminal substrates, in the lower respiratory epithelium.	Phenobarbital	119-126	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	38-43
31208318-4	2019	We also identified differential expression of the miR-99a/let-7c/miR-125b miRNA cluster as a marker for separation of the Luminal A and B subtypes.	Phenobarbital	122-129	microRNA 99a	Homo sapiens	50-57
31208318-4	2019	We also identified differential expression of the miR-99a/let-7c/miR-125b miRNA cluster as a marker for separation of the Luminal A and B subtypes.	Phenobarbital	122-129	microRNA let-7c	Homo sapiens	58-64
30878816-9	2019	CONCLUSIONS: These results demonstrate that the continuous ingestion of excessive fat and sucrose rapidly enhances the GLP-1 secretory response to luminal nutrients, and the HiFat diet may have a potent effect compared with the HiSuc diet on GLP-1 secretory responses.	Phenobarbital	147-154	glucagon	Rattus norvegicus	119-124
30317586-0	2019	A pH-sensitive luminal His-cluster promotes interaction of PAM with V-ATPase along the secretory and endocytic pathways of peptidergic cells.	Phenobarbital	15-22	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	59-62
30317586-6	2019	Peptidylglycine alpha-amidating mono-oxygenase (PAM; EC 1.14.17.3), a secretory pathway membrane enzyme which shares similar topology with two V-ATPase accessory proteins (Ac45 and prorenin receptor), has a pH-sensitive luminal linker region.	Phenobarbital	220-227	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	0-46
30317586-6	2019	Peptidylglycine alpha-amidating mono-oxygenase (PAM; EC 1.14.17.3), a secretory pathway membrane enzyme which shares similar topology with two V-ATPase accessory proteins (Ac45 and prorenin receptor), has a pH-sensitive luminal linker region.	Phenobarbital	220-227	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	48-51
30317586-6	2019	Peptidylglycine alpha-amidating mono-oxygenase (PAM; EC 1.14.17.3), a secretory pathway membrane enzyme which shares similar topology with two V-ATPase accessory proteins (Ac45 and prorenin receptor), has a pH-sensitive luminal linker region.	Phenobarbital	220-227	ATPase H+ transporting accessory protein 2	Homo sapiens	181-198
30317586-12	2019	Our analysis of the secretory and endocytic pathways of peptidergic cells supports the hypothesis that PAM serves as a luminal pH-sensor, regulating V-ATPase action by altering its assembly status.	Phenobarbital	119-126	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	103-106
31004845-11	2019	CD31+ expressing luminal structures suggestive of neovasculature were seen within MSS at 7 days and were more prevalent after 14 days.	Phenobarbital	17-24	platelet and endothelial cell adhesion molecule 1	Homo sapiens	0-4
30927613-3	2019	Intracoronary stents, either bare metal (BMS) or drug eluting (DES), can successfully treat luminal stenoses within the coronary arteries.	Phenobarbital	92-99	desmin	Homo sapiens	63-66
31003159-7	2019	Butoxamine, a selective beta2-adrenergic receptor antagonist, reversed SALB influence on the activity of PB.	Phenobarbital	105-107	adrenergic receptor, beta 2	Mus musculus	24-49
31142299-2	2019	CNs type II patients usually benefit from phenobarbital treatment that induces residual UGT1A1 activity.	Phenobarbital	42-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	88-94
31159302-10	2019	Anti-PD-L1 intervention increased survival of the animals that carried both primary and relapsed luminal noninvasive, muscular invasive, and relapsed luminal bladder cancer xenografts.	Phenobarbital	97-104	CD274 molecule	Homo sapiens	5-10
31034888-7	2019	The approach is applied to the 36-kDa luminal domain of the sialyltransferase, rST6Gal1, in which all phenylalanines are labeled with 15N, and the results are validated by elimination of resonances via single-point mutations of selected phenylalanines to tyrosines.	Phenobarbital	38-45	ST6 beta-galactoside alpha-2,6-sialyltransferase 1	Rattus norvegicus	79-87
31142299-5	2019	CONCLUSION: In newly diagnosed CNs patients with unconjugated bilirubin levels consistent with CNs type II but that are unresponsive to phenobarbital treatment, disruption of the HNF-1alpha binding site in the proximal promoter should be considered as a probable cause.	Phenobarbital	136-149	HNF1 homeobox A	Homo sapiens	179-189
31142299-6	2019	Upon confirming a mutation in the HNF-1alpha site, phenobarbital treatment should be stopped or at least be reconsidered because of its sedative effects and its teratogenic properties.	Phenobarbital	51-64	HNF1 homeobox A	Homo sapiens	34-44
31049530-3	2019	In this work, the influence of phosvitin on luminal microbiota composition and mucosal transcriptome was investigated with young (3-week) and adult (8-week) mouse models.	Phenobarbital	44-51	casein kinase 2, beta polypeptide	Mus musculus	31-40
30926317-5	2019	The recombinant rabbit DHRS11 reduced acetohexamide and 1,4-naphthoquinone, and was inhibited by tolbutamide and phenobarbital (RHAR-specific inhibitors), demonstrating its identity with RHAR.	Phenobarbital	113-126	LOW QUALITY PROTEIN: dehydrogenase/reductase SDR family member 11	Oryctolagus cuniculus	23-29
30926317-8	2019	The broad substrate specificity and inhibitor sensitivity were different from those of human DHRS11, which did not reduce aliphatic aldehydes and aromatic ketones despite its higher 3(17)beta-hydroxysteroid dehydrogenase activity, and was insensitive to tolbutamide, phenobarbital and diclofenac.	Phenobarbital	267-280	dehydrogenase/reductase 11	Homo sapiens	93-99
31072936-1	2019	Acetylation of K40 in alpha-tubulin is the sole posttranslational modification to mark the luminal surface of microtubules.	Phenobarbital	91-98	keratin 40	Homo sapiens	15-18
31072936-1	2019	Acetylation of K40 in alpha-tubulin is the sole posttranslational modification to mark the luminal surface of microtubules.	Phenobarbital	91-98	tubulin alpha 1b	Homo sapiens	22-35
30957988-5	2019	We find that PRMT5 mRNA and protein are expressed at comparable levels in TNBC, luminal breast tumors, and healthy mammary tissues.	Phenobarbital	80-87	protein arginine methyltransferase 5	Homo sapiens	13-18
30592088-10	2019	Exposure to phenobarbital resulted in an approximately twofold increase in CYP 2B6 enzyme activity.	Phenobarbital	12-25	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	75-82
30819798-4	2019	PRPH2 is expressed in the luminal membrane of the LE.	Phenobarbital	26-33	peripherin 2	Mus musculus	0-5
30991855-7	2019	Among conventional and newer AEDs, ACEA (a selective CB1 receptor agonist) enhanced the protective action of phenobarbital and levetiracetam without accompanying adverse effects or pharmacokinetic interactions.	Phenobarbital	109-122	cannabinoid receptor 1 (brain)	Mus musculus	53-56
31036156-3	2019	In full-fledged tumors, pharmacologic augmentation of Hedgehog (Hh) pathway activity impedes tumor growth, and this cancer-restraining effect of Hh signaling is mediated by the stromal response to Shh signals, which stimulates subtype conversion of basal to luminal-like urothelial carcinoma.	Phenobarbital	258-265	sonic hedgehog	Mus musculus	197-200
31044581-0	2019	Neuroprotective and reparative effects of endoplasmic reticulum luminal proteins - mesencephalic astrocyte-derived neurotrophic factor and cerebral dopamine neurotrophic factor.	Phenobarbital	64-71	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	83-134
31044581-0	2019	Neuroprotective and reparative effects of endoplasmic reticulum luminal proteins - mesencephalic astrocyte-derived neurotrophic factor and cerebral dopamine neurotrophic factor.	Phenobarbital	64-71	neurotrophin 3	Homo sapiens	115-134
31004013-5	2019	NOD2 and CYBB deficiencies led to marked accumulation of Mucispirillum, which was associated with impaired neutrophil recruitment and killing of the bacterium by luminal neutrophils.	Phenobarbital	162-169	nucleotide-binding oligomerization domain containing 2	Mus musculus	0-4
31009517-0	2019	STAT2 dependent Type I Interferon response promotes dysbiosis and luminal expansion of the enteric pathogen Salmonella Typhimurium.	Phenobarbital	66-73	signal transducer and activator of transcription 2	Mus musculus	0-5
31009517-8	2019	Furthermore, luminal expansion of S. Typhimurium in wild-type mice was blunted in Stat2-/- mice.	Phenobarbital	13-20	signal transducer and activator of transcription 2	Mus musculus	82-87
31009517-10	2019	Our results highlight STAT2 dependent type I IFN mediated inflammation in the gut as a novel mechanism promoting luminal expansion of S. Typhimurium.	Phenobarbital	113-120	signal transducer and activator of transcription 2	Mus musculus	22-27
30689138-4	2019	Since the induction of certain cytochrome P450 (CYP) enzymes accelerates warfarin metabolism, using CYP inducers, such as phenobarbital, to accelerate brodifacoum clearance seems plausible.	Phenobarbital	122-135	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	31-46
30527740-5	2019	Suppression of MFN1 expression leads to equal distribution of the fragmented mitochondria in both progenies that undergo symmetric luminal cell differentiation.	Phenobarbital	131-138	mitofusin 1	Homo sapiens	15-19
30703706-1	2019	The purpose of this study was to determine the direct effects of phenobarbital (PB) on receptor activator of nuclear factor kappa-B ligand (RANKL) induced osteoclast differentiation and function in vitro and in vivo.	Phenobarbital	65-78	TNF superfamily member 11	Homo sapiens	140-145
30703706-1	2019	The purpose of this study was to determine the direct effects of phenobarbital (PB) on receptor activator of nuclear factor kappa-B ligand (RANKL) induced osteoclast differentiation and function in vitro and in vivo.	Phenobarbital	80-82	TNF superfamily member 11	Homo sapiens	140-145
30703706-2	2019	Here, PB significantly inhibited osteoclast formation and bone resorption ability induced by RANKL in vitro.	Phenobarbital	6-8	TNF superfamily member 11	Homo sapiens	93-98
30316823-12	2019	IL-33 also boosted luminal NETosis and halted cytolytic antiviral activities but did not affect the TH2 response.	Phenobarbital	19-26	interleukin 33	Mus musculus	0-5
31531046-7	2019	The limits of detection for phenobarbital and carbamazepine were 0.017 and 0.010 microg L-1 and the limits of quantification were 0.056 and 0.033 microg mL-1, respectively.	Phenobarbital	28-41	immunoglobulin kappa variable 1-16	Homo sapiens	88-91
30573691-5	2019	As expected, basal-like tumors were associated with increased expression of the basal markers KRT5/6 and KRT14, and luminal-like tumors were associated with increased expression of the luminal markers KRT20.	Phenobarbital	116-123	keratin 20	Homo sapiens	201-206
30573691-5	2019	As expected, basal-like tumors were associated with increased expression of the basal markers KRT5/6 and KRT14, and luminal-like tumors were associated with increased expression of the luminal markers KRT20.	Phenobarbital	185-192	keratin 20	Homo sapiens	201-206
30922362-2	2019	In addition, HER2+ breast cancer is generally considered more immunogenic than hormone receptor-positive (HR+)/HER2-, and specific molecular HER2+ subgroups (e.g. HER2-enriched disease) are more immunogenic than others (e.g. Luminal A or B).	Phenobarbital	225-232	erb-b2 receptor tyrosine kinase 2	Homo sapiens	13-17
30565998-16	2019	Transport across luminal and basolateral membranes is likely mediated by SGLT4/5 and GLUT2, respectively.	Phenobarbital	17-24	solute carrier family 2 member 2	Rattus norvegicus	85-90
30632789-2	2019	The aim of this research was to observe the impacts of MDR1 (C3435T) variant on the efflux of phenytoin, carbamazepine, valproate, and phenobarbital in vitro.	Phenobarbital	135-148	ATP-binding cassette, sub-family B (MDR/TAP), member 1	Sus scrofa	55-59
30689138-4	2019	Since the induction of certain cytochrome P450 (CYP) enzymes accelerates warfarin metabolism, using CYP inducers, such as phenobarbital, to accelerate brodifacoum clearance seems plausible.	Phenobarbital	122-135	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	48-51
30689138-4	2019	Since the induction of certain cytochrome P450 (CYP) enzymes accelerates warfarin metabolism, using CYP inducers, such as phenobarbital, to accelerate brodifacoum clearance seems plausible.	Phenobarbital	122-135	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	100-103
30027304-6	2019	Phenobarbital clearance (CLPB) was calculated at steady state.	Phenobarbital	0-13	caseinolytic mitochondrial matrix peptidase chaperone subunit B	Homo sapiens	25-29
30944910-8	2019	A Kaplan-Meier survival curve showed a significantly increased mortality rate of DEN/PB-exposed Adk-tg mice compared with WT mice.	Phenobarbital	85-87	adenosine kinase	Mus musculus	96-99
31388363-0	2019	Concurrent Quinidine and Phenobarbital in the Treatment of a Patient with 2 KCNT1 Mutations.	Phenobarbital	25-38	potassium sodium-activated channel subfamily T member 1	Homo sapiens	76-81
31388363-4	2019	We report the case of an infant with 2 KCNT1 mutations who experienced minor relief with quinidine and discuss the drug"s important interaction with phenobarbital.	Phenobarbital	149-162	potassium sodium-activated channel subfamily T member 1	Homo sapiens	39-44
30779884-10	2019	Location of Twist2 during embryo implantation was detected by immunohistochemistry (IHC), which revealed that it was extensively expressed in endometrial glandular epithelium and luminal epithelium at implantation sites on Day 5.	Phenobarbital	179-186	twist basic helix-loop-helix transcription factor 2	Mus musculus	12-18
30397077-5	2019	When senescent, luminal cells activated stromal fibroblasts in an IL-8-dependent manner, through the activation of the STAT3 pathway.	Phenobarbital	16-23	C-X-C motif chemokine ligand 8	Homo sapiens	66-70
30481983-3	2019	The G allele of the c.-6-180T&gt;G variation in intron 1 of MDR1 (single nucleotide polymorphism [SNP] 180) causes P-glycoprotein over-expression, making epileptic dogs resistant to phenobarbital treatment.	Phenobarbital	182-195	ATP binding cassette subfamily B member 1	Canis lupus familiaris	60-64
30587340-10	2019	From the analysis of Ii-deletion mutants, we found that the luminal domain of Ii p41 is crucial for the production of sMHC II molecules.	Phenobarbital	60-67	erythrocyte membrane protein band 4.1	Mus musculus	81-84
30679694-2	2019	PGRMC1 consists of a short N-terminal extracellular or luminal domain, a single membrane-spanning domain, and a long cytoplasmic domain.	Phenobarbital	55-62	progesterone receptor membrane component 1	Homo sapiens	0-6
30559329-6	2019	Mechanistically, CANX acts as co-receptor that recognizes ER luminal misfolded procollagens and interacts with the ER-phagy receptor FAM134B.	Phenobarbital	61-68	calnexin	Homo sapiens	17-21
30559329-6	2019	Mechanistically, CANX acts as co-receptor that recognizes ER luminal misfolded procollagens and interacts with the ER-phagy receptor FAM134B.	Phenobarbital	61-68	epiregulin	Homo sapiens	58-60
30503582-7	2019	In addition, treatment with 3-methylcholanthrene, phenobarbital, and rifampin led to the induction of cytochrome P-450 (cyp) 1a1 and cyp1a2, cyp2b10, cyp3a11.	Phenobarbital	50-63	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	102-128
30503582-7	2019	In addition, treatment with 3-methylcholanthrene, phenobarbital, and rifampin led to the induction of cytochrome P-450 (cyp) 1a1 and cyp1a2, cyp2b10, cyp3a11.	Phenobarbital	50-63	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	133-139
30503582-7	2019	In addition, treatment with 3-methylcholanthrene, phenobarbital, and rifampin led to the induction of cytochrome P-450 (cyp) 1a1 and cyp1a2, cyp2b10, cyp3a11.	Phenobarbital	50-63	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	141-148
30503582-7	2019	In addition, treatment with 3-methylcholanthrene, phenobarbital, and rifampin led to the induction of cytochrome P-450 (cyp) 1a1 and cyp1a2, cyp2b10, cyp3a11.	Phenobarbital	50-63	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	150-157
30617224-3	2019	As disease normally resolved, neutralization of IL-22 caused luminal narrowing of the cecum-a feature reminiscent of fibrotic strictures seen in Crohn disease patients.	Phenobarbital	61-68	interleukin 22	Homo sapiens	48-53
30682134-8	2019	In addition, CsrB/C sRNA levels were greatly reduced under the simulated intracellular conditions and were responsive to nutritional factors that distinguish the intracellular and luminal environments.	Phenobarbital	180-187	mortality factor 4 (pseudogene)	Homo sapiens	13-17
30554919-2	2019	Herein DACH1 was detected among multipotent fetal mammary stem cells in the embryo, among mixed lineage precursors, and in adult basal cells and (ERalpha+) luminal progenitors.	Phenobarbital	156-163	dachshund family transcription factor 1	Homo sapiens	7-12
30397077-5	2019	When senescent, luminal cells activated stromal fibroblasts in an IL-8-dependent manner, through the activation of the STAT3 pathway.	Phenobarbital	16-23	signal transducer and activator of transcription 3	Homo sapiens	119-124
30397077-7	2019	These results show the role of senescent breast luminal cells in promoting the inflammatory/carcinogenic microenvironment through the activation of fibroblasts in an IL-8-dependent manner.	Phenobarbital	48-55	C-X-C motif chemokine ligand 8	Homo sapiens	166-170
30828081-7	2019	These findings indicated that the anesthetic effects of phenobarbital are potentiated in ARF rats, probably due to imbalanced cerebral expression of KCC2 and NKCC1, suggesting that altered cation-chloride handling in nerve cells is associated.	Phenobarbital	56-69	solute carrier family 12 member 5	Rattus norvegicus	149-153
30828081-7	2019	These findings indicated that the anesthetic effects of phenobarbital are potentiated in ARF rats, probably due to imbalanced cerebral expression of KCC2 and NKCC1, suggesting that altered cation-chloride handling in nerve cells is associated.	Phenobarbital	56-69	solute carrier family 12 member 2	Rattus norvegicus	158-163
30388696-7	2019	Phenobarbital was docked within the Fab domain of P1, P2, and P5 immobilized configurations and equilibrated with molecular dynamics for binding energy estimation.	Phenobarbital	0-13	exosome component 9	Homo sapiens	50-64
30315845-0	2019	Inhibition of BTF3 sensitizes luminal breast cancer cells to PI3Kalpha inhibition through the transcriptional regulation of ERalpha.	Phenobarbital	30-37	basic transcription factor 3	Homo sapiens	14-18
30315845-0	2019	Inhibition of BTF3 sensitizes luminal breast cancer cells to PI3Kalpha inhibition through the transcriptional regulation of ERalpha.	Phenobarbital	30-37	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	61-70
30315845-0	2019	Inhibition of BTF3 sensitizes luminal breast cancer cells to PI3Kalpha inhibition through the transcriptional regulation of ERalpha.	Phenobarbital	30-37	estrogen receptor 1	Homo sapiens	124-131
30315845-4	2019	Our TCGA analysis reveals high expression levels of BTF3 in luminal/ER + breast cancer and cell line models harboring ERalpha overexpression.	Phenobarbital	60-67	basic transcription factor 3	Homo sapiens	52-56
31670920-8	2019	EGFR expression was different in luminal A-like (Lum A, 1.3%) versus luminal B-like (Lum B, 11.4%) subtypes.	Phenobarbital	33-40	epidermal growth factor receptor	Homo sapiens	0-4
30575334-4	2019	We found that low-density lipoprotein receptor-related protein 8 (LRP8) was more strongly expressed in estrogen receptor-negative breast tumors, including TNBCs and those overexpressing HER2, than in luminal breast tumors and normal breast tissues.	Phenobarbital	200-207	LDL receptor related protein 8	Homo sapiens	66-70
31613724-3	2019	SGLT1 is apical membrane-constitutive and it is active at a low luminal glucose concentration, while at concentrations higher than 50 mM, glucose is mainly transported by GLUT2 (recruited from the basolateral membrane).	Phenobarbital	64-71	solute carrier family 5 member 1	Homo sapiens	0-5
30338550-0	2019	Pilot studies evaluating the nongenotoxic rodent carcinogens phenobarbital and clofibrate in the rat Pig-a assay.	Phenobarbital	61-74	phosphatidylinositol glycan anchor biosynthesis class A	Sus scrofa	101-106
30338550-3	2019	The purpose of the present study was to evaluate specificity of the Pig-a assay using two nongenotoxic and well-characterized rodent liver carcinogens, phenobarbital and clofibrate, in male F344/DuCrl rats.	Phenobarbital	152-165	phosphatidylinositol glycan anchor biosynthesis class A	Sus scrofa	68-73
30842367-5	2019	PB-BNF-induced S9 enhanced the micronucleus induction (MI) of benzo[a]pyrene (BaP), cyclophosphamide (CPA), and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine hydrochloride (PhIP), which are metabolized by CYP1A1, CYP2C6, and CYP1A2, respectively.	Phenobarbital	0-2	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	207-213
30842367-5	2019	PB-BNF-induced S9 enhanced the micronucleus induction (MI) of benzo[a]pyrene (BaP), cyclophosphamide (CPA), and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine hydrochloride (PhIP), which are metabolized by CYP1A1, CYP2C6, and CYP1A2, respectively.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	215-221
30842367-5	2019	PB-BNF-induced S9 enhanced the micronucleus induction (MI) of benzo[a]pyrene (BaP), cyclophosphamide (CPA), and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine hydrochloride (PhIP), which are metabolized by CYP1A1, CYP2C6, and CYP1A2, respectively.	Phenobarbital	0-2	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	227-233
31270302-3	2019	Slight hormone level changes, histopathological changes in thyroid gland or induction of UDP-glucuronosyltransferase in liver were observed in both the PB and DEHP groups.	Phenobarbital	152-154	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	89-116
30590041-1	2018	The SRC-family kinase LYN is highly expressed in triple-negative/basal-like breast cancer (TNBC) and in the cell of origin of these tumors, c-KIT-positive luminal progenitors.	Phenobarbital	155-162	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	140-145
31270302-7	2019	CYP2B and CYP3A, which are involved in testosterone metabolism, were induced in liver of the PB group.	Phenobarbital	93-95	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	10-15
31574503-2	2019	Conversely, elevated luminal shear stress (SS) promotes outward remodeling of arteries in vivo and prevents inward remodeling in culture in a nitric oxide synthase (NOS)-dependent manner.	Phenobarbital	21-28	nitric oxide synthase 1, neuronal	Mus musculus	142-163
30764626-4	2019	In hormone-dependent (HR+) HER2-positive tumors, the subgroup HER2-E represents 40-&#8202;50% of cases; others are luminal A and B subtypes.	Phenobarbital	115-122	erb-b2 receptor tyrosine kinase 2	Homo sapiens	62-66
31256150-2	2019	Phenobarbital is an inducer of cytochrome P450 (CYP) 3A, while midazolam is a CYP3A substrate.	Phenobarbital	0-13	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	31-55
31256150-11	2019	Phenobarbital co-administration increased midazolam clearance by a factor 2.3 (95% CI 1.9-2.9, p < 0.05).	Phenobarbital	0-13	transcription termination factor 2	Homo sapiens	67-75
31027466-3	2019	CFTR, an adenosine triphosphate binding anion channel, has multiple functions, but primarily regulates the movement of chloride anions, thiocyanate and bicarbonate across luminal cell membranes.	Phenobarbital	171-178	CF transmembrane conductance regulator	Homo sapiens	0-4
30361333-5	2019	We demonstrate CAR expression rescued the ability of Car-/- hepatocytes to respond to a wide range of CAR activators including phenobarbital.	Phenobarbital	127-140	nuclear receptor subfamily 1 group I member 3	Homo sapiens	15-18
30361333-5	2019	We demonstrate CAR expression rescued the ability of Car-/- hepatocytes to respond to a wide range of CAR activators including phenobarbital.	Phenobarbital	127-140	nuclear receptor subfamily 1 group I member 3	Homo sapiens	53-56
30590041-1	2018	The SRC-family kinase LYN is highly expressed in triple-negative/basal-like breast cancer (TNBC) and in the cell of origin of these tumors, c-KIT-positive luminal progenitors.	Phenobarbital	155-162	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	22-25
30581412-7	2018	Older AEDs, acting on cytochrome P450 isoenzymes, and especially on CYP3A4, such as phenobarbital, phenytoin, and carbamazepine are more likely to significantly reduce the anticoagulant effect of DOACs (especially rivaroxaban, apixaban, and edoxaban).	Phenobarbital	84-97	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	68-74
30566873-6	2018	In contrast, in luminal cells lacking PTEN, LY6D+ cells predominantly give rise to LY6D+ tumor cells, contributing to high-grade PIN lesions.	Phenobarbital	16-23	phosphatase and tensin homolog	Homo sapiens	38-42
30566873-6	2018	In contrast, in luminal cells lacking PTEN, LY6D+ cells predominantly give rise to LY6D+ tumor cells, contributing to high-grade PIN lesions.	Phenobarbital	16-23	lymphocyte antigen 6 family member D	Homo sapiens	44-48
30566873-6	2018	In contrast, in luminal cells lacking PTEN, LY6D+ cells predominantly give rise to LY6D+ tumor cells, contributing to high-grade PIN lesions.	Phenobarbital	16-23	lymphocyte antigen 6 family member D	Homo sapiens	83-87
30566873-8	2018	Our studies thus identify a subpopulation of luminal progenitors characterized by LY6D expression and intrinsic castration resistance.	Phenobarbital	45-52	lymphocyte antigen 6 family member D	Homo sapiens	82-86
30136373-5	2018	A model of PB-resistant ischemic seizures in postnatal day 7 (P7) CD-1 mice reported K-Cl cotransporter 2 (KCC2) degradation that has been shown to be due to activation of the TrkB pathway.	Phenobarbital	11-13	solute carrier family 12, member 5	Mus musculus	85-105
30397314-6	2018	Binding to lysosomal enzymes requires the second luminal loop of CLN8 and is abolished by some disease-causing mutations within this region.	Phenobarbital	49-56	CLN8 transmembrane ER and ERGIC protein	Homo sapiens	65-69
30136373-5	2018	A model of PB-resistant ischemic seizures in postnatal day 7 (P7) CD-1 mice reported K-Cl cotransporter 2 (KCC2) degradation that has been shown to be due to activation of the TrkB pathway.	Phenobarbital	11-13	solute carrier family 12, member 5	Mus musculus	107-111
30136373-5	2018	A model of PB-resistant ischemic seizures in postnatal day 7 (P7) CD-1 mice reported K-Cl cotransporter 2 (KCC2) degradation that has been shown to be due to activation of the TrkB pathway.	Phenobarbital	11-13	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	176-180
30485214-10	2018	The number and maximum luminal diameter of CD31-positive microvessels were also significantly correlated with the number of HIF-1alpha-positive cells (r = 0.85 and r = 0.89, respectively) and varied among the 3 plaque components (IPH > lipid-rich > fibrous).	Phenobarbital	23-30	platelet and endothelial cell adhesion molecule 1	Homo sapiens	43-47
30115646-3	2018	Here, we treated tumor-bearing mice with phenobarbital, an activator of the constitutive androstane receptor (CAR), to analyze the response of chemically induced Ha-ras- and B-raf-mutated mouse liver adenoma to CAR activation in vivo.	Phenobarbital	41-54	nuclear receptor subfamily 1, group I, member 3	Mus musculus	76-108
30115646-3	2018	Here, we treated tumor-bearing mice with phenobarbital, an activator of the constitutive androstane receptor (CAR), to analyze the response of chemically induced Ha-ras- and B-raf-mutated mouse liver adenoma to CAR activation in vivo.	Phenobarbital	41-54	nuclear receptor subfamily 1, group I, member 3	Mus musculus	110-113
30085095-7	2018	Finally, full protection against a phenobarbital-induced attack was achieved in AIP mice after the administration of 1 x 1011 gc/kg of rAAV2/8-PBGD-I291M/N340S vector; three times lower than the dose required to achieve full protection with the control rAAV2/8-hPBGD vector.	Phenobarbital	35-48	hydroxymethylbilane synthase	Mus musculus	143-147
29716964-0	2018	Nuclear Receptor CAR Suppresses GADD45B-p38 MAPK Signaling to Promote Phenobarbital-induced Proliferation in Mouse Liver.	Phenobarbital	70-83	nuclear receptor subfamily 1, group I, member 3	Mus musculus	17-20
30025153-0	2018	Phenobarbital-induced phosphorylation converts nuclear receptor RORalpha from a repressor to an activator of the estrogen sulfotransferase gene Sult1e1 in mouse livers.	Phenobarbital	0-13	RAR-related orphan receptor alpha	Mus musculus	64-72
30025153-0	2018	Phenobarbital-induced phosphorylation converts nuclear receptor RORalpha from a repressor to an activator of the estrogen sulfotransferase gene Sult1e1 in mouse livers.	Phenobarbital	0-13	sulfotransferase family 1E, member 1	Mus musculus	144-151
30025153-2	2018	Phenobarbital (PB), a clinical sedative, activates Sult1e1 gene transcription in mouse livers.	Phenobarbital	0-13	sulfotransferase family 1E, member 1	Mus musculus	51-58
30025153-2	2018	Phenobarbital (PB), a clinical sedative, activates Sult1e1 gene transcription in mouse livers.	Phenobarbital	15-17	sulfotransferase family 1E, member 1	Mus musculus	51-58
30025153-6	2018	Our findings suggest that PB signals CAR to communicate with RORalpha via serine 100 phosphorylation, converting RORalpha from transcription repressor to activator of the Sult1e1 gene and inducing SULT1E1 expression in mouse livers.	Phenobarbital	26-28	RAR-related orphan receptor alpha	Mus musculus	61-69
30025153-6	2018	Our findings suggest that PB signals CAR to communicate with RORalpha via serine 100 phosphorylation, converting RORalpha from transcription repressor to activator of the Sult1e1 gene and inducing SULT1E1 expression in mouse livers.	Phenobarbital	26-28	RAR-related orphan receptor alpha	Mus musculus	113-121
30025153-6	2018	Our findings suggest that PB signals CAR to communicate with RORalpha via serine 100 phosphorylation, converting RORalpha from transcription repressor to activator of the Sult1e1 gene and inducing SULT1E1 expression in mouse livers.	Phenobarbital	26-28	sulfotransferase family 1E, member 1	Mus musculus	171-178
30025153-6	2018	Our findings suggest that PB signals CAR to communicate with RORalpha via serine 100 phosphorylation, converting RORalpha from transcription repressor to activator of the Sult1e1 gene and inducing SULT1E1 expression in mouse livers.	Phenobarbital	26-28	sulfotransferase family 1E, member 1	Mus musculus	197-204
29806093-4	2018	Immunolocalization of the channels in the resting spermatic duct reveals that Aqp0a, -1aa, -4a, -7 and -10b are expressed in the monolayered luminal epithelium, Aqp8b and -9b in smooth muscle fibers, and Aqp1ab and -3a in different interstitial lamina cells.	Phenobarbital	141-148	aquaporin 7	Homo sapiens	78-107
29793206-8	2018	On the contrary, PB exposure repressed the mRNA expressions of CYP2AC2 in males and CYP2R1, CYP3A37, and CYP8B1 in females.	Phenobarbital	17-19	cytochrome P450, family 2, subfamily AC, polypeptide 2	Gallus gallus	63-70
29793206-8	2018	On the contrary, PB exposure repressed the mRNA expressions of CYP2AC2 in males and CYP2R1, CYP3A37, and CYP8B1 in females.	Phenobarbital	17-19	cytochrome P450 family 2 subfamily R member 1	Gallus gallus	84-90
29793206-8	2018	On the contrary, PB exposure repressed the mRNA expressions of CYP2AC2 in males and CYP2R1, CYP3A37, and CYP8B1 in females.	Phenobarbital	17-19	cytochrome P450 family 3 subfamily A member 5	Gallus gallus	92-99
29793206-8	2018	On the contrary, PB exposure repressed the mRNA expressions of CYP2AC2 in males and CYP2R1, CYP3A37, and CYP8B1 in females.	Phenobarbital	17-19	cytochrome P450 family 8 subfamily B member 1	Gallus gallus	105-111
29699863-6	2018	FGF12-related epileptic encephalopathy may exhibit diverse phenotypes and may respond to sodium channel blockers or high-dose PB.	Phenobarbital	126-128	fibroblast growth factor 12	Homo sapiens	0-5
30086303-5	2018	Reporters constructed to monitor each mechanism show that phenobarbital-induced ER membrane expansion depends on transmembrane domain-induced ATF6.	Phenobarbital	58-71	activating transcription factor 6	Homo sapiens	142-146
30127740-6	2018	In addition, repeated treatment with phenytoin (30 mg/kg, i.p., for 10 days) or phenobarbital (30 mg/kg, i.p., for 10 days) also elevated Kir4.1 expression region-specifically in the amygdala.	Phenobarbital	80-93	potassium inwardly-rectifying channel, subfamily J, member 10	Rattus norvegicus	138-144
30127740-8	2018	The present results demonstrated for the first time that the antiepileptic drugs effective for convulsive seizures (valproate, phenytoin, and phenobarbital) commonly elevate the astrocytic Kir4.1 channel expression in the limbic regions, which may be related to their antiepileptic actions.	Phenobarbital	142-155	potassium inwardly-rectifying channel, subfamily J, member 10	Rattus norvegicus	189-195
29716964-0	2018	Nuclear Receptor CAR Suppresses GADD45B-p38 MAPK Signaling to Promote Phenobarbital-induced Proliferation in Mouse Liver.	Phenobarbital	70-83	growth arrest and DNA-damage-inducible 45 beta	Mus musculus	32-39
29716964-0	2018	Nuclear Receptor CAR Suppresses GADD45B-p38 MAPK Signaling to Promote Phenobarbital-induced Proliferation in Mouse Liver.	Phenobarbital	70-83	mitogen-activated protein kinase 14	Mus musculus	40-43
29417440-5	2018	Phenobarbital also reduced expression of neuronal markers (doublecortin (DCX), calretinin, NeuN), neuronal transcription factors (Pax6, Sox2, Tbr1/2, Prox1), and neurotrophins (NGF, BDNF, NT-3) up to 24 h after the last administration.	Phenobarbital	0-13	doublecortin	Homo sapiens	73-76
29716964-2	2018	Nuclear receptor constitutive active/androstane receptor (NR1I3/CAR) regulates the induction and promotion activities of phenobarbital.	Phenobarbital	121-134	nuclear receptor subfamily 1, group I, member 3	Mus musculus	58-63
29417440-5	2018	Phenobarbital also reduced expression of neuronal markers (doublecortin (DCX), calretinin, NeuN), neuronal transcription factors (Pax6, Sox2, Tbr1/2, Prox1), and neurotrophins (NGF, BDNF, NT-3) up to 24 h after the last administration.	Phenobarbital	0-13	calbindin 2	Homo sapiens	79-89
29716964-2	2018	Nuclear receptor constitutive active/androstane receptor (NR1I3/CAR) regulates the induction and promotion activities of phenobarbital.	Phenobarbital	121-134	nuclear receptor subfamily 1, group I, member 3	Mus musculus	64-67
29417440-5	2018	Phenobarbital also reduced expression of neuronal markers (doublecortin (DCX), calretinin, NeuN), neuronal transcription factors (Pax6, Sox2, Tbr1/2, Prox1), and neurotrophins (NGF, BDNF, NT-3) up to 24 h after the last administration.	Phenobarbital	0-13	RNA binding fox-1 homolog 3	Homo sapiens	91-95
29716964-3	2018	Here, it is demonstrated that phenobarbital treatment results in dephosphorylation of a tumor suppressor p38 MAPK in the liver of C57BL/6 and C3H/HeNCrlBR mice.	Phenobarbital	30-43	mitogen-activated protein kinase 14	Mus musculus	105-113
29417440-5	2018	Phenobarbital also reduced expression of neuronal markers (doublecortin (DCX), calretinin, NeuN), neuronal transcription factors (Pax6, Sox2, Tbr1/2, Prox1), and neurotrophins (NGF, BDNF, NT-3) up to 24 h after the last administration.	Phenobarbital	0-13	paired box 6	Homo sapiens	130-134
29716964-5	2018	Phenobarbital-induced hepatocyte proliferation, as determined by BrdUrd incorporation, was significantly reduced in both male and female livers of GADD45B knockout (KO) mice compared with the wild-type mice.	Phenobarbital	0-13	growth arrest and DNA-damage-inducible 45 beta	Mus musculus	147-154
29417440-5	2018	Phenobarbital also reduced expression of neuronal markers (doublecortin (DCX), calretinin, NeuN), neuronal transcription factors (Pax6, Sox2, Tbr1/2, Prox1), and neurotrophins (NGF, BDNF, NT-3) up to 24 h after the last administration.	Phenobarbital	0-13	SRY-box transcription factor 2	Homo sapiens	136-140
29716964-6	2018	The phenobarbital-induced proliferation continued until 48 hours after phenobarbital injection in only the C57BL/6 males, but neither in males of GADD45B KO mice nor in females of C57BL/6 and GADD45B KO mice.	Phenobarbital	4-17	growth arrest and DNA-damage-inducible 45 beta	Mus musculus	192-199
29417440-5	2018	Phenobarbital also reduced expression of neuronal markers (doublecortin (DCX), calretinin, NeuN), neuronal transcription factors (Pax6, Sox2, Tbr1/2, Prox1), and neurotrophins (NGF, BDNF, NT-3) up to 24 h after the last administration.	Phenobarbital	0-13	T-box brain transcription factor 1	Homo sapiens	142-148
29716964-7	2018	Thus, these data reveal nuclear receptor CAR interacts with GADD45B to repress p38 MAPK signaling and elicit hepatocyte proliferation in male mice.Implications: This GADD45B-regulated male-predominant proliferation can be expanded as a phenobarbital promotion signal of HCC development in future studies.Visual Overview: http://mcr.aacrjournals.org/content/molcanres/16/8/1309/F1.large.jpg Mol Cancer Res; 16(8); 1309-18.	Phenobarbital	236-249	nuclear receptor subfamily 1, group I, member 3	Mus musculus	41-44
29417440-5	2018	Phenobarbital also reduced expression of neuronal markers (doublecortin (DCX), calretinin, NeuN), neuronal transcription factors (Pax6, Sox2, Tbr1/2, Prox1), and neurotrophins (NGF, BDNF, NT-3) up to 24 h after the last administration.	Phenobarbital	0-13	prospero homeobox 1	Homo sapiens	150-155
29716964-7	2018	Thus, these data reveal nuclear receptor CAR interacts with GADD45B to repress p38 MAPK signaling and elicit hepatocyte proliferation in male mice.Implications: This GADD45B-regulated male-predominant proliferation can be expanded as a phenobarbital promotion signal of HCC development in future studies.Visual Overview: http://mcr.aacrjournals.org/content/molcanres/16/8/1309/F1.large.jpg Mol Cancer Res; 16(8); 1309-18.	Phenobarbital	236-249	growth arrest and DNA-damage-inducible 45 beta	Mus musculus	60-67
29417440-5	2018	Phenobarbital also reduced expression of neuronal markers (doublecortin (DCX), calretinin, NeuN), neuronal transcription factors (Pax6, Sox2, Tbr1/2, Prox1), and neurotrophins (NGF, BDNF, NT-3) up to 24 h after the last administration.	Phenobarbital	0-13	nerve growth factor	Homo sapiens	177-180
29716964-7	2018	Thus, these data reveal nuclear receptor CAR interacts with GADD45B to repress p38 MAPK signaling and elicit hepatocyte proliferation in male mice.Implications: This GADD45B-regulated male-predominant proliferation can be expanded as a phenobarbital promotion signal of HCC development in future studies.Visual Overview: http://mcr.aacrjournals.org/content/molcanres/16/8/1309/F1.large.jpg Mol Cancer Res; 16(8); 1309-18.	Phenobarbital	236-249	growth arrest and DNA-damage-inducible 45 beta	Mus musculus	166-173
29417440-5	2018	Phenobarbital also reduced expression of neuronal markers (doublecortin (DCX), calretinin, NeuN), neuronal transcription factors (Pax6, Sox2, Tbr1/2, Prox1), and neurotrophins (NGF, BDNF, NT-3) up to 24 h after the last administration.	Phenobarbital	0-13	brain derived neurotrophic factor	Homo sapiens	182-186
29417440-7	2018	In contrast, caffeine alone reduced proliferative capacity and expression of the neuronal markers DCX and NeuN at 6 h, but increased expression of neurotrophins and neuronal transcription factors at 6 and 12 h. These results indicate that administration of phenobarbital during the vulnerable phase of brain development negatively interferes with neuronal development, which can be prevented in part by co-administration of caffeine.	Phenobarbital	257-270	doublecortin	Homo sapiens	98-101
29417440-7	2018	In contrast, caffeine alone reduced proliferative capacity and expression of the neuronal markers DCX and NeuN at 6 h, but increased expression of neurotrophins and neuronal transcription factors at 6 and 12 h. These results indicate that administration of phenobarbital during the vulnerable phase of brain development negatively interferes with neuronal development, which can be prevented in part by co-administration of caffeine.	Phenobarbital	257-270	RNA binding fox-1 homolog 3	Homo sapiens	106-110
29548889-2	2018	In this study the hepatic and thyroid gland effects of the constitutive androstane receptor (CAR) activator sodium phenobarbital (NaPB) were examined in male Sprague-Dawley wild type (WT) rats and in CAR knockout (CAR KO) rats and the effects of the pregnane X receptor (PXR) activator pregnenolone-16alpha-carbonitrile (PCN) were examined in WT and PXR knockout (PXR KO) rats.	Phenobarbital	108-128	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	93-96
29108398-10	2018	Results also showed that the administration of p75 antagonist alone or in combination with phenobarbital was able to significantly influence the behavioral responses.	Phenobarbital	91-104	nerve growth factor receptor	Rattus norvegicus	47-50
29898739-13	2018	RESULTS: Abluminal CX3CL1 production increased in 12-month-old AD BBB while CX3CL1 levels decreased in luminal lysates.	Phenobarbital	11-18	chemokine (C-X3-C motif) ligand 1	Mus musculus	19-25
29898739-14	2018	CCL3 in luminal compartment increased with aging and was significantly different compared to AD BBB at 12 months.	Phenobarbital	8-15	chemokine (C-C motif) ligand 3	Mus musculus	0-4
29649093-2	2018	The aim of this study was to estimate CYP3A4-inductive potency of EIAEDs by comparing CYP3A4 activity in patients treated with carbamazepine, phenobarbital, or phenytoin.	Phenobarbital	142-155	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	38-44
29649093-2	2018	The aim of this study was to estimate CYP3A4-inductive potency of EIAEDs by comparing CYP3A4 activity in patients treated with carbamazepine, phenobarbital, or phenytoin.	Phenobarbital	142-155	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	86-92
29649093-10	2018	CONCLUSIONS: This study shows that phenytoin and carbamazepine have approximately twice the CYP3A4-inducing potency of phenobarbital.	Phenobarbital	119-132	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	92-98
29649093-11	2018	The results indicate that 2-fold higher doses of CYP3A4-metabolized drugs may generally be required during concurrent treatment with phenytoin or carbamazepine compared with phenobarbital.	Phenobarbital	174-187	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	49-55
29548889-2	2018	In this study the hepatic and thyroid gland effects of the constitutive androstane receptor (CAR) activator sodium phenobarbital (NaPB) were examined in male Sprague-Dawley wild type (WT) rats and in CAR knockout (CAR KO) rats and the effects of the pregnane X receptor (PXR) activator pregnenolone-16alpha-carbonitrile (PCN) were examined in WT and PXR knockout (PXR KO) rats.	Phenobarbital	108-128	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	59-91
29548889-2	2018	In this study the hepatic and thyroid gland effects of the constitutive androstane receptor (CAR) activator sodium phenobarbital (NaPB) were examined in male Sprague-Dawley wild type (WT) rats and in CAR knockout (CAR KO) rats and the effects of the pregnane X receptor (PXR) activator pregnenolone-16alpha-carbonitrile (PCN) were examined in WT and PXR knockout (PXR KO) rats.	Phenobarbital	108-128	NSF attachment protein beta	Rattus norvegicus	130-134
29559914-6	2018	The clinical significance of alteration in P-GP function and expression was investigated by determining the distribution of the P-GP substrate phenobarbital (60 mg/kg, intravenous administration) in the brain and loss of righting reflex (LORR) induced by the drug (100 mg/kg).	Phenobarbital	143-156	phosphoglycolate phosphatase	Mus musculus	43-47
29704007-3	2018	Here we investigated the potential role of multidrug and toxin extrusion protein 1 (MATE1) for translocation of TMAO across the luminal membrane of proximal tubular cells.	Phenobarbital	128-135	solute carrier family 47 member 1	Canis lupus familiaris	43-82
29704007-3	2018	Here we investigated the potential role of multidrug and toxin extrusion protein 1 (MATE1) for translocation of TMAO across the luminal membrane of proximal tubular cells.	Phenobarbital	128-135	solute carrier family 47 member 1	Canis lupus familiaris	84-89
29550976-7	2018	In addition, the cocktail assay was applied for the determination of pharmacokinetic parameters against phenobarbital as a selective CYP2B inducer and ketoconazole as a strong CYP3A inhibitor.	Phenobarbital	104-117	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	133-138
29469947-6	2018	The inducers omeprazole, phenobarbital and rifampicin increased the levels of CYP1A2, 2B6 and 3A4 mRNAs by 110-fold, 12.5-fold and 5.4-fold, respectively, at day 2, compared with control human hepatocytes.	Phenobarbital	25-38	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	78-84
30090615-2	2018	Studies with the model CAR activator phenobarbital (PB) and its sodium salt (sodium phenobarbital; NaPB) have demonstrated that the key and associative events for rat and mouse liver tumour formation include CAR activation, increased hepatocyte replicative DNA synthesis (RDS), induction of cytochrome P450 CYP2B subfamily enzymes, liver hypertrophy, increased altered hepatic foci and hepatocellular adenomas/carcinomas.	Phenobarbital	37-50	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	23-26
30090615-2	2018	Studies with the model CAR activator phenobarbital (PB) and its sodium salt (sodium phenobarbital; NaPB) have demonstrated that the key and associative events for rat and mouse liver tumour formation include CAR activation, increased hepatocyte replicative DNA synthesis (RDS), induction of cytochrome P450 CYP2B subfamily enzymes, liver hypertrophy, increased altered hepatic foci and hepatocellular adenomas/carcinomas.	Phenobarbital	37-50	NSF attachment protein beta	Rattus norvegicus	99-103
30090615-2	2018	Studies with the model CAR activator phenobarbital (PB) and its sodium salt (sodium phenobarbital; NaPB) have demonstrated that the key and associative events for rat and mouse liver tumour formation include CAR activation, increased hepatocyte replicative DNA synthesis (RDS), induction of cytochrome P450 CYP2B subfamily enzymes, liver hypertrophy, increased altered hepatic foci and hepatocellular adenomas/carcinomas.	Phenobarbital	37-50	nuclear receptor subfamily 1, group I, member 3	Mus musculus	208-211
30090615-2	2018	Studies with the model CAR activator phenobarbital (PB) and its sodium salt (sodium phenobarbital; NaPB) have demonstrated that the key and associative events for rat and mouse liver tumour formation include CAR activation, increased hepatocyte replicative DNA synthesis (RDS), induction of cytochrome P450 CYP2B subfamily enzymes, liver hypertrophy, increased altered hepatic foci and hepatocellular adenomas/carcinomas.	Phenobarbital	52-54	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	23-26
30090615-2	2018	Studies with the model CAR activator phenobarbital (PB) and its sodium salt (sodium phenobarbital; NaPB) have demonstrated that the key and associative events for rat and mouse liver tumour formation include CAR activation, increased hepatocyte replicative DNA synthesis (RDS), induction of cytochrome P450 CYP2B subfamily enzymes, liver hypertrophy, increased altered hepatic foci and hepatocellular adenomas/carcinomas.	Phenobarbital	52-54	NSF attachment protein beta	Rattus norvegicus	99-103
30090615-2	2018	Studies with the model CAR activator phenobarbital (PB) and its sodium salt (sodium phenobarbital; NaPB) have demonstrated that the key and associative events for rat and mouse liver tumour formation include CAR activation, increased hepatocyte replicative DNA synthesis (RDS), induction of cytochrome P450 CYP2B subfamily enzymes, liver hypertrophy, increased altered hepatic foci and hepatocellular adenomas/carcinomas.	Phenobarbital	52-54	nuclear receptor subfamily 1, group I, member 3	Mus musculus	208-211
30090615-2	2018	Studies with the model CAR activator phenobarbital (PB) and its sodium salt (sodium phenobarbital; NaPB) have demonstrated that the key and associative events for rat and mouse liver tumour formation include CAR activation, increased hepatocyte replicative DNA synthesis (RDS), induction of cytochrome P450 CYP2B subfamily enzymes, liver hypertrophy, increased altered hepatic foci and hepatocellular adenomas/carcinomas.	Phenobarbital	77-97	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	23-26
30090615-2	2018	Studies with the model CAR activator phenobarbital (PB) and its sodium salt (sodium phenobarbital; NaPB) have demonstrated that the key and associative events for rat and mouse liver tumour formation include CAR activation, increased hepatocyte replicative DNA synthesis (RDS), induction of cytochrome P450 CYP2B subfamily enzymes, liver hypertrophy, increased altered hepatic foci and hepatocellular adenomas/carcinomas.	Phenobarbital	77-97	NSF attachment protein beta	Rattus norvegicus	99-103
30090615-2	2018	Studies with the model CAR activator phenobarbital (PB) and its sodium salt (sodium phenobarbital; NaPB) have demonstrated that the key and associative events for rat and mouse liver tumour formation include CAR activation, increased hepatocyte replicative DNA synthesis (RDS), induction of cytochrome P450 CYP2B subfamily enzymes, liver hypertrophy, increased altered hepatic foci and hepatocellular adenomas/carcinomas.	Phenobarbital	77-97	nuclear receptor subfamily 1, group I, member 3	Mus musculus	208-211
29559914-6	2018	The clinical significance of alteration in P-GP function and expression was investigated by determining the distribution of the P-GP substrate phenobarbital (60 mg/kg, intravenous administration) in the brain and loss of righting reflex (LORR) induced by the drug (100 mg/kg).	Phenobarbital	143-156	phosphoglycolate phosphatase	Mus musculus	128-132
29559914-12	2018	The attenuated function and expression of P-GP at the BBB might enhance phenobarbital distribution in the brain and increase phenobarbital efficacy on the CNS of ALF mice.	Phenobarbital	72-85	phosphoglycolate phosphatase	Mus musculus	42-46
29559914-12	2018	The attenuated function and expression of P-GP at the BBB might enhance phenobarbital distribution in the brain and increase phenobarbital efficacy on the CNS of ALF mice.	Phenobarbital	125-138	phosphoglycolate phosphatase	Mus musculus	42-46
29315524-0	2018	Neonatal phenobarbital exposure disrupts GABAergic synaptic maturation in rat CA1 neurons.	Phenobarbital	9-22	carbonic anhydrase 1	Rattus norvegicus	78-81
29270806-11	2018	MC from PB-treated rats produced and secreted enhanced levels of HBEGF and GDF15, factors found to suppress apoptosis and/or induce DNA synthesis in cultured HC and HCPREN.	Phenobarbital	8-10	heparin-binding EGF-like growth factor	Rattus norvegicus	65-70
29270806-11	2018	MC from PB-treated rats produced and secreted enhanced levels of HBEGF and GDF15, factors found to suppress apoptosis and/or induce DNA synthesis in cultured HC and HCPREN.	Phenobarbital	8-10	growth differentiation factor 15	Rattus norvegicus	75-80
29285606-9	2018	Regarding phase II metabolism, UGT2B7, 1A8 and 1A3 showed highest activity in glucuronidation of tamoxifen bisphenol and metabolite E. Anti-estrogenic metabolites (Z)-4-hydroxytamoxifen, (Z)-endoxifen and (Z)-norendoxifen inhibited the activity of CYP2C enzymes while tamoxifen bisphenol consistently induced CYPs similar to rifampicin and phenobarbital.	Phenobarbital	340-353	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	31-37
29269410-2	2018	Recently, it has been shown that in mouse hepatocytes, epidermal growth factor receptor (EGFR) plays a crucial role in the activation of the xenosensor constitutive androstane receptor (CAR) by the antiepileptic drug phenobarbital.	Phenobarbital	217-230	epidermal growth factor receptor	Mus musculus	55-87
29269410-2	2018	Recently, it has been shown that in mouse hepatocytes, epidermal growth factor receptor (EGFR) plays a crucial role in the activation of the xenosensor constitutive androstane receptor (CAR) by the antiepileptic drug phenobarbital.	Phenobarbital	217-230	epidermal growth factor receptor	Mus musculus	89-93
29269410-2	2018	Recently, it has been shown that in mouse hepatocytes, epidermal growth factor receptor (EGFR) plays a crucial role in the activation of the xenosensor constitutive androstane receptor (CAR) by the antiepileptic drug phenobarbital.	Phenobarbital	217-230	nuclear receptor subfamily 1, group I, member 3	Mus musculus	152-184
29269410-2	2018	Recently, it has been shown that in mouse hepatocytes, epidermal growth factor receptor (EGFR) plays a crucial role in the activation of the xenosensor constitutive androstane receptor (CAR) by the antiepileptic drug phenobarbital.	Phenobarbital	217-230	nuclear receptor subfamily 1, group I, member 3	Mus musculus	186-189
29269410-8	2018	Among these genes, only 15 were regulated by CITCO and one by phenobarbital in a CAR-dependent manner.	Phenobarbital	62-75	nuclear receptor subfamily 1 group I member 3	Homo sapiens	81-84
29269410-9	2018	Conversely, in the presence of EGF, CITCO and phenobarbital modulated gene expression only in a CAR-independent and PXR-dependent manner.	Phenobarbital	46-59	nuclear receptor subfamily 1 group I member 3	Homo sapiens	96-99
29269410-9	2018	Conversely, in the presence of EGF, CITCO and phenobarbital modulated gene expression only in a CAR-independent and PXR-dependent manner.	Phenobarbital	46-59	nuclear receptor subfamily 1 group I member 2	Homo sapiens	116-119
29425889-1	2018	Phenobarbital (PB), a constitutive androstane receptor (CAR) activator, produces liver tumours in rodents by a mitogenic mode of action involving CAR activation.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	22-54
29425889-1	2018	Phenobarbital (PB), a constitutive androstane receptor (CAR) activator, produces liver tumours in rodents by a mitogenic mode of action involving CAR activation.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	56-59
29425889-1	2018	Phenobarbital (PB), a constitutive androstane receptor (CAR) activator, produces liver tumours in rodents by a mitogenic mode of action involving CAR activation.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	146-149
29425889-1	2018	Phenobarbital (PB), a constitutive androstane receptor (CAR) activator, produces liver tumours in rodents by a mitogenic mode of action involving CAR activation.	Phenobarbital	15-17	nuclear receptor subfamily 1, group I, member 3	Mus musculus	22-54
29425889-1	2018	Phenobarbital (PB), a constitutive androstane receptor (CAR) activator, produces liver tumours in rodents by a mitogenic mode of action involving CAR activation.	Phenobarbital	15-17	nuclear receptor subfamily 1, group I, member 3	Mus musculus	56-59
29425889-1	2018	Phenobarbital (PB), a constitutive androstane receptor (CAR) activator, produces liver tumours in rodents by a mitogenic mode of action involving CAR activation.	Phenobarbital	15-17	nuclear receptor subfamily 1, group I, member 3	Mus musculus	146-149
29425889-2	2018	In this study, the hepatic effects of sodium phenobarbital (NaPB) were compared in male C57BL/6J wild type (WT) mice and in humanized mice, where both the mouse CAR and pregnane X receptor (PXR) have been replaced by their human counterparts (hCAR/hPXR mice).	Phenobarbital	38-58	N-ethylmaleimide sensitive fusion protein attachment protein beta	Mus musculus	60-64
29315524-8	2018	RESULTS: At P14 we found an increase in miniature inhibitory postsynaptic current (mIPSC) frequency in the phenobarbital-exposed as compared to the saline-exposed group.	Phenobarbital	107-120	SUB1 regulator of transcription	Rattus norvegicus	12-15
29095046-5	2018	METHODS: The interactions between phenobarbital and human serum albumin (HSA) and the effects of different alcohol concentrations on the binding behaviors of the phenobarbital-HSA system were investigated by molecular docking and spectroscopic methods, including fluorescence spectroscopy and UV-visible absorption spectroscopy.	Phenobarbital	34-47	albumin	Homo sapiens	58-71
29301444-4	2018	Another chemically diverse group of xenobiotics including phenobarbital, DDT, can activate the nuclear receptor CAR and in some cases estrogen receptors ESR1 and ESR2.	Phenobarbital	58-71	CXADR pseudogene 1	Homo sapiens	112-115
29301444-4	2018	Another chemically diverse group of xenobiotics including phenobarbital, DDT, can activate the nuclear receptor CAR and in some cases estrogen receptors ESR1 and ESR2.	Phenobarbital	58-71	estrogen receptor 1	Homo sapiens	153-157
29301444-4	2018	Another chemically diverse group of xenobiotics including phenobarbital, DDT, can activate the nuclear receptor CAR and in some cases estrogen receptors ESR1 and ESR2.	Phenobarbital	58-71	estrogen receptor 2	Homo sapiens	162-166
30141584-0	2018	Hypomethylation of the c-myc promoter region induced by phenobarbital in rat liver Background: The changes in DNA methylation are considered as one of the early events in hepatocarcinogenesis.	Phenobarbital	56-69	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	23-28
29357810-5	2018	mRNA expression levels and enzyme activities of CYP1A2, CYP2B6, and CYP3A in HepaRG cells treated with prototypical inducers of each CYP isoform [omeprazole (OME) for CYP1A2, phenobarbital (PB) for CYP2B6, and rifampicin (RIF) for CYP3A] were evaluated.	Phenobarbital	175-188	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	48-54
29357810-5	2018	mRNA expression levels and enzyme activities of CYP1A2, CYP2B6, and CYP3A in HepaRG cells treated with prototypical inducers of each CYP isoform [omeprazole (OME) for CYP1A2, phenobarbital (PB) for CYP2B6, and rifampicin (RIF) for CYP3A] were evaluated.	Phenobarbital	175-188	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	68-73
29357810-5	2018	mRNA expression levels and enzyme activities of CYP1A2, CYP2B6, and CYP3A in HepaRG cells treated with prototypical inducers of each CYP isoform [omeprazole (OME) for CYP1A2, phenobarbital (PB) for CYP2B6, and rifampicin (RIF) for CYP3A] were evaluated.	Phenobarbital	175-188	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	48-51
29357810-5	2018	mRNA expression levels and enzyme activities of CYP1A2, CYP2B6, and CYP3A in HepaRG cells treated with prototypical inducers of each CYP isoform [omeprazole (OME) for CYP1A2, phenobarbital (PB) for CYP2B6, and rifampicin (RIF) for CYP3A] were evaluated.	Phenobarbital	190-192	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	48-54
29357810-5	2018	mRNA expression levels and enzyme activities of CYP1A2, CYP2B6, and CYP3A in HepaRG cells treated with prototypical inducers of each CYP isoform [omeprazole (OME) for CYP1A2, phenobarbital (PB) for CYP2B6, and rifampicin (RIF) for CYP3A] were evaluated.	Phenobarbital	190-192	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	68-73
29357810-5	2018	mRNA expression levels and enzyme activities of CYP1A2, CYP2B6, and CYP3A in HepaRG cells treated with prototypical inducers of each CYP isoform [omeprazole (OME) for CYP1A2, phenobarbital (PB) for CYP2B6, and rifampicin (RIF) for CYP3A] were evaluated.	Phenobarbital	190-192	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	48-51
29357810-6	2018	RESULTS: Although the activities of CYP2B6 and CYP3A were induced by treatment with PB and RIF, we found that the activity of phenacetin O-deethylase (PHOD), which is known as a marker of the activity of CYP1A2, was also enhanced by treatment with these non-CYP1A2 inducers in HepaRG cells.	Phenobarbital	84-86	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	36-42
29357810-6	2018	RESULTS: Although the activities of CYP2B6 and CYP3A were induced by treatment with PB and RIF, we found that the activity of phenacetin O-deethylase (PHOD), which is known as a marker of the activity of CYP1A2, was also enhanced by treatment with these non-CYP1A2 inducers in HepaRG cells.	Phenobarbital	84-86	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	47-52
30141584-1	2018	Objective: We evaluated the ability of phenobarbital (PB) - the most widely used anticonvulsant worldwide and classical rodent liver carcinogen - to cause the promoter region of the c-myc protooncogene hypomethylation as well as changes of mRNA level of this gene.	Phenobarbital	39-52	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	182-187
30141584-1	2018	Objective: We evaluated the ability of phenobarbital (PB) - the most widely used anticonvulsant worldwide and classical rodent liver carcinogen - to cause the promoter region of the c-myc protooncogene hypomethylation as well as changes of mRNA level of this gene.	Phenobarbital	54-56	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	182-187
30141584-7	2018	Results: The study showed that phenobarbital stimulated persistent changes in DNA methylation, i.e. loss of methylation inthe promoter region of the c-myc gene and up-regulated its mRNA level.	Phenobarbital	31-44	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	149-154
30141584-10	2018	The c-myc over-expression by demethylation might represent an important, early events in the mechanism of action (MOA) of phenobarbital.	Phenobarbital	122-135	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	4-9
29133892-3	2017	Here, using proteomic and FRET analyses, we demonstrate that the ER protein membralin is an ERAD component, which mediates degradation of ER luminal and membrane substrates.	Phenobarbital	141-148	transmembrane protein 259	Mus musculus	76-85
29095046-0	2018	Molecular spectroscopic studies examining the interactions between phenobarbital and human serum albumin in alcohol consumption.	Phenobarbital	67-80	albumin	Homo sapiens	91-104
28776218-3	2017	Relative mRNA quantification using Taqman real-time PCR assay demonstrated higher expression of IL-1beta, TNF-alpha and iNOS, and lower expression of Nrf2 in methamphetamine intoxication and hyperthermia cases, higher expression of iNOS in phenobarbital intoxication cases, and higher expression of Nrf2 in phenobarbital intoxication and hypothermia cases.	Phenobarbital	240-253	NFE2 like bZIP transcription factor 2	Homo sapiens	150-154
28776218-3	2017	Relative mRNA quantification using Taqman real-time PCR assay demonstrated higher expression of IL-1beta, TNF-alpha and iNOS, and lower expression of Nrf2 in methamphetamine intoxication and hyperthermia cases, higher expression of iNOS in phenobarbital intoxication cases, and higher expression of Nrf2 in phenobarbital intoxication and hypothermia cases.	Phenobarbital	307-320	NFE2 like bZIP transcription factor 2	Homo sapiens	150-154
28856745-5	2017	RESULTS: A total of 10 publications were identified in which a CYP450 enzyme inducer was utilized intentionally to enhance CNI clearance in the setting of supratherapeutic concentrations; 7 case reports describe the use of phenytoin and 3 case reports describe the use of phenobarbital.	Phenobarbital	272-285	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	63-69
28821216-0	2017	Successful Treatment With Phenobarbital Following Lactase Supplementation in an Infant With Lactose Intolerance.	Phenobarbital	26-39	lactase	Homo sapiens	50-57
28495587-5	2017	Exposure to PB or CF resulted in dose-dependent increases in relative liver weights, hepatocellular hypertrophy and proliferation, and increases in Cyp2b1 and Cyp4a1 transcripts.	Phenobarbital	12-14	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	148-154
28495587-5	2017	Exposure to PB or CF resulted in dose-dependent increases in relative liver weights, hepatocellular hypertrophy and proliferation, and increases in Cyp2b1 and Cyp4a1 transcripts.	Phenobarbital	12-14	cytochrome P450, family 4, subfamily a, polypeptide 1	Rattus norvegicus	159-165
28643232-7	2017	Co-treatment with caffeine significantly decreased these upregulations at all time points investigated, while caffeine without phenobarbital resulted in increased expression of TNFalpha, IL-1beta, and IL-18, but not IFNgamma at 6 h. Downregulation of the adenosine A1 and A2a receptors, both of which bind caffeine, by 24 h of phenobarbital exposure was partly antagonized by caffeine.	Phenobarbital	327-340	tumor necrosis factor	Rattus norvegicus	177-185
28643232-6	2017	RNA expression of the pro-inflammatory cytokines TNFalpha, IFNgamma, and IL-1beta, but not IL-18, was upregulated by phenobarbital.	Phenobarbital	117-130	tumor necrosis factor	Rattus norvegicus	49-57
29054049-6	2017	Concomitant use of CYP inhibitors (e.g. paroxetine, fluoxetine and bupropion) or inducers (e.g. carbamazepine, phenobarbital and phenytoin) could counteract the clinical effect or trigger side effects of analgesics in the same manner as genetically determined differences in CYP2D6-mediated metabolism of many opioids.	Phenobarbital	111-124	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	275-281
28643232-6	2017	RNA expression of the pro-inflammatory cytokines TNFalpha, IFNgamma, and IL-1beta, but not IL-18, was upregulated by phenobarbital.	Phenobarbital	117-130	interleukin 18	Rattus norvegicus	59-67
28643232-6	2017	RNA expression of the pro-inflammatory cytokines TNFalpha, IFNgamma, and IL-1beta, but not IL-18, was upregulated by phenobarbital.	Phenobarbital	117-130	interleukin 1 beta	Rattus norvegicus	73-81
28873066-4	2017	This study"s objective was to determine the relationship between the maximum rate of metabolism of phenytoin (Vmax) and phenobarbital clearance (CLPB), which can serve as a guide to individualized drug therapy.	Phenobarbital	120-133	caseinolytic mitochondrial matrix peptidase chaperone subunit B	Homo sapiens	145-149
28873066-10	2017	CONCLUSIONS: Regression equations were established for estimating Vmax from CLPB, and vice versa in patients treated with combination of phenytoin and phenobarbital.	Phenobarbital	151-164	caseinolytic mitochondrial matrix peptidase chaperone subunit B	Homo sapiens	76-80
27458090-4	2017	Since phenobarbital indirectly activates Constitutive Androstane Receptor (CAR) by antagonizing growth factor binding to the epidermal growth factor receptor (EGFR), we hypothesized that PCBs may also diminish EGFR signaling.	Phenobarbital	6-19	epidermal growth factor receptor	Homo sapiens	125-157
27458090-4	2017	Since phenobarbital indirectly activates Constitutive Androstane Receptor (CAR) by antagonizing growth factor binding to the epidermal growth factor receptor (EGFR), we hypothesized that PCBs may also diminish EGFR signaling.	Phenobarbital	6-19	epidermal growth factor receptor	Homo sapiens	159-163
27458090-4	2017	Since phenobarbital indirectly activates Constitutive Androstane Receptor (CAR) by antagonizing growth factor binding to the epidermal growth factor receptor (EGFR), we hypothesized that PCBs may also diminish EGFR signaling.	Phenobarbital	6-19	epidermal growth factor receptor	Homo sapiens	210-214
30090543-2	2017	PB induces hepatocellular tumors by activating the constitutive androstane receptor (CAR).	Phenobarbital	0-2	nuclear receptor subfamily 1, group I, member 3	Mus musculus	51-83
30090543-2	2017	PB induces hepatocellular tumors by activating the constitutive androstane receptor (CAR).	Phenobarbital	0-2	nuclear receptor subfamily 1, group I, member 3	Mus musculus	85-88
28546505-0	2017	Role of CYP2B in Phenobarbital-Induced Hepatocyte Proliferation in Mice.	Phenobarbital	17-30	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	8-13
28058446-7	2017	Changes in the expression of classic CAR/PXR target genes such as Cyp2b10 were induced by cyproconazole and phenobarbital in both genotypes, while prochloraz treatment resulted in gene expression changes indicative of additional aryl hydrocarbon receptor activation, e.g. by up-regulation of Cyp1a1 expression.	Phenobarbital	108-121	nuclear receptor subfamily 1, group I, member 3	Mus musculus	37-40
28058446-7	2017	Changes in the expression of classic CAR/PXR target genes such as Cyp2b10 were induced by cyproconazole and phenobarbital in both genotypes, while prochloraz treatment resulted in gene expression changes indicative of additional aryl hydrocarbon receptor activation, e.g. by up-regulation of Cyp1a1 expression.	Phenobarbital	108-121	nuclear receptor subfamily 1, group I, member 2	Mus musculus	41-44
28058446-7	2017	Changes in the expression of classic CAR/PXR target genes such as Cyp2b10 were induced by cyproconazole and phenobarbital in both genotypes, while prochloraz treatment resulted in gene expression changes indicative of additional aryl hydrocarbon receptor activation, e.g. by up-regulation of Cyp1a1 expression.	Phenobarbital	108-121	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	66-73
28058446-7	2017	Changes in the expression of classic CAR/PXR target genes such as Cyp2b10 were induced by cyproconazole and phenobarbital in both genotypes, while prochloraz treatment resulted in gene expression changes indicative of additional aryl hydrocarbon receptor activation, e.g. by up-regulation of Cyp1a1 expression.	Phenobarbital	108-121	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	292-298
28546505-9	2017	These results indicate that CYP2B induction plays a significant, but partial, role in PB-induced hepatocyte proliferation in male mice.	Phenobarbital	86-88	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	28-33
28546505-1	2017	Phenobarbital (PB) promotes liver tumorigenesis in rodents, in part through activation of the constitutive androstane receptor (CAR) and the consequent changes in hepatic gene expression and increases in hepatocyte proliferation.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	94-126
28546505-1	2017	Phenobarbital (PB) promotes liver tumorigenesis in rodents, in part through activation of the constitutive androstane receptor (CAR) and the consequent changes in hepatic gene expression and increases in hepatocyte proliferation.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	128-131
28546505-1	2017	Phenobarbital (PB) promotes liver tumorigenesis in rodents, in part through activation of the constitutive androstane receptor (CAR) and the consequent changes in hepatic gene expression and increases in hepatocyte proliferation.	Phenobarbital	15-17	nuclear receptor subfamily 1, group I, member 3	Mus musculus	94-126
28546505-1	2017	Phenobarbital (PB) promotes liver tumorigenesis in rodents, in part through activation of the constitutive androstane receptor (CAR) and the consequent changes in hepatic gene expression and increases in hepatocyte proliferation.	Phenobarbital	15-17	nuclear receptor subfamily 1, group I, member 3	Mus musculus	128-131
28546505-2	2017	A typical effect of CAR activation by PB is a marked induction of Cyp2b10 expression in the liver; the latter has been suspected to be vital for PB-induced hepatocellular proliferation.	Phenobarbital	38-40	nuclear receptor subfamily 1, group I, member 3	Mus musculus	20-23
28546505-2	2017	A typical effect of CAR activation by PB is a marked induction of Cyp2b10 expression in the liver; the latter has been suspected to be vital for PB-induced hepatocellular proliferation.	Phenobarbital	38-40	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	66-73
28546505-2	2017	A typical effect of CAR activation by PB is a marked induction of Cyp2b10 expression in the liver; the latter has been suspected to be vital for PB-induced hepatocellular proliferation.	Phenobarbital	145-147	nuclear receptor subfamily 1, group I, member 3	Mus musculus	20-23
28546505-2	2017	A typical effect of CAR activation by PB is a marked induction of Cyp2b10 expression in the liver; the latter has been suspected to be vital for PB-induced hepatocellular proliferation.	Phenobarbital	145-147	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	66-73
28546505-5	2017	The liver-to-body weight ratio, an indicator of liver hypertrophy, was increased by 47% in male WT mice, but by only 22% in male Cyp2a(4/5)bgs-null mice, by the PB treatment.	Phenobarbital	161-163	cytochrome P450, family 2, subfamily a	Mus musculus	129-134
28218408-5	2017	In this study CAR-responsive genes Cyp3a11 and Cyp2b10 were induced in the liver of C57BL/6 (wild-type) mice by toxaphene (30-570-fold) (at the carcinogenic dose 320 ppm) and phenobarbital (positive control) (16-420-fold) following 14 days" dietary treatment.	Phenobarbital	175-188	nuclear receptor subfamily 1, group I, member 3	Mus musculus	14-17
28218408-5	2017	In this study CAR-responsive genes Cyp3a11 and Cyp2b10 were induced in the liver of C57BL/6 (wild-type) mice by toxaphene (30-570-fold) (at the carcinogenic dose 320 ppm) and phenobarbital (positive control) (16-420-fold) following 14 days" dietary treatment.	Phenobarbital	175-188	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	35-42
28218408-5	2017	In this study CAR-responsive genes Cyp3a11 and Cyp2b10 were induced in the liver of C57BL/6 (wild-type) mice by toxaphene (30-570-fold) (at the carcinogenic dose 320 ppm) and phenobarbital (positive control) (16-420-fold) following 14 days" dietary treatment.	Phenobarbital	175-188	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	47-54
28541575-3	2017	We previously demonstrated Constitutive Androstane Receptor (CAR) and WNT signaling-dependent up-regulation of the pluripotency associated Dlk1-Dio3 imprinted gene cluster noncoding RNAs (ncRNAs) in the liver of mice treated with tumor-promoting doses of phenobarbital (PB).	Phenobarbital	255-268	nuclear receptor subfamily 1, group I, member 3	Mus musculus	27-59
28520973-3	2017	To elucidate the MOA for rat hepatocellular tumor formation by momfluorothrin, this study was conducted to examine effects on key and associative events of the CAR-mediated MOA for phenobarbital based on the International Programme on Chemical Safety framework.	Phenobarbital	181-194	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	160-163
28520973-9	2017	A global gene expression profile analysis of the liver of male Wistar rats treated with momfluorothrin for 2 weeks also showed similarity to the prototypic CAR activator phenobarbital.	Phenobarbital	170-183	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	156-159
28541575-3	2017	We previously demonstrated Constitutive Androstane Receptor (CAR) and WNT signaling-dependent up-regulation of the pluripotency associated Dlk1-Dio3 imprinted gene cluster noncoding RNAs (ncRNAs) in the liver of mice treated with tumor-promoting doses of phenobarbital (PB).	Phenobarbital	255-268	nuclear receptor subfamily 1, group I, member 3	Mus musculus	61-64
28541575-3	2017	We previously demonstrated Constitutive Androstane Receptor (CAR) and WNT signaling-dependent up-regulation of the pluripotency associated Dlk1-Dio3 imprinted gene cluster noncoding RNAs (ncRNAs) in the liver of mice treated with tumor-promoting doses of phenobarbital (PB).	Phenobarbital	255-268	delta like non-canonical Notch ligand 1	Mus musculus	139-143
28541575-3	2017	We previously demonstrated Constitutive Androstane Receptor (CAR) and WNT signaling-dependent up-regulation of the pluripotency associated Dlk1-Dio3 imprinted gene cluster noncoding RNAs (ncRNAs) in the liver of mice treated with tumor-promoting doses of phenobarbital (PB).	Phenobarbital	255-268	deiodinase, iodothyronine type III	Mus musculus	144-148
28541575-3	2017	We previously demonstrated Constitutive Androstane Receptor (CAR) and WNT signaling-dependent up-regulation of the pluripotency associated Dlk1-Dio3 imprinted gene cluster noncoding RNAs (ncRNAs) in the liver of mice treated with tumor-promoting doses of phenobarbital (PB).	Phenobarbital	270-272	nuclear receptor subfamily 1, group I, member 3	Mus musculus	27-59
28541575-3	2017	We previously demonstrated Constitutive Androstane Receptor (CAR) and WNT signaling-dependent up-regulation of the pluripotency associated Dlk1-Dio3 imprinted gene cluster noncoding RNAs (ncRNAs) in the liver of mice treated with tumor-promoting doses of phenobarbital (PB).	Phenobarbital	270-272	nuclear receptor subfamily 1, group I, member 3	Mus musculus	61-64
28541575-3	2017	We previously demonstrated Constitutive Androstane Receptor (CAR) and WNT signaling-dependent up-regulation of the pluripotency associated Dlk1-Dio3 imprinted gene cluster noncoding RNAs (ncRNAs) in the liver of mice treated with tumor-promoting doses of phenobarbital (PB).	Phenobarbital	270-272	delta like non-canonical Notch ligand 1	Mus musculus	139-143
28541575-3	2017	We previously demonstrated Constitutive Androstane Receptor (CAR) and WNT signaling-dependent up-regulation of the pluripotency associated Dlk1-Dio3 imprinted gene cluster noncoding RNAs (ncRNAs) in the liver of mice treated with tumor-promoting doses of phenobarbital (PB).	Phenobarbital	270-272	deiodinase, iodothyronine type III	Mus musculus	144-148
28977209-9	2017	Antiepileptic drugs (lamotrigine, phenobarbital, and phenytoin) also inhibit aromatase.	Phenobarbital	34-47	cytochrome P450 family 19 subfamily A member 1	Homo sapiens	77-86
28729328-12	2017	The NMA on psychomotor developmental delay (11 cohort studies, 1145 children, 18 treatments) found that valproate (OR 4.16, CrI 2.04 to 8.75) and carbamazepine+phenobarbital+valproate (OR 19.12, CrI 1.49 to 337.50) were associated with significantly greater odds of psychomotor delay compared with control.	Phenobarbital	160-173	EP300 interacting inhibitor of differentiation 1	Homo sapiens	195-200
28977209-10	2017	Concomitant use of phenobarbital or valproate has a synergistic effect on aromatase inhibition.	Phenobarbital	19-32	cytochrome P450 family 19 subfamily A member 1	Homo sapiens	74-83
28414157-6	2017	The pro-inflammatory cytokine interleukin-6, tumor markers, angiogenesis markers, lipid peroxidation and nitric oxide (NO) were significantly increased in DEN/PB-induced rats.	Phenobarbital	159-161	interleukin 6	Rattus norvegicus	30-43
27832320-9	2017	Interestingly, in mouse hepatocytes, pretreatment with the protein phosphatase inhibitor okadaic acid prevented an increase in Cyp2b10 mRNA levels induced by phenobarbital as reported, but not that by PFOA.	Phenobarbital	158-171	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	127-134
28267557-4	2017	In addition, a recovery group and positive control groups for CAR or PPARalpha activation with either phenobarbital or diethylhexyl-phthalate were included in the 14-day study.	Phenobarbital	102-115	peroxisome proliferator activated receptor alpha	Mus musculus	69-78
28580885-8	2017	Our results indicated that beta-catenin mutations were not involved in early-stage hepatocarcinogenesis induced by PROTOX inhibitors in mice, although activation of beta-catenin and CAR is important in PB-induced tumorigenesis.	Phenobarbital	202-204	catenin (cadherin associated protein), beta 1	Mus musculus	165-177
28580885-8	2017	Our results indicated that beta-catenin mutations were not involved in early-stage hepatocarcinogenesis induced by PROTOX inhibitors in mice, although activation of beta-catenin and CAR is important in PB-induced tumorigenesis.	Phenobarbital	202-204	nuclear receptor subfamily 1, group I, member 3	Mus musculus	182-185
28215634-8	2017	We have confirmed that the hepatocyte-like cells prepared by our methods were able to increase gene expression of cytochrome P450 enzymes upon encountering rifampicin, phenobarbital, or omeprazole.	Phenobarbital	168-181	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	114-129
28265001-9	2017	Phenobarbital, which is not a CAR ligand, binds the EGF receptor, reversing the EGF signal to monomerize CAR for its indirect activation.	Phenobarbital	0-13	epidermal growth factor	Mus musculus	52-55
28265001-9	2017	Phenobarbital, which is not a CAR ligand, binds the EGF receptor, reversing the EGF signal to monomerize CAR for its indirect activation.	Phenobarbital	0-13	epidermal growth factor	Mus musculus	80-83
28265001-9	2017	Phenobarbital, which is not a CAR ligand, binds the EGF receptor, reversing the EGF signal to monomerize CAR for its indirect activation.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	105-108
28356313-3	2017	After nearly 50 years of investigation, the molecular target of phenobarbital induction has now been delineated to phosphorylation at threonine 38 of the constitutive androstane receptor (NR1I3), a member of the nuclear receptor superfamily.	Phenobarbital	64-77	nuclear receptor subfamily 1 group I member 3	Homo sapiens	188-193
28218408-7	2017	Cyp3a11 and Cyp2b10 were also induced in PXR-/- mice with toxaphene and phenobarbital but were not changed in treated PXR-/- /CAR-/- mice.	Phenobarbital	72-85	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	0-7
28218408-7	2017	Cyp3a11 and Cyp2b10 were also induced in PXR-/- mice with toxaphene and phenobarbital but were not changed in treated PXR-/- /CAR-/- mice.	Phenobarbital	72-85	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	12-19
28218408-7	2017	Cyp3a11 and Cyp2b10 were also induced in PXR-/- mice with toxaphene and phenobarbital but were not changed in treated PXR-/- /CAR-/- mice.	Phenobarbital	72-85	nuclear receptor subfamily 1, group I, member 2	Mus musculus	41-44
28218408-8	2017	Similarly, induction of liver pentoxyresorufin-O-deethylase (CAR activation) activity by toxaphene and phenobarbital was absent in CAR-/- and PXR-/- /CAR-/- mice treated with phenobarbital or toxaphene.	Phenobarbital	103-116	nuclear receptor subfamily 1, group I, member 3	Mus musculus	61-64
28218408-8	2017	Similarly, induction of liver pentoxyresorufin-O-deethylase (CAR activation) activity by toxaphene and phenobarbital was absent in CAR-/- and PXR-/- /CAR-/- mice treated with phenobarbital or toxaphene.	Phenobarbital	175-188	nuclear receptor subfamily 1, group I, member 3	Mus musculus	61-64
28218408-9	2017	Ethoxyresorufin-O-deethylase (EROD, represents aryl hydrocarbon receptor activation) activity in CAR-/- mice treated with toxaphene or phenobarbital was increased compared with untreated control, but lower overall in activity in comparison to the wild-type mouse.	Phenobarbital	135-148	nuclear receptor subfamily 1, group I, member 3	Mus musculus	97-100
28218408-10	2017	Liver EROD activity was also induced by both phenobarbital and toxaphene in the PXR-/- mice but not in the PXR-/- /CAR-/- mice.	Phenobarbital	45-58	nuclear receptor subfamily 1, group I, member 2	Mus musculus	80-83
28235604-5	2017	Primary cultures of RCMECs were treated with phenobarbital (PB) at various concentrations to induce P-gp overexpression.	Phenobarbital	45-58	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	100-104
28235604-5	2017	Primary cultures of RCMECs were treated with phenobarbital (PB) at various concentrations to induce P-gp overexpression.	Phenobarbital	60-62	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	100-104
28235604-10	2017	The mRNA and protein levels of P-gp increased as the concentration of PB increased, whereas miR-466b-1-3p levels decreased with increasing PB concentrations (P&lt;0.05).	Phenobarbital	70-72	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	31-35
28235604-10	2017	The mRNA and protein levels of P-gp increased as the concentration of PB increased, whereas miR-466b-1-3p levels decreased with increasing PB concentrations (P&lt;0.05).	Phenobarbital	139-141	microRNA mir-466b-1	Rattus norvegicus	92-102
28298240-10	2017	Inductions of Cyp2a5 activity by PYR and PB were accompanied by increases of Cyp2a4/5 mRNA.	Phenobarbital	41-43	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	14-20
28062541-6	2017	Importantly, HepatoCells retain a phenobarbital-responsive nuclear translocation of human constitutive androstane receptor from the cytoplasm, characteristic to primary hepatocytes.	Phenobarbital	34-47	nuclear receptor subfamily 1 group I member 3	Homo sapiens	90-122
27914986-4	2017	Among them, TMEM70 and UBE2E2 showed increased incidences of negative foci in GST-P+ foci by promotion of all examined TAA, beta-naphthoflavone, piperonyl butoxide, fenbendazole and phenobarbital, while HIST1H2AA and SLK did not respond to all promotive treatments.	Phenobarbital	182-195	transmembrane protein 70	Rattus norvegicus	12-18
28825041-4	2017	In the second part, documented effects of acetaminophen, hypolipidemic drugs, phenobarbital and methapyriline on connexin signaling are discussed.	Phenobarbital	78-91	LOC100128922	Homo sapiens	113-121
28118828-10	2017	In cohort C, a mean add-on dose of 1.5 mg/kg BID phenobarbital was sufficient to achieve a clinically meaningful effect.	Phenobarbital	49-62	BH3 interacting domain death agonist	Canis lupus familiaris	45-48
28118828-13	2017	CONCLUSION: A combination treatment of imepitoin and phenobarbital is a useful treatment option for a subpopulation of dogs with drug-resistant epilepsy, a low starting dose with 5 mg/kg BID is recommended.	Phenobarbital	53-66	BH3 interacting domain death agonist	Canis lupus familiaris	187-190
27914986-4	2017	Among them, TMEM70 and UBE2E2 showed increased incidences of negative foci in GST-P+ foci by promotion of all examined TAA, beta-naphthoflavone, piperonyl butoxide, fenbendazole and phenobarbital, while HIST1H2AA and SLK did not respond to all promotive treatments.	Phenobarbital	182-195	ubiquitin-conjugating enzyme E2E 2	Rattus norvegicus	23-29
27914986-4	2017	Among them, TMEM70 and UBE2E2 showed increased incidences of negative foci in GST-P+ foci by promotion of all examined TAA, beta-naphthoflavone, piperonyl butoxide, fenbendazole and phenobarbital, while HIST1H2AA and SLK did not respond to all promotive treatments.	Phenobarbital	182-195	glutathione S-transferase pi 1	Rattus norvegicus	78-83
29219065-10	2017	Furthermore by using both the LBD and full-length receptors, phenobarbital and midostaurin were found to be direct and indirect activators of PXR while human CAR activation by phenobarbital occurs by indirect mechanisms only.	Phenobarbital	61-74	nuclear receptor subfamily 1 group I member 2	Homo sapiens	142-145
27889497-8	2017	Taken together, our observations indicate that borneol is an in vivo inducer of rat hepatic CYP2B with different regulatory mechanism from phenobarbital-like inducers which caused CYP2B induction with CAR activation.	Phenobarbital	139-152	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	201-204
29219065-10	2017	Furthermore by using both the LBD and full-length receptors, phenobarbital and midostaurin were found to be direct and indirect activators of PXR while human CAR activation by phenobarbital occurs by indirect mechanisms only.	Phenobarbital	176-189	nuclear receptor subfamily 1 group I member 3	Homo sapiens	158-161
28785378-4	2017	This was coordinated with PB-induced significant elevation of 8-OHdG formation in DNA and cell proliferation in adjacent liver of Ogg1-/- mice.	Phenobarbital	26-28	8-oxoguanine DNA-glycosylase 1	Mus musculus	130-134
28785378-7	2017	Treatment of Ogg1-/- mice with PB resulted in significant elevation of cell proliferation in the liver.	Phenobarbital	31-33	8-oxoguanine DNA-glycosylase 1	Mus musculus	13-17
28785378-0	2017	Progression of Hepatic Adenoma to Carcinoma in Ogg1 Mutant Mice Induced by Phenobarbital.	Phenobarbital	75-88	8-oxoguanine DNA-glycosylase 1	Mus musculus	47-51
28785378-8	2017	These results indicate that PB induced progression from HCA to HCC in Ogg1-/- mice, due to persistent accumulation of DNA oxidative base modifications and suppression of Nrf2-mediated oxidative stress response, resulting in significant elevation of cell proliferation.	Phenobarbital	28-30	8-oxoguanine DNA-glycosylase 1	Mus musculus	70-74
28785378-1	2017	The carcinogenic potential of phenobarbital (PB) was assessed in a mouse line carrying a mutant Mmh allele of the Mmh/Ogg1 gene encoding the enzyme oxoguanine DNA glycosylase (Ogg1) responsible for the repair of 8-hydroxy-2"-deoxyguanosine (8-OHdG).	Phenobarbital	30-43	8-oxoguanine DNA-glycosylase 1	Mus musculus	176-180
28785378-3	2017	Hepatocellular carcinomas (HCCs) were found in PB-treated Ogg1-/- mice, while Ogg1+/+ animals developed only hepatocellular adenomas (HCAs) at the same rate.	Phenobarbital	47-49	8-oxoguanine DNA-glycosylase 1	Mus musculus	58-62
28785378-8	2017	These results indicate that PB induced progression from HCA to HCC in Ogg1-/- mice, due to persistent accumulation of DNA oxidative base modifications and suppression of Nrf2-mediated oxidative stress response, resulting in significant elevation of cell proliferation.	Phenobarbital	28-30	nuclear factor, erythroid derived 2, like 2	Mus musculus	170-174
27554620-9	2016	RESULTS: The carrier rates of HLA-A*01:01 and HLA-B*13:01 were significantly higher in the phenobarbital-induced SCARs than in the tolerant controls (18.5% vs. 1.85%, p = 0.01, odds ratio [OR] 11.66, 95% confidence interval [CI] 1.21-578.19; 37.04% vs. 11.11%, p = 0.009, OR 4.60, 95%CI 1.29-17.98).	Phenobarbital	91-104	major histocompatibility complex, class I, A	Homo sapiens	30-35
26377854-5	2016	PB, OA, and clofibrate elevated Lpar1 expression and inhibited cell motile activity.	Phenobarbital	0-2	lysophosphatidic acid receptor 1	Rattus norvegicus	32-37
26377854-7	2016	Lpar3 expression and cell motile activity were significantly elevated by the long-term DEN treatment with or without further PB treatment.	Phenobarbital	125-127	lysophosphatidic acid receptor 3	Rattus norvegicus	0-5
26377854-8	2016	In contrast, long-term PB treatment with or without further DEN elevated Lpar1 expression and inhibited cell motility.	Phenobarbital	23-25	lysophosphatidic acid receptor 1	Rattus norvegicus	73-78
27664318-10	2016	MIBK induced hepatic effects are consistent with a phenobarbital-like MOA where the initiating events are activation of the CAR and PXR nuclear receptors and resultant hepatocellular proliferation leading to rodent liver tumors.	Phenobarbital	51-64	nuclear receptor subfamily 1, group I, member 3	Mus musculus	124-127
27664318-10	2016	MIBK induced hepatic effects are consistent with a phenobarbital-like MOA where the initiating events are activation of the CAR and PXR nuclear receptors and resultant hepatocellular proliferation leading to rodent liver tumors.	Phenobarbital	51-64	nuclear receptor subfamily 1, group I, member 2	Mus musculus	132-135
27450623-6	2016	Carbamazepine, levetiracetam, phenobarbital, phenytoin and valproic acid might decrease the effect of NOACs by inducing P-glycoprotein (P-gp) activity.	Phenobarbital	30-43	ATP binding cassette subfamily B member 1	Homo sapiens	120-134
27450623-6	2016	Carbamazepine, levetiracetam, phenobarbital, phenytoin and valproic acid might decrease the effect of NOACs by inducing P-glycoprotein (P-gp) activity.	Phenobarbital	30-43	ATP binding cassette subfamily B member 1	Homo sapiens	136-140
27450623-7	2016	Carbamazepine, oxcarbazepine, phenytoin, phenobarbital and topiramate might decrease the effect of NOACs by inducing CYP3A4 activity.	Phenobarbital	41-54	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	117-123
27554620-9	2016	RESULTS: The carrier rates of HLA-A*01:01 and HLA-B*13:01 were significantly higher in the phenobarbital-induced SCARs than in the tolerant controls (18.5% vs. 1.85%, p = 0.01, odds ratio [OR] 11.66, 95% confidence interval [CI] 1.21-578.19; 37.04% vs. 11.11%, p = 0.009, OR 4.60, 95%CI 1.29-17.98).	Phenobarbital	91-104	major histocompatibility complex, class I, B	Homo sapiens	46-51
27554620-10	2016	There was a trend of a higher carrier rate of HLA-C*06:02 in the phenobarbital-induced SCARs when compared with those in the tolerant controls (29.63% vs. 11.11%, p = 0.059, OR 3.31, 95% CI 0.88-13.31).	Phenobarbital	65-78	major histocompatibility complex, class I, C	Homo sapiens	46-51
27554620-11	2016	In contrast to the phenobarbital-induced SCARs, only the HLA-A*01:01 carrier rate in the phenobarbital-induced MPs was significantly higher than those in the tolerant controls (20% vs. 1.85%, p = 0.017, OR 12.69, 95% CI 1.15-661.62).	Phenobarbital	89-102	major histocompatibility complex, class I, A	Homo sapiens	57-62
27554620-12	2016	SIGNIFICANCE: An association between phenobarbital hypersensitivity and HLA-A*01:01 and HLA-B*13:01 has been demonstrated in Thai children.	Phenobarbital	37-50	major histocompatibility complex, class I, A	Homo sapiens	72-77
27554620-12	2016	SIGNIFICANCE: An association between phenobarbital hypersensitivity and HLA-A*01:01 and HLA-B*13:01 has been demonstrated in Thai children.	Phenobarbital	37-50	major histocompatibility complex, class I, B	Homo sapiens	88-93
27713827-7	2016	Induction of CYP3A4 by PB, artemisinin, and phenytoin was also much reduced in PXR-KO cells, while the response to CITCO was maintained.	Phenobarbital	23-25	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	13-19
27530964-7	2016	Hepatocytes from all three species demonstrated CAR activation in response to the CAR agonists TCPOBOP, CITCO, and phenobarbital based on increased gene expression for Cyp2b isoforms.	Phenobarbital	115-128	nuclear receptor subfamily 1 group I member 3	Homo sapiens	48-51
27530964-7	2016	Hepatocytes from all three species demonstrated CAR activation in response to the CAR agonists TCPOBOP, CITCO, and phenobarbital based on increased gene expression for Cyp2b isoforms.	Phenobarbital	115-128	nuclear receptor subfamily 1 group I member 3	Homo sapiens	82-85
27530964-7	2016	Hepatocytes from all three species demonstrated CAR activation in response to the CAR agonists TCPOBOP, CITCO, and phenobarbital based on increased gene expression for Cyp2b isoforms.	Phenobarbital	115-128	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	168-173
27713827-7	2016	Induction of CYP3A4 by PB, artemisinin, and phenytoin was also much reduced in PXR-KO cells, while the response to CITCO was maintained.	Phenobarbital	23-25	nuclear receptor subfamily 1 group I member 2	Homo sapiens	79-82
27624558-9	2016	Phenobarbital pretreatment was used to induce hepatic Cyp3a and SLCO1B1 in rats.	Phenobarbital	0-13	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	54-59
27624558-9	2016	Phenobarbital pretreatment was used to induce hepatic Cyp3a and SLCO1B1 in rats.	Phenobarbital	0-13	solute carrier organic anion transporter family member 1B1	Homo sapiens	64-71
27235746-8	2016	In vitro co-application of an ineffective pattern of LFS (100 pulses at afterdischarge threshold intensity) and a sub-threshold dose of phenobarbital (100muM) which had no significant effect on GABAergic currents alone, increased the amplitude and area under curve of GABAergic currents in CA1 pyramidal neurons of hippocampal slices significantly.	Phenobarbital	136-149	carbonic anhydrase 1	Rattus norvegicus	290-293
27338863-8	2016	Finally, we show for the first time that cryo-HepaRG supports proper CAR cytosolic sequestration and translocation to hepatocyte nuclei in response to phenobarbital treatment.	Phenobarbital	151-164	nuclear receptor subfamily 1 group I member 3	Homo sapiens	69-72
27693619-0	2016	Inhibition of beta-catenin signaling by phenobarbital in hepatoma cells in vitro.	Phenobarbital	40-53	catenin (cadherin associated protein), beta 1	Mus musculus	14-26
27693619-1	2016	The antiepileptic drug phenobarbital (PB) exerts hepatic effect based on indirect activation of the constitutive androstane receptor (CAR) via inhibition of the epidermal growth factor receptor (EGFR) and the kinase Src.	Phenobarbital	23-36	nuclear receptor subfamily 1, group I, member 3	Mus musculus	100-132
27693619-1	2016	The antiepileptic drug phenobarbital (PB) exerts hepatic effect based on indirect activation of the constitutive androstane receptor (CAR) via inhibition of the epidermal growth factor receptor (EGFR) and the kinase Src.	Phenobarbital	23-36	nuclear receptor subfamily 1, group I, member 3	Mus musculus	134-137
27693619-1	2016	The antiepileptic drug phenobarbital (PB) exerts hepatic effect based on indirect activation of the constitutive androstane receptor (CAR) via inhibition of the epidermal growth factor receptor (EGFR) and the kinase Src.	Phenobarbital	23-36	epidermal growth factor receptor	Mus musculus	161-193
27693619-1	2016	The antiepileptic drug phenobarbital (PB) exerts hepatic effect based on indirect activation of the constitutive androstane receptor (CAR) via inhibition of the epidermal growth factor receptor (EGFR) and the kinase Src.	Phenobarbital	23-36	epidermal growth factor receptor	Mus musculus	195-199
27693619-1	2016	The antiepileptic drug phenobarbital (PB) exerts hepatic effect based on indirect activation of the constitutive androstane receptor (CAR) via inhibition of the epidermal growth factor receptor (EGFR) and the kinase Src.	Phenobarbital	23-36	Rous sarcoma oncogene	Mus musculus	216-219
27693619-1	2016	The antiepileptic drug phenobarbital (PB) exerts hepatic effect based on indirect activation of the constitutive androstane receptor (CAR) via inhibition of the epidermal growth factor receptor (EGFR) and the kinase Src.	Phenobarbital	38-40	nuclear receptor subfamily 1, group I, member 3	Mus musculus	100-132
27693619-1	2016	The antiepileptic drug phenobarbital (PB) exerts hepatic effect based on indirect activation of the constitutive androstane receptor (CAR) via inhibition of the epidermal growth factor receptor (EGFR) and the kinase Src.	Phenobarbital	38-40	nuclear receptor subfamily 1, group I, member 3	Mus musculus	134-137
27693619-1	2016	The antiepileptic drug phenobarbital (PB) exerts hepatic effect based on indirect activation of the constitutive androstane receptor (CAR) via inhibition of the epidermal growth factor receptor (EGFR) and the kinase Src.	Phenobarbital	38-40	epidermal growth factor receptor	Mus musculus	161-193
27693619-1	2016	The antiepileptic drug phenobarbital (PB) exerts hepatic effect based on indirect activation of the constitutive androstane receptor (CAR) via inhibition of the epidermal growth factor receptor (EGFR) and the kinase Src.	Phenobarbital	38-40	epidermal growth factor receptor	Mus musculus	195-199
27693619-1	2016	The antiepileptic drug phenobarbital (PB) exerts hepatic effect based on indirect activation of the constitutive androstane receptor (CAR) via inhibition of the epidermal growth factor receptor (EGFR) and the kinase Src.	Phenobarbital	38-40	Rous sarcoma oncogene	Mus musculus	216-219
27693619-2	2016	It has furthermore been observed that in mice PB suppresses the growth of hepatocellular carcinoma with overactive signaling through the oncogenic Wnt/beta-catenin pathway, thus suggesting an interference of PB with beta-catenin signaling.	Phenobarbital	46-48	catenin (cadherin associated protein), beta 1	Mus musculus	151-163
27693619-2	2016	It has furthermore been observed that in mice PB suppresses the growth of hepatocellular carcinoma with overactive signaling through the oncogenic Wnt/beta-catenin pathway, thus suggesting an interference of PB with beta-catenin signaling.	Phenobarbital	46-48	catenin (cadherin associated protein), beta 1	Mus musculus	216-228
27693619-2	2016	It has furthermore been observed that in mice PB suppresses the growth of hepatocellular carcinoma with overactive signaling through the oncogenic Wnt/beta-catenin pathway, thus suggesting an interference of PB with beta-catenin signaling.	Phenobarbital	208-210	catenin (cadherin associated protein), beta 1	Mus musculus	216-228
27693619-4	2016	PB efficiently inhibited signaling through beta-catenin.	Phenobarbital	0-2	catenin (cadherin associated protein), beta 1	Mus musculus	43-55
27693619-6	2016	Mechanistic analyses revealed that the effect of PB on beta-catenin signaling was independent of the activation of CAR and also independent of the cytosolic multi-protein complex responsible for physiological post-translation control of the beta-catenin pathway via initiation of beta-catenin degradation.	Phenobarbital	49-51	catenin (cadherin associated protein), beta 1	Mus musculus	55-67
27693619-6	2016	Mechanistic analyses revealed that the effect of PB on beta-catenin signaling was independent of the activation of CAR and also independent of the cytosolic multi-protein complex responsible for physiological post-translation control of the beta-catenin pathway via initiation of beta-catenin degradation.	Phenobarbital	49-51	nuclear receptor subfamily 1, group I, member 3	Mus musculus	115-118
27693619-6	2016	Mechanistic analyses revealed that the effect of PB on beta-catenin signaling was independent of the activation of CAR and also independent of the cytosolic multi-protein complex responsible for physiological post-translation control of the beta-catenin pathway via initiation of beta-catenin degradation.	Phenobarbital	49-51	catenin (cadherin associated protein), beta 1	Mus musculus	241-253
27693619-6	2016	Mechanistic analyses revealed that the effect of PB on beta-catenin signaling was independent of the activation of CAR and also independent of the cytosolic multi-protein complex responsible for physiological post-translation control of the beta-catenin pathway via initiation of beta-catenin degradation.	Phenobarbital	49-51	catenin (cadherin associated protein), beta 1	Mus musculus	241-253
27693619-7	2016	Instead, evidence is provided that PB diminishes beta-catenin protein production by inhibition of protein synthesis via signal transduction through EGFR and Src.	Phenobarbital	35-37	catenin (cadherin associated protein), beta 1	Mus musculus	49-61
27693619-7	2016	Instead, evidence is provided that PB diminishes beta-catenin protein production by inhibition of protein synthesis via signal transduction through EGFR and Src.	Phenobarbital	35-37	epidermal growth factor receptor	Mus musculus	148-152
27693619-7	2016	Instead, evidence is provided that PB diminishes beta-catenin protein production by inhibition of protein synthesis via signal transduction through EGFR and Src.	Phenobarbital	35-37	Rous sarcoma oncogene	Mus musculus	157-160
27693619-9	2016	Inhibition of beta-catenin signaling by PB through the proposed mechanism might explain the inhibitory effect of PB on the growth of specific sub-populations of mouse liver tumors.	Phenobarbital	40-42	catenin (cadherin associated protein), beta 1	Mus musculus	14-26
27693619-9	2016	Inhibition of beta-catenin signaling by PB through the proposed mechanism might explain the inhibitory effect of PB on the growth of specific sub-populations of mouse liver tumors.	Phenobarbital	113-115	catenin (cadherin associated protein), beta 1	Mus musculus	14-26
27693619-10	2016	In conclusion, the present data comprehensively characterize the effect of PB on beta-catenin signaling in mouse hepatoma cells in vitro and provides mechanistic insight into the molecular processes underlying the observed effect.	Phenobarbital	75-77	catenin (cadherin associated protein), beta 1	Mus musculus	81-93
28915576-5	2017	Hepatic Bcl-3 overexpression attenuated DEN/PB-induced hepatocarcinogenesis.	Phenobarbital	44-46	B cell leukemia/lymphoma 3	Mus musculus	8-13
33434982-3	2016	The luminal surfaces of ePTFE conduits were activated with plasma immersion ion implantation (PIII) treatment to facilitate covalent attachment of tropoelastin.	Phenobarbital	4-11	elastin	Homo sapiens	147-159
27490534-3	2016	Cytochrome P450 (CYP450) isoenzymes are induced by AEDs, especially the classical AEDs, such as benzodiazepines (BZDs), carbamazepine (CBZ), phenytoin (PT), phenobarbital (PB), and valproic acid (VPA).	Phenobarbital	157-170	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-15
27490534-3	2016	Cytochrome P450 (CYP450) isoenzymes are induced by AEDs, especially the classical AEDs, such as benzodiazepines (BZDs), carbamazepine (CBZ), phenytoin (PT), phenobarbital (PB), and valproic acid (VPA).	Phenobarbital	157-170	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	17-23
27490534-3	2016	Cytochrome P450 (CYP450) isoenzymes are induced by AEDs, especially the classical AEDs, such as benzodiazepines (BZDs), carbamazepine (CBZ), phenytoin (PT), phenobarbital (PB), and valproic acid (VPA).	Phenobarbital	172-174	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-15
27490534-3	2016	Cytochrome P450 (CYP450) isoenzymes are induced by AEDs, especially the classical AEDs, such as benzodiazepines (BZDs), carbamazepine (CBZ), phenytoin (PT), phenobarbital (PB), and valproic acid (VPA).	Phenobarbital	172-174	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	17-23
28915576-6	2017	Bcl-3Hep mice exhibited a lower number and smaller tumor nodules in response to DEN/PB at 40 weeks of age.	Phenobarbital	84-86	B cell leukemia/lymphoma 3	Mus musculus	0-5
28915576-9	2017	In parallel, the absolute number of intrahepatic macrophages, CD8+ T cells and activated B cells was reduced in DEN/PB-treated Bcl-3Hep mice mirroring a reduction of tumor-associated inflammation.	Phenobarbital	116-118	B cell leukemia/lymphoma 3	Mus musculus	127-132
28915576-11	2017	In summary, hepatocyte-restricted Bcl-3 overexpression reduced hepatocarcinogenesis related to prolonged liver injury early after tumor initiation likely due to decreased survival of DEN/PB-damaged, premalignant cells.	Phenobarbital	187-189	B cell leukemia/lymphoma 3	Mus musculus	34-39
26838046-2	2016	In mice, the tumor promoter phenobarbital (PB) selects for hepatocellular tumors with activating beta-catenin mutations via constitutive androstane receptor activation.	Phenobarbital	43-45	catenin (cadherin associated protein), beta 1	Mus musculus	97-109
27427493-6	2016	We also show that an extended treatment with PB in the B13/H cells produces a miRNA response similar to that seen in the rat in vivo, via the time-dependent induction of miR-182/96.	Phenobarbital	45-47	microRNA 182	Rattus norvegicus	170-177
27427493-9	2016	Finally, we also show that Car-associated miR-122 expression is decreased by PB treatment in B13/H cells, a PB-induced response that is common to the rat, mouse and human.	Phenobarbital	77-79	microRNA 122	Rattus norvegicus	42-49
27427493-9	2016	Finally, we also show that Car-associated miR-122 expression is decreased by PB treatment in B13/H cells, a PB-induced response that is common to the rat, mouse and human.	Phenobarbital	108-110	microRNA 122	Rattus norvegicus	42-49
26838046-0	2016	Tumor promotion and inhibition by phenobarbital in livers of conditional Apc-deficient mice.	Phenobarbital	34-47	APC, WNT signaling pathway regulator	Mus musculus	73-76
27155371-8	2016	The constitutive androstane receptor (CAR, NR1I3) was also reported to modulate MRP2 expression, phenobarbital being a typical activator.	Phenobarbital	97-110	nuclear receptor subfamily 1 group I member 3	Homo sapiens	4-36
27155371-8	2016	The constitutive androstane receptor (CAR, NR1I3) was also reported to modulate MRP2 expression, phenobarbital being a typical activator.	Phenobarbital	97-110	nuclear receptor subfamily 1 group I member 3	Homo sapiens	38-41
27155371-8	2016	The constitutive androstane receptor (CAR, NR1I3) was also reported to modulate MRP2 expression, phenobarbital being a typical activator.	Phenobarbital	97-110	nuclear receptor subfamily 1 group I member 3	Homo sapiens	43-48
27155371-8	2016	The constitutive androstane receptor (CAR, NR1I3) was also reported to modulate MRP2 expression, phenobarbital being a typical activator.	Phenobarbital	97-110	ATP binding cassette subfamily C member 2	Homo sapiens	80-84
26838046-2	2016	In mice, the tumor promoter phenobarbital (PB) selects for hepatocellular tumors with activating beta-catenin mutations via constitutive androstane receptor activation.	Phenobarbital	28-41	catenin (cadherin associated protein), beta 1	Mus musculus	97-109
26838046-3	2016	PB-dependent tumor promotion was studied in mice with genetic inactivation of Apc, a negative regulator of beta-catenin, to circumvent the problem of randomly induced mutations by chemical initiators and to allow monitoring of PB- and Wnt/beta-catenin-dependent tumorigenesis in the absence of unknown genomic alterations.	Phenobarbital	0-2	APC, WNT signaling pathway regulator	Mus musculus	78-81
26838046-3	2016	PB-dependent tumor promotion was studied in mice with genetic inactivation of Apc, a negative regulator of beta-catenin, to circumvent the problem of randomly induced mutations by chemical initiators and to allow monitoring of PB- and Wnt/beta-catenin-dependent tumorigenesis in the absence of unknown genomic alterations.	Phenobarbital	0-2	catenin (cadherin associated protein), beta 1	Mus musculus	107-119
26838046-3	2016	PB-dependent tumor promotion was studied in mice with genetic inactivation of Apc, a negative regulator of beta-catenin, to circumvent the problem of randomly induced mutations by chemical initiators and to allow monitoring of PB- and Wnt/beta-catenin-dependent tumorigenesis in the absence of unknown genomic alterations.	Phenobarbital	0-2	catenin (cadherin associated protein), beta 1	Mus musculus	239-251
26838046-4	2016	Moreover, the study was designed to investigate PB-induced proliferation of liver cells with activated beta-catenin.	Phenobarbital	48-50	catenin (cadherin associated protein), beta 1	Mus musculus	103-115
26838046-5	2016	PB treatment provided Apc-deficient hepatocytes with only a minor proliferative advantage, and additional connexin 32 deficiency did not affect the proliferative response.	Phenobarbital	0-2	APC, WNT signaling pathway regulator	Mus musculus	22-25
26838046-7	2016	The probability of tumor promotion by PB was calculated to be much lower for hepatocytes with loss of Apc, as compared to mutational beta-catenin activation.	Phenobarbital	38-40	APC, WNT signaling pathway regulator	Mus musculus	102-105
26946220-5	2016	Here we investigated the response of TK6 cells to higher percentages of Aroclor-, benzoflavone/phenobarbital-, or ethanol-induced rat liver S9 to expand TGx-28.65 biomarker applicability.	Phenobarbital	95-108	transglutaminase 5	Homo sapiens	153-156
26921222-1	2016	OBJECTIVE: The loop diuretic bumetanide has been reported to potentiate the antiseizure activity of phenobarbital in rodent models of neonatal seizures, most likely as a result of inhibition of the chloride importer Na-K-Cl cotransporter isoform 1 (NKCC1) in the brain.	Phenobarbital	100-113	solute carrier family 12, member 2	Mus musculus	216-247
26921222-1	2016	OBJECTIVE: The loop diuretic bumetanide has been reported to potentiate the antiseizure activity of phenobarbital in rodent models of neonatal seizures, most likely as a result of inhibition of the chloride importer Na-K-Cl cotransporter isoform 1 (NKCC1) in the brain.	Phenobarbital	100-113	solute carrier family 12, member 2	Mus musculus	249-254
27074912-4	2016	Here we have demonstrated that p38 MAPK forms a complex with CAR, enables it to bind to the response sequence, phenobarbital-responsive enhancer module (PBREM), within the CYP2B promoter, and thus recruits RNA polymerase II to activate transcription.	Phenobarbital	111-124	mitogen-activated protein kinase 14	Homo sapiens	31-34
27074912-4	2016	Here we have demonstrated that p38 MAPK forms a complex with CAR, enables it to bind to the response sequence, phenobarbital-responsive enhancer module (PBREM), within the CYP2B promoter, and thus recruits RNA polymerase II to activate transcription.	Phenobarbital	111-124	nuclear receptor subfamily 1 group I member 3	Homo sapiens	61-64
27074912-4	2016	Here we have demonstrated that p38 MAPK forms a complex with CAR, enables it to bind to the response sequence, phenobarbital-responsive enhancer module (PBREM), within the CYP2B promoter, and thus recruits RNA polymerase II to activate transcription.	Phenobarbital	111-124	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	172-177
26966071-7	2016	Treatment with dexamethasone, phenobarbital, rifampicin, or 1alpha,25-dihydroxyvitamin D3 resulted in 5.8-fold, 13.4-fold, 9.8-fold, or 95.0-fold induction of CYP3A4 expression relative to that in the untreated controls, respectively.	Phenobarbital	30-43	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	159-165
26994072-0	2016	Phenobarbital and Insulin Reciprocate Activation of the Nuclear Receptor Constitutive Androstane Receptor through the Insulin Receptor.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	73-105
26994072-0	2016	Phenobarbital and Insulin Reciprocate Activation of the Nuclear Receptor Constitutive Androstane Receptor through the Insulin Receptor.	Phenobarbital	0-13	insulin receptor	Mus musculus	118-134
26994072-1	2016	Phenobarbital (PB) antagonized insulin to inactivate the insulin receptor and attenuated the insulin receptor downstream protein kinase B (AKT)-forkhead box protein O1 and extracellular signal-regulated kinase 1/2 signals in mouse primary hepatocytes and HepG2 cells.	Phenobarbital	0-13	insulin	Homo sapiens	31-38
26994072-1	2016	Phenobarbital (PB) antagonized insulin to inactivate the insulin receptor and attenuated the insulin receptor downstream protein kinase B (AKT)-forkhead box protein O1 and extracellular signal-regulated kinase 1/2 signals in mouse primary hepatocytes and HepG2 cells.	Phenobarbital	0-13	insulin receptor	Mus musculus	57-73
26994072-1	2016	Phenobarbital (PB) antagonized insulin to inactivate the insulin receptor and attenuated the insulin receptor downstream protein kinase B (AKT)-forkhead box protein O1 and extracellular signal-regulated kinase 1/2 signals in mouse primary hepatocytes and HepG2 cells.	Phenobarbital	0-13	insulin	Homo sapiens	57-64
26994072-1	2016	Phenobarbital (PB) antagonized insulin to inactivate the insulin receptor and attenuated the insulin receptor downstream protein kinase B (AKT)-forkhead box protein O1 and extracellular signal-regulated kinase 1/2 signals in mouse primary hepatocytes and HepG2 cells.	Phenobarbital	0-13	thymoma viral proto-oncogene 1	Mus musculus	139-142
26994072-1	2016	Phenobarbital (PB) antagonized insulin to inactivate the insulin receptor and attenuated the insulin receptor downstream protein kinase B (AKT)-forkhead box protein O1 and extracellular signal-regulated kinase 1/2 signals in mouse primary hepatocytes and HepG2 cells.	Phenobarbital	0-13	mitogen-activated protein kinase 3	Mus musculus	172-213
26994072-1	2016	Phenobarbital (PB) antagonized insulin to inactivate the insulin receptor and attenuated the insulin receptor downstream protein kinase B (AKT)-forkhead box protein O1 and extracellular signal-regulated kinase 1/2 signals in mouse primary hepatocytes and HepG2 cells.	Phenobarbital	15-17	insulin	Homo sapiens	31-38
26994072-1	2016	Phenobarbital (PB) antagonized insulin to inactivate the insulin receptor and attenuated the insulin receptor downstream protein kinase B (AKT)-forkhead box protein O1 and extracellular signal-regulated kinase 1/2 signals in mouse primary hepatocytes and HepG2 cells.	Phenobarbital	15-17	insulin receptor	Mus musculus	57-73
26994072-1	2016	Phenobarbital (PB) antagonized insulin to inactivate the insulin receptor and attenuated the insulin receptor downstream protein kinase B (AKT)-forkhead box protein O1 and extracellular signal-regulated kinase 1/2 signals in mouse primary hepatocytes and HepG2 cells.	Phenobarbital	15-17	insulin	Homo sapiens	57-64
26994072-1	2016	Phenobarbital (PB) antagonized insulin to inactivate the insulin receptor and attenuated the insulin receptor downstream protein kinase B (AKT)-forkhead box protein O1 and extracellular signal-regulated kinase 1/2 signals in mouse primary hepatocytes and HepG2 cells.	Phenobarbital	15-17	thymoma viral proto-oncogene 1	Mus musculus	139-142
26994072-1	2016	Phenobarbital (PB) antagonized insulin to inactivate the insulin receptor and attenuated the insulin receptor downstream protein kinase B (AKT)-forkhead box protein O1 and extracellular signal-regulated kinase 1/2 signals in mouse primary hepatocytes and HepG2 cells.	Phenobarbital	15-17	mitogen-activated protein kinase 3	Mus musculus	172-213
26994072-2	2016	Hepatic AKT began dephosphorylation in an early stage of PB treatment, and blood glucose levels transiently increased in both wild-type and constitutive androstane receptor (CAR) knockout (KO) mice.	Phenobarbital	57-59	thymoma viral proto-oncogene 1	Mus musculus	8-11
27099654-7	2016	Phenobarbitone being an inducer of enzyme UDPGT is used as the first line of treatment and is not teratogenic in the low doses used.	Phenobarbital	0-14	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	42-47
26494205-10	2016	CONCLUSION: Our findings suggest that patients with LIS1-associated lissencephaly might benefit most from lamotrigine, valproate, vigabatrin or phenobarbital.	Phenobarbital	144-157	platelet activating factor acetylhydrolase 1b regulatory subunit 1	Homo sapiens	52-56
27595042-0	2016	SCN2A-Related Early-Onset Epileptic Encephalopathy Responsive to Phenobarbital.	Phenobarbital	65-78	sodium voltage-gated channel alpha subunit 2	Homo sapiens	0-5
26684499-0	2016	Effects of Phenobarbital on Expression of UDP-Glucuronosyltransferase 1a6 and 1a7 in Rat Brain.	Phenobarbital	11-24	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	42-73
26684499-3	2016	Phenobarbital (PB), a typical inducer of drug-metabolizing enzymes, has been reported to induce oxidative stress and epigenetic changes, which could alter UGT expression in the brain.	Phenobarbital	0-13	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	155-158
26684499-3	2016	Phenobarbital (PB), a typical inducer of drug-metabolizing enzymes, has been reported to induce oxidative stress and epigenetic changes, which could alter UGT expression in the brain.	Phenobarbital	15-17	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	155-158
26684499-4	2016	Here, we aimed to clarify the effects of PB on Ugt1a6 and Ugt1a7 gene expression in rat brains.	Phenobarbital	41-43	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	47-53
26684499-4	2016	Here, we aimed to clarify the effects of PB on Ugt1a6 and Ugt1a7 gene expression in rat brains.	Phenobarbital	41-43	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	58-64
26684499-9	2016	Measurement of oxidative stress markers suggested that PB induced oxidative stress in brain regions in which Ugt1a6 and Ugt1a7 mRNAs were increased.	Phenobarbital	55-57	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	109-115
26684499-9	2016	Measurement of oxidative stress markers suggested that PB induced oxidative stress in brain regions in which Ugt1a6 and Ugt1a7 mRNAs were increased.	Phenobarbital	55-57	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	120-126
26684499-12	2016	In summary, Ugt1a6 and Ugt1a7 mRNA levels were increased by PB treatment, which may alter pharmacokinetics in the brain.	Phenobarbital	60-62	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	12-18
26684499-12	2016	In summary, Ugt1a6 and Ugt1a7 mRNA levels were increased by PB treatment, which may alter pharmacokinetics in the brain.	Phenobarbital	60-62	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	23-29
26781906-2	2016	The T-3279G mutation in the phenobarbital responsive enhancer module (PBREM), the TA-insertion in the TATA box, creating the A(TA)7TAA motif instead of A(TA)6TAA and the G211A mutation in coding exon 1, particularly in Asian populations, of the human UGT1A1 gene are the three common genotypes found in patients with Gilbert"s syndrome.	Phenobarbital	28-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	251-257
26980803-0	2016	Correction to "Effects of Phenobarbital on Expression of UDP-Glucuronosyltransferase 1a6 and 1a7 in Rat Brain".	Phenobarbital	26-39	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	57-88
26764098-6	2016	In mouse cells, depletion of ER luminal FKBP10 was almost as potent as FK506 in attenuating expression of PrP(C).	Phenobarbital	32-39	FK506 binding protein 10	Mus musculus	40-46
26764098-6	2016	In mouse cells, depletion of ER luminal FKBP10 was almost as potent as FK506 in attenuating expression of PrP(C).	Phenobarbital	32-39	prion protein	Mus musculus	106-111
26496779-7	2016	Phenobarbital is metabolized in the liver by CYP2C9 with minor metabolism by CYP2C19 and CYP2E1.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	45-51
26351921-1	2016	The antiepileptic drug phenobarbital (PB) exerts hepatic effects related to cell proliferation and tumorigenesis which are closely linked to the Wnt/beta-catenin signaling pathway.	Phenobarbital	23-36	catenin (cadherin associated protein), beta 1	Mus musculus	149-161
26351921-1	2016	The antiepileptic drug phenobarbital (PB) exerts hepatic effects related to cell proliferation and tumorigenesis which are closely linked to the Wnt/beta-catenin signaling pathway.	Phenobarbital	38-40	catenin (cadherin associated protein), beta 1	Mus musculus	149-161
26351921-3	2016	We now identified PB as an inhibitor of Wnt/beta-catenin signaling in mouse hepatoma cells.	Phenobarbital	18-20	catenin (cadherin associated protein), beta 1	Mus musculus	44-56
26496779-7	2016	Phenobarbital is metabolized in the liver by CYP2C9 with minor metabolism by CYP2C19 and CYP2E1.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	77-84
26496779-7	2016	Phenobarbital is metabolized in the liver by CYP2C9 with minor metabolism by CYP2C19 and CYP2E1.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	89-95
27027306-11	2016	Subgroup analysis showed that only phenobarbitone doses at 20 mg/kg resulted in a significant reduction in the maximum seizure burden from T-1 to T+1 (p = 0.002).	Phenobarbital	35-49	CD5 molecule	Homo sapiens	139-142
27096699-6	2016	Molecular modeling studies showed that acetazolamide, ethosuxiamide, lamotrigine, oxcarbazepine, phenobarbital, phenytoin, primidone and sodium-valproate may induce ADR in HLA-B*15:02 carriers alike CBZ.	Phenobarbital	97-110	major histocompatibility complex, class I, B	Homo sapiens	172-177
27235785-5	2016	RESULTS: KCs decreased phenobarbital inducibility of CYP2B1/2 in a cell ratio dependent manner and activation of KCs by lipopolisacharide (LPS) amplified this effect.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	53-59
26400395-0	2015	Dose of Phenobarbital and Age of Treatment at Early Life are Two Key Factors for the Persistent Induction of Cytochrome P450 Enzymes in Adult Mouse Liver.	Phenobarbital	8-21	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	109-124
26378027-9	2015	PB treatment in vivo or in vitro elevated the production and release of tumor necrosis factor alpha from MC, which was identified as mainly responsible for the inhibition of apoptosis in HC.	Phenobarbital	0-2	tumor necrosis factor	Rattus norvegicus	72-99
26400395-2	2015	In the current study, we use phenobarbital as a model drug and mouse as an in vivo model to demonstrate that the dose of phenobarbital and age of treatment are two key factors for the persistent induction of gene expression and consequential increases of enzyme activities of Cyp2b, Cyp2c, and Cyp3a in adult livers.	Phenobarbital	29-42	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	276-281
26400395-2	2015	In the current study, we use phenobarbital as a model drug and mouse as an in vivo model to demonstrate that the dose of phenobarbital and age of treatment are two key factors for the persistent induction of gene expression and consequential increases of enzyme activities of Cyp2b, Cyp2c, and Cyp3a in adult livers.	Phenobarbital	29-42	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	283-288
26400395-2	2015	In the current study, we use phenobarbital as a model drug and mouse as an in vivo model to demonstrate that the dose of phenobarbital and age of treatment are two key factors for the persistent induction of gene expression and consequential increases of enzyme activities of Cyp2b, Cyp2c, and Cyp3a in adult livers.	Phenobarbital	29-42	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	294-299
26400395-2	2015	In the current study, we use phenobarbital as a model drug and mouse as an in vivo model to demonstrate that the dose of phenobarbital and age of treatment are two key factors for the persistent induction of gene expression and consequential increases of enzyme activities of Cyp2b, Cyp2c, and Cyp3a in adult livers.	Phenobarbital	121-134	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	276-281
26400395-2	2015	In the current study, we use phenobarbital as a model drug and mouse as an in vivo model to demonstrate that the dose of phenobarbital and age of treatment are two key factors for the persistent induction of gene expression and consequential increases of enzyme activities of Cyp2b, Cyp2c, and Cyp3a in adult livers.	Phenobarbital	121-134	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	283-288
26400395-2	2015	In the current study, we use phenobarbital as a model drug and mouse as an in vivo model to demonstrate that the dose of phenobarbital and age of treatment are two key factors for the persistent induction of gene expression and consequential increases of enzyme activities of Cyp2b, Cyp2c, and Cyp3a in adult livers.	Phenobarbital	121-134	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	294-299
26511920-7	2015	In the mice maximal electroshock-induced seizure screen, compound THb gave an ED50 of 11.8 mg/kg and a TD50 of 39.47 mg/kg, resulting in a good protection index (PI), that is, TD50/ED50, of 3.3 when compared to Phenobarbital and Valproate.	Phenobarbital	211-224	lymphocyte antigen 6 complex, locus D	Mus musculus	66-69
26421491-8	2015	CONCLUSIONS: rs776746 and rs15524 in the CYP3A5 gene tend to affect CBZ metabolism, and rs2032582, rs10234411 in the ABCB1 gene may contribute to inter-individual variation in CBZ and in CBZ-E transport among patients with epilepsy using CBZ in combination with PHT or PB.	Phenobarbital	269-271	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	41-47
26421491-8	2015	CONCLUSIONS: rs776746 and rs15524 in the CYP3A5 gene tend to affect CBZ metabolism, and rs2032582, rs10234411 in the ABCB1 gene may contribute to inter-individual variation in CBZ and in CBZ-E transport among patients with epilepsy using CBZ in combination with PHT or PB.	Phenobarbital	269-271	ATP binding cassette subfamily B member 1	Homo sapiens	117-122
26452067-0	2015	Acute TrkB inhibition rescues phenobarbital-resistant seizures in a mouse model of neonatal ischemia.	Phenobarbital	30-43	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	6-10
26452067-7	2015	A single dose of ANA12 + PB prevented the post-ischemic degradation of KCC2 for up to 24 h. As anticipated, ANA12 by itself had no anti-seizure properties and was unable to prevent KCC2 degradation at 24 h without follow-on PB.	Phenobarbital	25-27	solute carrier family 12, member 5	Mus musculus	71-75
26452067-9	2015	This study, for the first time as a proof-of-concept, reports the potential therapeutic value of KCC2 modulation for the management of PB-resistant seizures in neonates.	Phenobarbital	135-137	solute carrier family 12, member 5	Mus musculus	97-101
26348778-1	2015	The regulatory mechanism of phosphoenolpyruvate carboykinase (GTP) (EC 4.1.1.32) (PEPCK) gene expression and gluconeogenesis by phenobarbital (PB), which is known to induce drug-metabolizing enzymes, was investigated.	Phenobarbital	128-141	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	82-87
26215100-9	2015	AhR was suppressed by phenobarbital and 1,4-Bis[2-(3,5-dichloropyridyloxy)] benzene (TCPOBOP) in a constitutive activated receptor (CAR)-dependent manner and pregnenolone-16alpha-carbonitrile in a pregnane X receptor (PXR)-dependent manner.	Phenobarbital	22-35	aryl-hydrocarbon receptor	Mus musculus	0-3
26215100-9	2015	AhR was suppressed by phenobarbital and 1,4-Bis[2-(3,5-dichloropyridyloxy)] benzene (TCPOBOP) in a constitutive activated receptor (CAR)-dependent manner and pregnenolone-16alpha-carbonitrile in a pregnane X receptor (PXR)-dependent manner.	Phenobarbital	22-35	nuclear receptor subfamily 1, group I, member 2	Mus musculus	197-216
26215100-9	2015	AhR was suppressed by phenobarbital and 1,4-Bis[2-(3,5-dichloropyridyloxy)] benzene (TCPOBOP) in a constitutive activated receptor (CAR)-dependent manner and pregnenolone-16alpha-carbonitrile in a pregnane X receptor (PXR)-dependent manner.	Phenobarbital	22-35	nuclear receptor subfamily 1, group I, member 2	Mus musculus	218-221
26171734-5	2015	It has been shown that phenobarbital-mediated activation of constitutive androstane receptor (CAR), xenobiotic nuclear receptor, is associated with a decrease in miR-122 in the liver.	Phenobarbital	23-36	nuclear receptor subfamily 1, group I, member 3	Mus musculus	60-92
26348778-1	2015	The regulatory mechanism of phosphoenolpyruvate carboykinase (GTP) (EC 4.1.1.32) (PEPCK) gene expression and gluconeogenesis by phenobarbital (PB), which is known to induce drug-metabolizing enzymes, was investigated.	Phenobarbital	143-145	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	82-87
26348778-3	2015	We found that PB directly suppressed PEPCK gene expression in spherical hepatocytes on EHS-gel, but not in those on TIC.	Phenobarbital	14-16	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	37-42
26348778-4	2015	PB strongly suppressed cAMP-dependent induction of PEPCK gene expression.	Phenobarbital	0-2	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	51-56
26348778-6	2015	Chronic administration of PB reduced hepatic PEPCK mRNA in streptozotocin-induced diabetic and nondiabetic rats, and PB reduced blood glucose level in diabetic rats.	Phenobarbital	26-28	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	45-50
26348778-8	2015	These results indicated that PB-dependent reduction is specific to PEPCK.	Phenobarbital	29-31	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	67-72
26348778-10	2015	PEPCK gene promoter activity was suppressed by PB in HepG2 cells.	Phenobarbital	47-49	phosphoenolpyruvate carboxykinase 2, mitochondrial	Homo sapiens	0-5
26348778-11	2015	In conclusion, we found that spherical hepatocytes cultured on EHS-gel are capable to respond to PB to suppress PEPCK gene expression.	Phenobarbital	97-99	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	112-117
23572393-1	2015	The current study was aimed to scrutinize acetylcholinesterase (AchE) inhibitory profile of two antidepressants, diazepam and phenobarbitone.	Phenobarbital	126-140	acetylcholinesterase (Cartwright blood group)	Homo sapiens	42-62
23572393-1	2015	The current study was aimed to scrutinize acetylcholinesterase (AchE) inhibitory profile of two antidepressants, diazepam and phenobarbitone.	Phenobarbital	126-140	acetylcholinesterase (Cartwright blood group)	Homo sapiens	64-68
23572393-5	2015	Similar trend of antagonism was shown by phenobarbitone when it was subjected to the challenge of AchE with aKm and aVm values of 51.99% and 71.80%, respectively.	Phenobarbital	41-55	acetylcholinesterase (Cartwright blood group)	Homo sapiens	98-102
23572393-6	2015	It is concluded that diazepam and phenobarbitone exhibited prominent AchE attenuation apart from their well-established antidepressant activity, which could be more useful in related diseased conditions.	Phenobarbital	34-48	acetylcholinesterase (Cartwright blood group)	Homo sapiens	69-73
26171734-5	2015	It has been shown that phenobarbital-mediated activation of constitutive androstane receptor (CAR), xenobiotic nuclear receptor, is associated with a decrease in miR-122 in the liver.	Phenobarbital	23-36	nuclear receptor subfamily 1, group I, member 3	Mus musculus	94-97
26171734-5	2015	It has been shown that phenobarbital-mediated activation of constitutive androstane receptor (CAR), xenobiotic nuclear receptor, is associated with a decrease in miR-122 in the liver.	Phenobarbital	23-36	microRNA 122	Mus musculus	162-169
26775449-13	2015	Phenobarbital in SyrSpend SF PH4 retained above 90% of initial concentration for at least 154 days at room temperature.	Phenobarbital	0-13	prolyl 4-hydroxylase, transmembrane	Homo sapiens	29-32
26373282-8	2015	Consistently, the levels of intracellular/luminal vesicle and exosome marker flotillin-1 were significantly increased in frontal and temporal cortices of PPND/FTDP-17 patients with the N279K tau mutation, events that were not seen in the occipital cortex which is the most spared cortical region in the patients.	Phenobarbital	42-49	microtubule associated protein tau	Homo sapiens	159-166
26373282-8	2015	Consistently, the levels of intracellular/luminal vesicle and exosome marker flotillin-1 were significantly increased in frontal and temporal cortices of PPND/FTDP-17 patients with the N279K tau mutation, events that were not seen in the occipital cortex which is the most spared cortical region in the patients.	Phenobarbital	42-49	microtubule associated protein tau	Homo sapiens	191-194
26170821-5	2015	Hematoxylin-eosin and immunohistochemical staining revealed that phenobarbital and topiramate, individually or in combination, were cytotoxic to hippocampal CA1 neurons and inhibited the expression of GluR1 and NR2B, excitatory glutamate receptor subunits.	Phenobarbital	65-78	carbonic anhydrase 1	Homo sapiens	157-160
25846690-0	2015	Association of ABCB1 C3435T polymorphism with phenobarbital resistance in Thai patients with epilepsy.	Phenobarbital	46-59	ATP binding cassette subfamily B member 1	Homo sapiens	15-20
25846690-4	2015	Phenobarbital (PB), one of the most cost-effective and widely used AEDs in developing countries, has been reported to be transported by p-gp.	Phenobarbital	0-13	ATP binding cassette subfamily B member 1	Homo sapiens	136-140
25846690-4	2015	Phenobarbital (PB), one of the most cost-effective and widely used AEDs in developing countries, has been reported to be transported by p-gp.	Phenobarbital	15-17	ATP binding cassette subfamily B member 1	Homo sapiens	136-140
25846690-5	2015	This study aimed to investigate the association of a genetic variant, ABCB1 3435C&gt;T, and non-genetic factors with phenobarbital response in Thai patients with epilepsy.	Phenobarbital	117-130	ATP binding cassette subfamily B member 1	Homo sapiens	70-75
25846690-12	2015	The ABCB1 3435C&gt;T polymorphism and type of epilepsy were associated with response to PB.	Phenobarbital	88-90	ATP binding cassette subfamily B member 1	Homo sapiens	4-9
25846690-13	2015	Patients with PB-resistant epilepsy had a significantly higher frequency of ABCB1 3435CC genotype and had focal epilepsy more often than patients with PB-responsive epilepsy (adjusted OR = 3 962, 95% CI = 1 075-14 610, P-value = 0 039; adjusted OR = 5 936, 95% CI = 2 272-15 513, P-value &lt; 0 001, respectively).	Phenobarbital	14-16	ATP binding cassette subfamily B member 1	Homo sapiens	76-81
25846690-15	2015	WHAT IS NEW AND CONCLUSION: Thai patients of ABCB1 3435CC genotype and with focal epilepsy were more often PB resistant.	Phenobarbital	107-109	ATP binding cassette subfamily B member 1	Homo sapiens	45-50
25949234-4	2015	A gene expression biomarker signature of 83 CAR-dependent genes was identified using microarray profiles from the livers of wild-type and CAR-null mice after exposure to three structurally-diverse CAR activators (CITCO, phenobarbital, TCPOBOP).	Phenobarbital	220-233	nuclear receptor subfamily 1, group I, member 3	Mus musculus	44-47
25786523-1	2015	The effects of the peroxisome proliferator, dehydroepiandrosterone sulfate (DHEAS), and the typical cytochrome P450 (CYP) inducers phenobarbital (PB) and 3-methylcholanthrene (3-MC) on fatty liver were examined in rats.	Phenobarbital	131-144	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	117-120
25975989-2	2015	CAR activation can be elicited by a large variety of xenobiotics, including phenobarbital (PB) which is not a directly binding CAR ligand.	Phenobarbital	76-89	nuclear receptor subfamily 1 group I member 3	Homo sapiens	0-3
25975989-2	2015	CAR activation can be elicited by a large variety of xenobiotics, including phenobarbital (PB) which is not a directly binding CAR ligand.	Phenobarbital	91-93	nuclear receptor subfamily 1 group I member 3	Homo sapiens	0-3
26029047-8	2015	PB was an efficacious anti-seizure agent at P10 and P12, but not at P7.	Phenobarbital	0-2	S100 calcium binding protein A10 (calpactin)	Mus musculus	44-47
26029047-8	2015	PB was an efficacious anti-seizure agent at P10 and P12, but not at P7.	Phenobarbital	0-2	CDK2 (cyclin-dependent kinase 2)-associated protein 1	Mus musculus	52-55
26029047-9	2015	BTN failed as an adjunct, at all ages tested and significantly blunted PB-efficacy at P10.	Phenobarbital	71-73	S100 calcium binding protein A10 (calpactin)	Mus musculus	86-89
26029047-13	2015	The age-dependent profile of KCC2 expression and its post-insult downregulation may underlie the PB-resistance reported in this model.	Phenobarbital	97-99	solute carrier family 12, member 5	Mus musculus	29-33
26170821-5	2015	Hematoxylin-eosin and immunohistochemical staining revealed that phenobarbital and topiramate, individually or in combination, were cytotoxic to hippocampal CA1 neurons and inhibited the expression of GluR1 and NR2B, excitatory glutamate receptor subunits.	Phenobarbital	65-78	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	201-206
26170821-5	2015	Hematoxylin-eosin and immunohistochemical staining revealed that phenobarbital and topiramate, individually or in combination, were cytotoxic to hippocampal CA1 neurons and inhibited the expression of GluR1 and NR2B, excitatory glutamate receptor subunits.	Phenobarbital	65-78	glutamate ionotropic receptor NMDA type subunit 2B	Homo sapiens	211-215
25434925-10	2015	Tet alleviates the phenobarbital withdrawal symptoms and protects the brain cells against apoptosis, which may be a result of the regulation of the mRNA and protein expression levels of Bcl-2 and Bax.	Phenobarbital	19-32	BCL2, apoptosis regulator	Rattus norvegicus	186-191
25684626-2	2015	In this study, behavioral and electroencephalographic methods, as well as isobolographic analysis, are used to show that the CysLT1 inverse agonist montelukast synergistically increases the anticonvulsant action of phenobarbital against pentylenetetrazole-induced seizures.	Phenobarbital	215-228	cysteinyl leukotriene receptor 1	Mus musculus	125-131
25721668-5	2015	PRMT5 enhanced phenobarbital-mediated transactivation of a phenobarbital-responsive enhancer module (PBREM)-driven reporter gene in co-operation with PGC-1alpha in rat primary hepatocytes.	Phenobarbital	15-28	protein arginine methyltransferase 5	Rattus norvegicus	0-5
25721668-5	2015	PRMT5 enhanced phenobarbital-mediated transactivation of a phenobarbital-responsive enhancer module (PBREM)-driven reporter gene in co-operation with PGC-1alpha in rat primary hepatocytes.	Phenobarbital	15-28	PPARG coactivator 1 alpha	Rattus norvegicus	150-160
25721668-5	2015	PRMT5 enhanced phenobarbital-mediated transactivation of a phenobarbital-responsive enhancer module (PBREM)-driven reporter gene in co-operation with PGC-1alpha in rat primary hepatocytes.	Phenobarbital	59-72	protein arginine methyltransferase 5	Rattus norvegicus	0-5
25625231-3	2015	Nevertheless, it is not known if these flavonoids are direct CAR ligands or indirect phenobarbital-like CAR activators via the inhibition of epidermal growth factor receptor (EGFR) signaling.	Phenobarbital	85-98	nuclear receptor subfamily 1 group I member 3	Homo sapiens	104-107
25434925-10	2015	Tet alleviates the phenobarbital withdrawal symptoms and protects the brain cells against apoptosis, which may be a result of the regulation of the mRNA and protein expression levels of Bcl-2 and Bax.	Phenobarbital	19-32	BCL2 associated X, apoptosis regulator	Rattus norvegicus	196-199
25561733-5	2015	The Na(+)/H(+) exchanger NHE6 provides a leak pathway for protons, limiting luminal acidification by proton pumps.	Phenobarbital	76-83	solute carrier family 9 member A6	Homo sapiens	25-29
25489928-0	2015	Enhanced thyroid hormone breakdown in hepatocytes by mutual induction of the constitutive androstane receptor (CAR, NR1I3) and arylhydrocarbon receptor by benzo[a]pyrene and phenobarbital.	Phenobarbital	174-187	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	77-109
25661872-3	2015	These responses are strictly limited and are tightly linked, since beta-catenin is activated in nearly all of the CAR-dependent tumours generated by the tumour promoter phenobarbital.	Phenobarbital	169-182	catenin beta 1	Homo sapiens	67-79
25661872-3	2015	These responses are strictly limited and are tightly linked, since beta-catenin is activated in nearly all of the CAR-dependent tumours generated by the tumour promoter phenobarbital.	Phenobarbital	169-182	CXADR pseudogene 1	Homo sapiens	114-117
25489928-0	2015	Enhanced thyroid hormone breakdown in hepatocytes by mutual induction of the constitutive androstane receptor (CAR, NR1I3) and arylhydrocarbon receptor by benzo[a]pyrene and phenobarbital.	Phenobarbital	174-187	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	111-114
25489928-4	2015	Likewise, phenobarbital induced the AhR transcription.	Phenobarbital	10-23	aryl hydrocarbon receptor	Rattus norvegicus	36-39
25489928-5	2015	This mutual induction of the nuclear receptors enhanced the phenobarbital-dependent induction of the prototypic CAR target gene Cyp2b1 as well as the AhR-dependent induction of UDP-glucuronosyltransferases.	Phenobarbital	60-73	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	112-115
25489928-5	2015	This mutual induction of the nuclear receptors enhanced the phenobarbital-dependent induction of the prototypic CAR target gene Cyp2b1 as well as the AhR-dependent induction of UDP-glucuronosyltransferases.	Phenobarbital	60-73	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	128-134
25489928-7	2015	By inducing the AhR, phenobarbital enhanced the benzo[a]pyrene-dependent reduction of thyroid hormone half-life and the benzo[a]pyrene-dependent increase in the rate of thyroid hormone glucuronide formation in hepatocyte cultures.	Phenobarbital	21-34	aryl hydrocarbon receptor	Rattus norvegicus	16-19
25409894-0	2015	Characterization of CYP2B6 in a CYP2B6-humanized mouse model: inducibility in the liver by phenobarbital and dexamethasone and role in nicotine metabolism in vivo.	Phenobarbital	91-104	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	20-26
25409894-2	2015	The inducibility of CYP2B6 by phenobarbital (PB) and dexamethasone (DEX), known inducers of CYP2B6 in human liver, was examined in the TG mice, as well as in TG/Cyp2abfgs-null (or "CYP2B6-humanized") mice.	Phenobarbital	30-43	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	20-26
25409894-2	2015	The inducibility of CYP2B6 by phenobarbital (PB) and dexamethasone (DEX), known inducers of CYP2B6 in human liver, was examined in the TG mice, as well as in TG/Cyp2abfgs-null (or "CYP2B6-humanized") mice.	Phenobarbital	45-47	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	20-26
25409894-2	2015	The inducibility of CYP2B6 by phenobarbital (PB) and dexamethasone (DEX), known inducers of CYP2B6 in human liver, was examined in the TG mice, as well as in TG/Cyp2abfgs-null (or "CYP2B6-humanized") mice.	Phenobarbital	45-47	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	92-98
25409894-2	2015	The inducibility of CYP2B6 by phenobarbital (PB) and dexamethasone (DEX), known inducers of CYP2B6 in human liver, was examined in the TG mice, as well as in TG/Cyp2abfgs-null (or "CYP2B6-humanized") mice.	Phenobarbital	45-47	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	92-98
25409894-3	2015	Hepatic expression of CYP2B6 mRNA and protein was greatly induced by PB or DEX treatment in both TG and TG/Cyp2abfgs-null mice.	Phenobarbital	69-71	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	22-28
25409894-5	2015	In PB-treated mice, the rates of hepatic microsomal hydroxybupropion formation (at 50 muM bupropion) were &gt;4-fold higher in TG/Cyp2abfgs-null than in Cyp2abfgs-null mice (for both male and female mice); the rate difference was accompanied by a 5-fold higher catalytic efficiency in the TG/Cyp2abfgs-null mice and was abolished by an antibody to CYP2B6.	Phenobarbital	3-5	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	348-354
25528284-8	2015	When BP-3 was incubated with liver microsomes from untreated rats or phenobarbital-, 3-methylcholanthrene-, or acetone-treated rats in the presence of NADPH, estrogenic activity was increased.	Phenobarbital	69-82	Blood pressure QTL 3	Rattus norvegicus	5-9
25447507-0	2015	Cell expression patterns of CD147 in N-diethylnitrosamine/phenobarbital-induced mouse hepatocellular carcinoma.	Phenobarbital	58-71	basigin	Mus musculus	28-33
25336106-6	2015	Among the cells tested, HepG2 cells were highly responsive to CYP inducers, such as 3-methylcholanthrene for CYP1A2 and phenobarbital for CYP2B6 and CYP3A4.	Phenobarbital	120-133	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	62-65
25336106-6	2015	Among the cells tested, HepG2 cells were highly responsive to CYP inducers, such as 3-methylcholanthrene for CYP1A2 and phenobarbital for CYP2B6 and CYP3A4.	Phenobarbital	120-133	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	138-144
25600204-2	2015	To evaluate time-dependent cytochrome P450 induction precisely, induction of CYP1A2, CYP2B6, and CYP3A4 mRNA was confirmed (&gt;2-fold) by the treatment with omeprazole, phenobarbital, and rifampicin, respectively, for 24 or 48 h on day 3 from the start of culture.	Phenobarbital	170-183	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	77-83
25710017-5	2015	Administration of phenobarbital to male Wistar rats significantly increased levels of hepatic cytochrome P450 (CYP) 2B1/2 and microsomal pentoxyresorufin O-dealkylase (PROD) activity.	Phenobarbital	18-31	cytochrome P450 2B1	Rattus norvegicus	94-121
25600204-2	2015	To evaluate time-dependent cytochrome P450 induction precisely, induction of CYP1A2, CYP2B6, and CYP3A4 mRNA was confirmed (&gt;2-fold) by the treatment with omeprazole, phenobarbital, and rifampicin, respectively, for 24 or 48 h on day 3 from the start of culture.	Phenobarbital	170-183	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	85-91
25600204-2	2015	To evaluate time-dependent cytochrome P450 induction precisely, induction of CYP1A2, CYP2B6, and CYP3A4 mRNA was confirmed (&gt;2-fold) by the treatment with omeprazole, phenobarbital, and rifampicin, respectively, for 24 or 48 h on day 3 from the start of culture.	Phenobarbital	170-183	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	97-103
26574146-12	2015	Unlike CYP1 and 3 and other CYP2 members, CYP2D6 is resistant to typical inducers such as rifampin, phenobarbital and dexamethasone.	Phenobarbital	100-113	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	42-48
25408221-5	2015	AbetaPP/PS1 mice demonstrated no differences in intestinal motility or water absorption but elevated luminal IgA levels compared to wild type mice.	Phenobarbital	101-108	amyloid beta (A4) precursor protein	Mus musculus	0-7
25408221-5	2015	AbetaPP/PS1 mice demonstrated no differences in intestinal motility or water absorption but elevated luminal IgA levels compared to wild type mice.	Phenobarbital	101-108	presenilin 1	Mus musculus	8-11
25354764-8	2015	As expected, PB treatment produced an increase in number and relative size of the GSTP-positive lesions.	Phenobarbital	13-15	glutathione S-transferase pi 1	Rattus norvegicus	82-86
25542016-8	2014	Thus, CCRP confers phenobarbital-induced de-methylation capability to the promoter as well as the phenobarbital responsiveness of recruiting RNA polymerase II, but is not responsible for the binding between CAR and its cognate sequence, phenobarbital responsive element module.	Phenobarbital	19-32	DnaJ heat shock protein family (Hsp40) member C7	Mus musculus	6-10
25751380-5	2015	RESULTS: Sequencing of the Gilbert syndrome-associated gene, UGT 1A 1, revealed mutations in the upstream promoter phenobarbital-responsive element module (PBREM) (-3279 mutation, 23 cases), in the promoter TATA box (a TA insertion mutation, 21 cases), and in the coding region of exon 1 (a GGA-AGA Gly71Arg mutation, 18 cases); there was no statistical difference found for any of the three mutations among this patient population (x2 =1.640, P more than 0.05).	Phenobarbital	115-128	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	61-69
25542016-3	2014	Phenobarbital treatment greatly increased nuclear CAR accumulation in the livers of KO males as compared to those of wild type (WT) males.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	50-53
24865931-4	2014	Genetic polymorphisms of the UGT1A1 promoter, specifically the -3279 T G phenobarbital responsive enhancer module (rs4124874) and (TA)7 dinucleotide repeat (rs8175347) as well as the coding region variants (rs2306283 and rs4149056) of the OATP2 gene were significantly higher among the cases than the controls.	Phenobarbital	73-86	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	29-35
25542016-4	2014	Despite this accumulation, phenobarbital-induced activation of the Cyp2b10 gene was significantly attenuated.	Phenobarbital	27-40	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	67-74
25542016-5	2014	In ChIP assays, a CAR/retinoid X receptor-alpha (RXRalpha) heterodimer binding to the Cyp2b10 promoter was already increased before phenobarbital treatment and further pronounced after treatment.	Phenobarbital	132-145	nuclear receptor subfamily 1, group I, member 3	Mus musculus	18-21
25542016-5	2014	In ChIP assays, a CAR/retinoid X receptor-alpha (RXRalpha) heterodimer binding to the Cyp2b10 promoter was already increased before phenobarbital treatment and further pronounced after treatment.	Phenobarbital	132-145	retinoid X receptor alpha	Mus musculus	49-57
25542016-5	2014	In ChIP assays, a CAR/retinoid X receptor-alpha (RXRalpha) heterodimer binding to the Cyp2b10 promoter was already increased before phenobarbital treatment and further pronounced after treatment.	Phenobarbital	132-145	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	86-93
25542016-7	2014	Histone H3K27 on the Cyp2b10 promoter was de-methylated only after phenobarbital treatment in WT but was fully de-methylated before treatment in KO males.	Phenobarbital	67-80	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	21-28
25280786-4	2014	We tested the hypothesis that status epilepticus (SE) or exposure to phenytoin or phenobarbital affects brain expression of the metabolic enzyme CYP2E1.	Phenobarbital	82-95	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	145-151
25280786-8	2014	The effect of phenytoin, carbamazepine and phenobarbital on CYP2E1 expression was evaluated in vivo or by using organotypic hippocampal cultures in vitro.	Phenobarbital	43-56	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	60-66
25145657-1	2014	High doses of sodium phenobarbital (NaPB), a constitutive androstane receptor (CAR) activator, have been shown to produce hepatocellular tumors in rodents by a mitogenic mode of action (MOA) involving CAR activation.	Phenobarbital	14-34	N-ethylmaleimide sensitive fusion protein attachment protein beta	Mus musculus	36-40
25145657-1	2014	High doses of sodium phenobarbital (NaPB), a constitutive androstane receptor (CAR) activator, have been shown to produce hepatocellular tumors in rodents by a mitogenic mode of action (MOA) involving CAR activation.	Phenobarbital	14-34	nuclear receptor subfamily 1, group I, member 3	Mus musculus	45-77
25145657-1	2014	High doses of sodium phenobarbital (NaPB), a constitutive androstane receptor (CAR) activator, have been shown to produce hepatocellular tumors in rodents by a mitogenic mode of action (MOA) involving CAR activation.	Phenobarbital	14-34	nuclear receptor subfamily 1, group I, member 3	Mus musculus	79-82
25145657-1	2014	High doses of sodium phenobarbital (NaPB), a constitutive androstane receptor (CAR) activator, have been shown to produce hepatocellular tumors in rodents by a mitogenic mode of action (MOA) involving CAR activation.	Phenobarbital	14-34	nuclear receptor subfamily 1, group I, member 3	Mus musculus	201-204
24880085-11	2014	Future experimental and clinical studies should further evaluate the validity of TSPO PET data to predict the response to phenobarbital and other antiepileptic drugs in longitudinal studies with scanning before drug exposure and with a focus on the early phase following an epileptogenic brain insult.	Phenobarbital	122-135	translocator protein	Rattus norvegicus	81-85
25052955-2	2015	Phenobarbital (PB) has been widely used to induce CYP2B activity to investigate the drug-drug interaction of CYP2B substrate drugs.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	50-55
25052955-2	2015	Phenobarbital (PB) has been widely used to induce CYP2B activity to investigate the drug-drug interaction of CYP2B substrate drugs.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	109-114
25052955-2	2015	Phenobarbital (PB) has been widely used to induce CYP2B activity to investigate the drug-drug interaction of CYP2B substrate drugs.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	50-55
25052955-2	2015	Phenobarbital (PB) has been widely used to induce CYP2B activity to investigate the drug-drug interaction of CYP2B substrate drugs.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	109-114
25052955-9	2015	Accordingly, we suggest that leelamine is a novel substitute of PB for the selective induction of CYP2B activity in vivo.	Phenobarbital	64-66	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	98-103
24863967-0	2014	Phenobarbital-mediated tumor promotion in transgenic mice with humanized CAR and PXR.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	73-76
25063457-5	2014	dKeap1 and CncC binding at these loci was enhanced by phenobarbital, but not by tert-butylhydroquinone (tBHQ) or paraquat.	Phenobarbital	54-67	Keap1	Drosophila melanogaster	0-6
25063457-5	2014	dKeap1 and CncC binding at these loci was enhanced by phenobarbital, but not by tert-butylhydroquinone (tBHQ) or paraquat.	Phenobarbital	54-67	cap-n-collar	Drosophila melanogaster	11-15
24863967-0	2014	Phenobarbital-mediated tumor promotion in transgenic mice with humanized CAR and PXR.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 2	Mus musculus	81-84
24863967-1	2014	The nuclear receptors CAR (constitutive androstane receptor) and possibly PXR (pregnane X receptor) mediate the hepatic effects of phenobarbital (PB) and similar-acting compounds.	Phenobarbital	131-144	nuclear receptor subfamily 1, group I, member 3	Mus musculus	22-25
24863967-1	2014	The nuclear receptors CAR (constitutive androstane receptor) and possibly PXR (pregnane X receptor) mediate the hepatic effects of phenobarbital (PB) and similar-acting compounds.	Phenobarbital	131-144	nuclear receptor subfamily 1, group I, member 3	Mus musculus	27-59
24863967-1	2014	The nuclear receptors CAR (constitutive androstane receptor) and possibly PXR (pregnane X receptor) mediate the hepatic effects of phenobarbital (PB) and similar-acting compounds.	Phenobarbital	131-144	nuclear receptor subfamily 1, group I, member 2	Mus musculus	74-77
24863967-1	2014	The nuclear receptors CAR (constitutive androstane receptor) and possibly PXR (pregnane X receptor) mediate the hepatic effects of phenobarbital (PB) and similar-acting compounds.	Phenobarbital	131-144	nuclear receptor subfamily 1, group I, member 2	Mus musculus	79-98
24863967-1	2014	The nuclear receptors CAR (constitutive androstane receptor) and possibly PXR (pregnane X receptor) mediate the hepatic effects of phenobarbital (PB) and similar-acting compounds.	Phenobarbital	146-148	nuclear receptor subfamily 1, group I, member 3	Mus musculus	22-25
24863967-1	2014	The nuclear receptors CAR (constitutive androstane receptor) and possibly PXR (pregnane X receptor) mediate the hepatic effects of phenobarbital (PB) and similar-acting compounds.	Phenobarbital	146-148	nuclear receptor subfamily 1, group I, member 3	Mus musculus	27-59
24863967-1	2014	The nuclear receptors CAR (constitutive androstane receptor) and possibly PXR (pregnane X receptor) mediate the hepatic effects of phenobarbital (PB) and similar-acting compounds.	Phenobarbital	146-148	nuclear receptor subfamily 1, group I, member 2	Mus musculus	74-77
24863967-1	2014	The nuclear receptors CAR (constitutive androstane receptor) and possibly PXR (pregnane X receptor) mediate the hepatic effects of phenobarbital (PB) and similar-acting compounds.	Phenobarbital	146-148	nuclear receptor subfamily 1, group I, member 2	Mus musculus	79-98
24863967-5	2014	Analysis of liver tumor burden revealed that PB strongly promoted the outgrowth of hepatocellular adenoma driven by activated beta-catenin in WT mice, whereas the tumor-promoting effect of PB was much less pronounced in the humanized group.	Phenobarbital	45-47	catenin (cadherin associated protein), beta 1	Mus musculus	126-138
24675475-0	2014	Phenobarbital and propiconazole toxicogenomic profiles in mice show major similarities consistent with the key role that constitutive androstane receptor (CAR) activation plays in their mode of action.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	121-153
24999631-9	2014	Likewise, basal transcript expressions of the CYP monooxygenases 1A1, 2C8 and 3A4 were comparable as was their induction when treated with a cocktail that consisted of 3-methylcholantren, rifampicin and phenobarbital, with increased expression of CYP 1A1 and 3A4 mRNA while transcript expression of CYP 2C8 was only marginally changed.	Phenobarbital	203-216	solute carrier family 45 member 2	Homo sapiens	65-73
24999631-9	2014	Likewise, basal transcript expressions of the CYP monooxygenases 1A1, 2C8 and 3A4 were comparable as was their induction when treated with a cocktail that consisted of 3-methylcholantren, rifampicin and phenobarbital, with increased expression of CYP 1A1 and 3A4 mRNA while transcript expression of CYP 2C8 was only marginally changed.	Phenobarbital	203-216	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	247-254
24999631-9	2014	Likewise, basal transcript expressions of the CYP monooxygenases 1A1, 2C8 and 3A4 were comparable as was their induction when treated with a cocktail that consisted of 3-methylcholantren, rifampicin and phenobarbital, with increased expression of CYP 1A1 and 3A4 mRNA while transcript expression of CYP 2C8 was only marginally changed.	Phenobarbital	203-216	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	299-306
24675475-0	2014	Phenobarbital and propiconazole toxicogenomic profiles in mice show major similarities consistent with the key role that constitutive androstane receptor (CAR) activation plays in their mode of action.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	155-158
24675475-9	2014	Thus, with regard to the events which are hallmarks of CAR-induced effects that are key events in the mode of action (MOA) of mouse liver carcinogenesis with PB, PPZ-induced tumors can be viewed as being promoted by a similar PB-like CAR-dependent MOA.	Phenobarbital	158-160	nuclear receptor subfamily 1, group I, member 3	Mus musculus	55-58
24764148-8	2014	Dexamethasone (200 muM) and phenobarbital (500 muM) increased activity by 230 and 124%, whereas ketoconazole (10 muM) and lipopolysaccharide (LPS) (10 mug/ml) reduced activity by 90 and 92%, respectively.	Phenobarbital	28-41	latexin	Homo sapiens	47-50
24764148-8	2014	Dexamethasone (200 muM) and phenobarbital (500 muM) increased activity by 230 and 124%, whereas ketoconazole (10 muM) and lipopolysaccharide (LPS) (10 mug/ml) reduced activity by 90 and 92%, respectively.	Phenobarbital	28-41	latexin	Homo sapiens	47-50
24641623-9	2014	Induction of UGT1A4 and UGT1A3 gene expression was also determined in human hepatocytes treated with pregnane X receptor/constitutive androstane receptor agonists, such as rifampin, carbamazepine, and phenobarbital.	Phenobarbital	201-214	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	13-19
24967961-2	2014	Recently, it has been suggested that P-glycoprotein (P-gp), which is an efflux transporter expressed on the luminal membrane of the brain capillary endothelium, is capable of transporting Abeta out of the brain.	Phenobarbital	108-115	phosphoglycolate phosphatase	Mus musculus	37-51
24967961-2	2014	Recently, it has been suggested that P-glycoprotein (P-gp), which is an efflux transporter expressed on the luminal membrane of the brain capillary endothelium, is capable of transporting Abeta out of the brain.	Phenobarbital	108-115	phosphoglycolate phosphatase	Mus musculus	53-57
24967961-2	2014	Recently, it has been suggested that P-glycoprotein (P-gp), which is an efflux transporter expressed on the luminal membrane of the brain capillary endothelium, is capable of transporting Abeta out of the brain.	Phenobarbital	108-115	amyloid beta (A4) precursor protein	Mus musculus	188-193
24641623-9	2014	Induction of UGT1A4 and UGT1A3 gene expression was also determined in human hepatocytes treated with pregnane X receptor/constitutive androstane receptor agonists, such as rifampin, carbamazepine, and phenobarbital.	Phenobarbital	201-214	UDP glucuronosyltransferase family 1 member A3	Homo sapiens	24-30
24522554-7	2014	The activation of NF-kappaB induced by NDEA/PB treatment was suppressed by DMU-212 as evidenced by a reduction of p65 and p50 subunits translocation, DNA binding capacity, increased retention of IkappaB, and the reduced IKK activity.	Phenobarbital	44-46	synaptotagmin 1	Rattus norvegicus	114-117
24727425-3	2014	Both the mitochondrial enzyme, ALA synthase (ALAS) 1, involved in the first step of heme biosynthesis, which is closely linked to mitochondrial bioenergetic pathways, and the promise of an ALAS1 siRNA hepatic therapy in humans, led us to investigate hepatic energetic metabolism in Hmbs KO mice treated with phenobarbital.	Phenobarbital	308-321	5'-aminolevulinate synthase 1	Homo sapiens	189-194
24727425-8	2014	These results suggest a cataplerosis of the TCA cycle induced by phenobarbital, caused by the massive withdrawal of succinyl-CoA by ALAS induction, such that the TCA cycle is unable to supply the reduced cofactors to the RC.	Phenobarbital	65-78	aminolevulinic acid synthase 1	Mus musculus	132-136
24821812-7	2014	dose of Alas1-siRNA prevented the phenobarbital-induced biochemical acute attacks for approximately 2 wk.	Phenobarbital	34-47	aminolevulinic acid synthase 1	Mus musculus	8-13
24690595-1	2014	The constitutive androstane receptor (CAR) and the pregnane X receptor (PXR) are closely related nuclear receptors involved in drug metabolism and play important roles in the mechanism of phenobarbital (PB)-induced rodent nongenotoxic hepatocarcinogenesis.	Phenobarbital	188-201	nuclear receptor subfamily 1, group I, member 3	Mus musculus	4-36
24690595-1	2014	The constitutive androstane receptor (CAR) and the pregnane X receptor (PXR) are closely related nuclear receptors involved in drug metabolism and play important roles in the mechanism of phenobarbital (PB)-induced rodent nongenotoxic hepatocarcinogenesis.	Phenobarbital	188-201	nuclear receptor subfamily 1, group I, member 3	Mus musculus	38-41
24690595-1	2014	The constitutive androstane receptor (CAR) and the pregnane X receptor (PXR) are closely related nuclear receptors involved in drug metabolism and play important roles in the mechanism of phenobarbital (PB)-induced rodent nongenotoxic hepatocarcinogenesis.	Phenobarbital	188-201	nuclear receptor subfamily 1, group I, member 2	Mus musculus	51-70
24690595-1	2014	The constitutive androstane receptor (CAR) and the pregnane X receptor (PXR) are closely related nuclear receptors involved in drug metabolism and play important roles in the mechanism of phenobarbital (PB)-induced rodent nongenotoxic hepatocarcinogenesis.	Phenobarbital	188-201	nuclear receptor subfamily 1, group I, member 2	Mus musculus	72-75
24690595-1	2014	The constitutive androstane receptor (CAR) and the pregnane X receptor (PXR) are closely related nuclear receptors involved in drug metabolism and play important roles in the mechanism of phenobarbital (PB)-induced rodent nongenotoxic hepatocarcinogenesis.	Phenobarbital	203-205	nuclear receptor subfamily 1, group I, member 3	Mus musculus	4-36
24690595-1	2014	The constitutive androstane receptor (CAR) and the pregnane X receptor (PXR) are closely related nuclear receptors involved in drug metabolism and play important roles in the mechanism of phenobarbital (PB)-induced rodent nongenotoxic hepatocarcinogenesis.	Phenobarbital	203-205	nuclear receptor subfamily 1, group I, member 3	Mus musculus	38-41
24690595-1	2014	The constitutive androstane receptor (CAR) and the pregnane X receptor (PXR) are closely related nuclear receptors involved in drug metabolism and play important roles in the mechanism of phenobarbital (PB)-induced rodent nongenotoxic hepatocarcinogenesis.	Phenobarbital	203-205	nuclear receptor subfamily 1, group I, member 2	Mus musculus	51-70
24690595-1	2014	The constitutive androstane receptor (CAR) and the pregnane X receptor (PXR) are closely related nuclear receptors involved in drug metabolism and play important roles in the mechanism of phenobarbital (PB)-induced rodent nongenotoxic hepatocarcinogenesis.	Phenobarbital	203-205	nuclear receptor subfamily 1, group I, member 2	Mus musculus	72-75
24690595-4	2014	Wild-type and CAR(h)-PXR(h) mouse livers exhibited temporally and quantitatively similar transcriptional responses during 91 days of PB exposure including the sustained induction of the xenobiotic response gene Cyp2b10, the Wnt signaling inhibitor Wisp1, and noncoding RNA biomarkers from the Dlk1-Dio3 locus.	Phenobarbital	133-135	nuclear receptor subfamily 1, group I, member 2	Mus musculus	14-27
24690595-5	2014	Transient induction of DNA replication (Hells, Mcm6, and Esco2) and mitotic genes (Ccnb2, Cdc20, and Cdk1) and the proliferation-related nuclear antigen Mki67 were observed with peak expression occurring between 1 and 7 days PB exposure.	Phenobarbital	225-227	antigen identified by monoclonal antibody Ki 67	Mus musculus	153-158
24690595-6	2014	All these transcriptional responses were absent in CAR(KO)-PXR(KO) mouse livers and largely reversible in wild-type and CAR(h)-PXR(h) mouse livers following 91 days of PB exposure and a subsequent 4-week recovery period.	Phenobarbital	168-170	nuclear receptor subfamily 1, group I, member 2	Mus musculus	120-133
24690595-7	2014	Furthermore, PB-mediated upregulation of the noncoding RNA Meg3, which has recently been associated with cellular pluripotency, exhibited a similar dose response and perivenous hepatocyte-specific localization in both wild-type and CAR(h)-PXR(h) mice.	Phenobarbital	13-15	maternally expressed 3	Mus musculus	59-63
24690595-7	2014	Furthermore, PB-mediated upregulation of the noncoding RNA Meg3, which has recently been associated with cellular pluripotency, exhibited a similar dose response and perivenous hepatocyte-specific localization in both wild-type and CAR(h)-PXR(h) mice.	Phenobarbital	13-15	nuclear receptor subfamily 1, group I, member 2	Mus musculus	232-245
24690595-8	2014	Thus, mouse livers coexpressing human CAR and PXR support both the xenobiotic metabolizing and the proliferative transcriptional responses following exposure to PB.	Phenobarbital	161-163	nuclear receptor subfamily 1 group I member 3	Homo sapiens	38-41
24690595-8	2014	Thus, mouse livers coexpressing human CAR and PXR support both the xenobiotic metabolizing and the proliferative transcriptional responses following exposure to PB.	Phenobarbital	161-163	nuclear receptor subfamily 1 group I member 2	Homo sapiens	46-49
24699532-3	2014	To investigate the potential clinical applications for point-of-care detection and real-time monitoring, we perform SERS detection of ten pharmaceutical compounds (hydrocodone, levorphanol, morphine, oxycodone, methadone, phenobarbital, dopamine, diltiazem, promethazine, and mitoxantrone).	Phenobarbital	222-235	seryl-tRNA synthetase 2, mitochondrial	Homo sapiens	116-120
24886712-19	2014	Phenobarbital may be particularly helpful when weaning cIV-PTB.	Phenobarbital	0-13	polypyrimidine tract binding protein 1	Homo sapiens	59-62
24449422-2	2014	Phenobarbital (PB) is a prototypical nongenotoxic carcinogen that activates the constitutive androstane receptor (CAR) resulting in rodent liver tumors.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	80-112
24789201-3	2014	Upon activation by phenobarbital (PB) or the PB-like inducer 1,4-bis[2-(3,5-dichloropyridyloxy)]-benzene (TCPOBOP), CAR translocates into the nucleus.	Phenobarbital	19-32	nuclear receptor subfamily 1 group I member 3	Homo sapiens	116-119
24789201-3	2014	Upon activation by phenobarbital (PB) or the PB-like inducer 1,4-bis[2-(3,5-dichloropyridyloxy)]-benzene (TCPOBOP), CAR translocates into the nucleus.	Phenobarbital	34-36	nuclear receptor subfamily 1 group I member 3	Homo sapiens	116-119
24789201-3	2014	Upon activation by phenobarbital (PB) or the PB-like inducer 1,4-bis[2-(3,5-dichloropyridyloxy)]-benzene (TCPOBOP), CAR translocates into the nucleus.	Phenobarbital	45-47	nuclear receptor subfamily 1 group I member 3	Homo sapiens	116-119
24789201-12	2014	Collectively, these data suggest that ubiquitin-proteasomal regulation of CCRP and HSP70 are important contributors to the regulation of cytoplasmic CAR levels, and hence the ability of CAR to respond to PB or PB-like inducers.	Phenobarbital	204-206	heat shock protein family A (Hsp70) member 4	Homo sapiens	83-88
24789201-12	2014	Collectively, these data suggest that ubiquitin-proteasomal regulation of CCRP and HSP70 are important contributors to the regulation of cytoplasmic CAR levels, and hence the ability of CAR to respond to PB or PB-like inducers.	Phenobarbital	204-206	nuclear receptor subfamily 1 group I member 3	Homo sapiens	149-152
24789201-12	2014	Collectively, these data suggest that ubiquitin-proteasomal regulation of CCRP and HSP70 are important contributors to the regulation of cytoplasmic CAR levels, and hence the ability of CAR to respond to PB or PB-like inducers.	Phenobarbital	204-206	nuclear receptor subfamily 1 group I member 3	Homo sapiens	186-189
24789201-12	2014	Collectively, these data suggest that ubiquitin-proteasomal regulation of CCRP and HSP70 are important contributors to the regulation of cytoplasmic CAR levels, and hence the ability of CAR to respond to PB or PB-like inducers.	Phenobarbital	210-212	heat shock protein family A (Hsp70) member 4	Homo sapiens	83-88
24789201-12	2014	Collectively, these data suggest that ubiquitin-proteasomal regulation of CCRP and HSP70 are important contributors to the regulation of cytoplasmic CAR levels, and hence the ability of CAR to respond to PB or PB-like inducers.	Phenobarbital	210-212	nuclear receptor subfamily 1 group I member 3	Homo sapiens	149-152
24789201-12	2014	Collectively, these data suggest that ubiquitin-proteasomal regulation of CCRP and HSP70 are important contributors to the regulation of cytoplasmic CAR levels, and hence the ability of CAR to respond to PB or PB-like inducers.	Phenobarbital	210-212	nuclear receptor subfamily 1 group I member 3	Homo sapiens	186-189
24553381-5	2014	The results revealed that CYP1A2, CYP2B6, and CYP3A4 were induced (&gt;2.0-fold) by omeprazole, phenobarbital, and rifampicin, respectively, in all the hepatocyte lots tested at enzyme activity level (23 lots) and mRNA level (8 lots).	Phenobarbital	96-109	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	26-32
24553381-5	2014	The results revealed that CYP1A2, CYP2B6, and CYP3A4 were induced (&gt;2.0-fold) by omeprazole, phenobarbital, and rifampicin, respectively, in all the hepatocyte lots tested at enzyme activity level (23 lots) and mRNA level (8 lots).	Phenobarbital	96-109	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	34-40
24553381-5	2014	The results revealed that CYP1A2, CYP2B6, and CYP3A4 were induced (&gt;2.0-fold) by omeprazole, phenobarbital, and rifampicin, respectively, in all the hepatocyte lots tested at enzyme activity level (23 lots) and mRNA level (8 lots).	Phenobarbital	96-109	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	46-52
24522335-4	2014	Relative mRNA quantification using Taqman real-time PCR assay demonstrated higher expression of AQP4 and MMP9, lower expression of CLDN5 in METH intoxication cases and lower expression of MMP2 in phenobarbital intoxication cases.	Phenobarbital	196-209	matrix metallopeptidase 2	Homo sapiens	188-192
24464994-4	2014	Furthermore, transgenic mouse models enabled us to identify which of these regulatory activities was downstream of constitutive androstane receptor and beta-catenin signaling, both crucial components of PB-mediated liver tumorigenesis.	Phenobarbital	203-205	nuclear receptor subfamily 1, group I, member 3	Mus musculus	115-147
24464994-4	2014	Furthermore, transgenic mouse models enabled us to identify which of these regulatory activities was downstream of constitutive androstane receptor and beta-catenin signaling, both crucial components of PB-mediated liver tumorigenesis.	Phenobarbital	203-205	catenin (cadherin associated protein), beta 1	Mus musculus	152-164
24464994-5	2014	We propose novel roles for E2F and ZFP161 in PB-mediated hepatocyte proliferation and suggest that PB-mediated suppression of ESR1 activity contributes to the development of a tumor-prone environment.	Phenobarbital	45-47	zinc finger and BTB domain containing 14	Mus musculus	35-41
24464994-5	2014	We propose novel roles for E2F and ZFP161 in PB-mediated hepatocyte proliferation and suggest that PB-mediated suppression of ESR1 activity contributes to the development of a tumor-prone environment.	Phenobarbital	99-101	estrogen receptor 1 (alpha)	Mus musculus	126-130
24449422-2	2014	Phenobarbital (PB) is a prototypical nongenotoxic carcinogen that activates the constitutive androstane receptor (CAR) resulting in rodent liver tumors.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	114-117
24449422-2	2014	Phenobarbital (PB) is a prototypical nongenotoxic carcinogen that activates the constitutive androstane receptor (CAR) resulting in rodent liver tumors.	Phenobarbital	15-17	nuclear receptor subfamily 1, group I, member 3	Mus musculus	80-112
24449422-2	2014	Phenobarbital (PB) is a prototypical nongenotoxic carcinogen that activates the constitutive androstane receptor (CAR) resulting in rodent liver tumors.	Phenobarbital	15-17	nuclear receptor subfamily 1, group I, member 3	Mus musculus	114-117
24650251-2	2014	Administration of rats with DEN and PB caused an elevation in the levels of malondialde-hyde (MDA), DNAF, and activities of glutathione reductase (GSR) and caspase-3, while the activities of superoxide dismutase, glutathione S-transferase, total glutathione peroxidase (t-GPx), and glutathione (GSH) level were decreased in hepatocytes compared to the control.	Phenobarbital	36-38	glutathione-disulfide reductase	Rattus norvegicus	124-145
24650251-2	2014	Administration of rats with DEN and PB caused an elevation in the levels of malondialde-hyde (MDA), DNAF, and activities of glutathione reductase (GSR) and caspase-3, while the activities of superoxide dismutase, glutathione S-transferase, total glutathione peroxidase (t-GPx), and glutathione (GSH) level were decreased in hepatocytes compared to the control.	Phenobarbital	36-38	caspase 3	Rattus norvegicus	156-165
24650251-2	2014	Administration of rats with DEN and PB caused an elevation in the levels of malondialde-hyde (MDA), DNAF, and activities of glutathione reductase (GSR) and caspase-3, while the activities of superoxide dismutase, glutathione S-transferase, total glutathione peroxidase (t-GPx), and glutathione (GSH) level were decreased in hepatocytes compared to the control.	Phenobarbital	36-38	hematopoietic prostaglandin D synthase	Rattus norvegicus	213-238
24650251-3	2014	Treatment of rats with PJ pre, during, and post DEN and PB administration improved liver function and decreased the levels of MDA, DNAF, t-GPx, GSR, and caspase-3 activities, but the GSH level did not change compared to the D-P group.	Phenobarbital	56-58	caspase 3	Rattus norvegicus	153-162
24224465-3	2014	Release and subsequent nuclear translocation of CAR is triggered through either direct binding to ligand activators such as CITCO {6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime} or through indirect chemical activation, such as with PB (phenobarbital).	Phenobarbital	275-277	nuclear receptor subfamily 1 group I member 3	Homo sapiens	48-51
24710854-13	2014	The expression of Cyp2b10 was increased 35-fold by phenobarbital, and Cyp3a11 was increased 4.5-fold by rifampin.	Phenobarbital	51-64	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	18-25
24710854-15	2014	Both phenobarbital and rifampin increased Ugt1a1, Ugt1a6, Ugt1a9, and icariin but did not show any suppressive effects on the Ugt1 family genes.	Phenobarbital	5-18	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	42-48
24710854-15	2014	Both phenobarbital and rifampin increased Ugt1a1, Ugt1a6, Ugt1a9, and icariin but did not show any suppressive effects on the Ugt1 family genes.	Phenobarbital	5-18	UDP glucuronosyltransferase 1 family, polypeptide A6A	Mus musculus	50-56
24710854-15	2014	Both phenobarbital and rifampin increased Ugt1a1, Ugt1a6, Ugt1a9, and icariin but did not show any suppressive effects on the Ugt1 family genes.	Phenobarbital	5-18	UDP glucuronosyltransferase 1 family, polypeptide A9	Mus musculus	58-64
24710854-15	2014	Both phenobarbital and rifampin increased Ugt1a1, Ugt1a6, Ugt1a9, and icariin but did not show any suppressive effects on the Ugt1 family genes.	Phenobarbital	5-18	UDP glucuronosyltransferase 1 family, polypeptide A2	Mus musculus	42-46
24368200-7	2014	Both CAR and retinoid X receptor alpha (RXRalpha) were significantly dissociated from the phenobarbital-responsive enhancer module (PBREM) of the CYP2B1 promoter in the early stages of the acute stroke.	Phenobarbital	90-103	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	146-152
24224465-3	2014	Release and subsequent nuclear translocation of CAR is triggered through either direct binding to ligand activators such as CITCO {6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime} or through indirect chemical activation, such as with PB (phenobarbital).	Phenobarbital	279-292	nuclear receptor subfamily 1 group I member 3	Homo sapiens	48-51
24255117-9	2014	In the liver, phenobarbital induced CYP2B expression in both species.	Phenobarbital	14-27	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	36-41
25052003-3	2014	In this study, HepG2 cells transfected with expression plasmid of mouse constitutive androstane receptor (CAR) or PPARalpha were treated with CFA, phenobarbital (PB) or TCPOBOP.	Phenobarbital	147-160	nuclear receptor subfamily 1, group I, member 3	Mus musculus	72-104
24418717-7	2014	On the contrary, the mRNA levels of Cyp2b1/2 and Nqo1 were suppressed and enhanced, respectively, in the PB+I3C group in the isoadditive model, but there was no enhancement in the microsomal reactive oxygen species (ROS) production, thiobarbituric acid-reactive substance levels, and Ki-67(+) cell ratio in this group.	Phenobarbital	105-107	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	36-42
24418717-7	2014	On the contrary, the mRNA levels of Cyp2b1/2 and Nqo1 were suppressed and enhanced, respectively, in the PB+I3C group in the isoadditive model, but there was no enhancement in the microsomal reactive oxygen species (ROS) production, thiobarbituric acid-reactive substance levels, and Ki-67(+) cell ratio in this group.	Phenobarbital	105-107	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	49-53
24252946-5	2014	In human hepatocytes, metformin robustly suppressed the expression of CYP2B6 induced by both indirect (phenobarbital) and direct CITCO [6-(4-chlorophenyl)imidazo[2,1-b]1,3thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime] activators of human CAR.	Phenobarbital	103-116	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	70-76
24496695-2	2014	Here, we extended the study of HLA-B*1502 susceptibility to two different antiepileptic drugs, oxcarbazepine (OXC) and phenobarbital (PB).	Phenobarbital	119-132	major histocompatibility complex, class I, B	Homo sapiens	31-36
24496695-2	2014	Here, we extended the study of HLA-B*1502 susceptibility to two different antiepileptic drugs, oxcarbazepine (OXC) and phenobarbital (PB).	Phenobarbital	134-136	major histocompatibility complex, class I, B	Homo sapiens	31-36
24496695-6	2014	The data showed that HLA-B*1502 was positive in 5 of 6 cases of AEDs-induced SJS (4 CBZ, 1 OXC and 1 PB), which was significantly more frequent than AEDs-tolerant (2/32, 18 CBZ, 6 PB and 8 OXC) and normal controls (3/38).	Phenobarbital	101-103	major histocompatibility complex, class I, B	Homo sapiens	21-26
24496695-12	2014	It was suggested that the association between the CBZ-induced SJS and HLA-B*1502 allele in Han Chinese children can extend to other aromatic AEDs including OXC and PB related SJS.	Phenobarbital	164-166	major histocompatibility complex, class I, B	Homo sapiens	70-75
23641861-4	2014	RESULTS: We demonstrate that DNJ-27 is an ER luminal protein and that its expression is induced upon ER stress via IRE-1/XBP-1.	Phenobarbital	45-52	DnaJ homolog subfamily C member 10	Caenorhabditis elegans	29-35
24494203-5	2014	Nrf2(-/-) mice showed attenuated Cyp2b10 and Cyp2a5 induction by phenobarbital, a classical Cyp2b inducer.	Phenobarbital	65-78	nuclear factor, erythroid derived 2, like 2	Mus musculus	0-4
24494203-5	2014	Nrf2(-/-) mice showed attenuated Cyp2b10 and Cyp2a5 induction by phenobarbital, a classical Cyp2b inducer.	Phenobarbital	65-78	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	33-40
24494203-5	2014	Nrf2(-/-) mice showed attenuated Cyp2b10 and Cyp2a5 induction by phenobarbital, a classical Cyp2b inducer.	Phenobarbital	65-78	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	45-51
24494203-5	2014	Nrf2(-/-) mice showed attenuated Cyp2b10 and Cyp2a5 induction by phenobarbital, a classical Cyp2b inducer.	Phenobarbital	65-78	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	33-38
25052003-3	2014	In this study, HepG2 cells transfected with expression plasmid of mouse constitutive androstane receptor (CAR) or PPARalpha were treated with CFA, phenobarbital (PB) or TCPOBOP.	Phenobarbital	147-160	nuclear receptor subfamily 1, group I, member 3	Mus musculus	106-109
25052003-3	2014	In this study, HepG2 cells transfected with expression plasmid of mouse constitutive androstane receptor (CAR) or PPARalpha were treated with CFA, phenobarbital (PB) or TCPOBOP.	Phenobarbital	162-164	nuclear receptor subfamily 1, group I, member 3	Mus musculus	72-104
25052003-3	2014	In this study, HepG2 cells transfected with expression plasmid of mouse constitutive androstane receptor (CAR) or PPARalpha were treated with CFA, phenobarbital (PB) or TCPOBOP.	Phenobarbital	162-164	nuclear receptor subfamily 1, group I, member 3	Mus musculus	106-109
24674673-8	2014	Multiple factors may affect CYP3A expression and activity, such as inducers like rifampicin, phenobarbital, 3-methylcholantrene, beta-naphtoflavone, and dexamethasone.	Phenobarbital	93-106	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	28-33
25242409-5	2014	Combined treatment of 3 or 30 mg/kg of genotoxic DEN and PB induced marked increases in altered hepatocellular foci and a DEN dose-dependent increase in the number and area of glutathione S-transferase-placental form (GST-P)-positive foci.	Phenobarbital	57-59	glutathione S-transferase pi 1	Rattus norvegicus	176-216
25242409-5	2014	Combined treatment of 3 or 30 mg/kg of genotoxic DEN and PB induced marked increases in altered hepatocellular foci and a DEN dose-dependent increase in the number and area of glutathione S-transferase-placental form (GST-P)-positive foci.	Phenobarbital	57-59	glutathione S-transferase pi 1	Rattus norvegicus	218-223
24157574-5	2013	The main effect of PB treatment from days 1 to 90 on liver miRNA was found to be the persistent, progressive, and highly correlated induction of the miR-200a/200b/429 and miR-96/182 clusters, occurring after the termination of the xenobiotic-induced transient hyperplasia.	Phenobarbital	19-21	microRNA 200a	Rattus norvegicus	149-157
25374375-4	2014	The combination of DEN and PB induced marked increases in number and area of glutathione S-transferase-placental form (GST-P)-positive foci in the liver.	Phenobarbital	27-29	glutathione S-transferase pi 1	Rattus norvegicus	77-117
25374375-4	2014	The combination of DEN and PB induced marked increases in number and area of glutathione S-transferase-placental form (GST-P)-positive foci in the liver.	Phenobarbital	27-29	glutathione S-transferase pi 1	Rattus norvegicus	119-124
25247799-0	2014	The effect of phenobarbital on gene expression levels of p53 and Dnmt1 in the liver of Wistar rats.	Phenobarbital	14-27	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	57-60
25247799-0	2014	The effect of phenobarbital on gene expression levels of p53 and Dnmt1 in the liver of Wistar rats.	Phenobarbital	14-27	DNA methyltransferase 1	Rattus norvegicus	65-70
25247799-1	2014	BACKGROUND: Our previous studies have shown that short-term treatment with phenobarbital (PB) resulted in cytosine methylation of CpG sites on the p53 gene promoter in male Wistar rats" liver.	Phenobarbital	75-88	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	147-150
25247799-1	2014	BACKGROUND: Our previous studies have shown that short-term treatment with phenobarbital (PB) resulted in cytosine methylation of CpG sites on the p53 gene promoter in male Wistar rats" liver.	Phenobarbital	90-92	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	147-150
25247799-3	2014	OBJECTIVE: Since DNA methylation is involved in regulating gene transcription and that DNMT1 is implicated in regulating DNA methylation, this study assessed whether PB-induced hypermethylation of the p53 promoter region was associated with an altered expression of p53 and Dnmt1 genes.	Phenobarbital	166-168	DNA methyltransferase 1	Rattus norvegicus	87-92
25247799-3	2014	OBJECTIVE: Since DNA methylation is involved in regulating gene transcription and that DNMT1 is implicated in regulating DNA methylation, this study assessed whether PB-induced hypermethylation of the p53 promoter region was associated with an altered expression of p53 and Dnmt1 genes.	Phenobarbital	166-168	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	201-204
25247799-3	2014	OBJECTIVE: Since DNA methylation is involved in regulating gene transcription and that DNMT1 is implicated in regulating DNA methylation, this study assessed whether PB-induced hypermethylation of the p53 promoter region was associated with an altered expression of p53 and Dnmt1 genes.	Phenobarbital	166-168	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	266-269
25247799-3	2014	OBJECTIVE: Since DNA methylation is involved in regulating gene transcription and that DNMT1 is implicated in regulating DNA methylation, this study assessed whether PB-induced hypermethylation of the p53 promoter region was associated with an altered expression of p53 and Dnmt1 genes.	Phenobarbital	166-168	DNA methyltransferase 1	Rattus norvegicus	274-279
25247799-9	2014	CONCLUSIONS: Suppression of p53 mRNA and protein expression, which is probably a result of epigenetic changes, (in particular aberrant p53 promoter hypermethylation), can be associated with tumour promoting activity of phenobarbital.	Phenobarbital	219-232	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	28-31
25247799-9	2014	CONCLUSIONS: Suppression of p53 mRNA and protein expression, which is probably a result of epigenetic changes, (in particular aberrant p53 promoter hypermethylation), can be associated with tumour promoting activity of phenobarbital.	Phenobarbital	219-232	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	135-138
24157574-5	2013	The main effect of PB treatment from days 1 to 90 on liver miRNA was found to be the persistent, progressive, and highly correlated induction of the miR-200a/200b/429 and miR-96/182 clusters, occurring after the termination of the xenobiotic-induced transient hyperplasia.	Phenobarbital	19-21	microRNA 96	Rattus norvegicus	171-177
24090815-3	2013	Significant increase of P450 total content and hydroxyl radical levels by low, high doses of ETBE and PB treatments at weeks 1 and 2, and 8-OHdG formation at week 2, accompanied accumulation of CYP2B1/2B2, CYP3A1/3A2 and CYP2C6, and downregulation of DNA oxoguanine glycosylase 1, induction of apoptosis and cell cycle arrest in hepatocytes, respectively.	Phenobarbital	102-104	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	194-200
23994662-9	2013	Interactions between this PDE5 inhibitor and PB, CZP, ETS, TGB and OXC seem to be pharmacodynamic.	Phenobarbital	45-47	phosphodiesterase 5A, cGMP-specific	Mus musculus	26-30
24180433-0	2014	Mode of action and human relevance analysis for nuclear receptor-mediated liver toxicity: A case study with phenobarbital as a model constitutive androstane receptor (CAR) activator.	Phenobarbital	108-121	nuclear receptor subfamily 1 group I member 3	Homo sapiens	133-165
24180433-0	2014	Mode of action and human relevance analysis for nuclear receptor-mediated liver toxicity: A case study with phenobarbital as a model constitutive androstane receptor (CAR) activator.	Phenobarbital	108-121	nuclear receptor subfamily 1 group I member 3	Homo sapiens	167-170
24180433-2	2014	Phenobarbital (PB) is a non-genotoxic indirect CAR activator, which induces cytochrome P450 (CYP) and other xenobiotic metabolizing enzymes and is known to produce liver foci/tumors in mice and rats.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	47-50
24180433-2	2014	Phenobarbital (PB) is a non-genotoxic indirect CAR activator, which induces cytochrome P450 (CYP) and other xenobiotic metabolizing enzymes and is known to produce liver foci/tumors in mice and rats.	Phenobarbital	0-13	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	76-91
24180433-2	2014	Phenobarbital (PB) is a non-genotoxic indirect CAR activator, which induces cytochrome P450 (CYP) and other xenobiotic metabolizing enzymes and is known to produce liver foci/tumors in mice and rats.	Phenobarbital	0-13	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	93-96
24180433-2	2014	Phenobarbital (PB) is a non-genotoxic indirect CAR activator, which induces cytochrome P450 (CYP) and other xenobiotic metabolizing enzymes and is known to produce liver foci/tumors in mice and rats.	Phenobarbital	15-17	nuclear receptor subfamily 1, group I, member 3	Mus musculus	47-50
24180433-2	2014	Phenobarbital (PB) is a non-genotoxic indirect CAR activator, which induces cytochrome P450 (CYP) and other xenobiotic metabolizing enzymes and is known to produce liver foci/tumors in mice and rats.	Phenobarbital	15-17	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	76-91
24180433-2	2014	Phenobarbital (PB) is a non-genotoxic indirect CAR activator, which induces cytochrome P450 (CYP) and other xenobiotic metabolizing enzymes and is known to produce liver foci/tumors in mice and rats.	Phenobarbital	15-17	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	93-96
24180433-5	2014	The key events in the PB-induced liver tumor MOA comprise activation of CAR followed by altered gene expression specific to CAR activation, increased cell proliferation, formation of altered hepatic foci and ultimately the development of liver tumors.	Phenobarbital	22-24	nuclear receptor subfamily 1 group I member 3	Homo sapiens	72-75
24180433-5	2014	The key events in the PB-induced liver tumor MOA comprise activation of CAR followed by altered gene expression specific to CAR activation, increased cell proliferation, formation of altered hepatic foci and ultimately the development of liver tumors.	Phenobarbital	22-24	nuclear receptor subfamily 1 group I member 3	Homo sapiens	124-127
24570836-9	2013	PB markedly decreased AST and ALT levels and protected liver and small intestine against CAP-induced toxicity.	Phenobarbital	0-2	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	22-25
24090815-3	2013	Significant increase of P450 total content and hydroxyl radical levels by low, high doses of ETBE and PB treatments at weeks 1 and 2, and 8-OHdG formation at week 2, accompanied accumulation of CYP2B1/2B2, CYP3A1/3A2 and CYP2C6, and downregulation of DNA oxoguanine glycosylase 1, induction of apoptosis and cell cycle arrest in hepatocytes, respectively.	Phenobarbital	102-104	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	206-212
24090815-3	2013	Significant increase of P450 total content and hydroxyl radical levels by low, high doses of ETBE and PB treatments at weeks 1 and 2, and 8-OHdG formation at week 2, accompanied accumulation of CYP2B1/2B2, CYP3A1/3A2 and CYP2C6, and downregulation of DNA oxoguanine glycosylase 1, induction of apoptosis and cell cycle arrest in hepatocytes, respectively.	Phenobarbital	102-104	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	221-227
24107130-5	2013	More 5-OH-PCB 136 was formed in liver tissue slices obtained from animals pretreated with phenobarbital (P450 2B inducer) or, to a lesser extent, dexamethasone (P450 2B and 3A enzyme inducer) compared to tissue slices prepared from vehicle-pretreated animals.	Phenobarbital	90-103	pyruvate carboxylase	Mus musculus	10-13
24210819-5	2013	With live intravital two-photon microscopy, we demonstrate that patrolling monocytes are attracted to and crawl onto the luminal walls of Abeta-positive veins, but not on Abeta-positive arteries or Abeta-free blood vessels.	Phenobarbital	121-128	amyloid beta precursor protein	Homo sapiens	138-143
24236482-2	2013	PATIENTS &amp; METHODS: HLA class I and HLA-DRB1 loci were genotyped for Japanese patients with zonisamide-, phenobarbital- or phenytoin-induced SJS/TEN (n = 12, 8 and 9, respectively) and for healthy Japanese volunteers (n = 2878).	Phenobarbital	109-122	major histocompatibility complex, class II, DR beta 1	Homo sapiens	24-27
23978396-6	2013	IL-1beta production was significantly decreased by PRM, CBZ, LEV, LTG, OXC, PB and lithium.	Phenobarbital	76-78	interleukin 1 beta	Homo sapiens	0-8
23978396-7	2013	IL-2 significantly decreased by PRM, CBZ, LEV, LTG, VPA, OXC, TPM and PB.	Phenobarbital	70-72	interleukin 2	Homo sapiens	0-4
23992562-6	2013	Differential diagnosis of CN1 and CN2 was made on the basis of patient"s response to phenobarbitone.	Phenobarbital	85-99	5'-nucleotidase, cytosolic IA	Homo sapiens	26-29
23992562-6	2013	Differential diagnosis of CN1 and CN2 was made on the basis of patient"s response to phenobarbitone.	Phenobarbital	85-99	carnosine dipeptidase 2	Homo sapiens	34-37
24236482-2	2013	PATIENTS &amp; METHODS: HLA class I and HLA-DRB1 loci were genotyped for Japanese patients with zonisamide-, phenobarbital- or phenytoin-induced SJS/TEN (n = 12, 8 and 9, respectively) and for healthy Japanese volunteers (n = 2878).	Phenobarbital	109-122	major histocompatibility complex, class II, DR beta 1	Homo sapiens	40-48
24236482-4	2013	Carrier frequencies of HLA-B*51:01 in patients with phenobarbital- and phenytoin-induced SJS/TEN and in controls were 75.0, 55.6 and 15.2%, respectively.	Phenobarbital	52-65	major histocompatibility complex, class I, B	Homo sapiens	23-28
24236482-5	2013	HLA-A*02:07 and HLA-B*51:01, in a dominant model, were significantly associated with zonisamide- and phenobarbital-induced SJS/TEN, respectively (Pc = 0.0176 and 0.0042, respectively).	Phenobarbital	101-114	major histocompatibility complex, class I, A	Homo sapiens	0-5
24236482-5	2013	HLA-A*02:07 and HLA-B*51:01, in a dominant model, were significantly associated with zonisamide- and phenobarbital-induced SJS/TEN, respectively (Pc = 0.0176 and 0.0042, respectively).	Phenobarbital	101-114	major histocompatibility complex, class I, B	Homo sapiens	16-21
24236482-6	2013	CONCLUSION: Our data suggest that HLA-A*02:07 and HLA-B*51:01 are potential biomarkers for zonisamide- and phenobarbital-induced SJS/TEN, respectively, in Japanese individuals.	Phenobarbital	107-120	major histocompatibility complex, class I, A	Homo sapiens	34-39
24236482-6	2013	CONCLUSION: Our data suggest that HLA-A*02:07 and HLA-B*51:01 are potential biomarkers for zonisamide- and phenobarbital-induced SJS/TEN, respectively, in Japanese individuals.	Phenobarbital	107-120	major histocompatibility complex, class I, B	Homo sapiens	50-55
23581876-0	2013	Metabolism of 2,2",3,3",6,6"-hexachlorobiphenyl (PCB 136) atropisomers in tissue slices from phenobarbital or dexamethasone-induced rats is sex-dependent.	Phenobarbital	93-106	pyruvate carboxylase	Rattus norvegicus	49-52
23726801-8	2013	In the liver CYP2AA2 expression but not that of CYP2AA1, was increased by 1,4-bis [2-(3,5-dichloropyridyloxy)] benzene (TCPOBOP) and, to a lesser extent, by phenobarbital (PB).	Phenobarbital	157-170	y cytochrome P450, family 2, subfamily AA, polypeptide 2	Danio rerio	13-20
23958353-4	2013	Immunohistochemistry analyses of patient"s prostate adenocarcinoma revealed abundant mGluR1 expression in luminal acinar epithelial cells and binding of patient"s IgGs to tumoral mGluR1.	Phenobarbital	106-113	glutamate metabotropic receptor 1	Homo sapiens	85-91
23726801-8	2013	In the liver CYP2AA2 expression but not that of CYP2AA1, was increased by 1,4-bis [2-(3,5-dichloropyridyloxy)] benzene (TCPOBOP) and, to a lesser extent, by phenobarbital (PB).	Phenobarbital	172-174	y cytochrome P450, family 2, subfamily AA, polypeptide 2	Danio rerio	13-20
24098714-6	2013	qRT-PCR experiments showed that CYP2C45 was the most highly expressed isoform in chicken liver, while CYP2C23b was the most highly induced gene by phenobarbital.	Phenobarbital	147-160	cytochrome P450 family 2 subfamily C member 23b	Gallus gallus	102-110
23458726-6	2013	RESULTS: Despite low quality RNA, archival phenobarbital samples exhibited strong induction of the positive control genes Cyp2b9 and Cyp2b10 by quantitative real-time PCR (qPCR).	Phenobarbital	43-56	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	122-128
23458726-6	2013	RESULTS: Despite low quality RNA, archival phenobarbital samples exhibited strong induction of the positive control genes Cyp2b9 and Cyp2b10 by quantitative real-time PCR (qPCR).	Phenobarbital	43-56	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	133-140
23291559-0	2013	Nuclear receptor CAR specifically activates the two-pore K+ channel Kcnk1 gene in male mouse livers, which attenuates phenobarbital-induced hepatic hyperplasia.	Phenobarbital	118-131	nuclear receptor subfamily 1, group I, member 3	Mus musculus	17-20
23581556-9	2013	CYP3A12 and CYP2B11 induction after phenobarbital or rifampin treatment was robust in both cell types but stronger in S cells.	Phenobarbital	36-49	cytochrome P450 3A12	Canis lupus familiaris	0-7
23581556-9	2013	CYP3A12 and CYP2B11 induction after phenobarbital or rifampin treatment was robust in both cell types but stronger in S cells.	Phenobarbital	36-49	cytochrome P450 2B11	Canis lupus familiaris	12-19
22897113-5	2013	Only two of the seven PB-responsive target DTs (SLCO1B3 and SLC10A1) were not constitutively expressed in cattle extra-hepatic tissues.	Phenobarbital	22-24	solute carrier family 10 member 1	Bos taurus	60-67
23143187-8	2013	In contrast, miR-122 responses to phenobarbital and doxorubicin were low.	Phenobarbital	34-47	microRNA 122	Rattus norvegicus	13-20
23190297-9	2013	The oxidase activity affording 5-OH-BP-3 was enhanced in liver microsomes of dexamethasone-, phenobarbital- and 3-methylcholanthrene-treated rats.	Phenobarbital	93-106	Blood pressure QTL 3	Rattus norvegicus	36-40
23212742-4	2013	With human hepatocytes, treatment with phenobarbital, hyperforin, carbamazepine, and rifampin significantly increased the levels of CYP3A4, but not CYP24A1 or CYP27B1 mRNA.	Phenobarbital	39-52	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	132-138
23212742-4	2013	With human hepatocytes, treatment with phenobarbital, hyperforin, carbamazepine, and rifampin significantly increased the levels of CYP3A4, but not CYP24A1 or CYP27B1 mRNA.	Phenobarbital	39-52	cytochrome P450 family 24 subfamily A member 1	Homo sapiens	148-155
23212742-4	2013	With human hepatocytes, treatment with phenobarbital, hyperforin, carbamazepine, and rifampin significantly increased the levels of CYP3A4, but not CYP24A1 or CYP27B1 mRNA.	Phenobarbital	39-52	cytochrome P450 family 27 subfamily B member 1	Homo sapiens	159-166
23253155-5	2013	Replacing the lysine at the luminal membrane border (K28) with glutamic acid (K28E) increased Abeta37 and reduced Abeta42 production.	Phenobarbital	28-35	keratin 28	Homo sapiens	53-56
23551241-0	2013	Phenobarbital-induced severe cutaneous adverse drug reactions are associated with CYP2C19*2 in Thai children.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	82-89
23858795-3	2013	Pretreatment of phenobarbital (PB) resulted in a marked increase of M-1 in three animals and of M-2in guinea pigs.	Phenobarbital	16-29	myoregulin	Homo sapiens	68-71
23858795-3	2013	Pretreatment of phenobarbital (PB) resulted in a marked increase of M-1 in three animals and of M-2in guinea pigs.	Phenobarbital	31-33	myoregulin	Homo sapiens	68-71
23858795-9	2013	These results suggest that 3"-OH-CB146 is formed by PB-inducible cytochrome P450 (CYP2B enzymes) in animal and human livers and 4-OH-CB146 is a major metabolite in rat and human liver.	Phenobarbital	52-54	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	82-87
22897113-5	2013	Only two of the seven PB-responsive target DTs (SLCO1B3 and SLC10A1) were not constitutively expressed in cattle extra-hepatic tissues.	Phenobarbital	22-24	solute carrier organic anion transporter family member 1B3	Bos taurus	48-55
23588114-7	2013	In contrast, the Kpbrain values of phenobarbital, clobazam, zonisamide, gabapentin, tiagabine, and levetiracetam in the Mdr1a/1b(-/-)/Bcrp(-/-) mice were significantly higher than the corresponding ones in Mdr1a/1b(-/-) mice.	Phenobarbital	35-48	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	120-125
23528251-4	2013	Phenobarbital (PB), a typical CAR activator, increased the gene expression of HIF-target genes in the livers of mice, including erythropoietin, heme oxygenase-1 and vascular endothelial growth factor-a.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	30-33
23528251-4	2013	Phenobarbital (PB), a typical CAR activator, increased the gene expression of HIF-target genes in the livers of mice, including erythropoietin, heme oxygenase-1 and vascular endothelial growth factor-a.	Phenobarbital	0-13	erythropoietin	Mus musculus	128-142
23528251-4	2013	Phenobarbital (PB), a typical CAR activator, increased the gene expression of HIF-target genes in the livers of mice, including erythropoietin, heme oxygenase-1 and vascular endothelial growth factor-a.	Phenobarbital	0-13	heme oxygenase 1	Mus musculus	144-201
23528251-4	2013	Phenobarbital (PB), a typical CAR activator, increased the gene expression of HIF-target genes in the livers of mice, including erythropoietin, heme oxygenase-1 and vascular endothelial growth factor-a.	Phenobarbital	15-17	nuclear receptor subfamily 1, group I, member 3	Mus musculus	30-33
23528251-4	2013	Phenobarbital (PB), a typical CAR activator, increased the gene expression of HIF-target genes in the livers of mice, including erythropoietin, heme oxygenase-1 and vascular endothelial growth factor-a.	Phenobarbital	15-17	erythropoietin	Mus musculus	128-142
23528251-4	2013	Phenobarbital (PB), a typical CAR activator, increased the gene expression of HIF-target genes in the livers of mice, including erythropoietin, heme oxygenase-1 and vascular endothelial growth factor-a.	Phenobarbital	15-17	heme oxygenase 1	Mus musculus	144-201
23528251-5	2013	PB induced an accumulation of nuclear HIF-1alpha and an increase in the HIF-responsive element-mediated transactivation in HepG2 cells.	Phenobarbital	0-2	hypoxia inducible factor 1 subunit alpha	Homo sapiens	38-48
23528251-7	2013	Immunoprecipitation-immunoblot and chromatin immunoprecipitation analyses suggest that CAR binds to the PB-responsive enhancer module with HIF-1alpha in the liver of untreated mice and that the complex dissociates upon PB treatment.	Phenobarbital	104-106	nuclear receptor subfamily 1, group I, member 3	Mus musculus	87-90
23528251-7	2013	Immunoprecipitation-immunoblot and chromatin immunoprecipitation analyses suggest that CAR binds to the PB-responsive enhancer module with HIF-1alpha in the liver of untreated mice and that the complex dissociates upon PB treatment.	Phenobarbital	104-106	hypoxia inducible factor 1, alpha subunit	Mus musculus	139-149
23652202-2	2013	This finding provides a molecular basis for the suppression of hepatocyte EGFR signaling observed with PhB treatment, as previously noted in the context of tumor promotion.	Phenobarbital	103-106	epidermal growth factor receptor	Homo sapiens	74-78
23652203-0	2013	Phenobarbital indirectly activates the constitutive active androstane receptor (CAR) by inhibition of epidermal growth factor receptor signaling.	Phenobarbital	0-13	nuclear receptor subfamily 1 group I member 3	Homo sapiens	80-83
23652203-0	2013	Phenobarbital indirectly activates the constitutive active androstane receptor (CAR) by inhibition of epidermal growth factor receptor signaling.	Phenobarbital	0-13	epidermal growth factor receptor	Homo sapiens	102-134
23652203-1	2013	Phenobarbital is a central nervous system depressant that also indirectly activates nuclear receptor constitutive active androstane receptor (CAR), which promotes drug and energy metabolism, as well as cell growth (and death), in the liver.	Phenobarbital	0-13	nuclear receptor subfamily 1 group I member 3	Homo sapiens	142-145
23652203-2	2013	We found that phenobarbital activated CAR by inhibiting epidermal growth factor receptor (EGFR) signaling.	Phenobarbital	14-27	nuclear receptor subfamily 1 group I member 3	Homo sapiens	38-41
23652203-2	2013	We found that phenobarbital activated CAR by inhibiting epidermal growth factor receptor (EGFR) signaling.	Phenobarbital	14-27	epidermal growth factor receptor	Homo sapiens	56-88
23652203-2	2013	We found that phenobarbital activated CAR by inhibiting epidermal growth factor receptor (EGFR) signaling.	Phenobarbital	14-27	epidermal growth factor receptor	Homo sapiens	90-94
23652203-3	2013	Phenobarbital bound to EGFR and potently inhibited the binding of EGF, which prevented the activation of EGFR.	Phenobarbital	0-13	epidermal growth factor receptor	Homo sapiens	23-27
23652203-3	2013	Phenobarbital bound to EGFR and potently inhibited the binding of EGF, which prevented the activation of EGFR.	Phenobarbital	0-13	epidermal growth factor receptor	Homo sapiens	105-109
23652203-5	2013	The findings demonstrated that the phenobarbital-induced mechanism of CAR dephosphorylation and activation is mediated through its direct interaction with and inhibition of EGFR.	Phenobarbital	35-48	nuclear receptor subfamily 1 group I member 3	Homo sapiens	70-73
23652203-5	2013	The findings demonstrated that the phenobarbital-induced mechanism of CAR dephosphorylation and activation is mediated through its direct interaction with and inhibition of EGFR.	Phenobarbital	35-48	epidermal growth factor receptor	Homo sapiens	173-177
23551241-9	2013	In subgroup analysis, the patients with CYP2C19*2 variant were at four times increased risk of SCARs from phenobarbital more than the patients with CYP2C19 wild type (OR = 4.5, 95% CI (1.17-17.37) p &lt; 0.03).	Phenobarbital	106-119	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-47
23551241-11	2013	CONCLUSION: CYP2C19*2 variant may play a role in the genetic predisposition of SCARs from phenobarbital.	Phenobarbital	90-103	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	12-19
23569223-3	2013	This interaction requires TorsinA to be in the ATP-bound state, and can be attributed to the luminal domains of LAP1 and LULL1.	Phenobarbital	93-100	torsin family 1 member A	Homo sapiens	26-33
23569223-3	2013	This interaction requires TorsinA to be in the ATP-bound state, and can be attributed to the luminal domains of LAP1 and LULL1.	Phenobarbital	93-100	torsin 1A interacting protein 1	Homo sapiens	112-116
23569223-3	2013	This interaction requires TorsinA to be in the ATP-bound state, and can be attributed to the luminal domains of LAP1 and LULL1.	Phenobarbital	93-100	torsin 1A interacting protein 2	Homo sapiens	121-126
23122413-5	2013	In CAA, tTG and its cross-links at the abluminal side of the vessel were demonstrated to be either of astrocytic origin in parenchymal vessels, of fibroblastic origin in leptomeningeal vessels, and of endothelial origin at the luminal side of the deposited Abeta.	Phenobarbital	41-48	transglutaminase 2	Homo sapiens	8-11
23291559-0	2013	Nuclear receptor CAR specifically activates the two-pore K+ channel Kcnk1 gene in male mouse livers, which attenuates phenobarbital-induced hepatic hyperplasia.	Phenobarbital	118-131	potassium channel, subfamily K, member 1	Mus musculus	68-73
23291559-1	2013	KCNK1, a member of the family of two-pore K(+) ion channels, is specifically induced in the livers of male mice after phenobarbital treatment.	Phenobarbital	118-131	potassium channel, subfamily K, member 1	Mus musculus	0-5
23291559-2	2013	Here, we have determined the molecular mechanism of this male-specific activation of the Kcnk1 gene and characterized KCNK1 as a phenobarbital-inducible antihyperplasia factor.	Phenobarbital	129-142	potassium channel, subfamily K, member 1	Mus musculus	118-123
23291559-3	2013	Upon activation by phenobarbital, nuclear receptor CAR binds the 97-bp response element (-2441/-2345) within the Kcnk1 promoter.	Phenobarbital	19-32	nuclear receptor subfamily 1, group I, member 3	Mus musculus	51-54
23291559-3	2013	Upon activation by phenobarbital, nuclear receptor CAR binds the 97-bp response element (-2441/-2345) within the Kcnk1 promoter.	Phenobarbital	19-32	potassium channel, subfamily K, member 1	Mus musculus	113-118
23291559-5	2013	Hyperplasia further progressed in the livers of Kcnk1  (  -/-  ) male mice compared with those of Kcnk1  (  +/+  ) males after phenobarbital treatment.	Phenobarbital	127-140	potassium channel, subfamily K, member 1	Mus musculus	48-53
23291559-6	2013	Thus, KCNK1 suppresses phenobarbital-induced hyperplasia.	Phenobarbital	23-36	potassium channel, subfamily K, member 1	Mus musculus	6-11
23291559-7	2013	These results indicate that phenobarbital treatment induces KCNK1 to elicit a male-specific and growth-suppressing signal.	Phenobarbital	28-41	potassium channel, subfamily K, member 1	Mus musculus	60-65
23062940-6	2013	Phenobarbital-type (PB-type) inducer PCBs were prevalent, indicating the predominance of less toxic PCB congeners.	Phenobarbital	0-13	pyruvate carboxylase	Homo sapiens	37-40
23358146-1	2013	We previously demonstrated the super-induced expression of the Grin2c gene encoding the N-methyl-D-aspartate receptor 2C subunit during the development of liver enlargement with hepatocellular hypertrophy induced by phenobarbital, clofibrate, or piperonyl butoxide.	Phenobarbital	216-229	glutamate ionotropic receptor NMDA type subunit 2C	Rattus norvegicus	63-69
23091169-3	2013	Molecular profiling (mRNA, microRNA [miRNA], DNA methylation, and proteins) of mouse liver during 13 weeks of PB treatment revealed progressive increases in hepatic expression of long noncoding RNAs and miRNAs originating from the Dlk1-Dio3 imprinted gene cluster, a locus that has recently been associated with stem cell pluripotency in mice and various neoplasms in humans.	Phenobarbital	110-112	delta like non-canonical Notch ligand 1	Mus musculus	231-235
23091169-3	2013	Molecular profiling (mRNA, microRNA [miRNA], DNA methylation, and proteins) of mouse liver during 13 weeks of PB treatment revealed progressive increases in hepatic expression of long noncoding RNAs and miRNAs originating from the Dlk1-Dio3 imprinted gene cluster, a locus that has recently been associated with stem cell pluripotency in mice and various neoplasms in humans.	Phenobarbital	110-112	deiodinase, iodothyronine type III	Mus musculus	236-240
23091169-4	2013	PB induction of the Dlk1-Dio3 cluster noncoding RNA (ncRNA) Meg3 was localized to glutamine synthetase-positive hypertrophic perivenous hepatocytes, suggesting a role for beta-catenin signaling in the dysregulation of Dlk1-Dio3 ncRNAs.	Phenobarbital	0-2	delta like non-canonical Notch ligand 1	Mus musculus	20-24
23091169-4	2013	PB induction of the Dlk1-Dio3 cluster noncoding RNA (ncRNA) Meg3 was localized to glutamine synthetase-positive hypertrophic perivenous hepatocytes, suggesting a role for beta-catenin signaling in the dysregulation of Dlk1-Dio3 ncRNAs.	Phenobarbital	0-2	deiodinase, iodothyronine type III	Mus musculus	25-29
23091169-4	2013	PB induction of the Dlk1-Dio3 cluster noncoding RNA (ncRNA) Meg3 was localized to glutamine synthetase-positive hypertrophic perivenous hepatocytes, suggesting a role for beta-catenin signaling in the dysregulation of Dlk1-Dio3 ncRNAs.	Phenobarbital	0-2	maternally expressed 3	Mus musculus	60-64
23091169-4	2013	PB induction of the Dlk1-Dio3 cluster noncoding RNA (ncRNA) Meg3 was localized to glutamine synthetase-positive hypertrophic perivenous hepatocytes, suggesting a role for beta-catenin signaling in the dysregulation of Dlk1-Dio3 ncRNAs.	Phenobarbital	0-2	glutamate-ammonia ligase (glutamine synthetase)	Mus musculus	82-102
23091169-4	2013	PB induction of the Dlk1-Dio3 cluster noncoding RNA (ncRNA) Meg3 was localized to glutamine synthetase-positive hypertrophic perivenous hepatocytes, suggesting a role for beta-catenin signaling in the dysregulation of Dlk1-Dio3 ncRNAs.	Phenobarbital	0-2	catenin (cadherin associated protein), beta 1	Mus musculus	171-183
23091169-4	2013	PB induction of the Dlk1-Dio3 cluster noncoding RNA (ncRNA) Meg3 was localized to glutamine synthetase-positive hypertrophic perivenous hepatocytes, suggesting a role for beta-catenin signaling in the dysregulation of Dlk1-Dio3 ncRNAs.	Phenobarbital	0-2	delta like non-canonical Notch ligand 1	Mus musculus	218-222
23091169-4	2013	PB induction of the Dlk1-Dio3 cluster noncoding RNA (ncRNA) Meg3 was localized to glutamine synthetase-positive hypertrophic perivenous hepatocytes, suggesting a role for beta-catenin signaling in the dysregulation of Dlk1-Dio3 ncRNAs.	Phenobarbital	0-2	deiodinase, iodothyronine type III	Mus musculus	223-227
24302812-0	2013	High frequency of a single nucleotide substitution (c.-6-180T&gt;G) of the canine MDR1/ABCB1 gene associated with phenobarbital-resistant idiopathic epilepsy in Border Collie dogs.	Phenobarbital	114-127	ATP binding cassette subfamily B member 1	Canis lupus familiaris	82-86
24302812-0	2013	High frequency of a single nucleotide substitution (c.-6-180T&gt;G) of the canine MDR1/ABCB1 gene associated with phenobarbital-resistant idiopathic epilepsy in Border Collie dogs.	Phenobarbital	114-127	ATP binding cassette subfamily B member 1	Canis lupus familiaris	87-92
24302812-1	2013	A single nucleotide substitution (c.-6-180T&gt;G) associated with resistance to phenobarbital therapy has been found in the canine MDR1/ABCB1 gene in Border Collies with idiopathic epilepsy.	Phenobarbital	80-93	ATP binding cassette subfamily B member 1	Canis lupus familiaris	131-135
24302812-1	2013	A single nucleotide substitution (c.-6-180T&gt;G) associated with resistance to phenobarbital therapy has been found in the canine MDR1/ABCB1 gene in Border Collies with idiopathic epilepsy.	Phenobarbital	80-93	ATP binding cassette subfamily B member 1	Canis lupus familiaris	136-141
23294302-1	2013	Xenobiotics such as phenobarbital, 2,3,7,8-tetrachlorodibenzo-p-dioxin, and Aroclor 1254 significantly suppress the activity of a key gluconeogenic and glyceroneogenic enzyme, phosphoenolpyruvate carboxykinase (PEPCK), suggesting that xenobiotics disrupt hepatic glucose and fat metabolism.	Phenobarbital	20-33	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	176-209
24210059-8	2013	For patients who used CBZ in combination with an enzyme-inducing antiepileptic drug (AED: PHT or PB), individuals carrying the CYP3A5*1 allele (CYP3A5 expressers) showed a trend of having higher CBZ clearance and lower dose-adjusted CBZ level as compared to individuals carrying the CYP3A5*3 allele, even though no statistical significance was recorded.	Phenobarbital	97-99	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	127-133
24210059-8	2013	For patients who used CBZ in combination with an enzyme-inducing antiepileptic drug (AED: PHT or PB), individuals carrying the CYP3A5*1 allele (CYP3A5 expressers) showed a trend of having higher CBZ clearance and lower dose-adjusted CBZ level as compared to individuals carrying the CYP3A5*3 allele, even though no statistical significance was recorded.	Phenobarbital	97-99	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	144-150
24210059-8	2013	For patients who used CBZ in combination with an enzyme-inducing antiepileptic drug (AED: PHT or PB), individuals carrying the CYP3A5*1 allele (CYP3A5 expressers) showed a trend of having higher CBZ clearance and lower dose-adjusted CBZ level as compared to individuals carrying the CYP3A5*3 allele, even though no statistical significance was recorded.	Phenobarbital	97-99	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	144-150
23665940-8	2013	In the isoadditive model, the average values of the area of GST-P positive foci and PCNA positive hepatocyte ratio and Gstm3 mRNA level in the PB+ORPH group were significantly higher than the average values of those in the High PB and High ORPH groups.	Phenobarbital	143-145	glutathione S-transferase pi 1	Rattus norvegicus	60-65
23294302-1	2013	Xenobiotics such as phenobarbital, 2,3,7,8-tetrachlorodibenzo-p-dioxin, and Aroclor 1254 significantly suppress the activity of a key gluconeogenic and glyceroneogenic enzyme, phosphoenolpyruvate carboxykinase (PEPCK), suggesting that xenobiotics disrupt hepatic glucose and fat metabolism.	Phenobarbital	20-33	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	211-216
23824016-1	2013	We have previously demonstrated super-induced expression of the Grin2c gene encoding the N-methyl-D-aspartate receptor 2C subunit during the process of liver enlargement induced by phenobarbital, clofibrate, piperonyl butoxide, or lead nitrate.	Phenobarbital	181-194	glutamate ionotropic receptor NMDA type subunit 2C	Rattus norvegicus	64-70
23665940-8	2013	In the isoadditive model, the average values of the area of GST-P positive foci and PCNA positive hepatocyte ratio and Gstm3 mRNA level in the PB+ORPH group were significantly higher than the average values of those in the High PB and High ORPH groups.	Phenobarbital	143-145	glutathione S-transferase mu 3	Rattus norvegicus	119-124
24025784-9	2013	In the heteroadditive model, the net values of Cyp1a1 mRNA level and microsomal reactive oxygen species (ROS) production in the PB+PBO group were significantly lower than the sum of those in the Low PB or Low PBO groups.	Phenobarbital	128-130	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	47-53
24025784-8	2013	In the isoadditive model, the average values of the area of GST-P positive foci in the PB+PBO group were significantly lower than those in the High PB or High PBO groups.	Phenobarbital	87-89	glutathione S-transferase pi 1	Rattus norvegicus	60-65
23475686-3	2013	The cells are viable, can be transfected by DNA, and retain key properties of liver cells such as the induction of cytochrome P450 gene expression by drugs such as phenobarbital.	Phenobarbital	164-177	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	115-130
22827705-7	2012	Administration of [(14)C]-4BP to phenobarbital-induced rats resulted in covalent binding of 0.25, 0.33, and 0.42 nmol equiv 4BP/mg protein in the mitochondrial, microsomal, and cytosolic fractions, respectively.	Phenobarbital	33-46	complement component 4 binding protein, alpha	Rattus norvegicus	23-29
23536761-2	2013	The most common cause of neonatal seizures is hypoxic encephalopathy, and here we show in an established model of neonatal hypoxia-induced seizures that the NKCC1 inhibitor, bumetanide, in combination with phenobarbital is significantly more effective than phenobarbital alone.	Phenobarbital	206-219	solute carrier family 12 member 2	Rattus norvegicus	157-162
23536761-2	2013	The most common cause of neonatal seizures is hypoxic encephalopathy, and here we show in an established model of neonatal hypoxia-induced seizures that the NKCC1 inhibitor, bumetanide, in combination with phenobarbital is significantly more effective than phenobarbital alone.	Phenobarbital	257-270	solute carrier family 12 member 2	Rattus norvegicus	157-162
23531792-1	2013	The constitutive androstane receptor (CAR) is essential for Cyp2b induction, liver hypertrophy, and hepatocarcinogenesis in response to phenobarbital (PB).	Phenobarbital	136-149	nuclear receptor subfamily 1, group I, member 3	Mus musculus	4-36
23531792-1	2013	The constitutive androstane receptor (CAR) is essential for Cyp2b induction, liver hypertrophy, and hepatocarcinogenesis in response to phenobarbital (PB).	Phenobarbital	136-149	nuclear receptor subfamily 1, group I, member 3	Mus musculus	38-41
23531792-1	2013	The constitutive androstane receptor (CAR) is essential for Cyp2b induction, liver hypertrophy, and hepatocarcinogenesis in response to phenobarbital (PB).	Phenobarbital	136-149	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	60-65
23531792-1	2013	The constitutive androstane receptor (CAR) is essential for Cyp2b induction, liver hypertrophy, and hepatocarcinogenesis in response to phenobarbital (PB).	Phenobarbital	151-153	nuclear receptor subfamily 1, group I, member 3	Mus musculus	4-36
23531792-1	2013	The constitutive androstane receptor (CAR) is essential for Cyp2b induction, liver hypertrophy, and hepatocarcinogenesis in response to phenobarbital (PB).	Phenobarbital	151-153	nuclear receptor subfamily 1, group I, member 3	Mus musculus	38-41
23531792-1	2013	The constitutive androstane receptor (CAR) is essential for Cyp2b induction, liver hypertrophy, and hepatocarcinogenesis in response to phenobarbital (PB).	Phenobarbital	151-153	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	60-65
23531792-6	2013	In the wild-type mice, 4-week treatment with PBO, DBDE, or PB induced hepatocellular hypertrophy with increased Cyp2b10 messenger RNA and Cyp2b protein expression.	Phenobarbital	45-47	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	112-119
23531792-6	2013	In the wild-type mice, 4-week treatment with PBO, DBDE, or PB induced hepatocellular hypertrophy with increased Cyp2b10 messenger RNA and Cyp2b protein expression.	Phenobarbital	45-47	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	112-117
22581672-8	2012	Additionally, phenobarbital exposure impaired striatal-mediated behavior on P25.	Phenobarbital	14-27	lipocalin 2	Rattus norvegicus	76-79
22859313-9	2012	Phenobarbital, dibutyryl-cAMP, and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) overexpression stimulate heme biosynthesis and induce CYP2A5.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	170-176
22694178-5	2012	Phenobarbital significantly affected hepatic CYP2B22, 2C31, 2C87, 3A and UDP-glucuronosyltransferase 1A1-like, glutathione S-transferase A1-like and sulfotransferase 1A1-like (SULT1A1-like) mRNAs and apoprotein amounts; in extra-hepatic tissues, only duodenum showed a significant down-regulation of SULT1A1-like gene and apoprotein.	Phenobarbital	0-13	sulfotransferase 1A1	Bos taurus	176-183
22694178-5	2012	Phenobarbital significantly affected hepatic CYP2B22, 2C31, 2C87, 3A and UDP-glucuronosyltransferase 1A1-like, glutathione S-transferase A1-like and sulfotransferase 1A1-like (SULT1A1-like) mRNAs and apoprotein amounts; in extra-hepatic tissues, only duodenum showed a significant down-regulation of SULT1A1-like gene and apoprotein.	Phenobarbital	0-13	sulfotransferase 1A1	Bos taurus	300-307
22465049-4	2012	Differential pulse voltammetry peak currents of AC and PB increased linearly with their concentrations at the ranges of 0.5-100 muM and 0.4-60 muM, respectively.	Phenobarbital	55-57	latexin	Homo sapiens	128-131
22521463-1	2012	ATP-binding cassette (ABC) drug efflux transporters in the CNS are predominantly localized to the luminal surface of endothelial cells in capillaries to impede CNS accumulation of xenobiotics.	Phenobarbital	98-105	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	0-20
22521463-1	2012	ATP-binding cassette (ABC) drug efflux transporters in the CNS are predominantly localized to the luminal surface of endothelial cells in capillaries to impede CNS accumulation of xenobiotics.	Phenobarbital	98-105	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	22-25
22584684-5	2012	The three nuclear receptor-activating chemicals (phenobarbital, benzophenone, and diethylhexylphthalate) were characterized by the highly correlated induction of the miR-200a/200b/429, which is involved in protecting the epithelial status of cells and of the miR-96/182 clusters.	Phenobarbital	49-62	microRNA 200a	Rattus norvegicus	166-174
22584684-5	2012	The three nuclear receptor-activating chemicals (phenobarbital, benzophenone, and diethylhexylphthalate) were characterized by the highly correlated induction of the miR-200a/200b/429, which is involved in protecting the epithelial status of cells and of the miR-96/182 clusters.	Phenobarbital	49-62	microRNA 96	Rattus norvegicus	259-265
22466357-4	2012	In Drosophila melanogaster, (hormone receptor 96) HR96 responds to phenobarbital exposure and has been hypothesized as a toxicant receptor.	Phenobarbital	67-80	Hormone receptor-like in 96	Drosophila melanogaster	50-54
22513142-0	2012	Age-related inducibility of carboxylesterases by the antiepileptic agent phenobarbital and implications in drug metabolism and lipid accumulation.	Phenobarbital	73-86	carboxylesterase 1	Homo sapiens	28-45
22627700-4	2012	Protein disulfide isomerase (PDI) is a member of the thioredoxin superfamily and is believed to accelerate the folding of disulfide-bonded proteins in the luminal space of the endoplasmic reticulum.	Phenobarbital	155-162	prolyl 4-hydroxylase subunit beta	Homo sapiens	0-27
22627700-4	2012	Protein disulfide isomerase (PDI) is a member of the thioredoxin superfamily and is believed to accelerate the folding of disulfide-bonded proteins in the luminal space of the endoplasmic reticulum.	Phenobarbital	155-162	prolyl 4-hydroxylase subunit beta	Homo sapiens	29-32
22465049-5	2012	Also, the detection limits for AC and PB were 0.17 muM and 0.1 muM, respectively.	Phenobarbital	38-40	latexin	Homo sapiens	63-66
22465049-4	2012	Differential pulse voltammetry peak currents of AC and PB increased linearly with their concentrations at the ranges of 0.5-100 muM and 0.4-60 muM, respectively.	Phenobarbital	55-57	latexin	Homo sapiens	143-146
22465049-5	2012	Also, the detection limits for AC and PB were 0.17 muM and 0.1 muM, respectively.	Phenobarbital	38-40	latexin	Homo sapiens	51-54
22213127-11	2012	UGT1A transcriptional activation by dioxin, phenobarbital, and endotoxin was significantly reduced in SNP mice.	Phenobarbital	44-57	Ugt1a@	Mus musculus	0-5
22331680-0	2012	Effects of cytochrome P450 (CYP)2C19 polymorphisms on pharmacokinetics of phenobarbital in neonates and infants with seizures.	Phenobarbital	74-87	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	28-36
22331680-2	2012	It has been reported that PB metabolism was affected by cytochrome P450 (CYP)2C19 polymorphisms in adults requiring dose adjustment.	Phenobarbital	26-28	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	73-81
22331680-3	2012	AIM: This study aimed to evaluate the effects of CYP2C19 genetic polymorphisms on PB pharmacokinetics (PK) in neonates and infants with seizures.	Phenobarbital	82-84	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	49-56
22342565-6	2012	Our results are surprising, as phenobarbital, the N-desmethyl derivative of mephobarbital, has been shown to be a substrate of Pgp, which suggests that N-methylation abolishes Pgp affinity of barbiturates.	Phenobarbital	31-44	phosphoglycolate phosphatase	Mus musculus	127-130
22342565-6	2012	Our results are surprising, as phenobarbital, the N-desmethyl derivative of mephobarbital, has been shown to be a substrate of Pgp, which suggests that N-methylation abolishes Pgp affinity of barbiturates.	Phenobarbital	31-44	phosphoglycolate phosphatase	Mus musculus	176-179
22511793-6	2012	By differential membrane extraction and sequential mutagenesis of potential N-glycosylation sites, we identified TMEM106B as a type 2 integral membrane protein with a highly glycosylated luminal domain.	Phenobarbital	187-194	transmembrane protein 106B	Homo sapiens	113-121
22382228-5	2012	Blood gas O 2 saturation dropped after she received phenobarbital.	Phenobarbital	52-65	immunoglobulin kappa variable 1D-39	Homo sapiens	10-13
22398701-9	2012	DISCUSSION: These results provide evidence that NKCC1 inhibition amplifies PB bioactivity in the immature brain and suggest that coadministration of PB and BUM may represent a clinically feasible therapy to augment the neuroprotective efficacy of therapeutic HT in asphyxiated neonates.	Phenobarbital	75-77	solute carrier family 12 member 2	Rattus norvegicus	48-53
21851322-10	2012	Both midazolam and phenobarbital prevented the convulsions and suppressed the increase in both MDA level and HO-1 mRNA expression level in the brain.	Phenobarbital	19-32	heme oxygenase 1	Mus musculus	109-113
21851322-11	2012	CONCLUSION: In this study, both midazolam and phenobarbital suppressed PTZ-induced MDA and HO-1 reactions in the brain, suggesting that these drugs inhibit brain oxidative reactions in a convulsion model.	Phenobarbital	46-59	heme oxygenase 1	Mus musculus	91-95
22215515-5	2012	After exposure to the carcinogen diethylnitrosamine (DEN) and the tumor promoter phenobarbital, male Gpat1-/- mice, compared with controls (Gpat1+/+), had 93% fewer macroscopically visible nodules per liver at 21 weeks of age and 39% fewer at 34 weeks of age.	Phenobarbital	81-94	glycerol-3-phosphate acyltransferase, mitochondrial	Mus musculus	101-106
22245121-11	2012	By 28 days of treatment, K+ PFOS and PB increased liver activities of CYP2B and CYP3A as well as increased liver CYP2B1/2 and CYP3A1 proteins, and Wy 14,643 increased CYP2B enzyme activity to a slight extent.	Phenobarbital	37-39	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	80-85
22245121-11	2012	By 28 days of treatment, K+ PFOS and PB increased liver activities of CYP2B and CYP3A as well as increased liver CYP2B1/2 and CYP3A1 proteins, and Wy 14,643 increased CYP2B enzyme activity to a slight extent.	Phenobarbital	37-39	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	113-119
22245121-11	2012	By 28 days of treatment, K+ PFOS and PB increased liver activities of CYP2B and CYP3A as well as increased liver CYP2B1/2 and CYP3A1 proteins, and Wy 14,643 increased CYP2B enzyme activity to a slight extent.	Phenobarbital	37-39	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	126-132
22187485-4	2012	Serum T(4) concentrations were reduced by all treatments, but dramatic reductions occurred in response to Aroclor-1254, PCB-99 [phenobarbital (PB)-type congener], and PCB-118 (mixed-type congener).	Phenobarbital	128-141	pyruvate carboxylase	Rattus norvegicus	120-123
21437905-5	2012	Similarly to freshly isolated cells, cultured hepatocytes also retain the ability to respond to 3-methylcholanthrene (3MC) and phenobarbital (PB), two known CYP inducers.	Phenobarbital	127-140	peptidylprolyl isomerase G	Homo sapiens	157-160
22101211-2	2012	Constitutive androstane receptor (CAR), a member of the nuclear receptor superfamily, mediates various biological actions of phenobarbital.	Phenobarbital	125-138	nuclear receptor subfamily 1 group I member 3	Homo sapiens	0-32
22101211-2	2012	Constitutive androstane receptor (CAR), a member of the nuclear receptor superfamily, mediates various biological actions of phenobarbital.	Phenobarbital	125-138	nuclear receptor subfamily 1 group I member 3	Homo sapiens	34-37
22093699-1	2012	A previous report demonstrated that treatment of human hepatocytes with phenobarbital, an activator of nuclear receptor constitutive androstane receptor (CAR), increases mRNA levels of an efflux transporter ABCG2, which is involved in the excretion of xenobiotics in liver and intestine.	Phenobarbital	72-85	nuclear receptor subfamily 1 group I member 3	Homo sapiens	120-152
22093699-1	2012	A previous report demonstrated that treatment of human hepatocytes with phenobarbital, an activator of nuclear receptor constitutive androstane receptor (CAR), increases mRNA levels of an efflux transporter ABCG2, which is involved in the excretion of xenobiotics in liver and intestine.	Phenobarbital	72-85	nuclear receptor subfamily 1 group I member 3	Homo sapiens	154-157
22093699-1	2012	A previous report demonstrated that treatment of human hepatocytes with phenobarbital, an activator of nuclear receptor constitutive androstane receptor (CAR), increases mRNA levels of an efflux transporter ABCG2, which is involved in the excretion of xenobiotics in liver and intestine.	Phenobarbital	72-85	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	207-212
22642155-3	2012	At a flow rate of 2.0 ml x min(-1), a complete determination of phenobarbital, including sampling and washing, could be accomplished in 0.5 min, offering the sampling efficiency of 120 h(-1) accordingly.	Phenobarbital	64-77	CD59 molecule (CD59 blood group)	Homo sapiens	27-33
21437905-5	2012	Similarly to freshly isolated cells, cultured hepatocytes also retain the ability to respond to 3-methylcholanthrene (3MC) and phenobarbital (PB), two known CYP inducers.	Phenobarbital	142-144	peptidylprolyl isomerase G	Homo sapiens	157-160
22467018-6	2012	AR mRNA expression decreased in all the treated groups, but reduction was persistent only in PB group.	Phenobarbital	93-95	androgen receptor	Rattus norvegicus	0-2
22467018-0	2012	Estrogen and androgen receptor status in hepatocellular hypertrophy induced by phenobarbital, clofibrate, and piperonyl butoxide in F344 rats.	Phenobarbital	79-92	androgen receptor	Rattus norvegicus	13-30
21998292-9	2012	Quantification of the transcripts by RNA-Seq and real time quantitative PCR revealed that the CYP3A4 transcript with shorter 3"-UTR was preferentially expressed in developed livers, differentiated hepatocytes, and in rifampicin- and phenobarbital-induced hepatocytes.	Phenobarbital	233-246	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	94-100
22467018-8	2012	Thus, LIFR may be one of the key mediators of hepatic carcinogenesis induced by CF and PBO, but PB appears to act via different mechanisms.	Phenobarbital	87-89	LIF receptor subunit alpha	Rattus norvegicus	6-10
22815988-0	2012	MicroRNA-122 down-regulation is involved in phenobarbital-mediated activation of the constitutive androstane receptor.	Phenobarbital	44-57	nuclear receptor subfamily 1 group I member 3	Homo sapiens	85-117
22815988-2	2012	Phenobarbital activates CAR, at least in part, in an AMP-activated protein kinase (AMPK)-dependent manner.	Phenobarbital	0-13	nuclear receptor subfamily 1 group I member 3	Homo sapiens	24-27
22815988-4	2012	In the present study, it was demonstrated that phenobarbital administration to mice decreases hepatic miR-122, a liver-enriched microRNA involved in both hepatic differentiation and function.	Phenobarbital	47-60	microRNA 122	Mus musculus	102-109
22761658-9	2012	TCC was demonstrated to be a phenobarbital-like activator of CAR in receptor-based assays.	Phenobarbital	29-42	nuclear receptor subfamily 1 group I member 3	Homo sapiens	61-64
22815988-5	2012	The time-course change in the phenobarbital-mediated down-regulation of miR-122 was inversely correlated with AMPK activation.	Phenobarbital	30-43	microRNA 122	Homo sapiens	72-79
22815988-6	2012	Phenobarbital decreased primary miR-122 to approximately 25% of the basal level as early as 1 h and suppressed transactivity of mir-122 promoter in HuH-7 cells, suggesting that the down-regulation occurred at the transcriptional level.	Phenobarbital	0-13	microRNA 122	Homo sapiens	32-39
22815988-6	2012	Phenobarbital decreased primary miR-122 to approximately 25% of the basal level as early as 1 h and suppressed transactivity of mir-122 promoter in HuH-7 cells, suggesting that the down-regulation occurred at the transcriptional level.	Phenobarbital	0-13	microRNA 122	Homo sapiens	128-135
22815988-8	2012	An inhibitory RNA specific for miR-122 increased activated AMPK and CAR-mediated trancactivation of the phenobarbital-responsive enhancer module in HepG2 cells.	Phenobarbital	104-117	microRNA 122	Homo sapiens	31-38
22761897-11	2012	Thus, DEN/PB enhanced HCC in mice lacking beta-catenin in the liver may be due to their ineptness at regulating cell survival, leading to enhanced fibrosis and regeneration through PDGFRalpha activation.	Phenobarbital	10-12	catenin (cadherin associated protein), beta 1	Mus musculus	42-54
22815988-8	2012	An inhibitory RNA specific for miR-122 increased activated AMPK and CAR-mediated trancactivation of the phenobarbital-responsive enhancer module in HepG2 cells.	Phenobarbital	104-117	nuclear receptor subfamily 1 group I member 3	Homo sapiens	68-71
22761897-11	2012	Thus, DEN/PB enhanced HCC in mice lacking beta-catenin in the liver may be due to their ineptness at regulating cell survival, leading to enhanced fibrosis and regeneration through PDGFRalpha activation.	Phenobarbital	10-12	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	181-191
22815988-12	2012	Taken together, these results suggest that phenobarbital-mediated down-regulation of miR-122 is an early and important event in the AMPK-dependent CAR activation and transactivation of its target genes.	Phenobarbital	43-56	microRNA 122	Homo sapiens	85-92
22815988-12	2012	Taken together, these results suggest that phenobarbital-mediated down-regulation of miR-122 is an early and important event in the AMPK-dependent CAR activation and transactivation of its target genes.	Phenobarbital	43-56	nuclear receptor subfamily 1 group I member 3	Homo sapiens	147-150
21970748-3	2011	Additionally, CYP2S1 expression was examined after treatments with the classic CYP-inducers beta-naphthoflavone (beta-NF, AhR activator), phenobarbital (PB, CAR activator) and dexamethasone (Dex, PXR activator).	Phenobarbital	153-155	cytochrome P450, family 2, subfamily s, polypeptide 1	Rattus norvegicus	14-20
21988088-2	2011	As observed in liver, pretreatment of phenobarbital (PB) or phenytoin were found to increase the expression of CYP2B1, CYP2B2 and associated enzyme activity in PBL.	Phenobarbital	38-51	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	111-117
21988088-2	2011	As observed in liver, pretreatment of phenobarbital (PB) or phenytoin were found to increase the expression of CYP2B1, CYP2B2 and associated enzyme activity in PBL.	Phenobarbital	38-51	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	119-125
21988088-2	2011	As observed in liver, pretreatment of phenobarbital (PB) or phenytoin were found to increase the expression of CYP2B1, CYP2B2 and associated enzyme activity in PBL.	Phenobarbital	53-55	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	111-117
21988088-2	2011	As observed in liver, pretreatment of phenobarbital (PB) or phenytoin were found to increase the expression of CYP2B1, CYP2B2 and associated enzyme activity in PBL.	Phenobarbital	53-55	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	119-125
22761897-0	2012	beta-Catenin loss in hepatocytes promotes hepatocellular cancer after diethylnitrosamine and phenobarbital administration to mice.	Phenobarbital	93-106	catenin (cadherin associated protein), beta 1	Mus musculus	0-12
22359658-4	2012	Thiopental, pentobarbital, and phenobarbital were all found to bind to apoferritin with affinities ranging from 10-500 microM, approximately matching the concentrations required to produce anesthetic and GABAergic responses.	Phenobarbital	31-44	ferritin heavy chain	Equus caballus	71-82
22382835-7	2012	From these experiments, it was suggested that the phenobarbital-induced changes in cyp2c29 and mrp3 are regulated by miR-30a and miR-29b, respectively.	Phenobarbital	50-63	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	83-90
22382835-7	2012	From these experiments, it was suggested that the phenobarbital-induced changes in cyp2c29 and mrp3 are regulated by miR-30a and miR-29b, respectively.	Phenobarbital	50-63	prolactin family 2, subfamily c, member 4	Mus musculus	95-99
22382835-7	2012	From these experiments, it was suggested that the phenobarbital-induced changes in cyp2c29 and mrp3 are regulated by miR-30a and miR-29b, respectively.	Phenobarbital	50-63	microRNA 30a	Mus musculus	117-124
22382835-8	2012	In addition, we obtained evidence that indicates a phenobarbital-mediated decrease in miR-122, a highly abundant liver-specific miRNA, leads to the activation of the transcription factor CAR and thereby induces drug-metabolizing enzymes.	Phenobarbital	51-64	microRNA 122	Mus musculus	86-93
21926048-9	2011	However, phenobarbital appeared to be associated with a higher rate of adverse drug reaction related withdrawal (ADR-related withdraw), compared to carbamazepine, valproic acid and phenytoin.	Phenobarbital	9-22	aldo-keto reductase family 1 member B	Homo sapiens	113-116
21970748-3	2011	Additionally, CYP2S1 expression was examined after treatments with the classic CYP-inducers beta-naphthoflavone (beta-NF, AhR activator), phenobarbital (PB, CAR activator) and dexamethasone (Dex, PXR activator).	Phenobarbital	138-151	cytochrome P450, family 2, subfamily s, polypeptide 1	Rattus norvegicus	14-20
21968144-2	2011	Phenobarbital (PB) is the typical inducer of cytochrome P450.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	45-60
21968144-2	2011	Phenobarbital (PB) is the typical inducer of cytochrome P450.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	45-60
21968144-4	2011	Firstly, we made a phenobarbital-induced cytochrome P450 rat model.	Phenobarbital	19-32	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	41-56
21745122-3	2011	Protein disulfide isomerase (PDI) is a member of the thioredoxin superfamily and is believed to accelerate the folding of disulfide-bonded proteins by catalyzing the disulfide interchange reaction, which is the rate-limiting step during protein folding in the luminal space of the endoplasmic reticulum.	Phenobarbital	260-267	prolyl 4-hydroxylase subunit beta	Homo sapiens	0-27
21745122-3	2011	Protein disulfide isomerase (PDI) is a member of the thioredoxin superfamily and is believed to accelerate the folding of disulfide-bonded proteins by catalyzing the disulfide interchange reaction, which is the rate-limiting step during protein folding in the luminal space of the endoplasmic reticulum.	Phenobarbital	260-267	prolyl 4-hydroxylase subunit beta	Homo sapiens	29-32
21763762-7	2011	NDEA treatment following PB exposure increased CYP2B1 mRNA expression under all tested concentrations and also increased CYP2B2 expression at 21 and 105 mug/mL.	Phenobarbital	25-27	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	47-53
21807095-5	2011	In this paper we show that, in Drosophila melanogaster, the induction response of the P450 gene Cyp6g1 to the xenobiotic Phenobarbital (PB) requires the presence of both tissue specific enhancers and a distinct CRE.	Phenobarbital	121-134	Cyp6a9-rAF4-2	Drosophila melanogaster	86-90
21807095-5	2011	In this paper we show that, in Drosophila melanogaster, the induction response of the P450 gene Cyp6g1 to the xenobiotic Phenobarbital (PB) requires the presence of both tissue specific enhancers and a distinct CRE.	Phenobarbital	121-134	Cyp6g1	Drosophila melanogaster	96-102
21807095-5	2011	In this paper we show that, in Drosophila melanogaster, the induction response of the P450 gene Cyp6g1 to the xenobiotic Phenobarbital (PB) requires the presence of both tissue specific enhancers and a distinct CRE.	Phenobarbital	121-134	mirror	Drosophila melanogaster	211-214
21807095-5	2011	In this paper we show that, in Drosophila melanogaster, the induction response of the P450 gene Cyp6g1 to the xenobiotic Phenobarbital (PB) requires the presence of both tissue specific enhancers and a distinct CRE.	Phenobarbital	136-138	Cyp6a9-rAF4-2	Drosophila melanogaster	86-90
21807095-5	2011	In this paper we show that, in Drosophila melanogaster, the induction response of the P450 gene Cyp6g1 to the xenobiotic Phenobarbital (PB) requires the presence of both tissue specific enhancers and a distinct CRE.	Phenobarbital	136-138	Cyp6g1	Drosophila melanogaster	96-102
21807095-5	2011	In this paper we show that, in Drosophila melanogaster, the induction response of the P450 gene Cyp6g1 to the xenobiotic Phenobarbital (PB) requires the presence of both tissue specific enhancers and a distinct CRE.	Phenobarbital	136-138	mirror	Drosophila melanogaster	211-214
21807095-7	2011	Site-directed mutagenesis of sequences within the CRE, sequences similar to mouse PB induction sequences, reduces the level of induction by PB, suggesting some degree of mechanistic conservation between flies and mice.	Phenobarbital	82-84	mirror	Drosophila melanogaster	50-53
21807095-7	2011	Site-directed mutagenesis of sequences within the CRE, sequences similar to mouse PB induction sequences, reduces the level of induction by PB, suggesting some degree of mechanistic conservation between flies and mice.	Phenobarbital	140-142	mirror	Drosophila melanogaster	50-53
21862659-8	2011	By comparison, phenobarbital activated hCAR-WT, whereas DEHP activated hCAR-SV23, hCAR-SV24 (with exogenous RXRalpha supplementation), and hCAR-WT.	Phenobarbital	15-28	CXADR Ig-like cell adhesion molecule	Homo sapiens	39-43
21763762-7	2011	NDEA treatment following PB exposure increased CYP2B1 mRNA expression under all tested concentrations and also increased CYP2B2 expression at 21 and 105 mug/mL.	Phenobarbital	25-27	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	121-127
21763762-8	2011	Our data suggest that the alteration of CYP2B1/2 expression by PB increased the cytotoxicity and genotoxicity of NDEA leading to the final genotoxic metabolite.	Phenobarbital	63-65	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	40-46
21741702-6	2011	For example, cytochrome P450 (CYP1A2, CYP2B2 and CYP3A2) activities were significantly elevated in spheroids exposed to beta-naphthoflavone, phenobarbital, or pregnenolone-16alpha-carbonitrile, respectively.	Phenobarbital	141-154	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	13-36
21896647-2	2011	Mutant Htt (mHtt) in the cytoplasm has been linked to induction of the luminal endoplasmic reticulum (ER) stress pathway, the unfolded protein response (UPR).	Phenobarbital	71-78	huntingtin	Homo sapiens	7-10
21726593-0	2011	Effect of vitamin E on hepatic cell proliferation and apoptosis in mice deficient in the p50 subunit of NF-kappaB after treatment with phenobarbital.	Phenobarbital	135-148	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	89-113
21726593-3	2011	We previously found that PB activates NF-kappaB and that dietary vitamin E is effective in decreasing PB-induced NF-kappaB DNA binding.	Phenobarbital	25-27	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	38-47
21726593-3	2011	We previously found that PB activates NF-kappaB and that dietary vitamin E is effective in decreasing PB-induced NF-kappaB DNA binding.	Phenobarbital	102-104	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	113-122
21726593-4	2011	We therefore hypothesized that dietary vitamin E influences PB-induced changes in cell proliferation and apoptosis through its action on NF-kappaB.	Phenobarbital	60-62	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	137-146
21689057-2	2011	Protein disulfide isomerase (PDI) is a member of the thioredoxin superfamily and is believed to accelerate the folding of disulfide-bonded proteins by catalyzing the disulfide interchange reaction, which is the rate-limiting step during protein folding in the luminal space of the endoplasmic reticulum (ER).	Phenobarbital	260-267	prolyl 4-hydroxylase subunit beta	Homo sapiens	0-27
21689057-2	2011	Protein disulfide isomerase (PDI) is a member of the thioredoxin superfamily and is believed to accelerate the folding of disulfide-bonded proteins by catalyzing the disulfide interchange reaction, which is the rate-limiting step during protein folding in the luminal space of the endoplasmic reticulum (ER).	Phenobarbital	260-267	prolyl 4-hydroxylase subunit beta	Homo sapiens	29-32
21896647-2	2011	Mutant Htt (mHtt) in the cytoplasm has been linked to induction of the luminal endoplasmic reticulum (ER) stress pathway, the unfolded protein response (UPR).	Phenobarbital	71-78	huntingtin	Mus musculus	12-16
21737571-4	2011	Because we have demonstrated that PB reduces activity of MTX influx carrier reduced folate carrier (Rfc1) in liver, we investigated the influence of the AEDs PB, carbamazepine (CBZ), or gabapentin on Rfc1-mediated MTX transport in CP.	Phenobarbital	34-36	replication factor C subunit 1	Rattus norvegicus	100-104
22008536-5	2011	Genes encoding DNA damage-inducible 45 (GADD45) family proteins, in particular GADD45g (GADD45 gamma) were down-regulated by treatment with either PB or CF for 4 and 13 weeks.	Phenobarbital	147-149	growth arrest and DNA-damage-inducible, alpha	Rattus norvegicus	40-46
22008536-5	2011	Genes encoding DNA damage-inducible 45 (GADD45) family proteins, in particular GADD45g (GADD45 gamma) were down-regulated by treatment with either PB or CF for 4 and 13 weeks.	Phenobarbital	147-149	growth arrest and DNA-damage-inducible, gamma	Rattus norvegicus	79-86
22008536-5	2011	Genes encoding DNA damage-inducible 45 (GADD45) family proteins, in particular GADD45g (GADD45 gamma) were down-regulated by treatment with either PB or CF for 4 and 13 weeks.	Phenobarbital	147-149	growth arrest and DNA-damage-inducible, gamma	Rattus norvegicus	88-100
22008536-7	2011	Additionally, DNA microarray data indicated that cell cycle-related genes such as cyclins CCNB1 and CCNA2 and cyclin-dependent kinase inhibitor CDKN3 were also down-regulated by treatment with either PB or CF at 13 weeks.	Phenobarbital	200-202	cyclin B1	Rattus norvegicus	90-95
22008536-7	2011	Additionally, DNA microarray data indicated that cell cycle-related genes such as cyclins CCNB1 and CCNA2 and cyclin-dependent kinase inhibitor CDKN3 were also down-regulated by treatment with either PB or CF at 13 weeks.	Phenobarbital	200-202	cyclin A2	Rattus norvegicus	100-105
22008536-7	2011	Additionally, DNA microarray data indicated that cell cycle-related genes such as cyclins CCNB1 and CCNA2 and cyclin-dependent kinase inhibitor CDKN3 were also down-regulated by treatment with either PB or CF at 13 weeks.	Phenobarbital	200-202	cyclin-dependent kinase inhibitor 3	Rattus norvegicus	144-149
21737571-8	2011	PB and CBZ but not gabapentin significantly inhibited Rfc1-mediated uptake of MTX in CP cells.	Phenobarbital	0-2	replication factor C subunit 1	Rattus norvegicus	54-58
21737571-9	2011	Studies on the regulatory mechanism showed that PB significantly inhibited Rfc1 translation but did not alter carrier gene expression.	Phenobarbital	48-50	replication factor C subunit 1	Rattus norvegicus	75-79
21737571-11	2011	Antiepileptic treatment with PB or CBZ causes post-transcriptional down-regulation of Rfc1 activity in CP.	Phenobarbital	29-31	replication factor C subunit 1	Rattus norvegicus	86-90
21564387-1	2011	BACKGROUND: Phenobarbital induces specific hepatic cytochrome P-450 enzyme pathways causing increased clearance of hepatically metabolized drugs.	Phenobarbital	12-25	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	51-67
21737571-4	2011	Because we have demonstrated that PB reduces activity of MTX influx carrier reduced folate carrier (Rfc1) in liver, we investigated the influence of the AEDs PB, carbamazepine (CBZ), or gabapentin on Rfc1-mediated MTX transport in CP.	Phenobarbital	34-36	replication factor C subunit 1	Rattus norvegicus	200-204
21896655-5	2011	A binding site for CncC and its heterodimer partner Maf (muscle aponeurosis fibromatosis) is sufficient and necessary for robust transcriptional responses to three xenobiotic compounds: phenobarbital (PB), chlorpromazine, and caffeine.	Phenobarbital	186-199	cap-n-collar	Drosophila melanogaster	19-23
21896655-5	2011	A binding site for CncC and its heterodimer partner Maf (muscle aponeurosis fibromatosis) is sufficient and necessary for robust transcriptional responses to three xenobiotic compounds: phenobarbital (PB), chlorpromazine, and caffeine.	Phenobarbital	201-203	cap-n-collar	Drosophila melanogaster	19-23
21494841-16	2011	Phenobarbital is the most cost-effective drug and can be used to control the seizures of JME when antiepileptic drugs are limited or too costly.	Phenobarbital	0-13	myoclonic epilepsy, juvenile, 2	Homo sapiens	89-92
21832258-5	2011	In the 96-well plate induction assay, the CYP3A4 inducers rifampin, phenobarbital, carbamazepine, phenytoin, troglitazone, rosiglitazone, and pioglitazone yielded dose-dependent induction of LIPA metabolism, whereas the CYP1A2 inducers omeprazole and 3-methylcholanthrene did not display any induction in the CYP3A4 activity.	Phenobarbital	68-81	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	42-48
21445586-3	2011	The PB-induced increase in the number and area of glutathione S-transferase placental form-positive foci and the proliferating cell nuclear antigen-positive ratio was significantly suppressed by EMIQ.	Phenobarbital	4-6	hematopoietic prostaglandin D synthase	Rattus norvegicus	50-75
21574168-0	2011	Hepatocyte proliferation and hepatomegaly induced by phenobarbital and 1,4-bis [2-(3,5-dichloropyridyloxy)] benzene is suppressed in hepatocyte-targeted glypican 3 transgenic mice.	Phenobarbital	53-66	glypican 3	Mus musculus	153-163
21574168-4	2011	This study investigates the role of GPC3 in hepatocyte proliferation and hepatomegaly induced by the xenobiotic mitogens phenobarbital (PB) and TCPOBOP (1, 4-bis [2-(3, 5-dichloropyridyloxy)] benzene).	Phenobarbital	121-134	glypican 3	Mus musculus	36-40
21574168-4	2011	This study investigates the role of GPC3 in hepatocyte proliferation and hepatomegaly induced by the xenobiotic mitogens phenobarbital (PB) and TCPOBOP (1, 4-bis [2-(3, 5-dichloropyridyloxy)] benzene).	Phenobarbital	136-138	glypican 3	Mus musculus	36-40
21574168-6	2011	At day 5 the WT mice showed a 2.2- and 3.0-fold increase in liver weight, whereas the GPC3 TG mice showed a 1.3- and 1.6-fold increase in liver weight after PB and TCPOBOP administration, respectively.	Phenobarbital	157-159	glypican 3	Mus musculus	86-90
21481568-0	2011	Different effects of high- and low-dose phenobarbital on post-stroke seizure suppression and recovery in immature CD1 mice.	Phenobarbital	40-53	CD1 antigen complex	Mus musculus	114-117
21169640-14	2011	CONCLUSION: Phenobarbital (40 mg/kg) given in the first two hours of life in term neonates with perinatal asphyxia led to a decrease in CSF levels of lipid peroxides and antioxidant enzymes at 12 +- 2 hours of life.	Phenobarbital	12-25	colony stimulating factor 2	Homo sapiens	136-139
21492891-8	2011	Our work showed that adverse effects in epileptics under high doses of AVP was related to the association of the AVP with other antiepileptic in particular carbamazepine, phenobarbital and benzodiazepines rather than supra-therapeutic plasmatic concentrations of AVP.	Phenobarbital	171-184	arginine vasopressin	Homo sapiens	71-74
21492891-8	2011	Our work showed that adverse effects in epileptics under high doses of AVP was related to the association of the AVP with other antiepileptic in particular carbamazepine, phenobarbital and benzodiazepines rather than supra-therapeutic plasmatic concentrations of AVP.	Phenobarbital	171-184	arginine vasopressin	Homo sapiens	113-116
21492891-8	2011	Our work showed that adverse effects in epileptics under high doses of AVP was related to the association of the AVP with other antiepileptic in particular carbamazepine, phenobarbital and benzodiazepines rather than supra-therapeutic plasmatic concentrations of AVP.	Phenobarbital	171-184	arginine vasopressin	Homo sapiens	113-116
21492891-10	2011	CONCLUSION: Consequently, clinical signs of liver toxicity may be present in AVP concentrations generally considered in the therapeutic range especially when used in high doses and or combined with antiepileptic drugs like phenobarbital or carbamazepine.	Phenobarbital	223-236	arginine vasopressin	Homo sapiens	77-80
21420387-2	2011	Differential induction of liver microsomal CYP activities following treatment of rats with aryl hydrocarbons or phenobarbital, discovered over 50 years ago, initiated studies to characterize multiple CYPs and the transcription factors Ah receptor (AhR) and CAR, respectively.	Phenobarbital	112-125	aryl hydrocarbon receptor	Rattus norvegicus	235-246
21420387-2	2011	Differential induction of liver microsomal CYP activities following treatment of rats with aryl hydrocarbons or phenobarbital, discovered over 50 years ago, initiated studies to characterize multiple CYPs and the transcription factors Ah receptor (AhR) and CAR, respectively.	Phenobarbital	112-125	aryl hydrocarbon receptor	Rattus norvegicus	248-251
21872825-1	2011	Phenobarbital (PB), a nongenotoxic carcinogen, activates the nuclear constitutive active/androstane receptor (CAR), resulting in the transcriptional induction or repression of various hepatic genes.	Phenobarbital	0-13	nuclear receptor subfamily 1 group I member 3	Homo sapiens	110-113
21872825-1	2011	Phenobarbital (PB), a nongenotoxic carcinogen, activates the nuclear constitutive active/androstane receptor (CAR), resulting in the transcriptional induction or repression of various hepatic genes.	Phenobarbital	15-17	nuclear receptor subfamily 1 group I member 3	Homo sapiens	69-108
21872825-1	2011	Phenobarbital (PB), a nongenotoxic carcinogen, activates the nuclear constitutive active/androstane receptor (CAR), resulting in the transcriptional induction or repression of various hepatic genes.	Phenobarbital	15-17	nuclear receptor subfamily 1 group I member 3	Homo sapiens	110-113
21872825-2	2011	We previously demonstrated that liver tumors developed after chronic PB treatment only when CAR is present.	Phenobarbital	69-71	nuclear receptor subfamily 1 group I member 3	Homo sapiens	92-95
21872825-5	2011	Tuba8 mRNA was induced with PB treatment in mouse livers before tumor development as well as in tumor tissues.	Phenobarbital	28-30	tubulin, alpha 8	Mus musculus	0-5
21424122-1	2011	The nuclear xenobiotic receptor CAR is a phenobarbital (PB)-activated transcription factor.	Phenobarbital	41-54	nuclear receptor subfamily 1, group I, member 3	Mus musculus	32-35
21424122-2	2011	Using a mouse model of two-step liver tumorigenesis, in which tumor growth was initiated by diethyl nitrosamine (DEN) and promoted by chronic treatment with PB, we previously demonstrated that tumors developed only in the presence of CAR.	Phenobarbital	157-159	nuclear receptor subfamily 1, group I, member 3	Mus musculus	234-237
21424122-3	2011	Here, we have identified the FAM84A (family with sequence similarity 84, member A) gene as a CAR-regulated gene that is over-expressed during development of phenobarbital-promoted mouse liver tumors.	Phenobarbital	157-170	LRAT domain containing 1	Mus musculus	29-35
21424122-3	2011	Here, we have identified the FAM84A (family with sequence similarity 84, member A) gene as a CAR-regulated gene that is over-expressed during development of phenobarbital-promoted mouse liver tumors.	Phenobarbital	157-170	nuclear receptor subfamily 1, group I, member 3	Mus musculus	93-96
21424122-4	2011	FAM84A mRNA was induced in the liver of DEN/PB-treated mice prior to the development of liver tumors and this induction continued in the non-tumor as well as tumor tissues of a tumor-bearing liver.	Phenobarbital	44-46	LRAT domain containing 1	Mus musculus	0-6
21424122-5	2011	Western blotting demonstated that FAM84A protein expression increased in mouse liver after PB treatment; however, the FAM84A protein in liver and liver tumors was not phosphorylated at the serine 38 residue, which has been reported to correlate with morphological changes in cells.	Phenobarbital	91-93	LRAT domain containing 1	Mus musculus	34-40
21872825-1	2011	Phenobarbital (PB), a nongenotoxic carcinogen, activates the nuclear constitutive active/androstane receptor (CAR), resulting in the transcriptional induction or repression of various hepatic genes.	Phenobarbital	0-13	nuclear receptor subfamily 1 group I member 3	Homo sapiens	69-108
21765560-6	2011	We examined the PB inducibility of CYP6D1v1 promoter from LPR using dual luciferase reporter assays in Drosophila S2 cells and found the CYP6D1v1 promoter was able to mediate PB induction, similar to the CYP6D1v2 promoter from the insecticide susceptible CS strain.	Phenobarbital	16-18	Liprin-alpha	Drosophila melanogaster	58-61
21765560-8	2011	HR96 has been implicated in having a role in PB induction in Drosophila melanogaster and M. domestica.	Phenobarbital	45-47	Hormone receptor-like in 96	Drosophila melanogaster	0-4
21455306-0	2011	Phenobarbital mediates an epigenetic switch at the constitutive androstane receptor (CAR) target gene Cyp2b10 in the liver of B6C3F1 mice.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	51-83
21111054-4	2011	METHODS: To evaluate the xenobiotic-mediated induction of hepatocellular gene expression, the prototypical inducers rifampicin (10 muM) and phenobarbital (1 mM) were used for CYP3A4, CITCO (1 muM) and artemisinin (50 muM) were used for CYP2B6, and 3-methylcholanthrene (1 muM) and omeprazole (50 muM) were utilized for induction of CYP1A2.	Phenobarbital	140-153	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	175-181
21111054-4	2011	METHODS: To evaluate the xenobiotic-mediated induction of hepatocellular gene expression, the prototypical inducers rifampicin (10 muM) and phenobarbital (1 mM) were used for CYP3A4, CITCO (1 muM) and artemisinin (50 muM) were used for CYP2B6, and 3-methylcholanthrene (1 muM) and omeprazole (50 muM) were utilized for induction of CYP1A2.	Phenobarbital	140-153	latexin	Homo sapiens	192-195
21111054-4	2011	METHODS: To evaluate the xenobiotic-mediated induction of hepatocellular gene expression, the prototypical inducers rifampicin (10 muM) and phenobarbital (1 mM) were used for CYP3A4, CITCO (1 muM) and artemisinin (50 muM) were used for CYP2B6, and 3-methylcholanthrene (1 muM) and omeprazole (50 muM) were utilized for induction of CYP1A2.	Phenobarbital	140-153	latexin	Homo sapiens	192-195
21111054-4	2011	METHODS: To evaluate the xenobiotic-mediated induction of hepatocellular gene expression, the prototypical inducers rifampicin (10 muM) and phenobarbital (1 mM) were used for CYP3A4, CITCO (1 muM) and artemisinin (50 muM) were used for CYP2B6, and 3-methylcholanthrene (1 muM) and omeprazole (50 muM) were utilized for induction of CYP1A2.	Phenobarbital	140-153	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	236-242
21111054-4	2011	METHODS: To evaluate the xenobiotic-mediated induction of hepatocellular gene expression, the prototypical inducers rifampicin (10 muM) and phenobarbital (1 mM) were used for CYP3A4, CITCO (1 muM) and artemisinin (50 muM) were used for CYP2B6, and 3-methylcholanthrene (1 muM) and omeprazole (50 muM) were utilized for induction of CYP1A2.	Phenobarbital	140-153	latexin	Homo sapiens	192-195
21111054-4	2011	METHODS: To evaluate the xenobiotic-mediated induction of hepatocellular gene expression, the prototypical inducers rifampicin (10 muM) and phenobarbital (1 mM) were used for CYP3A4, CITCO (1 muM) and artemisinin (50 muM) were used for CYP2B6, and 3-methylcholanthrene (1 muM) and omeprazole (50 muM) were utilized for induction of CYP1A2.	Phenobarbital	140-153	latexin	Homo sapiens	192-195
21111054-4	2011	METHODS: To evaluate the xenobiotic-mediated induction of hepatocellular gene expression, the prototypical inducers rifampicin (10 muM) and phenobarbital (1 mM) were used for CYP3A4, CITCO (1 muM) and artemisinin (50 muM) were used for CYP2B6, and 3-methylcholanthrene (1 muM) and omeprazole (50 muM) were utilized for induction of CYP1A2.	Phenobarbital	140-153	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	332-338
21130899-8	2011	Analysis of sequence and synteny identifies cormorant and finch CYPs that are apparent orthologs of phenobarbital-inducible chicken CYP2C45.	Phenobarbital	100-113	cytochrome P450 family 2 subfamily C member 18	Gallus gallus	132-139
21336540-11	2011	Our results suggested that VER may regulate the transport of PB across BBB in a concentration-dependently biphasic manner and the biphasic regulation may be involved in P-gp function.	Phenobarbital	61-63	phosphoglycolate phosphatase	Rattus norvegicus	169-173
21488961-0	2011	Polymorphisms in the ABCB1 gene in phenobarbital responsive and resistant idiopathic epileptic Border Collies.	Phenobarbital	35-48	ATP binding cassette subfamily B member 1	Canis lupus familiaris	21-26
21488961-2	2011	HYPOTHESIS/OBJECTIVES: Variation in the ABCB1 gene encoding the permeability-glycoprotein could have an influence on phenobarbital (PB) resistance, which occurs with high frequency in idiopathic epileptic Border Collies (BCs).	Phenobarbital	117-130	ATP binding cassette subfamily B member 1	Canis lupus familiaris	40-45
21488961-2	2011	HYPOTHESIS/OBJECTIVES: Variation in the ABCB1 gene encoding the permeability-glycoprotein could have an influence on phenobarbital (PB) resistance, which occurs with high frequency in idiopathic epileptic Border Collies (BCs).	Phenobarbital	132-134	ATP binding cassette subfamily B member 1	Canis lupus familiaris	40-45
20661683-2	2011	The aim of the present study was to investigate potential involvement of selected MMPs in the pathogenesis of neuronal apoptosis induced by the NMDA antagonist MK-801 (dizocilpine) or the GABA(A) agonist phenobarbital in infant rats, transgenic rats overexpressing MMP-9 and MMP-9 knockout mice.	Phenobarbital	204-217	matrix metallopeptidase 2	Rattus norvegicus	82-86
20661683-9	2011	The extent of neurodegeneration induced by MK-801 or phenobarbital was not altered in MMP-9 transgenic rats and was increased in MMP-9 knockout mice compared to wild-type rats and mice.	Phenobarbital	53-66	matrix metallopeptidase 9	Rattus norvegicus	129-134
21338669-6	2011	AEDs can induce various hormonal abnormalities; in particular, the use of the liver enzyme inducing AEDs, such as phenobarbital, phenytoin and carbamazepine, which increases serum sex hormone binding globulin (SHBG) concentrations.	Phenobarbital	114-127	sex hormone binding globulin	Homo sapiens	180-208
21338669-6	2011	AEDs can induce various hormonal abnormalities; in particular, the use of the liver enzyme inducing AEDs, such as phenobarbital, phenytoin and carbamazepine, which increases serum sex hormone binding globulin (SHBG) concentrations.	Phenobarbital	114-127	sex hormone binding globulin	Homo sapiens	210-214
21455306-0	2011	Phenobarbital mediates an epigenetic switch at the constitutive androstane receptor (CAR) target gene Cyp2b10 in the liver of B6C3F1 mice.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	85-88
21455306-0	2011	Phenobarbital mediates an epigenetic switch at the constitutive androstane receptor (CAR) target gene Cyp2b10 in the liver of B6C3F1 mice.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	102-109
21455306-6	2011	However, the constitutive androstane receptor (CAR) target gene Cyp2b10 was found to be concomitantly hypomethylated and transcriptionally activated in a liver tissue-specific manner following PB treatment.	Phenobarbital	193-195	nuclear receptor subfamily 1, group I, member 3	Mus musculus	13-45
21455306-6	2011	However, the constitutive androstane receptor (CAR) target gene Cyp2b10 was found to be concomitantly hypomethylated and transcriptionally activated in a liver tissue-specific manner following PB treatment.	Phenobarbital	193-195	nuclear receptor subfamily 1, group I, member 3	Mus musculus	47-50
21455306-6	2011	However, the constitutive androstane receptor (CAR) target gene Cyp2b10 was found to be concomitantly hypomethylated and transcriptionally activated in a liver tissue-specific manner following PB treatment.	Phenobarbital	193-195	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	64-71
21455306-8	2011	Our data reveal that PB-induced transcriptional perturbations are not generally associated with broad changes in the DNA methylation status at proximal promoters and suggest that the drug-inducible CAR pathway regulates an epigenetic switch from repressive to active chromatin at the target gene Cyp2b10.	Phenobarbital	21-23	nuclear receptor subfamily 1, group I, member 3	Mus musculus	198-201
21455306-8	2011	Our data reveal that PB-induced transcriptional perturbations are not generally associated with broad changes in the DNA methylation status at proximal promoters and suggest that the drug-inducible CAR pathway regulates an epigenetic switch from repressive to active chromatin at the target gene Cyp2b10.	Phenobarbital	21-23	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	296-303
21912117-9	2011	CONCLUSIONS: Our results demonstrate that PB treatment causes downregulation of Rfc1 activity through PKC-dependent accelerated degradation of the Rfc1 protein by the ubiqutin-proteasome pathway.	Phenobarbital	42-44	replication factor C subunit 1	Homo sapiens	147-151
21246600-6	2011	Treatment with phenobarbital, pregabalin, primidone, or topiramate was associated with lower vitamin B12 levels compared with the entire group of patients.	Phenobarbital	15-28	NADH:ubiquinone oxidoreductase subunit B3	Homo sapiens	101-104
21204821-4	2011	The use of the liver enzyme-inducing AEDs--such as phenobarbital, phenytoin, and carbamazepine--can increase serum sex hormone-binding globulin concentrations, leading to diminished bioactivity of testosterone (T) and estradiol.	Phenobarbital	51-64	sex hormone binding globulin	Homo sapiens	115-143
21343881-6	2011	Neuromelanin-laden C1q-positive cells were also attached to the luminal surfaces of blood vessels in the SNc in PD.	Phenobarbital	64-71	complement C1q A chain	Homo sapiens	19-22
20877347-7	2011	Full protection against induced phenobarbital-attacks was achieved in animals showing over 10% of hepatocytes expressing high amounts of PBGD.	Phenobarbital	32-45	hydroxymethylbilane synthase	Mus musculus	137-141
20877347-8	2011	More importantly, sustained hepatic expression of hPBGD protected against loss of large-caliber axons in the sciatic nerve and disturbances in nerve conduction velocity as induced by recurrent phenobarbital administrations.	Phenobarbital	193-206	hydroxymethylbilane synthase	Homo sapiens	50-55
21356386-4	2011	We have used three different complementary approaches: i) diethylnitrosamine (DEN)-induced chemical hepatocarcinogenesis in COX-2 Tg mice, ii) DEN/phenobarbital treatment of human COX-2 Tg hepatocyte-like cells, and iii) COX-2 Tg hepatocyte-like cells implants in nude mice.	Phenobarbital	147-160	prostaglandin-endoperoxide synthase 2	Mus musculus	180-185
21356386-4	2011	We have used three different complementary approaches: i) diethylnitrosamine (DEN)-induced chemical hepatocarcinogenesis in COX-2 Tg mice, ii) DEN/phenobarbital treatment of human COX-2 Tg hepatocyte-like cells, and iii) COX-2 Tg hepatocyte-like cells implants in nude mice.	Phenobarbital	147-160	prostaglandin-endoperoxide synthase 2	Mus musculus	180-185
21029232-0	2011	Hormone receptor-like in 96 and Broad-Complex modulate phenobarbital induced transcription of cytochrome P450 CYP6D1 in Drosophila S2 cells.	Phenobarbital	55-68	Hormone receptor-like in 96	Drosophila melanogaster	0-27
21029232-0	2011	Hormone receptor-like in 96 and Broad-Complex modulate phenobarbital induced transcription of cytochrome P450 CYP6D1 in Drosophila S2 cells.	Phenobarbital	55-68	Cytochrome P450-4d1	Drosophila melanogaster	110-116
21029232-7	2011	RNA interference (RNAi) treatment of S2 cells in conjunction with CYP6D1 promoter assays showed that suppression of Drosophila HR96 and BR-C transcription in S2 cells resulted in a significant decrease and increase, respectively, of PB induction.	Phenobarbital	233-235	Hormone receptor-like in 96	Drosophila melanogaster	127-131
21029232-8	2011	Effects of HR96 and BR-C in mediating PB induction were PB specific and PB dependent.	Phenobarbital	38-40	Hormone receptor-like in 96	Drosophila melanogaster	11-15
21029232-8	2011	Effects of HR96 and BR-C in mediating PB induction were PB specific and PB dependent.	Phenobarbital	56-58	Hormone receptor-like in 96	Drosophila melanogaster	11-15
20637316-1	2011	Mammalian cytochrome P450 2B4 (CYP2B4) is a phenobarbital-inducible rabbit hepatic monooxygenase that catalyzes the N-demethylation of benzphetamine and metabolism of numerous other compounds.	Phenobarbital	44-57	cytochrome P450 2B4	Oryctolagus cuniculus	10-29
20637316-1	2011	Mammalian cytochrome P450 2B4 (CYP2B4) is a phenobarbital-inducible rabbit hepatic monooxygenase that catalyzes the N-demethylation of benzphetamine and metabolism of numerous other compounds.	Phenobarbital	44-57	cytochrome P450 2B4	Oryctolagus cuniculus	31-37
21047994-1	2011	The antiepileptic drug phenobarbital (PB) is a potent tumor promoter in mouse liver, where it stimulates the selective outgrowth of tumor populations harboring activating mutations in Ctnnb1, encoding beta-catenin.	Phenobarbital	23-36	catenin (cadherin associated protein), beta 1	Mus musculus	184-190
21047994-1	2011	The antiepileptic drug phenobarbital (PB) is a potent tumor promoter in mouse liver, where it stimulates the selective outgrowth of tumor populations harboring activating mutations in Ctnnb1, encoding beta-catenin.	Phenobarbital	23-36	catenin (cadherin associated protein), beta 1	Mus musculus	201-213
21047994-1	2011	The antiepileptic drug phenobarbital (PB) is a potent tumor promoter in mouse liver, where it stimulates the selective outgrowth of tumor populations harboring activating mutations in Ctnnb1, encoding beta-catenin.	Phenobarbital	38-40	catenin (cadherin associated protein), beta 1	Mus musculus	184-190
21047994-1	2011	The antiepileptic drug phenobarbital (PB) is a potent tumor promoter in mouse liver, where it stimulates the selective outgrowth of tumor populations harboring activating mutations in Ctnnb1, encoding beta-catenin.	Phenobarbital	38-40	catenin (cadherin associated protein), beta 1	Mus musculus	201-213
21047994-5	2011	PB strongly enhanced liver tumor formation in Ctnnb1 wild-type mice, and 90% of the PB-promoted tumors were Ctnnb1-mutated.	Phenobarbital	0-2	catenin (cadherin associated protein), beta 1	Mus musculus	46-52
21047994-5	2011	PB strongly enhanced liver tumor formation in Ctnnb1 wild-type mice, and 90% of the PB-promoted tumors were Ctnnb1-mutated.	Phenobarbital	84-86	catenin (cadherin associated protein), beta 1	Mus musculus	108-114
21047994-10	2011	In summary, our data demonstrate that (i) liver tumor promotion by PB requires functional beta-catenin signaling and (ii) absence of beta-catenin enhances carcinogen-induced hepatocarcinogenesis and induces a pre-cirrhotic phenotype in mouse liver.	Phenobarbital	67-69	catenin (cadherin associated protein), beta 1	Mus musculus	90-102
21912117-5	2011	Pretreatment with PB significantly reduced Rfc1-mediated MTX uptake and shortened the carrier protein half-life.	Phenobarbital	18-20	replication factor C subunit 1	Homo sapiens	43-47
21912117-8	2011	Finally, we demonstrated that PB treatment resulted in enhanced levels of Rfc1 polyubiquitin conjugates.	Phenobarbital	30-32	replication factor C subunit 1	Homo sapiens	74-78
21912117-9	2011	CONCLUSIONS: Our results demonstrate that PB treatment causes downregulation of Rfc1 activity through PKC-dependent accelerated degradation of the Rfc1 protein by the ubiqutin-proteasome pathway.	Phenobarbital	42-44	replication factor C subunit 1	Homo sapiens	80-84
20932986-4	2010	Significant increases in the level and activity of hepatic T(4)-UDP-glucuronosyltransferase (UGT1A) after the PB administration occurred in mice, hamsters, and rats, while the increase in the amount of biliary [(125)I]T(4)-glucuronide after an intravenous injection of [(125)I]T(4) to the PB-pretreated animals occurred only in rats.	Phenobarbital	110-112	Ugt1a@	Mus musculus	93-98
21083847-7	2011	In P3-P5 slices, valproic acid and phenobarbital increased both tonic and clonic seizure-like activities in the CA3, whereas phenytoin and carbamazepine blocked tonic-like but prolonged clonic-like activity.	Phenobarbital	35-48	carbonic anhydrase 3	Rattus norvegicus	112-115
20932986-4	2010	Significant increases in the level and activity of hepatic T(4)-UDP-glucuronosyltransferase (UGT1A) after the PB administration occurred in mice, hamsters, and rats, while the increase in the amount of biliary [(125)I]T(4)-glucuronide after an intravenous injection of [(125)I]T(4) to the PB-pretreated animals occurred only in rats.	Phenobarbital	289-291	Ugt1a@	Mus musculus	93-98
21098752-13	2010	Cytochrome P450 enzyme induction by phenobarbital could be responsible for the production of reactive metabolites of lamotrigine that might be causative for the observed hematologic effects.	Phenobarbital	36-49	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-15
20583967-0	2010	A multi-endpoint evaluation of cytochrome P450 1A2, 2B6 and 3A4 induction response in human hepatocyte cultures after treatment with beta-naphthoflavone, phenobarbital and rifampicin.	Phenobarbital	154-167	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	31-50
20583967-3	2010	The concentration-dependent response and time-course for the induction of CYP1A2, CYP2B6 and CYP3A4 by inducing agents beta-naphthoflavone, phenobarbital and rifampicin, respectively were examined in two or more donors using multiple end-points (mRNA, enzyme activity and Western blot analysis).	Phenobarbital	140-153	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	74-80
20583967-3	2010	The concentration-dependent response and time-course for the induction of CYP1A2, CYP2B6 and CYP3A4 by inducing agents beta-naphthoflavone, phenobarbital and rifampicin, respectively were examined in two or more donors using multiple end-points (mRNA, enzyme activity and Western blot analysis).	Phenobarbital	140-153	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	82-88
20583967-3	2010	The concentration-dependent response and time-course for the induction of CYP1A2, CYP2B6 and CYP3A4 by inducing agents beta-naphthoflavone, phenobarbital and rifampicin, respectively were examined in two or more donors using multiple end-points (mRNA, enzyme activity and Western blot analysis).	Phenobarbital	140-153	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	93-99
20837660-4	2010	The efficacy of MG132 was increased by inclusion of ketoconazole in the hepatocyte incubations and decreased by prior treatment of the cultures with the CYP3A inducers phenobarbital or rifampicin.	Phenobarbital	168-181	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	153-158
20816911-8	2010	Phenobarbital did not modify the Cyp6g1 levels but increased the Cyp6a2 and CYP450s basal activity.	Phenobarbital	0-13	Cytochrome P450-6a2	Drosophila melanogaster	65-71
20871212-0	2010	Estrogen modulates transactivations of SXR-mediated liver X receptor response element and CAR-mediated phenobarbital response element in HepG2 cells.	Phenobarbital	103-116	nuclear receptor subfamily 1 group I member 3	Homo sapiens	90-93
20871212-2	2010	The present study demonstrates modulatory actions of estrogen in transactivations of SXR-mediated liver X receptor response element (LXRE) and CAR-mediated phenobarbital response element (PBRU).	Phenobarbital	156-169	nuclear receptor subfamily 1 group I member 3	Homo sapiens	143-146
20585144-7	2010	However, increased liver alkaline phosphatase or gamma glutamyltransferase activity in dogs treated with phenobarbital or corticosteroids suggests that direct or indirect induction of select hepatobiliary injury markers can occur both in the absence of liver injury and independently of induction of DME activity.	Phenobarbital	105-118	gamma-glutamyltransferase 1	Rattus norvegicus	49-74
20624854-7	2010	Mechanistic studies revealed that C/EBPalpha plays an important role in such synergism by directly interacting with PXR; enhancing RIF-mediated recruitment of PXR to the -82T C harboring CYP2B6 promoter; and looping the PXR-bound distal phenobarbital-responsive enhancer module toward the proximal C/EBP binding site.	Phenobarbital	237-250	CCAAT enhancer binding protein alpha	Homo sapiens	34-44
20624854-7	2010	Mechanistic studies revealed that C/EBPalpha plays an important role in such synergism by directly interacting with PXR; enhancing RIF-mediated recruitment of PXR to the -82T C harboring CYP2B6 promoter; and looping the PXR-bound distal phenobarbital-responsive enhancer module toward the proximal C/EBP binding site.	Phenobarbital	237-250	CCAAT enhancer binding protein alpha	Homo sapiens	34-39
20816995-6	2010	KEY FINDINGS: we found a 2.3-fold increase of CAR DNA-binding activity in response to phenobarbital in the sensitive C3H/He mice, but no change in the relatively resistant C57BL/6J and CC57BR/Mv mice.	Phenobarbital	86-99	nuclear receptor subfamily 1, group I, member 3	Mus musculus	46-49
20816995-8	2010	In the sensitive C3H/He mice only, the expression of a CAR target gene encoding sulfotransferase Sult2a1, the thyroid hormone inactivation enzyme, increased by 260-fold after phenobarbital administration.	Phenobarbital	175-188	nuclear receptor subfamily 1, group I, member 3	Mus musculus	55-58
20816995-9	2010	The expression of another CAR target gene, Mdm2, was also increased by phenobarbital treatment in C3H/He mice.	Phenobarbital	71-84	nuclear receptor subfamily 1, group I, member 3	Mus musculus	26-29
20816995-9	2010	The expression of another CAR target gene, Mdm2, was also increased by phenobarbital treatment in C3H/He mice.	Phenobarbital	71-84	transformed mouse 3T3 cell double minute 2	Mus musculus	43-47
20816995-10	2010	SIGNIFICANCE: we have shown that phenobarbital activates CAR and increases the expression of its target genes thereby accelerating the metabolism of thyroid hormones only in mice susceptible to liver tumor promotion by phenobarbital, but not in relatively resistant animals.	Phenobarbital	33-46	nuclear receptor subfamily 1, group I, member 3	Mus musculus	57-60
20417680-3	2010	The aim of the present study was to investigate the role of ABCB1 polymorphisms: C1236T, G2677T/A and C3435T in determining drug response to first line antiepileptic drugs (AEDs) namely phenobarbitone, phenytoin, carbamazepine and valproate in North Indian cohort of epilepsy patients.	Phenobarbital	186-200	ATP binding cassette subfamily B member 1	Homo sapiens	60-65
20551240-8	2010	In particular, Ugt1a6 and Cyp2b1 were increased by BNF, Cyp1a1, Cyp3a1, and Ugt2b1 by PB, and Cyp3a1 and Ugt2b1 by CLO.	Phenobarbital	86-88	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	15-21
20551240-8	2010	In particular, Ugt1a6 and Cyp2b1 were increased by BNF, Cyp1a1, Cyp3a1, and Ugt2b1 by PB, and Cyp3a1 and Ugt2b1 by CLO.	Phenobarbital	86-88	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	26-32
20551240-8	2010	In particular, Ugt1a6 and Cyp2b1 were increased by BNF, Cyp1a1, Cyp3a1, and Ugt2b1 by PB, and Cyp3a1 and Ugt2b1 by CLO.	Phenobarbital	86-88	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	56-62
20551240-8	2010	In particular, Ugt1a6 and Cyp2b1 were increased by BNF, Cyp1a1, Cyp3a1, and Ugt2b1 by PB, and Cyp3a1 and Ugt2b1 by CLO.	Phenobarbital	86-88	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	64-70
20551240-8	2010	In particular, Ugt1a6 and Cyp2b1 were increased by BNF, Cyp1a1, Cyp3a1, and Ugt2b1 by PB, and Cyp3a1 and Ugt2b1 by CLO.	Phenobarbital	86-88	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	76-82
20550946-6	2010	Protein disulfide isomerase (PDI) is a member of the thioredoxin (TX) superfamily and is believed to accelerate the folding of disulfide-bonded proteins by catalyzing the disulfide interchange reaction, which is the rate-limiting step during protein folding in the luminal space of the endoplasmic reticulum (ER).	Phenobarbital	265-272	prolyl 4-hydroxylase subunit beta	Homo sapiens	0-27
20550946-6	2010	Protein disulfide isomerase (PDI) is a member of the thioredoxin (TX) superfamily and is believed to accelerate the folding of disulfide-bonded proteins by catalyzing the disulfide interchange reaction, which is the rate-limiting step during protein folding in the luminal space of the endoplasmic reticulum (ER).	Phenobarbital	265-272	prolyl 4-hydroxylase subunit beta	Homo sapiens	29-32
20550946-6	2010	Protein disulfide isomerase (PDI) is a member of the thioredoxin (TX) superfamily and is believed to accelerate the folding of disulfide-bonded proteins by catalyzing the disulfide interchange reaction, which is the rate-limiting step during protein folding in the luminal space of the endoplasmic reticulum (ER).	Phenobarbital	265-272	thioredoxin	Homo sapiens	53-64
20550946-6	2010	Protein disulfide isomerase (PDI) is a member of the thioredoxin (TX) superfamily and is believed to accelerate the folding of disulfide-bonded proteins by catalyzing the disulfide interchange reaction, which is the rate-limiting step during protein folding in the luminal space of the endoplasmic reticulum (ER).	Phenobarbital	265-272	thioredoxin	Homo sapiens	66-68
27713373-5	2010	The defective alleles of CYP2C9 and/or CYP2C19 were also found to have clinically significant effects on the inter-individual variabilities in the population pharmacokinetics of phenobarbital, valproic acid and zonisamide.	Phenobarbital	178-191	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	25-31
27713373-5	2010	The defective alleles of CYP2C9 and/or CYP2C19 were also found to have clinically significant effects on the inter-individual variabilities in the population pharmacokinetics of phenobarbital, valproic acid and zonisamide.	Phenobarbital	178-191	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	39-46
20488228-3	2010	Rifampicin and phenobarbital have been shown to induce P-gp in hepatic and intestinal cells through the activation of the nuclear receptors PXR and CAR.	Phenobarbital	15-28	ATP binding cassette subfamily B member 1	Homo sapiens	55-59
20488228-3	2010	Rifampicin and phenobarbital have been shown to induce P-gp in hepatic and intestinal cells through the activation of the nuclear receptors PXR and CAR.	Phenobarbital	15-28	nuclear receptor subfamily 1 group I member 2	Homo sapiens	140-143
20488228-3	2010	Rifampicin and phenobarbital have been shown to induce P-gp in hepatic and intestinal cells through the activation of the nuclear receptors PXR and CAR.	Phenobarbital	15-28	CXADR pseudogene 1	Homo sapiens	148-151
20478346-2	2010	The CAR is normally located in the cytoplasmic compartment of untreated liver cells and translocates to the nucleus after exposure to phenobarbital (PB) or PB-like chemicals.	Phenobarbital	134-147	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	4-7
20478346-2	2010	The CAR is normally located in the cytoplasmic compartment of untreated liver cells and translocates to the nucleus after exposure to phenobarbital (PB) or PB-like chemicals.	Phenobarbital	149-151	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	4-7
20478346-2	2010	The CAR is normally located in the cytoplasmic compartment of untreated liver cells and translocates to the nucleus after exposure to phenobarbital (PB) or PB-like chemicals.	Phenobarbital	156-158	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	4-7
20478346-7	2010	IPO13 was shown to be involved in the PB-mediated nuclear translocation of CAR, which was found to be susceptible to inhibition by a dominant negative mutant of IPO13 in primary hepatocytes.	Phenobarbital	38-40	importin 13	Rattus norvegicus	0-5
20478346-7	2010	IPO13 was shown to be involved in the PB-mediated nuclear translocation of CAR, which was found to be susceptible to inhibition by a dominant negative mutant of IPO13 in primary hepatocytes.	Phenobarbital	38-40	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	75-78
20478346-7	2010	IPO13 was shown to be involved in the PB-mediated nuclear translocation of CAR, which was found to be susceptible to inhibition by a dominant negative mutant of IPO13 in primary hepatocytes.	Phenobarbital	38-40	importin 13	Rattus norvegicus	161-166
20683948-6	2010	Conditional knockout of c-jun and stat3 in hepatocytes achieves a nearly complete, additive effect on prevention of core-induced spontaneous HCC or core-enhanced HCC incidence caused by DEN/Pb.	Phenobarbital	190-192	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	24-29
20683948-6	2010	Conditional knockout of c-jun and stat3 in hepatocytes achieves a nearly complete, additive effect on prevention of core-induced spontaneous HCC or core-enhanced HCC incidence caused by DEN/Pb.	Phenobarbital	190-192	signal transducer and activator of transcription 3	Homo sapiens	34-39
20686344-4	2010	CAR is activated by phenobarbital (PB) treatment.	Phenobarbital	20-33	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	0-3
20686344-4	2010	CAR is activated by phenobarbital (PB) treatment.	Phenobarbital	35-37	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	0-3
20686344-5	2010	It has been recently reported that AMPK is involved in PB-mediated CYP2B induction both in vitro and in vivo.	Phenobarbital	55-57	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	35-39
20686344-7	2010	The AMPK-activator 5-aminoimidazole-4-Carboxamide-1-beta-Ribofuranoside (AICAR) unexpectedly repressed PB-induced CYP2B mRNA expression as well as AMPK-inhibitor compound C. In contrast, both the AMPK-activator metformin and the constitutive active form of AMPK enhanced PB-induced PB-responsive enhancer module-driven reporter gene expression.	Phenobarbital	103-105	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	4-8
20686344-7	2010	The AMPK-activator 5-aminoimidazole-4-Carboxamide-1-beta-Ribofuranoside (AICAR) unexpectedly repressed PB-induced CYP2B mRNA expression as well as AMPK-inhibitor compound C. In contrast, both the AMPK-activator metformin and the constitutive active form of AMPK enhanced PB-induced PB-responsive enhancer module-driven reporter gene expression.	Phenobarbital	271-273	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	4-8
20686344-7	2010	The AMPK-activator 5-aminoimidazole-4-Carboxamide-1-beta-Ribofuranoside (AICAR) unexpectedly repressed PB-induced CYP2B mRNA expression as well as AMPK-inhibitor compound C. In contrast, both the AMPK-activator metformin and the constitutive active form of AMPK enhanced PB-induced PB-responsive enhancer module-driven reporter gene expression.	Phenobarbital	271-273	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	4-8
20686344-9	2010	AICAR might be a convenient probe for studying the mechanisms of PB-induced activation, especially nuclear translocation, of CAR in rat primary hepatocytes.	Phenobarbital	65-67	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	2-5
20403969-11	2010	Induction of the CAR and PXR target genes, Cyp2b10 and Cyp3a11, was observed in both WT and huPXR/huCAR mouse lines following treatment with PB or chlordane.	Phenobarbital	141-143	CXADR Ig-like cell adhesion molecule	Homo sapiens	17-20
20403969-11	2010	Induction of the CAR and PXR target genes, Cyp2b10 and Cyp3a11, was observed in both WT and huPXR/huCAR mouse lines following treatment with PB or chlordane.	Phenobarbital	141-143	nuclear receptor subfamily 1, group I, member 2	Mus musculus	25-28
20403969-11	2010	Induction of the CAR and PXR target genes, Cyp2b10 and Cyp3a11, was observed in both WT and huPXR/huCAR mouse lines following treatment with PB or chlordane.	Phenobarbital	141-143	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	43-50
20403969-11	2010	Induction of the CAR and PXR target genes, Cyp2b10 and Cyp3a11, was observed in both WT and huPXR/huCAR mouse lines following treatment with PB or chlordane.	Phenobarbital	141-143	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	55-62
20886225-7	2010	Nonetheless, beta-catenin-positive hepatocytes had no striking proliferative advantage, but started to grow out on treatment with phenobarbital, a tumor-promoting agent known to facilitate the formation of mouse liver adenoma with activating mutations of Ctnnb1.	Phenobarbital	130-143	catenin (cadherin associated protein), beta 1	Mus musculus	13-25
20886225-7	2010	Nonetheless, beta-catenin-positive hepatocytes had no striking proliferative advantage, but started to grow out on treatment with phenobarbital, a tumor-promoting agent known to facilitate the formation of mouse liver adenoma with activating mutations of Ctnnb1.	Phenobarbital	130-143	catenin (cadherin associated protein), beta 1	Mus musculus	255-261
20886225-10	2010	In summary, our data demonstrate that the zone-specificity of a hepatocyte"s gene expression profile is dependent on the presence of beta-catenin, and that beta-catenin provides a proliferative advantage to hepatocytes when promoted with phenobarbital, or in a pre-cirrhotic environment.	Phenobarbital	238-251	catenin (cadherin associated protein), beta 1	Mus musculus	156-168
21155392-4	2010	BCP N-glucuronidation activities were studied using hepatic microsomes prepared from Wistar rats pretreated with PB (primarily induces UGT1A1, 1A6 and 2B1) or with clofibric acid (CF, primarily induces UGT1A1 and 1A6), and from Gunn rats (deficiency of UGT1A family), and the results were compared with those of untreated rat microsomes.The plasma elimination clearance value of BCP in PB-pretreated rats was approximately 1.4 times greater than that of untreated rats.	Phenobarbital	113-115	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	135-141
21155392-4	2010	BCP N-glucuronidation activities were studied using hepatic microsomes prepared from Wistar rats pretreated with PB (primarily induces UGT1A1, 1A6 and 2B1) or with clofibric acid (CF, primarily induces UGT1A1 and 1A6), and from Gunn rats (deficiency of UGT1A family), and the results were compared with those of untreated rat microsomes.The plasma elimination clearance value of BCP in PB-pretreated rats was approximately 1.4 times greater than that of untreated rats.	Phenobarbital	113-115	Ugt1a@	Rattus norvegicus	135-140
20516253-6	2010	HDAC inhibitors activated the phenobarbital-responsive enhancer module of the CYP2B6 promoter in transient transfection reporter assays with Ym17 cells.	Phenobarbital	30-43	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	78-84
20547735-4	2010	Exposing rat brain capillaries to the CAR activator, phenobarbital (PB), increased the transport activity and protein expression (Western blots) of P-glycoprotein, Mrp2, and BCRP.	Phenobarbital	53-66	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	38-41
20547735-4	2010	Exposing rat brain capillaries to the CAR activator, phenobarbital (PB), increased the transport activity and protein expression (Western blots) of P-glycoprotein, Mrp2, and BCRP.	Phenobarbital	53-66	ATP binding cassette subfamily C member 2	Rattus norvegicus	164-168
20547735-4	2010	Exposing rat brain capillaries to the CAR activator, phenobarbital (PB), increased the transport activity and protein expression (Western blots) of P-glycoprotein, Mrp2, and BCRP.	Phenobarbital	68-70	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	38-41
20547735-4	2010	Exposing rat brain capillaries to the CAR activator, phenobarbital (PB), increased the transport activity and protein expression (Western blots) of P-glycoprotein, Mrp2, and BCRP.	Phenobarbital	68-70	ATP binding cassette subfamily C member 2	Rattus norvegicus	164-168
20573785-8	2010	The marked T(4) reductions occurred in response to Aroclor 1254, PCB 99 (a PB-type congener), and PCB 118 (a mixed-type congener).	Phenobarbital	75-77	pyruvate carboxylase	Rattus norvegicus	65-68
20509749-0	2010	Expression and inducibility by phenobarbital of CYP2C33, CYP2C42, CYP2C49, CYP2B22, and CYP3As in porcine liver, kidney, small intestine, and nasal tissues.	Phenobarbital	31-44	cytochrome P450 family 2 subfamily C member 33	Sus scrofa	48-55
20509749-2	2010	PB treatment resulted in an up-regulation of mRNA levels of all analyzed CYPs in liver, of CYP2C42 and CYP2C49 in kidney, of CYP2C42, CYP2C49, CYP2B22, and CYP3As in small intestine.	Phenobarbital	0-2	cytochrome P450 2C42	Sus scrofa	91-98
20509749-1	2010	In this study, the expression and inducibility of CYP2C33, CYP2C42, CYP2C49, CYP2B22, CYP3A22, CYP3A29, and CYP3A46 were investigated at activity and/or transcriptional level in liver, kidney, small intestine, respiratory, and olfactory nasal mucosa of control and phenobarbital (PB)-treated pigs.	Phenobarbital	265-278	cytochrome P450 family 2 subfamily C member 33	Sus scrofa	50-57
20509749-1	2010	In this study, the expression and inducibility of CYP2C33, CYP2C42, CYP2C49, CYP2B22, CYP3A22, CYP3A29, and CYP3A46 were investigated at activity and/or transcriptional level in liver, kidney, small intestine, respiratory, and olfactory nasal mucosa of control and phenobarbital (PB)-treated pigs.	Phenobarbital	280-282	cytochrome P450 family 2 subfamily C member 33	Sus scrofa	50-57
20509749-2	2010	PB treatment resulted in an up-regulation of mRNA levels of all analyzed CYPs in liver, of CYP2C42 and CYP2C49 in kidney, of CYP2C42, CYP2C49, CYP2B22, and CYP3As in small intestine.	Phenobarbital	0-2	cytochrome P450 2C49	Sus scrofa	103-110
20509749-2	2010	PB treatment resulted in an up-regulation of mRNA levels of all analyzed CYPs in liver, of CYP2C42 and CYP2C49 in kidney, of CYP2C42, CYP2C49, CYP2B22, and CYP3As in small intestine.	Phenobarbital	0-2	cytochrome P450 2C42	Sus scrofa	125-132
20509749-2	2010	PB treatment resulted in an up-regulation of mRNA levels of all analyzed CYPs in liver, of CYP2C42 and CYP2C49 in kidney, of CYP2C42, CYP2C49, CYP2B22, and CYP3As in small intestine.	Phenobarbital	0-2	cytochrome P450 2C49	Sus scrofa	134-141
20509749-2	2010	PB treatment resulted in an up-regulation of mRNA levels of all analyzed CYPs in liver, of CYP2C42 and CYP2C49 in kidney, of CYP2C42, CYP2C49, CYP2B22, and CYP3As in small intestine.	Phenobarbital	0-2	cytochrome P450 family 2 subfamily B member 6B	Sus scrofa	143-150
20509749-3	2010	In liver microsomes from PB-treated pigs, these transcriptional activations were accompanied by an increase of various marker activities of human CYP2B6, CYP3As, CYP2C9, CYP2C19.	Phenobarbital	25-27	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	146-152
20509749-3	2010	In liver microsomes from PB-treated pigs, these transcriptional activations were accompanied by an increase of various marker activities of human CYP2B6, CYP3As, CYP2C9, CYP2C19.	Phenobarbital	25-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	162-168
20509749-3	2010	In liver microsomes from PB-treated pigs, these transcriptional activations were accompanied by an increase of various marker activities of human CYP2B6, CYP3As, CYP2C9, CYP2C19.	Phenobarbital	25-27	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	170-177
20509749-4	2010	Among the extrahepatic tissues, a significant induction by PB was observed only in kidney for the marker activities of CYP2C9.	Phenobarbital	59-61	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
20509749-5	2010	Taken together, our results demonstrated that the PB administration in pigs induced at least in liver, in addition to CYP2B22 and CYP3As, the expression of CYP2C33, CYP2C42, and CYP2C49 at transcriptional and activity levels.	Phenobarbital	50-52	cytochrome P450 family 2 subfamily B member 6B	Sus scrofa	118-125
20509749-5	2010	Taken together, our results demonstrated that the PB administration in pigs induced at least in liver, in addition to CYP2B22 and CYP3As, the expression of CYP2C33, CYP2C42, and CYP2C49 at transcriptional and activity levels.	Phenobarbital	50-52	cytochrome P450 family 2 subfamily C member 33	Sus scrofa	156-163
20509749-5	2010	Taken together, our results demonstrated that the PB administration in pigs induced at least in liver, in addition to CYP2B22 and CYP3As, the expression of CYP2C33, CYP2C42, and CYP2C49 at transcriptional and activity levels.	Phenobarbital	50-52	cytochrome P450 2C42	Sus scrofa	165-172
20509749-5	2010	Taken together, our results demonstrated that the PB administration in pigs induced at least in liver, in addition to CYP2B22 and CYP3As, the expression of CYP2C33, CYP2C42, and CYP2C49 at transcriptional and activity levels.	Phenobarbital	50-52	cytochrome P450 2C49	Sus scrofa	178-185
20371638-2	2010	We have now found that CYP2C55 is induced by phenobarbital (PB) and pregnenolone 16alpha-carbonitrile (PCN) in both mouse kidney and liver.	Phenobarbital	45-58	cytochrome P450, family 2, subfamily c, polypeptide 55	Mus musculus	23-30
20590600-4	2010	EXPERIMENTAL APPROACH: Effects of the selective cyclooxygenase-2 inhibitor celecoxib on the response to the P-glycoprotein substrate, phenobarbital, was evaluated in a chronic model of drug-resistant temporal lobe epilepsy in rats.	Phenobarbital	134-147	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	48-64
20590600-4	2010	EXPERIMENTAL APPROACH: Effects of the selective cyclooxygenase-2 inhibitor celecoxib on the response to the P-glycoprotein substrate, phenobarbital, was evaluated in a chronic model of drug-resistant temporal lobe epilepsy in rats.	Phenobarbital	134-147	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	108-122
20590600-8	2010	CONCLUSIONS AND IMPLICATIONS: Pretreatment with the cyclooxygenase-2 inhibitor restored the anticonvulsant activity of phenobarbital in rats that failed to exhibit a relevant response before celecoxib treatment.	Phenobarbital	119-132	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	52-68
20371638-5	2010	Chronic PB treatment increased hepatic microsomal CYP2C55 protein and serum 19-HETE levels.	Phenobarbital	8-10	cytochrome P450, family 2, subfamily c, polypeptide 55	Mus musculus	50-57
20371638-2	2010	We have now found that CYP2C55 is induced by phenobarbital (PB) and pregnenolone 16alpha-carbonitrile (PCN) in both mouse kidney and liver.	Phenobarbital	60-62	cytochrome P450, family 2, subfamily c, polypeptide 55	Mus musculus	23-30
20371638-3	2010	The nuclear xenobiotic receptors constitutive active/androstane receptor (CAR) and pregnane X receptor (PXR) regulate these drug inductions: CYP2C55 mRNA was increased 25-fold in PB-treated Car(+/+) but not in Car(-/-) mice and was induced in Pxr(+/+) but not Pxr(-/-) mice after PCN treatment.	Phenobarbital	179-181	nuclear receptor subfamily 1, group I, member 3	Mus musculus	74-77
20371638-3	2010	The nuclear xenobiotic receptors constitutive active/androstane receptor (CAR) and pregnane X receptor (PXR) regulate these drug inductions: CYP2C55 mRNA was increased 25-fold in PB-treated Car(+/+) but not in Car(-/-) mice and was induced in Pxr(+/+) but not Pxr(-/-) mice after PCN treatment.	Phenobarbital	179-181	nuclear receptor subfamily 1, group I, member 2	Mus musculus	83-102
20371638-3	2010	The nuclear xenobiotic receptors constitutive active/androstane receptor (CAR) and pregnane X receptor (PXR) regulate these drug inductions: CYP2C55 mRNA was increased 25-fold in PB-treated Car(+/+) but not in Car(-/-) mice and was induced in Pxr(+/+) but not Pxr(-/-) mice after PCN treatment.	Phenobarbital	179-181	nuclear receptor subfamily 1, group I, member 2	Mus musculus	104-107
20371638-3	2010	The nuclear xenobiotic receptors constitutive active/androstane receptor (CAR) and pregnane X receptor (PXR) regulate these drug inductions: CYP2C55 mRNA was increased 25-fold in PB-treated Car(+/+) but not in Car(-/-) mice and was induced in Pxr(+/+) but not Pxr(-/-) mice after PCN treatment.	Phenobarbital	179-181	cytochrome P450, family 2, subfamily c, polypeptide 55	Mus musculus	141-148
20371638-3	2010	The nuclear xenobiotic receptors constitutive active/androstane receptor (CAR) and pregnane X receptor (PXR) regulate these drug inductions: CYP2C55 mRNA was increased 25-fold in PB-treated Car(+/+) but not in Car(-/-) mice and was induced in Pxr(+/+) but not Pxr(-/-) mice after PCN treatment.	Phenobarbital	179-181	nuclear receptor subfamily 1, group I, member 3	Mus musculus	190-193
20371638-3	2010	The nuclear xenobiotic receptors constitutive active/androstane receptor (CAR) and pregnane X receptor (PXR) regulate these drug inductions: CYP2C55 mRNA was increased 25-fold in PB-treated Car(+/+) but not in Car(-/-) mice and was induced in Pxr(+/+) but not Pxr(-/-) mice after PCN treatment.	Phenobarbital	179-181	nuclear receptor subfamily 1, group I, member 3	Mus musculus	210-213
20371638-3	2010	The nuclear xenobiotic receptors constitutive active/androstane receptor (CAR) and pregnane X receptor (PXR) regulate these drug inductions: CYP2C55 mRNA was increased 25-fold in PB-treated Car(+/+) but not in Car(-/-) mice and was induced in Pxr(+/+) but not Pxr(-/-) mice after PCN treatment.	Phenobarbital	179-181	nuclear receptor subfamily 1, group I, member 2	Mus musculus	243-246
20371638-3	2010	The nuclear xenobiotic receptors constitutive active/androstane receptor (CAR) and pregnane X receptor (PXR) regulate these drug inductions: CYP2C55 mRNA was increased 25-fold in PB-treated Car(+/+) but not in Car(-/-) mice and was induced in Pxr(+/+) but not Pxr(-/-) mice after PCN treatment.	Phenobarbital	179-181	nuclear receptor subfamily 1, group I, member 2	Mus musculus	260-263
20404936-2	2010	PB activates nuclear xenobiotic receptor Constitutive Active/Androstane Receptor (CAR; NR1I3) and this activation is shown to determine PB promotion of HCC in mice.	Phenobarbital	0-2	nuclear receptor subfamily 1, group I, member 3	Mus musculus	41-80
20461738-8	2010	The phenobarbital-inducible cytochrome P450 mRNA level was decreased in rats treated with &gt;10 mg XN/kg/day, in agreement with reduced CAR protein.	Phenobarbital	4-17	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	137-140
20979879-3	2010	The phenobarbital-responsive enhancer module (PBREM), TATA box and common mutation sites in exons of UGT1A1 gene were amplified by polymerase chain reaction (PCR) and the products screened by direct DNA sequencing.	Phenobarbital	4-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	101-107
20417647-6	2010	MDCK-MDR1 cells transported PB when initial concentrations were 10 or 20, but not 5microg/ml.	Phenobarbital	28-30	ATP binding cassette subfamily B member 1	Canis lupus familiaris	5-9
20417647-11	2010	SIGNIFICANCE: Human P-gp transports PHT and PB, but not ESM, in a concentration dependent manner.	Phenobarbital	44-46	phosphoglycolate phosphatase	Homo sapiens	20-24
20582327-3	2010	We also compared various insecticides and xenobiotics for their ability to induce this cytochrome P450 gene, and show that the pattern of Cyp6a2 inducibility is comparable to that of vertebrate CYP2B genes, and different from that of vertebrate CYP1A genes, suggesting a degree of evolutionary conservation for the "phenobarbital-type" induction mechanism.	Phenobarbital	316-329	Cyp6a9-rAF4-2	Drosophila melanogaster	98-102
20582327-3	2010	We also compared various insecticides and xenobiotics for their ability to induce this cytochrome P450 gene, and show that the pattern of Cyp6a2 inducibility is comparable to that of vertebrate CYP2B genes, and different from that of vertebrate CYP1A genes, suggesting a degree of evolutionary conservation for the "phenobarbital-type" induction mechanism.	Phenobarbital	316-329	Cytochrome P450-6a2	Drosophila melanogaster	138-144
20307138-6	2010	Female livers and livers exposed to inducers (phenobarbital and/or dexamethasone) were associated with higher CYP2B6.	Phenobarbital	46-59	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	110-116
20124398-3	2010	The well characterized substrate for UGT1A1, 7-ethyl-10-hydroxy-camptothecin (SN-38), showed the greatest difference in parent drug exposure ( approximately 3-fold increase) and clearance ( approximately 3-fold decrease) in Tg(UGT1(A1*28)) Ugt1(-/-) mice after intravenous administration compared with wild-type and phenobarbital-treated animals.	Phenobarbital	316-329	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	37-43
20124398-3	2010	The well characterized substrate for UGT1A1, 7-ethyl-10-hydroxy-camptothecin (SN-38), showed the greatest difference in parent drug exposure ( approximately 3-fold increase) and clearance ( approximately 3-fold decrease) in Tg(UGT1(A1*28)) Ugt1(-/-) mice after intravenous administration compared with wild-type and phenobarbital-treated animals.	Phenobarbital	316-329	UDP glucuronosyltransferase 1 family, polypeptide A2	Mus musculus	37-41
20404936-2	2010	PB activates nuclear xenobiotic receptor Constitutive Active/Androstane Receptor (CAR; NR1I3) and this activation is shown to determine PB promotion of HCC in mice.	Phenobarbital	0-2	nuclear receptor subfamily 1, group I, member 3	Mus musculus	82-85
20404936-2	2010	PB activates nuclear xenobiotic receptor Constitutive Active/Androstane Receptor (CAR; NR1I3) and this activation is shown to determine PB promotion of HCC in mice.	Phenobarbital	0-2	nuclear receptor subfamily 1, group I, member 3	Mus musculus	87-92
20404936-2	2010	PB activates nuclear xenobiotic receptor Constitutive Active/Androstane Receptor (CAR; NR1I3) and this activation is shown to determine PB promotion of HCC in mice.	Phenobarbital	136-138	nuclear receptor subfamily 1, group I, member 3	Mus musculus	41-80
20404936-2	2010	PB activates nuclear xenobiotic receptor Constitutive Active/Androstane Receptor (CAR; NR1I3) and this activation is shown to determine PB promotion of HCC in mice.	Phenobarbital	136-138	nuclear receptor subfamily 1, group I, member 3	Mus musculus	82-85
20404936-2	2010	PB activates nuclear xenobiotic receptor Constitutive Active/Androstane Receptor (CAR; NR1I3) and this activation is shown to determine PB promotion of HCC in mice.	Phenobarbital	136-138	nuclear receptor subfamily 1, group I, member 3	Mus musculus	87-92
20404936-5	2010	METHODOLOGY/PRINCIPAL FINDINGS: PB activation of nuclear xenobiotic receptor CAR is found to induce the Gadd45b gene in mouse liver throughout the development of HCC as well as in liver tumors.	Phenobarbital	32-34	nuclear receptor subfamily 1, group I, member 3	Mus musculus	77-80
20404936-5	2010	METHODOLOGY/PRINCIPAL FINDINGS: PB activation of nuclear xenobiotic receptor CAR is found to induce the Gadd45b gene in mouse liver throughout the development of HCC as well as in liver tumors.	Phenobarbital	32-34	growth arrest and DNA-damage-inducible 45 beta	Mus musculus	104-111
20404936-13	2010	The present finding that CAR can repress cell death via its interaction with GADD45B provides an insight for further investigations into the CAR-regulated molecular mechanism by which PB promotes development of HCC.	Phenobarbital	184-186	nuclear receptor subfamily 1, group I, member 3	Mus musculus	25-28
20404936-13	2010	The present finding that CAR can repress cell death via its interaction with GADD45B provides an insight for further investigations into the CAR-regulated molecular mechanism by which PB promotes development of HCC.	Phenobarbital	184-186	growth arrest and DNA-damage-inducible 45 beta	Mus musculus	77-84
20404936-13	2010	The present finding that CAR can repress cell death via its interaction with GADD45B provides an insight for further investigations into the CAR-regulated molecular mechanism by which PB promotes development of HCC.	Phenobarbital	184-186	nuclear receptor subfamily 1, group I, member 3	Mus musculus	141-144
20166883-0	2010	Cytochrome P450 induction by phenobarbital exacerbates warm hepatic ischemia-reperfusion injury in rat livers.	Phenobarbital	29-42	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-15
20233212-0	2010	Combined effects of epileptic seizure and phenobarbital induced overexpression of P-glycoprotein in brain of chemically kindled rats.	Phenobarbital	42-55	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	82-96
20233212-10	2010	Good associations were found among P-glycoprotein activity, expression and phenobarbital concentration in the hippocampus.	Phenobarbital	75-88	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	35-49
20233212-11	2010	Short-term treatment with phenobarbital showed good anti-epileptic effect; the maximum effect occurred on day 14 when overexpression of P-glycoprotein was reversed.	Phenobarbital	26-39	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	136-150
20233212-12	2010	Continuous treatment with phenobarbital had a gradually reduced anti-epileptic effect and on day 40, phenobarbital exhibited no anti-epileptic effect; this was accompanied by both a re-enhancement of P-glycoprotein expression and decreased phenobarbital concentration in the hippocampus.	Phenobarbital	26-39	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	200-214
20233212-13	2010	P-glycoprotein function and expression were also increased in age-matched normal rats treated with phenobarbital.	Phenobarbital	99-112	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-14
20185760-3	2010	In this study, we show that CAR activators]phenobarbital and 6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime] induce the lipogenic gene thyroid hormone-responsive spot 14 protein (THRSP) (or Spot14, S14) expression in human hepatocytes.	Phenobarbital	43-56	nuclear receptor subfamily 1 group I member 3	Homo sapiens	28-31
20185760-3	2010	In this study, we show that CAR activators]phenobarbital and 6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime] induce the lipogenic gene thyroid hormone-responsive spot 14 protein (THRSP) (or Spot14, S14) expression in human hepatocytes.	Phenobarbital	43-56	thyroid hormone responsive	Homo sapiens	221-226
20185760-3	2010	In this study, we show that CAR activators]phenobarbital and 6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime] induce the lipogenic gene thyroid hormone-responsive spot 14 protein (THRSP) (or Spot14, S14) expression in human hepatocytes.	Phenobarbital	43-56	thyroid hormone responsive	Homo sapiens	232-238
20185760-3	2010	In this study, we show that CAR activators]phenobarbital and 6-(4-chlorophenyl)imidazo[2,1-b][1,3]thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime] induce the lipogenic gene thyroid hormone-responsive spot 14 protein (THRSP) (or Spot14, S14) expression in human hepatocytes.	Phenobarbital	43-56	thyroid hormone responsive	Homo sapiens	240-243
20185760-4	2010	In addition, we report that treatment of wild-type mice with mCAR activators (phenobarbital and 1,4-Bis[2-(3,5-dichloropyridyloxy)]benzene) efficiently increases thrsp expression, in contrast to CAR null mice.	Phenobarbital	78-91	coxsackie virus and adenovirus receptor	Mus musculus	61-65
20185760-4	2010	In addition, we report that treatment of wild-type mice with mCAR activators (phenobarbital and 1,4-Bis[2-(3,5-dichloropyridyloxy)]benzene) efficiently increases thrsp expression, in contrast to CAR null mice.	Phenobarbital	78-91	thyroid hormone responsive	Mus musculus	162-167
20185760-4	2010	In addition, we report that treatment of wild-type mice with mCAR activators (phenobarbital and 1,4-Bis[2-(3,5-dichloropyridyloxy)]benzene) efficiently increases thrsp expression, in contrast to CAR null mice.	Phenobarbital	78-91	nuclear receptor subfamily 1, group I, member 3	Mus musculus	62-65
19920070-0	2010	Liver-specific ablation of integrin-linked kinase in mice results in enhanced and prolonged cell proliferation and hepatomegaly after phenobarbital administration.	Phenobarbital	134-147	integrin linked kinase	Mus musculus	27-49
19394173-5	2010	Long-term treatment with Phenobarbital (40mg/kg), valproate (100mg/kg) and topiramate (40mg/kg) reduces BDNF and NT-3 mRNA expression in the developing brain, while lamotrigine reduces mRNA expression only at high dose level (80mg/kg).	Phenobarbital	25-38	brain derived neurotrophic factor	Homo sapiens	104-108
19394173-5	2010	Long-term treatment with Phenobarbital (40mg/kg), valproate (100mg/kg) and topiramate (40mg/kg) reduces BDNF and NT-3 mRNA expression in the developing brain, while lamotrigine reduces mRNA expression only at high dose level (80mg/kg).	Phenobarbital	25-38	neurotrophin 3	Homo sapiens	113-117
20369030-7	2010	AEDs, such as phenytoin, phenobarbital, carbamazepine, felbamate, topiramate, oxcarbazepine and primidone, induce cytochrome P450 3A4, leading to enhanced metabolism of either or both the estrogenic and progestogenic component of OCs, thereby reducing their efficacy in preventing pregnancy.	Phenobarbital	25-38	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	114-133
19760798-8	2010	PB induced all phase I and phase II gene transcripts except for Cyp1a1 and Cyp2b9.	Phenobarbital	0-2	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	64-70
19760798-8	2010	PB induced all phase I and phase II gene transcripts except for Cyp1a1 and Cyp2b9.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	75-81
19833192-7	2010	The results demonstrate that transcriptional activation of CYP2B6 gene is mediated mainly by the pregnane X receptor (PXR) and the Phenobarbital Responsive Element Module (PBREM).	Phenobarbital	131-144	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	59-65
19737542-0	2010	Werner"s syndrome helicase participates in transcription of phenobarbital-inducible CYP2B genes in rat and mouse liver.	Phenobarbital	60-73	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	84-89
19737542-7	2010	The rat CYP2B2 gene and its closely related mouse homolog, Cyp2b10, are both strongly induced in liver by phenobarbital.	Phenobarbital	106-119	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	8-14
19737542-7	2010	The rat CYP2B2 gene and its closely related mouse homolog, Cyp2b10, are both strongly induced in liver by phenobarbital.	Phenobarbital	106-119	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	59-66
19737542-8	2010	We found that there is phenobarbital-dependent recruitment of WRN to the promoter of the CYP2B2 gene as demonstrated by chromatin immunoprecipitation analysis.	Phenobarbital	23-36	Werner syndrome RecQ like helicase	Mus musculus	62-65
19737542-8	2010	We found that there is phenobarbital-dependent recruitment of WRN to the promoter of the CYP2B2 gene as demonstrated by chromatin immunoprecipitation analysis.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	89-95
19737542-9	2010	Mice homozygous for a Wrn mutation deleting part of the helicase domain showed a decrease in basal and phenobarbital-induced CYP2B10 mRNA levels compared to wild type animals.	Phenobarbital	103-116	Werner syndrome RecQ like helicase	Mus musculus	22-25
19737542-9	2010	Mice homozygous for a Wrn mutation deleting part of the helicase domain showed a decrease in basal and phenobarbital-induced CYP2B10 mRNA levels compared to wild type animals.	Phenobarbital	103-116	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	125-132
19737542-10	2010	The phenobarbital-induced level of CYP2B10 protein was also reduced in the mutant mice.	Phenobarbital	4-17	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	35-42
19831498-1	2010	Differential induction of rat-liver microsomal uridine diphospho-glucuronosyltransferase (UGT) activities by 3-methylcholanthrene or phenobarbital provided the model to separate and purify the corresponding UGT enzymes, initially termed GT1 and GT2, respectively.	Phenobarbital	133-146	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	90-93
20002224-0	2010	Functional analysis of the cis-acting elements responsible for the induction of the Cyp6a8 and Cyp6g1 genes of Drosophila melanogaster by DDT, phenobarbital and caffeine.	Phenobarbital	143-156	Cytochrome P450-6a8	Drosophila melanogaster	84-90
20002224-0	2010	Functional analysis of the cis-acting elements responsible for the induction of the Cyp6a8 and Cyp6g1 genes of Drosophila melanogaster by DDT, phenobarbital and caffeine.	Phenobarbital	143-156	Cyp6g1	Drosophila melanogaster	95-101
20002224-1	2010	Many Drosophila cytochrome P450 or Cyp genes are induced by caffeine and phenobarbital (PB).	Phenobarbital	73-86	disembodied	Drosophila melanogaster	35-38
20002224-1	2010	Many Drosophila cytochrome P450 or Cyp genes are induced by caffeine and phenobarbital (PB).	Phenobarbital	88-90	disembodied	Drosophila melanogaster	35-38
20002224-5	2010	However, the 0.2-, 0.5- and 0.8-kb DNAs of Cyp6a8 showed 13-24-, 4-5- and 2.2-2.7-fold induction with caffeine, PB and DDT, respectively.	Phenobarbital	112-114	Cytochrome P450-6a8	Drosophila melanogaster	43-49
19920082-0	2010	Dependence on the microtubule network and 90-kDa heat shock protein of phenobarbital-induced nuclear translocation of the rat constitutive androstane receptor.	Phenobarbital	71-84	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	126-158
19920082-1	2010	The role of the microtubule network in the constitutive androstane receptor (CAR)-mediated transactivation of CYP2B induced by phenobarbital (PB) in rat primary hepatocytes was investigated using the microtubule-disrupting agent nocodazole (NCZ).	Phenobarbital	127-140	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	43-75
19920082-1	2010	The role of the microtubule network in the constitutive androstane receptor (CAR)-mediated transactivation of CYP2B induced by phenobarbital (PB) in rat primary hepatocytes was investigated using the microtubule-disrupting agent nocodazole (NCZ).	Phenobarbital	127-140	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	77-80
19920082-1	2010	The role of the microtubule network in the constitutive androstane receptor (CAR)-mediated transactivation of CYP2B induced by phenobarbital (PB) in rat primary hepatocytes was investigated using the microtubule-disrupting agent nocodazole (NCZ).	Phenobarbital	142-144	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	43-75
19920082-1	2010	The role of the microtubule network in the constitutive androstane receptor (CAR)-mediated transactivation of CYP2B induced by phenobarbital (PB) in rat primary hepatocytes was investigated using the microtubule-disrupting agent nocodazole (NCZ).	Phenobarbital	142-144	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	77-80
19920082-5	2010	Furthermore, the transactivation of the PB-responsive enhancer module-luciferase reporter gene and the nuclear transport of CAR induced by PB were also repressed in the presence of NCZ.	Phenobarbital	40-42	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	124-127
19920082-5	2010	Furthermore, the transactivation of the PB-responsive enhancer module-luciferase reporter gene and the nuclear transport of CAR induced by PB were also repressed in the presence of NCZ.	Phenobarbital	139-141	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	124-127
19920082-6	2010	Based on these findings, microtubular integrity might be required for PB-induced nuclear translocation of CAR in rat primary hepatocytes.	Phenobarbital	70-72	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	106-109
19427778-0	2010	Docosahexaenoic acid down-regulates phenobarbital-induced cytochrome P450 2B1 gene expression in rat primary hepatocytes via the sphingomyelinase/ceramide pathway.	Phenobarbital	36-49	cytochrome P450 2B1	Rattus norvegicus	58-77
19427778-5	2010	In addition, the cAMP-dependent PKA pathway down-regulates CYP 2B1 expression induced by phenobarbital (PB).	Phenobarbital	89-102	cytochrome P450 2B1	Rattus norvegicus	59-66
19427778-5	2010	In addition, the cAMP-dependent PKA pathway down-regulates CYP 2B1 expression induced by phenobarbital (PB).	Phenobarbital	104-106	cytochrome P450 2B1	Rattus norvegicus	59-66
19427778-6	2010	In the present study, we determined the effect of DHA on SMase transactivation and the downstream pathway in CYP 2B1 expression induced by PB.	Phenobarbital	139-141	cytochrome P450 2B1	Rattus norvegicus	109-116
19427778-7	2010	SMase was activated by DHA 2 h after treatment, and D609 (an SMase inhibitor) attenuated the inhibition of PB-induced CYP 2B1 expression by DHA.	Phenobarbital	107-109	cytochrome P450 2B1	Rattus norvegicus	118-125
19427778-9	2010	C2-ceramide dose-dependently inhibited PB-induced CYP 2B1 expression and increased intracellular cAMP concentrations.	Phenobarbital	39-41	cytochrome P450 2B1	Rattus norvegicus	50-57
19427778-10	2010	SQ22536 (an adenylyl cyclase inhibitor) and H89 (a PKA-specific inhibitor) partially reversed the inhibition of PB-induced CYP 2B1 expression by C2-ceramide.	Phenobarbital	112-114	cytochrome P450 2B1	Rattus norvegicus	123-130
20071449-1	2010	We have reported previously that the hepatic heme-regulated inhibitor (HRI)-eukaryotic initiation factor 2 alpha (eIF2 alpha) kinase is activated in acute heme-deficient states, resulting in translational shut-off of global hepatic protein synthesis, including phenobarbital (PB)-mediated induction of CYP2B enzymes in rats.	Phenobarbital	261-274	eukaryotic translation initiation factor 2 alpha kinase 1	Homo sapiens	71-74
20071449-1	2010	We have reported previously that the hepatic heme-regulated inhibitor (HRI)-eukaryotic initiation factor 2 alpha (eIF2 alpha) kinase is activated in acute heme-deficient states, resulting in translational shut-off of global hepatic protein synthesis, including phenobarbital (PB)-mediated induction of CYP2B enzymes in rats.	Phenobarbital	261-274	eukaryotic translation initiation factor 2A	Rattus norvegicus	114-124
20071449-1	2010	We have reported previously that the hepatic heme-regulated inhibitor (HRI)-eukaryotic initiation factor 2 alpha (eIF2 alpha) kinase is activated in acute heme-deficient states, resulting in translational shut-off of global hepatic protein synthesis, including phenobarbital (PB)-mediated induction of CYP2B enzymes in rats.	Phenobarbital	276-278	eukaryotic translation initiation factor 2 alpha kinase 1	Homo sapiens	71-74
20071449-1	2010	We have reported previously that the hepatic heme-regulated inhibitor (HRI)-eukaryotic initiation factor 2 alpha (eIF2 alpha) kinase is activated in acute heme-deficient states, resulting in translational shut-off of global hepatic protein synthesis, including phenobarbital (PB)-mediated induction of CYP2B enzymes in rats.	Phenobarbital	276-278	eukaryotic translation initiation factor 2A	Rattus norvegicus	114-124
20071449-1	2010	We have reported previously that the hepatic heme-regulated inhibitor (HRI)-eukaryotic initiation factor 2 alpha (eIF2 alpha) kinase is activated in acute heme-deficient states, resulting in translational shut-off of global hepatic protein synthesis, including phenobarbital (PB)-mediated induction of CYP2B enzymes in rats.	Phenobarbital	276-278	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	302-307
20071449-8	2010	Furthermore, because HRI exists in both human and rat liver in its heme-sensitive form and is inducible by cytochrome P450 inducers such as PB, these findings are clinically relevant to acute heme-deficient states, such as the acute hepatic porphyrias.	Phenobarbital	140-142	eukaryotic translation initiation factor 2 alpha kinase 1	Homo sapiens	21-24
20019244-2	2010	In the present study, we carefully analyzed mRNA expression and activity of the major P450s and their responsiveness to three prototypical inducers, phenobarbital, rifampicin, and omeprazole, in differentiated HepaRG cell cultures over a 4-week period after low and high seeding.	Phenobarbital	149-162	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	86-91
20019244-7	2010	Thus, CYP1A2, CYP2B6, and CYP3A4 were found to accurately respond to their respective prototypical inducers, i.e., omeprazole, phenobarbital, and rifampicin.	Phenobarbital	127-140	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	6-12
20019244-7	2010	Thus, CYP1A2, CYP2B6, and CYP3A4 were found to accurately respond to their respective prototypical inducers, i.e., omeprazole, phenobarbital, and rifampicin.	Phenobarbital	127-140	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	14-20
20019244-7	2010	Thus, CYP1A2, CYP2B6, and CYP3A4 were found to accurately respond to their respective prototypical inducers, i.e., omeprazole, phenobarbital, and rifampicin.	Phenobarbital	127-140	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	26-32
20012030-6	2010	Livers exposed to dexamethasone and phenobarbital had higher CYP2A6 expression and activity, however the difference was not statistically significant.	Phenobarbital	36-49	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	61-67
19958760-1	2010	Several major antiepileptic drugs, including carbamazepine, phenytoin and phenobarbital, induce xenobiotic metabolizing enzymes via activation of nuclear receptors, including pregnane X receptor (NR1I2) and constitutive androstane receptor (NR1I3).	Phenobarbital	74-87	nuclear receptor subfamily 1, group I, member 2	Rattus norvegicus	196-201
19958760-1	2010	Several major antiepileptic drugs, including carbamazepine, phenytoin and phenobarbital, induce xenobiotic metabolizing enzymes via activation of nuclear receptors, including pregnane X receptor (NR1I2) and constitutive androstane receptor (NR1I3).	Phenobarbital	74-87	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	241-246
19958760-5	2010	In the present study, we studied the effects of exposure to phenobarbital, phenytoin and carbamazepine on Pgp expression and functionality in the rat brain endothelial cell line GPNT.	Phenobarbital	60-73	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	106-109
19920070-2	2010	This study investigates the role of ILK in liver enlargement induced by phenobarbital (PB).	Phenobarbital	72-85	integrin linked kinase	Mus musculus	36-39
19920070-2	2010	This study investigates the role of ILK in liver enlargement induced by phenobarbital (PB).	Phenobarbital	87-89	integrin linked kinase	Mus musculus	36-39
19920070-7	2010	There were slightly increased proliferating cell nuclear antigen-positive cells in the ILK/liver-/- animals at day 2 as compared to WT after PB administration.	Phenobarbital	141-143	integrin linked kinase	Mus musculus	87-90
19920070-10	2010	ILK/liver-/- mice also showed increased expression of key genes involved in hepatocyte proliferation at different time points during PB administration.	Phenobarbital	133-135	integrin linked kinase	Mus musculus	0-3
19920070-12	2010	Lack of ILK in the hepatocytes imparts prolonged proliferative response not only to stimuli related to liver regeneration but also to xenobiotic chemical mitogens, such as PB.	Phenobarbital	172-174	integrin linked kinase	Mus musculus	8-11
19661216-7	2009	However, HGF prevented constitutive androstane receptor-related up-regulation of MRP2 occurring in phenobarbital-treated hepatocytes.	Phenobarbital	99-112	hepatocyte growth factor	Homo sapiens	9-12
19682433-1	2010	Phenobarbital has long been known to increase cellular levels of CYP1A1 and CYP1A2 possibly through a pathway(s) independent of aryl hydrocarbon receptor.	Phenobarbital	0-13	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	65-71
19682433-1	2010	Phenobarbital has long been known to increase cellular levels of CYP1A1 and CYP1A2 possibly through a pathway(s) independent of aryl hydrocarbon receptor.	Phenobarbital	0-13	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	76-82
20201778-3	2010	The system was then validated using known ligands of PXR, rifampicin (RIF), clotrimazole (CLOT) sulfinpyrazone (SPZ) and phenobarbital (PB), which produced dose dependent induction of UGT1A1 luciferase activity by 4.4, 5.3, 4.7 and 3.7 fold, respectively, relative to the vehicle control, 0.1 % dimethylsulfoxide (DMSO).	Phenobarbital	121-134	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	184-190
19895823-3	2009	KEY FINDINGS: Phenobarbital-like inducer administration significantly up-regulated CYP2B activity in rat and mouse liver in a species-specific manner, in contrast to the effects on CYP2B in lungs, kidneys and brains.	Phenobarbital	14-27	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	83-88
19895823-4	2009	In parallel, Western blot analysis showed that the species-specific increase of PROD in liver is related to the high content of CYP2B: phenobarbital (PB) and TPD increased CYP2B in rat liver, PB and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) - in mouse liver.	Phenobarbital	135-148	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	128-133
19895823-4	2009	In parallel, Western blot analysis showed that the species-specific increase of PROD in liver is related to the high content of CYP2B: phenobarbital (PB) and TPD increased CYP2B in rat liver, PB and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) - in mouse liver.	Phenobarbital	135-148	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	172-177
19895823-4	2009	In parallel, Western blot analysis showed that the species-specific increase of PROD in liver is related to the high content of CYP2B: phenobarbital (PB) and TPD increased CYP2B in rat liver, PB and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) - in mouse liver.	Phenobarbital	150-152	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	128-133
19895823-4	2009	In parallel, Western blot analysis showed that the species-specific increase of PROD in liver is related to the high content of CYP2B: phenobarbital (PB) and TPD increased CYP2B in rat liver, PB and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) - in mouse liver.	Phenobarbital	150-152	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	172-177
19915937-4	2010	Following exposure of PICM-19H cells to either 3-methylcholanthrene, rifampicin or phenobarbital, the induced activities of cytochrome P450 (CYP450) isozymes CYP-1A, -2, and-3A were assessed.	Phenobarbital	83-96	cytochrome P450 family 2 subfamily D member 6	Sus scrofa	124-139
19915937-4	2010	Following exposure of PICM-19H cells to either 3-methylcholanthrene, rifampicin or phenobarbital, the induced activities of cytochrome P450 (CYP450) isozymes CYP-1A, -2, and-3A were assessed.	Phenobarbital	83-96	cytochrome P450 family 2 subfamily D member 6	Sus scrofa	141-147
20645062-3	2010	Rifampicin, a nuclear pregnane X receptor (PXR) ligand; CITCO, a nuclear constitutive androstane receptor (CAR) ligand; and phenobarbital, which activates both CAR and PXR, have been used.	Phenobarbital	124-137	nuclear receptor subfamily 1 group I member 3	Homo sapiens	107-110
20645062-3	2010	Rifampicin, a nuclear pregnane X receptor (PXR) ligand; CITCO, a nuclear constitutive androstane receptor (CAR) ligand; and phenobarbital, which activates both CAR and PXR, have been used.	Phenobarbital	124-137	nuclear receptor subfamily 1 group I member 3	Homo sapiens	160-163
20645062-3	2010	Rifampicin, a nuclear pregnane X receptor (PXR) ligand; CITCO, a nuclear constitutive androstane receptor (CAR) ligand; and phenobarbital, which activates both CAR and PXR, have been used.	Phenobarbital	124-137	nuclear receptor subfamily 1 group I member 2	Homo sapiens	168-171
20051697-3	2010	METHODS: The patch-clamp technique was used combining an ultrafast solution exchange system to investigate the interaction of riluzole and phenobarbital with recombinant AMPA-type glutamate receptor channels (homomeric GluR2flipGQ or nondesensitizing GluR2L504Y).	Phenobarbital	139-152	glutamate ionotropic receptor AMPA type subunit 2	Homo sapiens	219-224
19850644-3	2010	We hypothesized that some PPC, including DEHP, induce transcriptional changes independent of PPARalpha but dependent on other nuclear receptors, including the constitutive-activated receptor (CAR) that mediates phenobarbital (PB) effects on hepatocyte growth and liver tumor induction.	Phenobarbital	211-224	nuclear receptor subfamily 1, group I, member 3	Mus musculus	159-190
19850644-3	2010	We hypothesized that some PPC, including DEHP, induce transcriptional changes independent of PPARalpha but dependent on other nuclear receptors, including the constitutive-activated receptor (CAR) that mediates phenobarbital (PB) effects on hepatocyte growth and liver tumor induction.	Phenobarbital	211-224	nuclear receptor subfamily 1, group I, member 3	Mus musculus	192-195
19850644-3	2010	We hypothesized that some PPC, including DEHP, induce transcriptional changes independent of PPARalpha but dependent on other nuclear receptors, including the constitutive-activated receptor (CAR) that mediates phenobarbital (PB) effects on hepatocyte growth and liver tumor induction.	Phenobarbital	226-228	nuclear receptor subfamily 1, group I, member 3	Mus musculus	159-190
19850644-3	2010	We hypothesized that some PPC, including DEHP, induce transcriptional changes independent of PPARalpha but dependent on other nuclear receptors, including the constitutive-activated receptor (CAR) that mediates phenobarbital (PB) effects on hepatocyte growth and liver tumor induction.	Phenobarbital	226-228	nuclear receptor subfamily 1, group I, member 3	Mus musculus	192-195
19895823-4	2009	In parallel, Western blot analysis showed that the species-specific increase of PROD in liver is related to the high content of CYP2B: phenobarbital (PB) and TPD increased CYP2B in rat liver, PB and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) - in mouse liver.	Phenobarbital	192-194	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	128-133
19858220-7	2009	Immunohistochemical study using an anti-phospho-threonine 38 peptide antibody has, in fact, demonstrated that the classic CAR activator phenobarbital dephosphorylates the corresponding threonine 48 of mouse CAR in the cytoplasm of mouse liver and translocates CAR into the nucleus.	Phenobarbital	136-149	nuclear receptor subfamily 1, group I, member 3	Mus musculus	122-125
19858220-7	2009	Immunohistochemical study using an anti-phospho-threonine 38 peptide antibody has, in fact, demonstrated that the classic CAR activator phenobarbital dephosphorylates the corresponding threonine 48 of mouse CAR in the cytoplasm of mouse liver and translocates CAR into the nucleus.	Phenobarbital	136-149	nuclear receptor subfamily 1, group I, member 3	Mus musculus	207-210
19858220-7	2009	Immunohistochemical study using an anti-phospho-threonine 38 peptide antibody has, in fact, demonstrated that the classic CAR activator phenobarbital dephosphorylates the corresponding threonine 48 of mouse CAR in the cytoplasm of mouse liver and translocates CAR into the nucleus.	Phenobarbital	136-149	nuclear receptor subfamily 1, group I, member 3	Mus musculus	207-210
19732027-0	2009	Glucocorticoids and phenobarbital induce murine CYP2B genes by independent mechanisms.	Phenobarbital	20-33	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	48-53
19732027-1	2009	BACKGROUND: Genes for CYP of the 2B subfamily (CYP2B genes) have long been known to be inducible in murine liver by phenobarbital and phenobarbital-like inducers.	Phenobarbital	116-129	peptidyl-prolyl isomerase G (cyclophilin G)	Mus musculus	22-25
19732027-1	2009	BACKGROUND: Genes for CYP of the 2B subfamily (CYP2B genes) have long been known to be inducible in murine liver by phenobarbital and phenobarbital-like inducers.	Phenobarbital	116-129	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	47-52
19732027-1	2009	BACKGROUND: Genes for CYP of the 2B subfamily (CYP2B genes) have long been known to be inducible in murine liver by phenobarbital and phenobarbital-like inducers.	Phenobarbital	134-147	peptidyl-prolyl isomerase G (cyclophilin G)	Mus musculus	22-25
19732027-1	2009	BACKGROUND: Genes for CYP of the 2B subfamily (CYP2B genes) have long been known to be inducible in murine liver by phenobarbital and phenobarbital-like inducers.	Phenobarbital	134-147	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	47-52
19732027-4	2009	METHODS: The mechanism of action of phenobarbital-like inducers of murine CYP2B genes is first briefly summarized.	Phenobarbital	36-49	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	74-79
19841609-5	2009	A case-control association study of 125 epileptic dogs identified five genes with suggestive association to phenobarbital drug response: KCNQ3, P=0.0003; SNC2A2, P=0.0008; EPOX HYD, P=0.0005; ABCC4, P=0.0091; and GABRA2, P=0.0130.	Phenobarbital	108-121	potassium voltage-gated channel subfamily Q member 3	Canis lupus familiaris	137-142
19841609-5	2009	A case-control association study of 125 epileptic dogs identified five genes with suggestive association to phenobarbital drug response: KCNQ3, P=0.0003; SNC2A2, P=0.0008; EPOX HYD, P=0.0005; ABCC4, P=0.0091; and GABRA2, P=0.0130.	Phenobarbital	108-121	ATP binding cassette subfamily C member 4	Canis lupus familiaris	192-197
19841609-5	2009	A case-control association study of 125 epileptic dogs identified five genes with suggestive association to phenobarbital drug response: KCNQ3, P=0.0003; SNC2A2, P=0.0008; EPOX HYD, P=0.0005; ABCC4, P=0.0091; and GABRA2, P=0.0130.	Phenobarbital	108-121	gamma-aminobutyric acid type A receptor subunit alpha2	Canis lupus familiaris	213-219
19406444-0	2009	Long-lasting enhancement of CYP activity after discontinuation of repeated administration of phenobarbital in dogs.	Phenobarbital	93-106	Cytochrome P450 1A1	Canis lupus familiaris	28-31
19406444-1	2009	We investigated how long in vivo hepatic cytochrome P450 (CYP) activity is enhanced even after discontinuation of repeated oral administration of phenobarbital (PB) in dogs using antipyrine clearance, which reflects hepatic CYP activity.	Phenobarbital	146-159	Cytochrome P450 1A1	Canis lupus familiaris	58-61
19406444-4	2009	The result suggests that hepatic CYP activity was enhanced by the repeated administration of PB, and this enhancement may last for at least 4 weeks even after its discontinuation.	Phenobarbital	93-95	Cytochrome P450 1A1	Canis lupus familiaris	33-36
19661216-7	2009	However, HGF prevented constitutive androstane receptor-related up-regulation of MRP2 occurring in phenobarbital-treated hepatocytes.	Phenobarbital	99-112	ATP binding cassette subfamily C member 2	Homo sapiens	81-85
19666990-8	2009	RT-PCR and Western immunoblotting analysis showed that the inducibility of Cyp1a, Cyp2b, and Cyp3a by 3-methylcholanthrene, phenobarbital, and dexamethasone, respectively, was similar between nontumor- and tumor-bearing mice.	Phenobarbital	124-137	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	82-87
19666990-8	2009	RT-PCR and Western immunoblotting analysis showed that the inducibility of Cyp1a, Cyp2b, and Cyp3a by 3-methylcholanthrene, phenobarbital, and dexamethasone, respectively, was similar between nontumor- and tumor-bearing mice.	Phenobarbital	124-137	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	93-98
19663741-3	2009	At the BBB level, due to its luminal localisation, ABCB1 limits drug transport and is important in central detoxification.	Phenobarbital	29-36	ATP binding cassette subfamily B member 1	Homo sapiens	51-56
19845433-9	2009	In microsomes prepared from phenobarbital-treated Tg-UGT1 animals, 13-fold higher CL(int) (Vmax/K(m)) value was observed as compared with the untreated transgenic mice.	Phenobarbital	28-41	UDP glucuronosyltransferase 1 family, polypeptide A2	Mus musculus	53-57
19451401-7	2009	LIPA metabolism in human hepatocytes was found to be induced by the treatment of human hepatocytes with the prototypical CYP3A4 inducers rifampin, carbamazepine, omeprazole, phenobarbital, and phenytoin but not by the CYP1A2 inducer 3-methylcholanthrene.	Phenobarbital	174-187	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	121-127
19631232-5	2009	We have recently shown, that PPAR alpha agonists synergize with phenobarbital to induce another prototypical CAR target gene, CYP2B1.	Phenobarbital	64-77	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	126-132
19631232-6	2009	Therefore, it was tested whether a PPAR alpha agonist could enhance the phenobarbital-dependent acceleration of thyroid hormone elimination.	Phenobarbital	72-85	peroxisome proliferator activated receptor alpha	Rattus norvegicus	35-45
19541828-0	2009	Genetic polymorphisms in the TATA box and upstream phenobarbital-responsive enhancer module of the UGT1A1 promoter have combined effects on UDP-glucuronosyltransferase 1A1 transcription mediated by constitutive androstane receptor, pregnane X receptor, or glucocorticoid receptor in human liver.	Phenobarbital	51-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
19541828-0	2009	Genetic polymorphisms in the TATA box and upstream phenobarbital-responsive enhancer module of the UGT1A1 promoter have combined effects on UDP-glucuronosyltransferase 1A1 transcription mediated by constitutive androstane receptor, pregnane X receptor, or glucocorticoid receptor in human liver.	Phenobarbital	51-64	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	140-171
19541828-0	2009	Genetic polymorphisms in the TATA box and upstream phenobarbital-responsive enhancer module of the UGT1A1 promoter have combined effects on UDP-glucuronosyltransferase 1A1 transcription mediated by constitutive androstane receptor, pregnane X receptor, or glucocorticoid receptor in human liver.	Phenobarbital	51-64	nuclear receptor subfamily 1 group I member 3	Homo sapiens	198-230
19541828-0	2009	Genetic polymorphisms in the TATA box and upstream phenobarbital-responsive enhancer module of the UGT1A1 promoter have combined effects on UDP-glucuronosyltransferase 1A1 transcription mediated by constitutive androstane receptor, pregnane X receptor, or glucocorticoid receptor in human liver.	Phenobarbital	51-64	nuclear receptor subfamily 1 group I member 2	Homo sapiens	232-251
19541828-0	2009	Genetic polymorphisms in the TATA box and upstream phenobarbital-responsive enhancer module of the UGT1A1 promoter have combined effects on UDP-glucuronosyltransferase 1A1 transcription mediated by constitutive androstane receptor, pregnane X receptor, or glucocorticoid receptor in human liver.	Phenobarbital	51-64	nuclear receptor subfamily 3 group C member 1	Homo sapiens	256-279
19541828-2	2009	The purpose of this study was to determine whether the genetic polymorphisms in the RNA polymerase II core promoter and the upstream phenobarbital-responsive element module (PBREM) of the UGT1A1 promoter have combined effects on UGT1A1 transcription mediated by the transcription factors.	Phenobarbital	133-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	188-194
19541828-2	2009	The purpose of this study was to determine whether the genetic polymorphisms in the RNA polymerase II core promoter and the upstream phenobarbital-responsive element module (PBREM) of the UGT1A1 promoter have combined effects on UGT1A1 transcription mediated by the transcription factors.	Phenobarbital	133-146	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	229-235
19708687-0	2009	Transcriptional activation of PPARalpha by phenobarbital in the absence of CAR and PXR.	Phenobarbital	43-56	peroxisome proliferator activated receptor alpha	Mus musculus	30-39
19708687-1	2009	The nuclear receptors CAR (constitutive androstane receptor) and PXR (pregnane X receptor) mediate the effects of phenobarbital on gene transcription.	Phenobarbital	114-127	nuclear receptor subfamily 1, group I, member 3	Mus musculus	22-59
19708687-1	2009	The nuclear receptors CAR (constitutive androstane receptor) and PXR (pregnane X receptor) mediate the effects of phenobarbital on gene transcription.	Phenobarbital	114-127	nuclear receptor subfamily 1, group I, member 2	Mus musculus	65-68
19708687-1	2009	The nuclear receptors CAR (constitutive androstane receptor) and PXR (pregnane X receptor) mediate the effects of phenobarbital on gene transcription.	Phenobarbital	114-127	nuclear receptor subfamily 1, group I, member 2	Mus musculus	70-89
19708687-4	2009	In the absence of CAR and PXR, phenobarbital unexpectedly induced mRNAs of several nuclear receptors, including PPARalpha and its target genes Cyp4a10 and Cyp4a14.	Phenobarbital	31-44	peroxisome proliferator activated receptor alpha	Mus musculus	112-121
19708687-4	2009	In the absence of CAR and PXR, phenobarbital unexpectedly induced mRNAs of several nuclear receptors, including PPARalpha and its target genes Cyp4a10 and Cyp4a14.	Phenobarbital	31-44	cytochrome P450, family 4, subfamily a, polypeptide 10	Mus musculus	143-150
19708687-4	2009	In the absence of CAR and PXR, phenobarbital unexpectedly induced mRNAs of several nuclear receptors, including PPARalpha and its target genes Cyp4a10 and Cyp4a14.	Phenobarbital	31-44	cytochrome P450, family 4, subfamily a, polypeptide 14	Mus musculus	155-162
19708687-5	2009	Interestingly, in primary cultures of hepatocytes isolated from CAR/PXR(-/-) knockout mice, phenobarbital increased HNF-4alpha levels.	Phenobarbital	92-105	nuclear receptor subfamily 1, group I, member 3	Mus musculus	64-67
19708687-5	2009	Interestingly, in primary cultures of hepatocytes isolated from CAR/PXR(-/-) knockout mice, phenobarbital increased HNF-4alpha levels.	Phenobarbital	92-105	nuclear receptor subfamily 1, group I, member 2	Mus musculus	68-71
19708687-5	2009	Interestingly, in primary cultures of hepatocytes isolated from CAR/PXR(-/-) knockout mice, phenobarbital increased HNF-4alpha levels.	Phenobarbital	92-105	hepatic nuclear factor 4, alpha	Mus musculus	116-126
19708687-6	2009	In further experiments in these hepatocyte cultures we provide evidence that phenobarbital directly induces transcription of the PPARalpha gene via its HNF-4alpha response element, and indirectly by lack of inhibitory crosstalk of AMPK, CAR and PXR with HNF-4alpha.	Phenobarbital	77-90	peroxisome proliferator activated receptor alpha	Mus musculus	129-138
19708687-6	2009	In further experiments in these hepatocyte cultures we provide evidence that phenobarbital directly induces transcription of the PPARalpha gene via its HNF-4alpha response element, and indirectly by lack of inhibitory crosstalk of AMPK, CAR and PXR with HNF-4alpha.	Phenobarbital	77-90	hepatic nuclear factor 4, alpha	Mus musculus	152-162
19708687-6	2009	In further experiments in these hepatocyte cultures we provide evidence that phenobarbital directly induces transcription of the PPARalpha gene via its HNF-4alpha response element, and indirectly by lack of inhibitory crosstalk of AMPK, CAR and PXR with HNF-4alpha.	Phenobarbital	77-90	nuclear receptor subfamily 1, group I, member 2	Mus musculus	245-248
19708687-6	2009	In further experiments in these hepatocyte cultures we provide evidence that phenobarbital directly induces transcription of the PPARalpha gene via its HNF-4alpha response element, and indirectly by lack of inhibitory crosstalk of AMPK, CAR and PXR with HNF-4alpha.	Phenobarbital	77-90	hepatic nuclear factor 4, alpha	Mus musculus	254-264
19708687-7	2009	Our results provide further insight into CAR and PXR-independent effects of phenobarbital and the crosstalk between different nuclear receptor signaling pathways.	Phenobarbital	76-89	nuclear receptor subfamily 1, group I, member 3	Mus musculus	41-44
19708687-7	2009	Our results provide further insight into CAR and PXR-independent effects of phenobarbital and the crosstalk between different nuclear receptor signaling pathways.	Phenobarbital	76-89	nuclear receptor subfamily 1, group I, member 2	Mus musculus	49-52
19520777-7	2009	Moreover, CYP2B1 expression was induced by administration of phenobarbital.	Phenobarbital	61-74	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	10-16
19494186-8	2009	After withdrawal of the EP1 receptor antagonist, a low dose of the P-glycoprotein substrate phenobarbital resulted in an anticonvulsant effect in this pretreated group, whereas the same dosage of phenobarbital did not exert a significant effect in the respective control group.	Phenobarbital	92-105	prostaglandin E receptor 1	Rattus norvegicus	24-27
19494186-8	2009	After withdrawal of the EP1 receptor antagonist, a low dose of the P-glycoprotein substrate phenobarbital resulted in an anticonvulsant effect in this pretreated group, whereas the same dosage of phenobarbital did not exert a significant effect in the respective control group.	Phenobarbital	92-105	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	67-81
19648928-0	2009	Aberrant luminal progenitors as the candidate target population for basal tumor development in BRCA1 mutation carriers.	Phenobarbital	9-16	BRCA1 DNA repair associated	Homo sapiens	95-100
19648928-4	2009	Unexpectedly, we found that breast tissue from BRCA1 mutation carriers harbors an expanded luminal progenitor population that shows factor-independent growth in vitro.	Phenobarbital	91-98	BRCA1 DNA repair associated	Homo sapiens	47-52
19648928-6	2009	The c-KIT tyrosine kinase receptor (encoded by KIT) emerged as a key marker of luminal progenitor cells and was more highly expressed in BRCA1-associated preneoplastic tissue and tumors.	Phenobarbital	79-86	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	6-9
19648928-7	2009	Our findings suggest that an aberrant luminal progenitor population is a target for transformation in BRCA1-associated basal tumors .	Phenobarbital	38-45	BRCA1 DNA repair associated	Homo sapiens	102-107
19482888-0	2009	The constitutive active/androstane receptor facilitates unique phenobarbital-induced expression changes of genes involved in key pathways in precancerous liver and liver tumors.	Phenobarbital	63-76	nuclear receptor subfamily 1, group I, member 3	Mus musculus	4-43
19482888-2	2009	PB-elicited unique expression changes of genes, including some of those identified previously as exhibiting regions of altered DNA methylation, were discerned in precancerous liver tissue and/or individual liver tumors from susceptible constitutive active/androstane receptor (CAR) wild-type (WT) compared with resistant CAR knockout (KO) mice.	Phenobarbital	0-2	nuclear receptor subfamily 1, group I, member 3	Mus musculus	236-275
19482888-2	2009	PB-elicited unique expression changes of genes, including some of those identified previously as exhibiting regions of altered DNA methylation, were discerned in precancerous liver tissue and/or individual liver tumors from susceptible constitutive active/androstane receptor (CAR) wild-type (WT) compared with resistant CAR knockout (KO) mice.	Phenobarbital	0-2	nuclear receptor subfamily 1, group I, member 3	Mus musculus	277-280
19482888-2	2009	PB-elicited unique expression changes of genes, including some of those identified previously as exhibiting regions of altered DNA methylation, were discerned in precancerous liver tissue and/or individual liver tumors from susceptible constitutive active/androstane receptor (CAR) wild-type (WT) compared with resistant CAR knockout (KO) mice.	Phenobarbital	0-2	nuclear receptor subfamily 1, group I, member 3	Mus musculus	321-324
19622001-1	2009	Phenobarbitone and related compounds induce hepatic microsomal cytochrome P450 (CYP) 2B forms (mediated by the constitutive androstane receptor), whereas peroxisome proliferators induce CYP4A forms (mediated by the peroxisome proliferator-activated receptor alpha) in rats and mice.	Phenobarbital	0-14	peroxisome proliferator activated receptor alpha	Rattus norvegicus	215-263
19702536-3	2009	A variety of xenobiotics such as phenobarbital, rifampicin, and hyperforin have been shown to induce the transcriptional expression of CYP2C genes in primary human hepatocytes and to increase the metabolism of CYP2C substrates in vivo in man.	Phenobarbital	33-46	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	135-140
19702536-3	2009	A variety of xenobiotics such as phenobarbital, rifampicin, and hyperforin have been shown to induce the transcriptional expression of CYP2C genes in primary human hepatocytes and to increase the metabolism of CYP2C substrates in vivo in man.	Phenobarbital	33-46	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	210-215
19359405-7	2009	Treatment of mice with the CAR activator 1,4-bis[2-(3,5-dichloropyridyloxy)] benzene also induced expression of Ces6 in duodenum and liver in a CAR-dependent manner, whereas treatment with phenobarbital produced induction of Ces6 exclusively in liver.	Phenobarbital	189-202	nuclear receptor subfamily 1, group I, member 3	Mus musculus	27-30
19761046-1	2009	Chronic feeding of carcinogens p-dimethylamino azobenzene (initiator) and phenobarbital (promoter) for 90 and 120 days elevated activities of acid and alkaline phosphatases, levels of blood glucose and cortisol and decreased the activities of glutathione reductase, succinate dehydrogenase, and blood cholesterol and hemoglobin contents, and levels of serum estradiol and testosterone in mice.	Phenobarbital	74-87	glutathione reductase	Mus musculus	243-264
19409407-2	2009	Furthermore, formation of CK8 and CK18 complexes due to CK8 phosphorylation at Ser73 and Ser431 was found to be strongly associated with promotion of hepatocarcinogenesis by PB and the development of hepatocellular carcinomas.	Phenobarbital	174-176	keratin 8	Rattus norvegicus	26-29
19409407-2	2009	Furthermore, formation of CK8 and CK18 complexes due to CK8 phosphorylation at Ser73 and Ser431 was found to be strongly associated with promotion of hepatocarcinogenesis by PB and the development of hepatocellular carcinomas.	Phenobarbital	174-176	keratin 18	Rattus norvegicus	34-38
19409407-2	2009	Furthermore, formation of CK8 and CK18 complexes due to CK8 phosphorylation at Ser73 and Ser431 was found to be strongly associated with promotion of hepatocarcinogenesis by PB and the development of hepatocellular carcinomas.	Phenobarbital	174-176	keratin 8	Rattus norvegicus	56-59
19047470-12	2009	In summary, there are at least two independent mechanisms of CYP2B induction: one involving phenobarbital and phenobarbital-like inducers and another involving glucocorticoids that induce via the glucocorticoid receptor with CAR acting as an accessory factor.	Phenobarbital	92-105	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	61-66
19383836-5	2009	Immunohistochemical studies with cerumen gland-containing tissue specimens revealed that the ABCC11 WT protein was localized in intracellular granules and large vacuoles, as well as at the luminal membrane of secretory cells in the cerumen gland, whereas granular or vacuolar localization was not detected for the SNP (Arg180) variant.	Phenobarbital	189-196	ATP binding cassette subfamily C member 11	Homo sapiens	93-99
19212336-3	2009	Indeed, we have shown that functional Rfc1 activity is significantly reduced by clinically relevant concentrations of the anticonvulsant drugs PB or carbamazepine in an adequate in vitro model.	Phenobarbital	143-145	replication factor C subunit 1	Homo sapiens	38-42
19212336-4	2009	As PB is known to regulate carrier-associated transport by the nuclear receptor constitutive androstane receptor (CAR), we investigated the involvement of the CAR signaling cascade and the mode of PB-induced downregulation of Rfc1 activity.	Phenobarbital	197-199	replication factor C subunit 1	Homo sapiens	226-230
19212336-5	2009	CAR activation by PB or the CAR agonist 1,4-bis[2-(3,5-dichloro- pyridyloxy)]-benzene resulted in translocation of Ca(2+)-dependent protein kinase Calpha (cPKCalpha) to the plasma membrane related to significantly elevated PKC activities.	Phenobarbital	18-20	protein kinase C delta	Homo sapiens	156-159
19212336-7	2009	Studies on intracellular distribution of the Rfc1 protein indicated that PB-induced activation of cPKCalpha was associated with carrier internalization from the plasma membrane into the cytosol independent of the Rfc1 phosphorylation status.	Phenobarbital	73-75	replication factor C subunit 1	Homo sapiens	45-49
19420747-4	2009	Here, we examined the induction of CYP gene expression by an inducer by examining the effect of phenobarbital treatment on CYP gene expression in the co-culture system.	Phenobarbital	96-109	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	35-38
19420747-4	2009	Here, we examined the induction of CYP gene expression by an inducer by examining the effect of phenobarbital treatment on CYP gene expression in the co-culture system.	Phenobarbital	96-109	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	123-126
19196849-5	2009	This pathology was absent in WT mice pretreated with PB and TCPOBOP, indicating CAR-dependent hepatoprotection.	Phenobarbital	53-55	nuclear receptor subfamily 1, group I, member 3	Mus musculus	80-83
19588850-4	2009	Addition of antiserum against CYP2B4, a constitutive and PB-inducible rabbit P450 isoform, to a microsomal incubation system resulted in almost complete inhibition of the formation of 3-OH-, 4-OH- and 3,4-diOH-metabolites.	Phenobarbital	57-59	cytochrome P450 2B4	Oryctolagus cuniculus	30-36
19123478-7	2009	Tumour promotion by PB led to significant increases in the number of preneoplastic and neoplastic lesions in liver of both wild-type and c-met knockout mice, with only minor differences in response.	Phenobarbital	20-22	met proto-oncogene	Mus musculus	137-142
19382721-4	2009	CCl4-treated animals showed significant increase in the levels of liver enzymes, phenobarbitone-induced sleeping time and revealed fatty changes and centrizonal necrosis on histological examination of liver indicating hepatic damage.	Phenobarbital	81-95	chemokine (C-C motif) ligand 4	Mus musculus	0-4
19233941-0	2009	Multiple genes exhibit phenobarbital-induced constitutive active/androstane receptor-mediated DNA methylation changes during liver tumorigenesis and in liver tumors.	Phenobarbital	23-36	nuclear receptor subfamily 1, group I, member 3	Mus musculus	45-84
19233941-1	2009	The constitutive active/androstane receptor (CAR) mediates responses to the nongenotoxic rodent liver tumor promoter phenobarbital (PB), including certain gene expression changes, hepatomegaly, and tumor formation.	Phenobarbital	117-130	nuclear receptor subfamily 1, group I, member 3	Mus musculus	4-43
19233941-1	2009	The constitutive active/androstane receptor (CAR) mediates responses to the nongenotoxic rodent liver tumor promoter phenobarbital (PB), including certain gene expression changes, hepatomegaly, and tumor formation.	Phenobarbital	117-130	nuclear receptor subfamily 1, group I, member 3	Mus musculus	45-48
19233941-1	2009	The constitutive active/androstane receptor (CAR) mediates responses to the nongenotoxic rodent liver tumor promoter phenobarbital (PB), including certain gene expression changes, hepatomegaly, and tumor formation.	Phenobarbital	132-134	nuclear receptor subfamily 1, group I, member 3	Mus musculus	4-43
19233941-1	2009	The constitutive active/androstane receptor (CAR) mediates responses to the nongenotoxic rodent liver tumor promoter phenobarbital (PB), including certain gene expression changes, hepatomegaly, and tumor formation.	Phenobarbital	132-134	nuclear receptor subfamily 1, group I, member 3	Mus musculus	45-48
19233941-3	2009	Previously, 146 unique PB-induced regions of altered DNA methylation (RAMs) were observed in liver tumor-susceptible CAR wild-type (WT) mice (in 23 weeks, precancerous tissue, and 32 weeks, tumor tissue), as compared to the resistant knockout (KO).	Phenobarbital	23-25	nuclear receptor subfamily 1, group I, member 3	Mus musculus	117-120
19233941-8	2009	Importantly, 11 of these genes were identified from identical, unique RAMs discerned in both the sensitive B6C3F1 and CAR WT mice, thus representing an initial, potential candidate "fingerprint" which might serve as a biomarker for PB-induced tumorigenesis.	Phenobarbital	232-234	nuclear receptor subfamily 1, group I, member 3	Mus musculus	118-121
19233941-9	2009	These two studies reveal "new" genes whose epigenetic statuses changed uniquely in liver tumor-susceptible mice (B6C3F1 and CAR WT), as compared to their resistant counterparts (C57BL/6 and CAR KO, respectively), within a continuum of PB-induced tumorigenesis.	Phenobarbital	235-237	nuclear receptor subfamily 1, group I, member 3	Mus musculus	124-127
19047470-3	2009	Expression of murine CYP2B genes is strongly activated by treatment with phenobarbital or phenobarbital-like inducers, and a detectable response requires the presence of the constitutive androstane receptor (CAR).	Phenobarbital	73-86	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	21-26
19047470-3	2009	Expression of murine CYP2B genes is strongly activated by treatment with phenobarbital or phenobarbital-like inducers, and a detectable response requires the presence of the constitutive androstane receptor (CAR).	Phenobarbital	73-86	nuclear receptor subfamily 1, group I, member 3	Mus musculus	208-211
19047470-3	2009	Expression of murine CYP2B genes is strongly activated by treatment with phenobarbital or phenobarbital-like inducers, and a detectable response requires the presence of the constitutive androstane receptor (CAR).	Phenobarbital	90-103	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	21-26
19047470-7	2009	Given the well known observation that CYP2B genes are not phenobarbital-responsive in cultured cell lines, the dexamethasone responsiveness of CYP2B reporter constructs in cell lines demonstrates in itself that the mechanism of dexamethasone induction is distinct from that of phenobarbital.	Phenobarbital	277-290	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	143-148
19084987-4	2009	When WIF-B9 cells were treated with phenobarbital, claudin-2 expression and tight junction strands were markedly increased together with induction of canalicular formation with a biliary secretion function.	Phenobarbital	36-49	claudin 2	Homo sapiens	51-60
19084987-5	2009	Knockdown of claudin-2 prevented bile canalicular formation after treatment with or without phenobarbital.	Phenobarbital	92-105	claudin 2	Homo sapiens	13-22
19136022-1	2009	Constitutive androstane receptor (CAR) and peroxisome proliferator activated receptor (PPAR)alpha are transcription factors known to be primary mediators of liver effects, including carcinogenesis, by phenobarbital-like compounds and peroxisome proliferators, respectively, in rodents.	Phenobarbital	201-214	nuclear receptor subfamily 1, group I, member 3	Mus musculus	34-37
19136022-1	2009	Constitutive androstane receptor (CAR) and peroxisome proliferator activated receptor (PPAR)alpha are transcription factors known to be primary mediators of liver effects, including carcinogenesis, by phenobarbital-like compounds and peroxisome proliferators, respectively, in rodents.	Phenobarbital	201-214	peroxisome proliferator activated receptor alpha	Mus musculus	87-97
19286836-5	2009	Phenobarbital suppressed the expression of CYP2R1 in fibroblasts and CYP2J2 in LNCaP cells.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily R member 1	Homo sapiens	43-49
19286836-5	2009	Phenobarbital suppressed the expression of CYP2R1 in fibroblasts and CYP2J2 in LNCaP cells.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily J member 2	Homo sapiens	69-75
19270015-1	2009	At 2 and 4 weeks following treatment with phenobarbital (PB), the classical nongenotoxic rodent liver carcinogen, we elucidated unique gene expression changes (both induction and repression) in liver tumor-susceptible B6C3F1 mice, as compared with the relatively resistant C57BL/6.	Phenobarbital	42-55	serine (or cysteine) peptidase inhibitor, clade B, member 9d	Mus musculus	0-4
19270015-1	2009	At 2 and 4 weeks following treatment with phenobarbital (PB), the classical nongenotoxic rodent liver carcinogen, we elucidated unique gene expression changes (both induction and repression) in liver tumor-susceptible B6C3F1 mice, as compared with the relatively resistant C57BL/6.	Phenobarbital	57-59	serine (or cysteine) peptidase inhibitor, clade B, member 9d	Mus musculus	0-4
19270015-4	2009	Additionally, three DNA methyltransferase genes (Dnmt1, Dnmt3a, and Dnmt3b) were repressed uniquely in the tumor-prone B6C3F1 mice, and all possess putative CAREs, providing a potential direct link between PB and expression of key genes that regulate DNA methylation status.	Phenobarbital	206-208	DNA methyltransferase (cytosine-5) 1	Mus musculus	49-54
19270015-4	2009	Additionally, three DNA methyltransferase genes (Dnmt1, Dnmt3a, and Dnmt3b) were repressed uniquely in the tumor-prone B6C3F1 mice, and all possess putative CAREs, providing a potential direct link between PB and expression of key genes that regulate DNA methylation status.	Phenobarbital	206-208	DNA methyltransferase 3A	Mus musculus	56-62
19270015-4	2009	Additionally, three DNA methyltransferase genes (Dnmt1, Dnmt3a, and Dnmt3b) were repressed uniquely in the tumor-prone B6C3F1 mice, and all possess putative CAREs, providing a potential direct link between PB and expression of key genes that regulate DNA methylation status.	Phenobarbital	206-208	DNA methyltransferase 3B	Mus musculus	68-74
19270015-5	2009	Previously, we demonstrated that PB-elicited unique regions of altered methylation (RAMs) in B6C3F1 mice, as compared with the relatively resistant C57BL/6, at 2 and 4 weeks, and annotation of the regions harboring these changes revealed 51 genes.	Phenobarbital	33-35	serine (or cysteine) peptidase inhibitor, clade B, member 9d	Mus musculus	148-167
19297538-8	2009	Experiment 3 investigated whether phenobarbital, like other nonphotic zeitgebers, suppresses SCN Period1 and Period2 transcription.	Phenobarbital	34-47	period circadian regulator 2	Homo sapiens	109-116
19196849-3	2009	CAR activators phenobarbital (PB) and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) or corn oil (CO) were administered to C57BL/6 wild-type (WT) and CAR knockout (CAR-null) mice before and during induction of intrahepatic cholestasis using the secondary bile acid, lithocholic acid (LCA).	Phenobarbital	15-28	nuclear receptor subfamily 1, group I, member 3	Mus musculus	0-3
19196849-3	2009	CAR activators phenobarbital (PB) and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) or corn oil (CO) were administered to C57BL/6 wild-type (WT) and CAR knockout (CAR-null) mice before and during induction of intrahepatic cholestasis using the secondary bile acid, lithocholic acid (LCA).	Phenobarbital	30-32	nuclear receptor subfamily 1, group I, member 3	Mus musculus	0-3
19378387-3	2009	Treatment with 50 microM MTF and 50 microM PB for 72 h increased CYP2B1 mRNA levels in male Wistar rat hepatocytes and CYP2B6 mRNA levels in human hepatocytes.	Phenobarbital	43-45	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	65-71
19378387-3	2009	Treatment with 50 microM MTF and 50 microM PB for 72 h increased CYP2B1 mRNA levels in male Wistar rat hepatocytes and CYP2B6 mRNA levels in human hepatocytes.	Phenobarbital	43-45	cytochrome P450, family 2, subfamily b, polypeptide 3	Rattus norvegicus	119-125
19171675-4	2009	In cultured rat hepatocytes treated with phenobarbital, IL-1beta stimulation failed to down-regulate CYP3A1 mRNA within 24 h of treatment, whereas CYP3A protein was down-regulated to 40% of control within 6 h, showing the post-transcriptional down-regulation of CYP3A1 protein.	Phenobarbital	41-54	interleukin 1 beta	Rattus norvegicus	56-64
19429015-2	2009	The aim of the present work was to assess the involvement of P-glycoprotein in carbamazepine and phenobarbital hippocampal pharmacokinetics in an experimental model of epilepsy, induced by repetitive MP administration.	Phenobarbital	97-110	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	61-75
19429015-15	2009	Conversely, hippocampal levels of phenobarbital are reduced in MP rats with regard to non-epileptic rats, suggesting a potential role of P-gp overexpression in pharmacoresistance to phenobarbital.	Phenobarbital	34-47	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	137-141
19429015-15	2009	Conversely, hippocampal levels of phenobarbital are reduced in MP rats with regard to non-epileptic rats, suggesting a potential role of P-gp overexpression in pharmacoresistance to phenobarbital.	Phenobarbital	182-195	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	137-141
18798224-9	2009	The administration of PB suppressed CYP1A2 apoprotein levels in CD rats, whereas the drug had no effect on NF rats.	Phenobarbital	22-24	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	36-42
18798224-10	2009	The PB-induced up-regulation of CYP2B, CYP2E1 and CYP1A1 isozymes was markedly higher in CD than in NF rats.	Phenobarbital	4-6	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	39-45
18798224-10	2009	The PB-induced up-regulation of CYP2B, CYP2E1 and CYP1A1 isozymes was markedly higher in CD than in NF rats.	Phenobarbital	4-6	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	50-56
19047470-12	2009	In summary, there are at least two independent mechanisms of CYP2B induction: one involving phenobarbital and phenobarbital-like inducers and another involving glucocorticoids that induce via the glucocorticoid receptor with CAR acting as an accessory factor.	Phenobarbital	110-123	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	61-66
18983865-6	2009	The strong and overlapping inductive role of phenobarbital strengthens the participation of CYP2B6 and CYP3A in diazepam N-demethylation and CYP3A in temazepam formation.	Phenobarbital	45-58	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	92-98
18983865-6	2009	The strong and overlapping inductive role of phenobarbital strengthens the participation of CYP2B6 and CYP3A in diazepam N-demethylation and CYP3A in temazepam formation.	Phenobarbital	45-58	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	103-108
18983865-6	2009	The strong and overlapping inductive role of phenobarbital strengthens the participation of CYP2B6 and CYP3A in diazepam N-demethylation and CYP3A in temazepam formation.	Phenobarbital	45-58	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	141-146
19515014-10	2009	CYP2C9 is subject to induction by rifampin, phenobarbital, and dexamethasone, indicating the involvement of pregnane X receptor, constitutive androstane receptor and glucocorticoid receptor in the regulation of CYP2C9.	Phenobarbital	44-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	0-6
19515014-10	2009	CYP2C9 is subject to induction by rifampin, phenobarbital, and dexamethasone, indicating the involvement of pregnane X receptor, constitutive androstane receptor and glucocorticoid receptor in the regulation of CYP2C9.	Phenobarbital	44-57	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	211-217
19202563-3	2009	Clotrimazole, rifampin, ritonavir, phenytoin, and phenobarbital induced CYP2C9 consistent with previous findings for CYP3A4.	Phenobarbital	50-63	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	72-78
19202563-3	2009	Clotrimazole, rifampin, ritonavir, phenytoin, and phenobarbital induced CYP2C9 consistent with previous findings for CYP3A4.	Phenobarbital	50-63	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	117-123
18573861-9	2008	Metabolism of 17-OHPC was significantly greater in FHH treated with the CYP3A inducers, rifampin and phenobarbital.	Phenobarbital	101-114	calcium sensing receptor	Homo sapiens	51-54
18587059-3	2008	We demonstrated that a 1-day treatment of infant mice at postnatal day 6 (P6) with the NMDAR antagonist dizocilpine or the GABA(A)R agonist phenobarbital not only has acute but also long term effects on the cerebral cortex.	Phenobarbital	140-153	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 2	Mus musculus	123-131
18824002-6	2008	Direct comparison of the conventional bi-directional (concentration gradient) assay with the CETA, using MDR1-transfected LLC cells, demonstrated that CETA, but not the conventional assay, identified phenytoin and phenobarbital as substrates of human Pgp.	Phenobarbital	214-227	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	105-109
18824002-6	2008	Direct comparison of the conventional bi-directional (concentration gradient) assay with the CETA, using MDR1-transfected LLC cells, demonstrated that CETA, but not the conventional assay, identified phenytoin and phenobarbital as substrates of human Pgp.	Phenobarbital	214-227	ATP binding cassette subfamily B member 1	Homo sapiens	251-254
18824002-9	2008	However, transport of phenobarbital and levetiracetam was also inhibited by MK571, which preferentially blocks transport by multidrug resistance transporters (MRPs), indicating that, in addition to Pgp, these AEDs are substrates of MRPs.	Phenobarbital	22-35	ATP binding cassette subfamily B member 1	Homo sapiens	198-201
18796496-0	2008	Global liver proteomics of rats exposed for 5 days to phenobarbital identifies changes associated with cancer and with CYP metabolism.	Phenobarbital	54-67	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	119-122
18796496-6	2008	The GO results suggested that PB"s mechanism of nongenotoxic carcinogenesis involves both increased xenobiotic metabolism, especially induction of the 2B subfamily of CYP enzymes, and increased cell cycle activity.	Phenobarbital	30-32	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	167-170
18616970-2	2008	A PB promoting regimen (0.05% in the diet) stimulated the outgrowth of FB(1)-induced placental glutathione S-transferase (GSTP) positive initiated hepatocytes.	Phenobarbital	2-4	hematopoietic prostaglandin D synthase	Rattus norvegicus	95-120
18616970-2	2008	A PB promoting regimen (0.05% in the diet) stimulated the outgrowth of FB(1)-induced placental glutathione S-transferase (GSTP) positive initiated hepatocytes.	Phenobarbital	2-4	glutathione S-transferase pi 1	Rattus norvegicus	122-126
19601803-7	2009	CYP2D6 is largely uninducible by prototypical CYP inducers such as phenobarbital, rifampin and dexamethasone, but it is regulated by hepatocyte nuclear factor-4alpha, a nuclear receptor.	Phenobarbital	67-80	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	0-6
19601803-7	2009	CYP2D6 is largely uninducible by prototypical CYP inducers such as phenobarbital, rifampin and dexamethasone, but it is regulated by hepatocyte nuclear factor-4alpha, a nuclear receptor.	Phenobarbital	67-80	peptidylprolyl isomerase G	Homo sapiens	0-3
18989830-4	2008	CYP3A4 mRNA and activity were induced by the prototypical pregnane X receptor (PXR) ligands, rifampicin (E(max) = 36- and 6-fold, respectively, and EC(50) = 4 microM) and phenobarbital (E(max) = 12- and 4-fold, respectively, and EC(50) = 205 microM).	Phenobarbital	171-184	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
18989830-4	2008	CYP3A4 mRNA and activity were induced by the prototypical pregnane X receptor (PXR) ligands, rifampicin (E(max) = 36- and 6-fold, respectively, and EC(50) = 4 microM) and phenobarbital (E(max) = 12- and 4-fold, respectively, and EC(50) = 205 microM).	Phenobarbital	171-184	nuclear receptor subfamily 1 group I member 2	Homo sapiens	58-77
18989830-4	2008	CYP3A4 mRNA and activity were induced by the prototypical pregnane X receptor (PXR) ligands, rifampicin (E(max) = 36- and 6-fold, respectively, and EC(50) = 4 microM) and phenobarbital (E(max) = 12- and 4-fold, respectively, and EC(50) = 205 microM).	Phenobarbital	171-184	nuclear receptor subfamily 1 group I member 2	Homo sapiens	79-82
18782568-1	2008	Rat CYP2B1 and CYP2B2 and mouse CYP2B10 are dramatically induced by phenobarbital (PB) in liver.	Phenobarbital	68-81	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	32-39
18782568-1	2008	Rat CYP2B1 and CYP2B2 and mouse CYP2B10 are dramatically induced by phenobarbital (PB) in liver.	Phenobarbital	83-85	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	32-39
18782568-2	2008	PB responsiveness requires the constitutive androstane receptor (CAR).	Phenobarbital	0-2	nuclear receptor subfamily 1, group I, member 3	Mus musculus	31-63
18782568-2	2008	PB responsiveness requires the constitutive androstane receptor (CAR).	Phenobarbital	0-2	nuclear receptor subfamily 1, group I, member 3	Mus musculus	65-68
17418998-4	2008	Results showed that the expressions of PCNA and iNOS were induced by DEN plus PB in liver tissues.	Phenobarbital	78-80	proliferating cell nuclear antigen	Rattus norvegicus	39-43
17418998-4	2008	Results showed that the expressions of PCNA and iNOS were induced by DEN plus PB in liver tissues.	Phenobarbital	78-80	nitric oxide synthase 2	Rattus norvegicus	48-52
18437444-4	2008	PCB 136 levels were significantly lower in phenobarbital- and, to a lesser extent, in dexamethasone-pretreated animals, presumably due to the induction of PCB 136 metabolizing enzymes.	Phenobarbital	43-56	pyruvate carboxylase	Mus musculus	0-3
18437444-4	2008	PCB 136 levels were significantly lower in phenobarbital- and, to a lesser extent, in dexamethasone-pretreated animals, presumably due to the induction of PCB 136 metabolizing enzymes.	Phenobarbital	43-56	pyruvate carboxylase	Mus musculus	155-158
18437444-6	2008	Fecal PCB levels and enantiomeric fraction values changed over time in a manner consistent with slower digestive motility in the mice pretreated with phenobarbital and dexamethasone.	Phenobarbital	150-163	pyruvate carboxylase	Mus musculus	6-9
18827444-3	2008	Treatment with phenobarbital, a potent CYP inducer, increased the predominance of expression of these three mRNAs in WI rats (by 26-, 4-, and 2-fold, respectively) along with the predominance of increased microsomal total P450 contents and smooth-surface endoplasmic reticulum in the centrilobular hepatocytes.	Phenobarbital	15-28	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-42
18677425-7	2008	To demonstrate the utility of this panel of mice, we used the mice to show that the in vivo induction of Cyp3a11 and Cyp2b10 by phenobarbital was only mediated by CAR, although this compound is described as a PXR and CAR activator in vitro.	Phenobarbital	128-141	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	105-112
18677425-7	2008	To demonstrate the utility of this panel of mice, we used the mice to show that the in vivo induction of Cyp3a11 and Cyp2b10 by phenobarbital was only mediated by CAR, although this compound is described as a PXR and CAR activator in vitro.	Phenobarbital	128-141	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	117-124
18677425-7	2008	To demonstrate the utility of this panel of mice, we used the mice to show that the in vivo induction of Cyp3a11 and Cyp2b10 by phenobarbital was only mediated by CAR, although this compound is described as a PXR and CAR activator in vitro.	Phenobarbital	128-141	nuclear receptor subfamily 1, group I, member 3	Mus musculus	163-166
18677425-7	2008	To demonstrate the utility of this panel of mice, we used the mice to show that the in vivo induction of Cyp3a11 and Cyp2b10 by phenobarbital was only mediated by CAR, although this compound is described as a PXR and CAR activator in vitro.	Phenobarbital	128-141	nuclear receptor subfamily 1, group I, member 2	Mus musculus	209-212
18677425-7	2008	To demonstrate the utility of this panel of mice, we used the mice to show that the in vivo induction of Cyp3a11 and Cyp2b10 by phenobarbital was only mediated by CAR, although this compound is described as a PXR and CAR activator in vitro.	Phenobarbital	128-141	nuclear receptor subfamily 1, group I, member 3	Mus musculus	217-220
18670162-2	2008	In Experiment 1, oral administration of PB (0, 25, 50, 100 or 150 mg/kg/day) for 2 weeks induced increases in hepatic cytochrome P450 content and CYP2B expression, prolongation of coagulation time (activated partial thromboplastin time (APTT) and Thrombotest (TBT)) and an increase in anti-thrombin III (AT III) concentration in a dose-dependent manner.	Phenobarbital	40-42	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	146-151
18329296-0	2008	The influence of C3435T polymorphism of ABCB1 gene on penetration of phenobarbital across the blood-brain barrier in patients with generalized epilepsy.	Phenobarbital	69-82	ATP binding cassette subfamily B member 1	Homo sapiens	40-45
18329296-4	2008	OBJECTIVE: To analyze the effect of two ABCB1 gene polymorphisms, C3435T and G2677T/A, on phenobarbital (PB) concentrations in the cerebrospinal fluid (CSF) and serum (S) and to assess the relationship of ABCB1 polymorphisms to phenobarbital penetration across BBB in vivo and seizure frequency.	Phenobarbital	90-103	ATP binding cassette subfamily B member 1	Homo sapiens	40-45
18329296-4	2008	OBJECTIVE: To analyze the effect of two ABCB1 gene polymorphisms, C3435T and G2677T/A, on phenobarbital (PB) concentrations in the cerebrospinal fluid (CSF) and serum (S) and to assess the relationship of ABCB1 polymorphisms to phenobarbital penetration across BBB in vivo and seizure frequency.	Phenobarbital	105-107	ATP binding cassette subfamily B member 1	Homo sapiens	40-45
18329296-6	2008	CSF/S PB concentration ratio was calculated as an index of phenobarbital penetration across BBB.	Phenobarbital	59-72	surfactant protein B	Homo sapiens	4-8
18803983-9	2008	Carbamazepine, phenytoin, phenobarbital, and primidone were found to have prominent cytochrome P450 (CYP) enzyme-induction effects, while valproic acid had an inhibitory effect.	Phenobarbital	26-39	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	84-99
18803983-9	2008	Carbamazepine, phenytoin, phenobarbital, and primidone were found to have prominent cytochrome P450 (CYP) enzyme-induction effects, while valproic acid had an inhibitory effect.	Phenobarbital	26-39	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	101-104
18474683-7	2008	OPZ also induced transcription of the human CYP2B6 promoter-reporter containing the phenobarbital (PB) responsive element in mouse liver using an in vivo transcription assay.	Phenobarbital	84-97	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	44-50
18474683-7	2008	OPZ also induced transcription of the human CYP2B6 promoter-reporter containing the phenobarbital (PB) responsive element in mouse liver using an in vivo transcription assay.	Phenobarbital	99-101	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	44-50
18670162-2	2008	In Experiment 1, oral administration of PB (0, 25, 50, 100 or 150 mg/kg/day) for 2 weeks induced increases in hepatic cytochrome P450 content and CYP2B expression, prolongation of coagulation time (activated partial thromboplastin time (APTT) and Thrombotest (TBT)) and an increase in anti-thrombin III (AT III) concentration in a dose-dependent manner.	Phenobarbital	40-42	serpin family C member 1	Rattus norvegicus	285-302
18670162-2	2008	In Experiment 1, oral administration of PB (0, 25, 50, 100 or 150 mg/kg/day) for 2 weeks induced increases in hepatic cytochrome P450 content and CYP2B expression, prolongation of coagulation time (activated partial thromboplastin time (APTT) and Thrombotest (TBT)) and an increase in anti-thrombin III (AT III) concentration in a dose-dependent manner.	Phenobarbital	40-42	serpin family C member 1	Rattus norvegicus	304-310
18670162-3	2008	In Experiment 2, PB administration (100 mg/kg/day) for up to 14 days produced time-dependent increases in hepatic cytochrome P450 content and CYP2B (CYP2B1 and CYP2B2) expression.	Phenobarbital	17-19	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	142-147
18670162-3	2008	In Experiment 2, PB administration (100 mg/kg/day) for up to 14 days produced time-dependent increases in hepatic cytochrome P450 content and CYP2B (CYP2B1 and CYP2B2) expression.	Phenobarbital	17-19	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	149-155
18670162-3	2008	In Experiment 2, PB administration (100 mg/kg/day) for up to 14 days produced time-dependent increases in hepatic cytochrome P450 content and CYP2B (CYP2B1 and CYP2B2) expression.	Phenobarbital	17-19	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	160-166
18332078-8	2008	CYP3A4 and CYP2B6 induction in Fa2N-4 cells were also low for phenytoin, phenobarbital, and efavirenz, which are dual activators of PXR/CAR.	Phenobarbital	73-86	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
18486294-0	2008	Inhibitory effects of a dietary phytochemical 3,3"-diindolylmethane on the phenobarbital-induced hepatic CYP mRNA expression and CYP-catalyzed reactions in female rats.	Phenobarbital	75-88	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	105-108
18486294-5	2008	Evaluation of the effects of co-treatment of rats with PB and DIM by a full factorial ANOVA showed that DIM decreased the PB-induced CYP2B1 and CYP2B2 mRNA expression levels, and the rates of 2- and 4-hydroxylation of E2, and total E2 metabolite formation.	Phenobarbital	55-57	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	133-139
18486294-5	2008	Evaluation of the effects of co-treatment of rats with PB and DIM by a full factorial ANOVA showed that DIM decreased the PB-induced CYP2B1 and CYP2B2 mRNA expression levels, and the rates of 2- and 4-hydroxylation of E2, and total E2 metabolite formation.	Phenobarbital	55-57	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	144-150
18486294-5	2008	Evaluation of the effects of co-treatment of rats with PB and DIM by a full factorial ANOVA showed that DIM decreased the PB-induced CYP2B1 and CYP2B2 mRNA expression levels, and the rates of 2- and 4-hydroxylation of E2, and total E2 metabolite formation.	Phenobarbital	122-124	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	133-139
18486294-5	2008	Evaluation of the effects of co-treatment of rats with PB and DIM by a full factorial ANOVA showed that DIM decreased the PB-induced CYP2B1 and CYP2B2 mRNA expression levels, and the rates of 2- and 4-hydroxylation of E2, and total E2 metabolite formation.	Phenobarbital	122-124	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	144-150
23055876-5	2008	RESULTS: THE FOLLOWING DRUGS WERE DEEMED COMPATIBLE WITH IBUPROFEN LYSINE: ceftazidime, epinephrine, furosemide, heparin lock flush, diluted insulin, morphine sulfate, phenobarbital, potassium chloride, and sodium bicarbonate.	Phenobarbital	168-181	insulin	Homo sapiens	141-148
18558634-5	2008	RESULTS: Genetic polymorphisms of the UGT1A1 promoter, specifically the T-3279G phenobarbital responsive enhancer module and the (thymidine-adenine)(7) dinucleotide repeat TATAA box variants, were common.	Phenobarbital	80-93	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44
18442974-11	2008	PB also down-regulated glutathione peroxidase and glutathione reductase, which together constitute a key enzymatic system that uses NADPH in protecting against oxidative stress.	Phenobarbital	0-2	glutathione reductase	Mus musculus	50-71
19099828-14	2008	(3) Significantly increased expression of Bax protein and ratio of Bax/Bcl-2 was only found in infant rats treated with PB, CNP or VPA compared with control (P &lt; 0.05), the results of TUNEL was in accordance with immunohistochemistry.	Phenobarbital	120-122	BCL2 associated X, apoptosis regulator	Homo sapiens	42-45
19099828-14	2008	(3) Significantly increased expression of Bax protein and ratio of Bax/Bcl-2 was only found in infant rats treated with PB, CNP or VPA compared with control (P &lt; 0.05), the results of TUNEL was in accordance with immunohistochemistry.	Phenobarbital	120-122	BCL2 associated X, apoptosis regulator	Homo sapiens	67-70
19099828-14	2008	(3) Significantly increased expression of Bax protein and ratio of Bax/Bcl-2 was only found in infant rats treated with PB, CNP or VPA compared with control (P &lt; 0.05), the results of TUNEL was in accordance with immunohistochemistry.	Phenobarbital	120-122	BCL2 apoptosis regulator	Homo sapiens	71-76
18440557-0	2008	Effect of 21-day exposure of phenobarbital, carbamazepine and phenytoin on P-glycoprotein expression and activity in the rat brain.	Phenobarbital	29-42	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	75-89
18337461-4	2008	The presence of WT and mutant SOD1 species in luminal structures was further confirmed by immunoblotting analysis of microsomal fractions from spinal cord lysates of SOD1 transgenic mice prepared by sucrose density-gradient ultracentrifugation.	Phenobarbital	46-53	superoxide dismutase 1, soluble	Mus musculus	30-34
18337461-6	2008	Cell-free translocation assays provided evidence that monomeric SOD1 is a molecular form that can be translocated into luminal structures in the presence of ATP.	Phenobarbital	119-126	superoxide dismutase 1, soluble	Mus musculus	64-68
18468591-5	2008	Additionally, infected hepatocytes retain the capacity for CYP3A4 induction in response to treatment with phenobarbital, a uniquely sensitive indicator of hepatic differentiation status.	Phenobarbital	106-119	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	59-65
18332078-8	2008	CYP3A4 and CYP2B6 induction in Fa2N-4 cells were also low for phenytoin, phenobarbital, and efavirenz, which are dual activators of PXR/CAR.	Phenobarbital	73-86	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	11-17
18332078-8	2008	CYP3A4 and CYP2B6 induction in Fa2N-4 cells were also low for phenytoin, phenobarbital, and efavirenz, which are dual activators of PXR/CAR.	Phenobarbital	73-86	nuclear receptor subfamily 1 group I member 2	Homo sapiens	132-135
18332078-8	2008	CYP3A4 and CYP2B6 induction in Fa2N-4 cells were also low for phenytoin, phenobarbital, and efavirenz, which are dual activators of PXR/CAR.	Phenobarbital	73-86	nuclear receptor subfamily 1 group I member 3	Homo sapiens	136-139
18332083-6	2008	These results were confirmed in cultured human hepatocytes, where the cooperation of ATF5 and CAR not only increased CYP2B6 basal expression but also enhanced the induced levels after phenobarbital or 6-(4-chloropheny-l)-imidazo[2,1-b][1,3]thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime (CITCO).	Phenobarbital	184-197	activating transcription factor 5	Homo sapiens	85-89
18332083-6	2008	These results were confirmed in cultured human hepatocytes, where the cooperation of ATF5 and CAR not only increased CYP2B6 basal expression but also enhanced the induced levels after phenobarbital or 6-(4-chloropheny-l)-imidazo[2,1-b][1,3]thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime (CITCO).	Phenobarbital	184-197	nuclear receptor subfamily 1 group I member 3	Homo sapiens	94-97
18172616-2	2008	A 290-bp distal enhancer module, phenobarbital-responsive enhancer module of UGT1A1 (gtPBREM), fully accounts for constitutive androstane receptor (CAR)-, pregnane X receptor (PXR)-, glucocorticoid receptor (GR)-, and aryl hydrocarbon receptor (AhR)-mediated activation of the UGT1A1 gene.	Phenobarbital	33-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	77-83
18172616-2	2008	A 290-bp distal enhancer module, phenobarbital-responsive enhancer module of UGT1A1 (gtPBREM), fully accounts for constitutive androstane receptor (CAR)-, pregnane X receptor (PXR)-, glucocorticoid receptor (GR)-, and aryl hydrocarbon receptor (AhR)-mediated activation of the UGT1A1 gene.	Phenobarbital	33-46	nuclear receptor subfamily 1 group I member 3	Homo sapiens	114-146
18172616-2	2008	A 290-bp distal enhancer module, phenobarbital-responsive enhancer module of UGT1A1 (gtPBREM), fully accounts for constitutive androstane receptor (CAR)-, pregnane X receptor (PXR)-, glucocorticoid receptor (GR)-, and aryl hydrocarbon receptor (AhR)-mediated activation of the UGT1A1 gene.	Phenobarbital	33-46	nuclear receptor subfamily 1 group I member 3	Homo sapiens	148-151
18172616-2	2008	A 290-bp distal enhancer module, phenobarbital-responsive enhancer module of UGT1A1 (gtPBREM), fully accounts for constitutive androstane receptor (CAR)-, pregnane X receptor (PXR)-, glucocorticoid receptor (GR)-, and aryl hydrocarbon receptor (AhR)-mediated activation of the UGT1A1 gene.	Phenobarbital	33-46	nuclear receptor subfamily 1 group I member 2	Homo sapiens	155-174
18172616-2	2008	A 290-bp distal enhancer module, phenobarbital-responsive enhancer module of UGT1A1 (gtPBREM), fully accounts for constitutive androstane receptor (CAR)-, pregnane X receptor (PXR)-, glucocorticoid receptor (GR)-, and aryl hydrocarbon receptor (AhR)-mediated activation of the UGT1A1 gene.	Phenobarbital	33-46	nuclear receptor subfamily 1 group I member 2	Homo sapiens	176-179
18172616-2	2008	A 290-bp distal enhancer module, phenobarbital-responsive enhancer module of UGT1A1 (gtPBREM), fully accounts for constitutive androstane receptor (CAR)-, pregnane X receptor (PXR)-, glucocorticoid receptor (GR)-, and aryl hydrocarbon receptor (AhR)-mediated activation of the UGT1A1 gene.	Phenobarbital	33-46	nuclear receptor subfamily 3 group C member 1	Homo sapiens	183-206
18560012-3	2008	High level of expression, luminal membrane location, multispecificity, and high transport potency make P-glycoprotein a selective gatekeeper of the blood-brain barrier and thus a primary obstacle to drug delivery into the brain.	Phenobarbital	26-33	ATP binding cassette subfamily B member 1	Homo sapiens	103-117
18528841-5	2008	PF2D was also found to be useful for the semiquantification of some representative cytochrome P450 family proteins (e.g., cytochrome P450 2B2) that were induced by PB treatment compared with untreated controls.	Phenobarbital	164-166	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	122-141
18308698-2	2008	We recently demonstrated that Cx32 is essential for phenobarbital (PB)-mediated tumor promotion in mouse liver.	Phenobarbital	52-65	gap junction protein, beta 1	Mus musculus	30-34
18308698-2	2008	We recently demonstrated that Cx32 is essential for phenobarbital (PB)-mediated tumor promotion in mouse liver.	Phenobarbital	67-69	gap junction protein, beta 1	Mus musculus	30-34
18308698-8	2008	The tumor response in PB-treated mice of both strains was quite similar, but the number of smaller tumors and of enzyme-altered neoplastic lesions was somewhat larger in PB-treated Cx26 knockout (Cx26 KO) compared with wild-type mice, whereas the volume fraction of enzyme-altered lesions was slightly reduced in PB-treated Cx26-deficient mice.	Phenobarbital	170-172	gap junction protein, beta 2	Mus musculus	181-185
18308698-8	2008	The tumor response in PB-treated mice of both strains was quite similar, but the number of smaller tumors and of enzyme-altered neoplastic lesions was somewhat larger in PB-treated Cx26 knockout (Cx26 KO) compared with wild-type mice, whereas the volume fraction of enzyme-altered lesions was slightly reduced in PB-treated Cx26-deficient mice.	Phenobarbital	170-172	gap junction protein, beta 2	Mus musculus	196-200
18308698-8	2008	The tumor response in PB-treated mice of both strains was quite similar, but the number of smaller tumors and of enzyme-altered neoplastic lesions was somewhat larger in PB-treated Cx26 knockout (Cx26 KO) compared with wild-type mice, whereas the volume fraction of enzyme-altered lesions was slightly reduced in PB-treated Cx26-deficient mice.	Phenobarbital	170-172	gap junction protein, beta 2	Mus musculus	196-200
18308698-8	2008	The tumor response in PB-treated mice of both strains was quite similar, but the number of smaller tumors and of enzyme-altered neoplastic lesions was somewhat larger in PB-treated Cx26 knockout (Cx26 KO) compared with wild-type mice, whereas the volume fraction of enzyme-altered lesions was slightly reduced in PB-treated Cx26-deficient mice.	Phenobarbital	170-172	gap junction protein, beta 2	Mus musculus	181-185
18308698-8	2008	The tumor response in PB-treated mice of both strains was quite similar, but the number of smaller tumors and of enzyme-altered neoplastic lesions was somewhat larger in PB-treated Cx26 knockout (Cx26 KO) compared with wild-type mice, whereas the volume fraction of enzyme-altered lesions was slightly reduced in PB-treated Cx26-deficient mice.	Phenobarbital	170-172	gap junction protein, beta 2	Mus musculus	196-200
18308698-8	2008	The tumor response in PB-treated mice of both strains was quite similar, but the number of smaller tumors and of enzyme-altered neoplastic lesions was somewhat larger in PB-treated Cx26 knockout (Cx26 KO) compared with wild-type mice, whereas the volume fraction of enzyme-altered lesions was slightly reduced in PB-treated Cx26-deficient mice.	Phenobarbital	170-172	gap junction protein, beta 2	Mus musculus	196-200
18473823-3	2008	Carbamazepine, phenobarbital and phenytoin induced the highest levels of P-gp and MPRs expression that was associated with increased activation of PXR and CAR receptors as compared to levetiracetam, tiagabine and topiramate.	Phenobarbital	15-28	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	73-77
18172616-2	2008	A 290-bp distal enhancer module, phenobarbital-responsive enhancer module of UGT1A1 (gtPBREM), fully accounts for constitutive androstane receptor (CAR)-, pregnane X receptor (PXR)-, glucocorticoid receptor (GR)-, and aryl hydrocarbon receptor (AhR)-mediated activation of the UGT1A1 gene.	Phenobarbital	33-46	nuclear receptor subfamily 3 group C member 1	Homo sapiens	208-210
18172616-2	2008	A 290-bp distal enhancer module, phenobarbital-responsive enhancer module of UGT1A1 (gtPBREM), fully accounts for constitutive androstane receptor (CAR)-, pregnane X receptor (PXR)-, glucocorticoid receptor (GR)-, and aryl hydrocarbon receptor (AhR)-mediated activation of the UGT1A1 gene.	Phenobarbital	33-46	aryl hydrocarbon receptor	Homo sapiens	218-243
18172616-2	2008	A 290-bp distal enhancer module, phenobarbital-responsive enhancer module of UGT1A1 (gtPBREM), fully accounts for constitutive androstane receptor (CAR)-, pregnane X receptor (PXR)-, glucocorticoid receptor (GR)-, and aryl hydrocarbon receptor (AhR)-mediated activation of the UGT1A1 gene.	Phenobarbital	33-46	aryl hydrocarbon receptor	Homo sapiens	245-248
18172616-2	2008	A 290-bp distal enhancer module, phenobarbital-responsive enhancer module of UGT1A1 (gtPBREM), fully accounts for constitutive androstane receptor (CAR)-, pregnane X receptor (PXR)-, glucocorticoid receptor (GR)-, and aryl hydrocarbon receptor (AhR)-mediated activation of the UGT1A1 gene.	Phenobarbital	33-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	277-283
18473823-3	2008	Carbamazepine, phenobarbital and phenytoin induced the highest levels of P-gp and MPRs expression that was associated with increased activation of PXR and CAR receptors as compared to levetiracetam, tiagabine and topiramate.	Phenobarbital	15-28	nuclear receptor subfamily 1, group I, member 2	Rattus norvegicus	147-150
18473823-3	2008	Carbamazepine, phenobarbital and phenytoin induced the highest levels of P-gp and MPRs expression that was associated with increased activation of PXR and CAR receptors as compared to levetiracetam, tiagabine and topiramate.	Phenobarbital	15-28	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	155-158
18473823-4	2008	We conclude that P-gp and MRPs are differently overexpressed in GPNT and RBE4 by various AEDs and both PXR and CAR are involved in the drug-resistant epilepsy induced by carbamazepine, phenobarbital and phenytoin.	Phenobarbital	185-198	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	17-21
18473823-4	2008	We conclude that P-gp and MRPs are differently overexpressed in GPNT and RBE4 by various AEDs and both PXR and CAR are involved in the drug-resistant epilepsy induced by carbamazepine, phenobarbital and phenytoin.	Phenobarbital	185-198	nuclear receptor subfamily 1, group I, member 2	Rattus norvegicus	103-106
18473823-4	2008	We conclude that P-gp and MRPs are differently overexpressed in GPNT and RBE4 by various AEDs and both PXR and CAR are involved in the drug-resistant epilepsy induced by carbamazepine, phenobarbital and phenytoin.	Phenobarbital	185-198	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	111-114
18281256-9	2008	There was excellent correlation between the transcript profile of PPAR alpha-independent PFOA genes and those of activators of CAR including phenobarbital and 1,4-bis[2-(3,5-dichloropyridyloxy)] benzene (TCPOBOP) but not those regulated by the Nrf2 activator, dithiol-3-thione.	Phenobarbital	141-154	peroxisome proliferator activated receptor alpha	Mus musculus	66-76
18281256-9	2008	There was excellent correlation between the transcript profile of PPAR alpha-independent PFOA genes and those of activators of CAR including phenobarbital and 1,4-bis[2-(3,5-dichloropyridyloxy)] benzene (TCPOBOP) but not those regulated by the Nrf2 activator, dithiol-3-thione.	Phenobarbital	141-154	nuclear receptor subfamily 1, group I, member 3	Mus musculus	127-130
18328680-6	2008	PB induced CYP3A4, 3A5, 2B6 and 2A6, UGT1A1 and all transporters.	Phenobarbital	0-2	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	11-17
18328680-6	2008	PB induced CYP3A4, 3A5, 2B6 and 2A6, UGT1A1 and all transporters.	Phenobarbital	0-2	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
18328680-9	2008	7-Ethoxycoumarin O-deethylation activity, mediated predominantly by CYP 1A1/1A2 but also by other CYPs, was increased after 24h with PB.	Phenobarbital	133-135	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	68-75
17959350-5	2008	The drugs inhibiting CYP19 were: lamotrigine, oxcarbazepine, tiagabine, phenobarbital, phenytoin, ethosuximide, and valproate.	Phenobarbital	72-85	cytochrome P450 family 19 subfamily A member 1	Homo sapiens	21-26
18164277-0	2008	Cell shape, cell-cell contact, cell-extracellular matrix contact and cell polarity are all required for the maximum induction of CYP2B1 and CYP2B2 gene expression by phenobarbital in adult rat cultured hepatocytes.	Phenobarbital	166-179	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	129-135
18164277-0	2008	Cell shape, cell-cell contact, cell-extracellular matrix contact and cell polarity are all required for the maximum induction of CYP2B1 and CYP2B2 gene expression by phenobarbital in adult rat cultured hepatocytes.	Phenobarbital	166-179	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	140-146
18164277-1	2008	The effect of cell shape, cell density, contact with extracellular matrix and cell polarity on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes was investigated.	Phenobarbital	99-112	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	145-151
18164277-1	2008	The effect of cell shape, cell density, contact with extracellular matrix and cell polarity on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes was investigated.	Phenobarbital	99-112	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	156-162
18164277-1	2008	The effect of cell shape, cell density, contact with extracellular matrix and cell polarity on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes was investigated.	Phenobarbital	99-112	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	164-174
18164277-1	2008	The effect of cell shape, cell density, contact with extracellular matrix and cell polarity on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes was investigated.	Phenobarbital	114-116	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	145-151
18164277-1	2008	The effect of cell shape, cell density, contact with extracellular matrix and cell polarity on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes was investigated.	Phenobarbital	114-116	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	156-162
18164277-1	2008	The effect of cell shape, cell density, contact with extracellular matrix and cell polarity on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes was investigated.	Phenobarbital	114-116	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	164-174
18164277-3	2008	Hepatocytes cultured on EHS gel showed a spherical cell shape and highly enhanced the induction of CYP2B1/2B2 gene expression by PB.	Phenobarbital	129-131	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	99-109
18164277-8	2008	On the other hand, when hepatocytes were cultured on dishes coated with lower concentrations of laminin, they became round and greater induction of CYP2B1/2B2 gene expression by PB was observed.	Phenobarbital	178-180	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	148-158
18094037-11	2008	Phenobarbital (constitutive androstane receptor activator) induced CYP3A4 (4.1-fold, only in jejunum), CYP2B6 (4.9-fold in colon and 2.3-fold in proximal jejunum), and MDR1/ABCB1 mRNA and CYP3A4 activity (2-fold only proximal jejunum).	Phenobarbital	0-13	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	67-73
18094037-11	2008	Phenobarbital (constitutive androstane receptor activator) induced CYP3A4 (4.1-fold, only in jejunum), CYP2B6 (4.9-fold in colon and 2.3-fold in proximal jejunum), and MDR1/ABCB1 mRNA and CYP3A4 activity (2-fold only proximal jejunum).	Phenobarbital	0-13	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	103-109
18094037-11	2008	Phenobarbital (constitutive androstane receptor activator) induced CYP3A4 (4.1-fold, only in jejunum), CYP2B6 (4.9-fold in colon and 2.3-fold in proximal jejunum), and MDR1/ABCB1 mRNA and CYP3A4 activity (2-fold only proximal jejunum).	Phenobarbital	0-13	ATP binding cassette subfamily B member 1	Homo sapiens	168-172
18094037-11	2008	Phenobarbital (constitutive androstane receptor activator) induced CYP3A4 (4.1-fold, only in jejunum), CYP2B6 (4.9-fold in colon and 2.3-fold in proximal jejunum), and MDR1/ABCB1 mRNA and CYP3A4 activity (2-fold only proximal jejunum).	Phenobarbital	0-13	ATP binding cassette subfamily B member 1	Homo sapiens	173-178
18094037-11	2008	Phenobarbital (constitutive androstane receptor activator) induced CYP3A4 (4.1-fold, only in jejunum), CYP2B6 (4.9-fold in colon and 2.3-fold in proximal jejunum), and MDR1/ABCB1 mRNA and CYP3A4 activity (2-fold only proximal jejunum).	Phenobarbital	0-13	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	188-194
18202305-12	2008	Taken together, R16A at the membrane may mediate the PB signal to initiate CAR nuclear translocation, through a mechanism including its dimerization and inhibition of PP1beta activity, providing a novel model for the translocation of nuclear receptors in which direct interaction of ligands and the receptors may not be crucial.	Phenobarbital	53-55	nuclear receptor subfamily 1, group I, member 3	Mus musculus	75-78
18164216-5	2008	The use of the liver enzyme inducing AEDs phenobarbital, phenytoin and carbamazepine increases serum sex hormone binding globulin (SHBG) concentrations in both men and women with epilepsy.	Phenobarbital	42-55	sex hormone binding globulin	Homo sapiens	101-129
18164216-5	2008	The use of the liver enzyme inducing AEDs phenobarbital, phenytoin and carbamazepine increases serum sex hormone binding globulin (SHBG) concentrations in both men and women with epilepsy.	Phenobarbital	42-55	sex hormone binding globulin	Homo sapiens	131-135
17963809-3	2008	We previously found that PB administration increased hepatic NF-kappaB DNA binding activity.	Phenobarbital	25-27	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	61-70
17963809-4	2008	In this study we examined the hypothesis that the effects of PB on cell proliferation and apoptosis are dependent on NF-kappaB.	Phenobarbital	61-63	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	117-126
18022748-4	2008	In rat hepatocytes both Pyrethrins and Phenobarbital produced an induction of 7-benzyloxy-4-trifluoromethylcoumarin O-debenzylase activity (a CYP1A/2B form marker) and CYP2B1 and CYP2B1/2 mRNA levels.	Phenobarbital	39-52	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	168-174
18092747-6	2008	beta-Glucuronidase activity increased significantly in the liver by 1.2-fold in the DEN/PB group compared to the activity in a saline group.	Phenobarbital	88-90	glucuronidase, beta	Rattus norvegicus	0-18
18022748-4	2008	In rat hepatocytes both Pyrethrins and Phenobarbital produced an induction of 7-benzyloxy-4-trifluoromethylcoumarin O-debenzylase activity (a CYP1A/2B form marker) and CYP2B1 and CYP2B1/2 mRNA levels.	Phenobarbital	39-52	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	179-185
18022748-5	2008	Pyrethrins and Phenobarbital also induced CYP3A-dependent testosterone 6beta-hydroxylase activity in rat hepatocytes.	Phenobarbital	15-28	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	42-47
18022748-6	2008	In human hepatocytes Pyrethrins and Phenobarbital induced both testosterone 6beta-hydroxylase activity and CYP3A4 mRNA levels and also increased CYP2B6 mRNA levels.	Phenobarbital	36-49	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	107-113
18022748-6	2008	In human hepatocytes Pyrethrins and Phenobarbital induced both testosterone 6beta-hydroxylase activity and CYP3A4 mRNA levels and also increased CYP2B6 mRNA levels.	Phenobarbital	36-49	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	145-151
17904175-0	2007	DHA down-regulates phenobarbital-induced cytochrome P450 2B1 gene expression in rat primary hepatocytes by attenuating CAR translocation.	Phenobarbital	19-32	cytochrome P450 2B1	Rattus norvegicus	41-60
19227257-0	2008	[Phenobarbital-induced hypermethylation of the p53 promoter region in the liver of Wistar rats].	Phenobarbital	1-14	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	47-50
19227257-2	2008	The effect of phenobarbital (PB), a rodent liver carcinogen on the methylation level of the p53 promoter region in rat liver was studied.	Phenobarbital	14-27	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	92-95
19227257-2	2008	The effect of phenobarbital (PB), a rodent liver carcinogen on the methylation level of the p53 promoter region in rat liver was studied.	Phenobarbital	29-31	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	92-95
19227257-6	2008	We have demonstrated that PB increased the methylation of the p53 gene.	Phenobarbital	26-28	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	62-65
19227257-11	2008	It is proposed that PB-induced de novo methylation of the p53 gene was not associated with DNMTs activity.	Phenobarbital	20-22	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	58-61
18488805-5	2008	Compounds 4, 5, 9 and 11 exhibited a similar anticonvulsant activity as the reference drug phenobarbital (CAS 50-06-6).	Phenobarbital	91-104	BCAR1 scaffold protein, Cas family member	Homo sapiens	106-109
18540476-5	2008	Compounds 4, 6 and 9 exhibited a similar anticonvulsant activity as the reference drug phenobarbital (CAS 50-06-6).	Phenobarbital	87-100	breast cancer anti-estrogen resistance 1	Mus musculus	102-105
18986100-0	2008	Influence of stable, long-term treatment with phenobarbital on the activity of serum alanine aminotransferase and gamma-glutamyltransferase.	Phenobarbital	46-59	glutamic--pyruvic transaminase	Homo sapiens	85-109
17826359-3	2008	In the present study, we determined the in vivo and in vitro effects of typical mammalian CYP3A inducers (rifampicin, phenobarbital and dexamethasone) on CYP3A-related enzyme activities in a freshwater teleost, the grass carp (Ctenopharyngodon idellus).	Phenobarbital	118-131	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	90-95
17826359-3	2008	In the present study, we determined the in vivo and in vitro effects of typical mammalian CYP3A inducers (rifampicin, phenobarbital and dexamethasone) on CYP3A-related enzyme activities in a freshwater teleost, the grass carp (Ctenopharyngodon idellus).	Phenobarbital	118-131	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	154-159
18063342-0	2008	P-glycoprotein-mediated efflux of phenobarbital at the blood-brain barrier evidence from transport experiments in vitro.	Phenobarbital	34-47	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-14
18063342-6	2008	P-gp modulators, cyclosporin A (CsA), ketoconazole and metabolic inhibitor dinitrophenol, increased the PB steady-state uptake by more than 50% (p &lt; 0.01), and decreased the PB efflux by more than 50% (p &lt; 0.01).	Phenobarbital	104-106	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-4
18063342-6	2008	P-gp modulators, cyclosporin A (CsA), ketoconazole and metabolic inhibitor dinitrophenol, increased the PB steady-state uptake by more than 50% (p &lt; 0.01), and decreased the PB efflux by more than 50% (p &lt; 0.01).	Phenobarbital	177-179	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-4
18063342-10	2008	Overall, these findings suggest that P-gp may contribute to the efflux transport of PB across BBB.	Phenobarbital	84-86	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	37-41
18058858-5	2008	The method was linear in the range of 0.5-25 mg/L for PEMA and LAM; 1.25-25 mg/L for PD and CMZ; 0.625-12.5 mg/L for EPO; 1.5-60 mg/L for PB; and 1.25-50 mg/L for DPH, respectively.	Phenobarbital	138-140	selectin L	Homo sapiens	63-69
17904175-10	2007	The EMSA results showed that PB-induced CAR binding to NR-1 was attenuated by DHA.	Phenobarbital	29-31	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	40-43
17904175-11	2007	Taken together, these results suggest that attenuation of CAR translocation and decreased subsequent binding to NR-1 are involved in DHA"s down-regulation of PB-induced CYP 2B1 expression.	Phenobarbital	158-160	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	58-61
17904175-11	2007	Taken together, these results suggest that attenuation of CAR translocation and decreased subsequent binding to NR-1 are involved in DHA"s down-regulation of PB-induced CYP 2B1 expression.	Phenobarbital	158-160	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	169-176
18023279-6	2007	The PPARalpha-dependent increase in CAR potentiated the phenobarbital-induced transcription of the prototypical CAR-dependent gene CYP2B1.	Phenobarbital	56-69	peroxisome proliferator activated receptor alpha	Rattus norvegicus	4-13
18023279-6	2007	The PPARalpha-dependent increase in CAR potentiated the phenobarbital-induced transcription of the prototypical CAR-dependent gene CYP2B1.	Phenobarbital	56-69	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	36-39
18023279-6	2007	The PPARalpha-dependent increase in CAR potentiated the phenobarbital-induced transcription of the prototypical CAR-dependent gene CYP2B1.	Phenobarbital	56-69	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	112-115
18023279-6	2007	The PPARalpha-dependent increase in CAR potentiated the phenobarbital-induced transcription of the prototypical CAR-dependent gene CYP2B1.	Phenobarbital	56-69	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	131-137
17950690-2	2007	Each of the p160 coactivators enhanced mouse CAR (mCAR) transactivation of the CYP2B1 phenobarbital (PB)-responsive enhancer in transfected cultured cells and mouse hepatocytes in vivo.	Phenobarbital	86-99	MYB binding protein (P160) 1a	Mus musculus	12-16
17950690-2	2007	Each of the p160 coactivators enhanced mouse CAR (mCAR) transactivation of the CYP2B1 phenobarbital (PB)-responsive enhancer in transfected cultured cells and mouse hepatocytes in vivo.	Phenobarbital	86-99	nuclear receptor subfamily 1, group I, member 3	Mus musculus	45-48
17950690-2	2007	Each of the p160 coactivators enhanced mouse CAR (mCAR) transactivation of the CYP2B1 phenobarbital (PB)-responsive enhancer in transfected cultured cells and mouse hepatocytes in vivo.	Phenobarbital	86-99	coxsackie virus and adenovirus receptor	Mus musculus	50-54
17950690-2	2007	Each of the p160 coactivators enhanced mouse CAR (mCAR) transactivation of the CYP2B1 phenobarbital (PB)-responsive enhancer in transfected cultured cells and mouse hepatocytes in vivo.	Phenobarbital	101-103	MYB binding protein (P160) 1a	Mus musculus	12-16
17950690-2	2007	Each of the p160 coactivators enhanced mouse CAR (mCAR) transactivation of the CYP2B1 phenobarbital (PB)-responsive enhancer in transfected cultured cells and mouse hepatocytes in vivo.	Phenobarbital	101-103	nuclear receptor subfamily 1, group I, member 3	Mus musculus	45-48
17950690-2	2007	Each of the p160 coactivators enhanced mouse CAR (mCAR) transactivation of the CYP2B1 phenobarbital (PB)-responsive enhancer in transfected cultured cells and mouse hepatocytes in vivo.	Phenobarbital	101-103	coxsackie virus and adenovirus receptor	Mus musculus	50-54
17950690-5	2007	Induction of Cyp2b10 gene expression by PB was equivalent or greater in mice null for each of the p160 coactivators than in wild type mice.	Phenobarbital	40-42	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	13-20
17904175-0	2007	DHA down-regulates phenobarbital-induced cytochrome P450 2B1 gene expression in rat primary hepatocytes by attenuating CAR translocation.	Phenobarbital	19-32	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	119-122
17904175-2	2007	Phenobarbital (PB) induction of human CYP 2B6 and mouse CYP 2b10 has been shown to be mediated by CAR.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	38-45
17904175-2	2007	Phenobarbital (PB) induction of human CYP 2B6 and mouse CYP 2b10 has been shown to be mediated by CAR.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	56-64
17904175-2	2007	Phenobarbital (PB) induction of human CYP 2B6 and mouse CYP 2b10 has been shown to be mediated by CAR.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	98-101
17904175-2	2007	Phenobarbital (PB) induction of human CYP 2B6 and mouse CYP 2b10 has been shown to be mediated by CAR.	Phenobarbital	15-17	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	38-45
17904175-2	2007	Phenobarbital (PB) induction of human CYP 2B6 and mouse CYP 2b10 has been shown to be mediated by CAR.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	56-64
17904175-2	2007	Phenobarbital (PB) induction of human CYP 2B6 and mouse CYP 2b10 has been shown to be mediated by CAR.	Phenobarbital	15-17	nuclear receptor subfamily 1, group I, member 3	Mus musculus	98-101
17904175-3	2007	Our previous study showed that PB-induced CYP 2B1 expression in rat primary hepatocytes is down-regulated by both n-6 and n-3 polyunsaturated fatty acids (PUFAs), especially docosahexaenoic acid (DHA); however, the mechanism for this down-regulation by DHA was previously unknown.	Phenobarbital	31-33	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	42-49
17904175-4	2007	The objective of the present study was to determine whether change in CAR translocation is involved in the down-regulation by n-6 and n-3 PUFAs of PB-induced CYP 2B1 expression in rat primary hepatocytes.	Phenobarbital	147-149	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	70-73
17904175-4	2007	The objective of the present study was to determine whether change in CAR translocation is involved in the down-regulation by n-6 and n-3 PUFAs of PB-induced CYP 2B1 expression in rat primary hepatocytes.	Phenobarbital	147-149	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	158-165
17904175-6	2007	PB triggered the translocation of CAR from the cytosol into the nucleus in a dose-dependent and time-dependent manner in our hepatocyte system, and the CAR distribution in rat primary hepatocytes was significantly affected by DHA.	Phenobarbital	0-2	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	34-37
17904175-6	2007	PB triggered the translocation of CAR from the cytosol into the nucleus in a dose-dependent and time-dependent manner in our hepatocyte system, and the CAR distribution in rat primary hepatocytes was significantly affected by DHA.	Phenobarbital	0-2	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	152-155
17904175-7	2007	DHA treatment decreased PB-inducible accumulation of CAR in the nuclear fraction and increased it in the cytosolic fraction in a dose-dependent manner.	Phenobarbital	24-26	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	53-56
21783825-5	2007	In order to assess the induction of the CYP subfamilies 1A1/2, 2B1/2, 2E1 and 3A2 in the gastrointestinal tract, male Wistar rats were treated with phenobarbital/beta-naphthoflavone (PB/NF), cyclohexanol/albendazole (CH/ABZ) or toluene (TL).	Phenobarbital	148-161	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	40-43
18032674-7	2007	Suppression of these seizures with phenobarbital reversed the change in the voltage dependence of I(h), the current produced by HCN channels, but did not affect the loss of HCN channel expression.	Phenobarbital	35-48	cyclic nucleotide gated channel subunit alpha 1	Rattus norvegicus	128-131
17888866-3	2007	In this study, we performed DNA microarray experiments, together with quantitative reverse transcriptase PCR analyses and enzymatic activity determinations to identify human CTSE as a novel target gene for regulation by the constitutive androstane receptor (CAR), a nuclear receptor activated by the liver tumor promoting agent, phenobarbital.	Phenobarbital	329-342	cathepsin E	Homo sapiens	174-178
17888866-3	2007	In this study, we performed DNA microarray experiments, together with quantitative reverse transcriptase PCR analyses and enzymatic activity determinations to identify human CTSE as a novel target gene for regulation by the constitutive androstane receptor (CAR), a nuclear receptor activated by the liver tumor promoting agent, phenobarbital.	Phenobarbital	329-342	nuclear receptor subfamily 1 group I member 3	Homo sapiens	224-256
17888866-3	2007	In this study, we performed DNA microarray experiments, together with quantitative reverse transcriptase PCR analyses and enzymatic activity determinations to identify human CTSE as a novel target gene for regulation by the constitutive androstane receptor (CAR), a nuclear receptor activated by the liver tumor promoting agent, phenobarbital.	Phenobarbital	329-342	nuclear receptor subfamily 1 group I member 3	Homo sapiens	258-261
17916406-1	2007	Retinal dehydrogenase type 1 (RALDH1) catalyzes the oxidation of all-trans and 9-cis retinal to the respective retinoic acids (RAs), whereas another member of the aldehyde dehydrogenase family, the phenobarbital-induced aldehyde dehydrogenase (PB-ALDH), is very poorly active.	Phenobarbital	198-211	aldehyde dehydrogenase 1 family member A1	Homo sapiens	0-28
17916406-1	2007	Retinal dehydrogenase type 1 (RALDH1) catalyzes the oxidation of all-trans and 9-cis retinal to the respective retinoic acids (RAs), whereas another member of the aldehyde dehydrogenase family, the phenobarbital-induced aldehyde dehydrogenase (PB-ALDH), is very poorly active.	Phenobarbital	198-211	aldehyde dehydrogenase 1 family member A1	Homo sapiens	30-36
17658503-17	2007	The liver and erythrocyte glutathione-S-transferase (GST) activity increased in all the groups treated with NDEA and PB.	Phenobarbital	117-119	hematopoietic prostaglandin D synthase	Rattus norvegicus	26-51
17965553-6	2007	In fact, WY-14,643, clofibrate, gemfibrozil and benzbromarone, reported to be PPARalpha activators, distributed to the former, whereas propylthiouracil, omeprazole, phenobarbital, thioacetamide, methapyrilene, sulfasalazine and coumarin did to the latter.	Phenobarbital	165-178	peroxisome proliferator activated receptor alpha	Rattus norvegicus	78-87
17845805-1	2007	The purposes of this study were to investigate whether P-glycoprotein (P-GP) is overexpressed in the brain of pentylenetetrazole (PTZ)-kindled rats, and to investigate the effects of P-GP up-regulation on the distribution of phenobarbital (PB) in brain and its antiepileptic effects.	Phenobarbital	225-238	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	71-75
17845805-1	2007	The purposes of this study were to investigate whether P-glycoprotein (P-GP) is overexpressed in the brain of pentylenetetrazole (PTZ)-kindled rats, and to investigate the effects of P-GP up-regulation on the distribution of phenobarbital (PB) in brain and its antiepileptic effects.	Phenobarbital	240-242	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	71-75
17907271-6	2007	DmGSTD2 was detected only after pretreatment of the flies with Phenobarbital (PhB).	Phenobarbital	63-76	Glutathione S transferase D2	Drosophila melanogaster	0-7
17907271-6	2007	DmGSTD2 was detected only after pretreatment of the flies with Phenobarbital (PhB).	Phenobarbital	78-81	Glutathione S transferase D2	Drosophila melanogaster	0-7
17706854-0	2007	The effect of phenobarbital on the methylation level of the p16 promoter region in rat liver.	Phenobarbital	14-27	cyclin-dependent kinase inhibitor 2A	Rattus norvegicus	60-63
17706854-2	2007	We studied the effects of phenobarbital (PB) -- a non-genotoxic rodent liver carcinogen -- on the methylation level of the promoter region of the p16 suppressor gene, as well as on hepatomegaly, DNA synthesis, and DNA-methyltransferase (DNMTs) activity in the rat liver.	Phenobarbital	26-39	cyclin-dependent kinase inhibitor 2A	Rattus norvegicus	146-149
17706854-2	2007	We studied the effects of phenobarbital (PB) -- a non-genotoxic rodent liver carcinogen -- on the methylation level of the promoter region of the p16 suppressor gene, as well as on hepatomegaly, DNA synthesis, and DNA-methyltransferase (DNMTs) activity in the rat liver.	Phenobarbital	41-43	cyclin-dependent kinase inhibitor 2A	Rattus norvegicus	146-149
17706854-12	2007	Thus, transient changes in methylation of the p16 gene, although their direct role in the mechanisms of PB toxicity, including its carcinogenic action, remains doubtful, may therefore be a significant element of such processes.	Phenobarbital	104-106	cyclin-dependent kinase inhibitor 2A	Rattus norvegicus	46-49
17904126-1	2007	Various drugs such as phenobarbital (PB) trigger translocation of constitutive active/adrostane receptor (CAR) from the cytoplasm into the nucleus of mouse liver cells without directly binding to the receptor.	Phenobarbital	22-35	nuclear receptor subfamily 1, group I, member 3	Mus musculus	66-104
17904126-1	2007	Various drugs such as phenobarbital (PB) trigger translocation of constitutive active/adrostane receptor (CAR) from the cytoplasm into the nucleus of mouse liver cells without directly binding to the receptor.	Phenobarbital	22-35	nuclear receptor subfamily 1, group I, member 3	Mus musculus	106-109
17904126-1	2007	Various drugs such as phenobarbital (PB) trigger translocation of constitutive active/adrostane receptor (CAR) from the cytoplasm into the nucleus of mouse liver cells without directly binding to the receptor.	Phenobarbital	37-39	nuclear receptor subfamily 1, group I, member 3	Mus musculus	66-104
17904126-1	2007	Various drugs such as phenobarbital (PB) trigger translocation of constitutive active/adrostane receptor (CAR) from the cytoplasm into the nucleus of mouse liver cells without directly binding to the receptor.	Phenobarbital	37-39	nuclear receptor subfamily 1, group I, member 3	Mus musculus	106-109
17904126-2	2007	We have now characterized the guanine nucleotide exchange factor epithelial cell-transforming gene 2 (ECT2) as a PB-inducible factor as well as a cellular signal that represses PB-triggered nuclear translocation of CAR.	Phenobarbital	113-115	ect2 oncogene	Mus musculus	65-100
17904126-2	2007	We have now characterized the guanine nucleotide exchange factor epithelial cell-transforming gene 2 (ECT2) as a PB-inducible factor as well as a cellular signal that represses PB-triggered nuclear translocation of CAR.	Phenobarbital	113-115	ect2 oncogene	Mus musculus	102-106
17904126-6	2007	Thus, ECT2 may comprise a part of the PB response signal regulating the intracellular trafficking of CAR.	Phenobarbital	38-40	ect2 oncogene	Mus musculus	6-10
17904126-6	2007	Thus, ECT2 may comprise a part of the PB response signal regulating the intracellular trafficking of CAR.	Phenobarbital	38-40	nuclear receptor subfamily 1, group I, member 3	Mus musculus	101-104
17658503-17	2007	The liver and erythrocyte glutathione-S-transferase (GST) activity increased in all the groups treated with NDEA and PB.	Phenobarbital	117-119	hematopoietic prostaglandin D synthase	Rattus norvegicus	53-56
17599282-4	2007	In the present study, the effects of the flavone chrysin and six natural coumarins isolated from various Rutaceous plants on UGT1A6-dependent P-nitrophenol and/or UGT1A1-dependent bilirubin glucuronoconjugation activities were evaluated in cultured rat and human hepatocytes and compared to those of the prototypical UGT1A inducers beta-naphthoflavone, phenobarbital and clofibric acid.	Phenobarbital	353-366	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	125-131
17845805-10	2007	The present study demonstrated that chronic PTZ-kindling might increase P-GP expression and function in brain of rat, resulting in decrease of Rho 123 and PB levels in brain tissues.	Phenobarbital	155-157	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	72-76
17845805-11	2007	Co-administration of CsA increased PB levels in brain and enhanced anticonvulsive effects of PB by inhibiting P-GP function.	Phenobarbital	93-95	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	110-114
17517822-0	2007	Spatial distribution of CYP2B1/2 messenger RNA within the rat liver acinus following exposure to the inducers phenobarbital and dieldrin.	Phenobarbital	110-123	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	24-30
17517822-2	2007	In this study, the CYP2B1/2 messenger RNA (mRNA) in the hepatocytes was compared following treatment of rats with either of two inducers, phenobarbital (PB), or dieldrin.	Phenobarbital	138-151	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	19-25
17517822-8	2007	Whole liver mRNA samples exhibited significant induction in CYP2B1/2 transcript levels: sixfold for PB and 2200-fold for dieldrin.	Phenobarbital	100-102	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	60-66
17586480-6	2007	In contrast, BROD activity measured in hepatic microsomes from PB-treated rats was inhibited by PCB 47, PCB 52 and PCB 54 but not by PCB 77.	Phenobarbital	63-65	pyruvate carboxylase	Rattus norvegicus	96-99
17586480-6	2007	In contrast, BROD activity measured in hepatic microsomes from PB-treated rats was inhibited by PCB 47, PCB 52 and PCB 54 but not by PCB 77.	Phenobarbital	63-65	pyruvate carboxylase	Rattus norvegicus	104-107
17586480-6	2007	In contrast, BROD activity measured in hepatic microsomes from PB-treated rats was inhibited by PCB 47, PCB 52 and PCB 54 but not by PCB 77.	Phenobarbital	63-65	pyruvate carboxylase	Rattus norvegicus	104-107
17586480-6	2007	In contrast, BROD activity measured in hepatic microsomes from PB-treated rats was inhibited by PCB 47, PCB 52 and PCB 54 but not by PCB 77.	Phenobarbital	63-65	pyruvate carboxylase	Rattus norvegicus	104-107
17567731-1	2007	Translocation of constitutive androstane receptor (CAR) from the cytoplasm to the nucleus is induced by phenobarbital-like drugs.	Phenobarbital	104-117	nuclear receptor subfamily 1, group I, member 3	Mus musculus	17-49
17567731-1	2007	Translocation of constitutive androstane receptor (CAR) from the cytoplasm to the nucleus is induced by phenobarbital-like drugs.	Phenobarbital	104-117	nuclear receptor subfamily 1, group I, member 3	Mus musculus	51-54
17557908-2	2007	The constitutive androstane receptor (CAR) has been shown to play a significant role in the overall mode of action for several nongenotoxic rodent carcinogens such as phenobarbital.	Phenobarbital	167-180	nuclear receptor subfamily 1, group I, member 3	Mus musculus	4-36
17557908-2	2007	The constitutive androstane receptor (CAR) has been shown to play a significant role in the overall mode of action for several nongenotoxic rodent carcinogens such as phenobarbital.	Phenobarbital	167-180	nuclear receptor subfamily 1, group I, member 3	Mus musculus	38-41
17557908-10	2007	In Car-null mice, the effects noted with either cyproconazole or phenobarbital were absent or greatly diminished.	Phenobarbital	65-78	nuclear receptor subfamily 1, group I, member 3	Mus musculus	3-6
17992728-13	2007	Kinetic analysis showed that the Km values for the formation of fenchone, 6-exo- hydroxyfenchol and 10-hydroxyfenchol in rats treated with phenobarbital were 0.06, 0.03 and 0.03 mM, and Vmax values were 2.94, 6.1 and 13.8 nmol min-1 nmol-1 P450, respectively.	Phenobarbital	139-152	CD59 molecule (CD59 blood group)	Homo sapiens	227-232
17992728-13	2007	Kinetic analysis showed that the Km values for the formation of fenchone, 6-exo- hydroxyfenchol and 10-hydroxyfenchol in rats treated with phenobarbital were 0.06, 0.03 and 0.03 mM, and Vmax values were 2.94, 6.1 and 13.8 nmol min-1 nmol-1 P450, respectively.	Phenobarbital	139-152	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	240-244
17672909-11	2007	Phenobarbital significantly accelerated SPWs at 50 and 100 muM whereas it reduced their rate at 200 and 400 muM.	Phenobarbital	0-13	latexin	Homo sapiens	59-62
17672909-11	2007	Phenobarbital significantly accelerated SPWs at 50 and 100 muM whereas it reduced their rate at 200 and 400 muM.	Phenobarbital	0-13	latexin	Homo sapiens	108-111
17306917-5	2007	As with the PB-promoted case, both numbers and areas of glutathione S-transferase placental form-positive liver cell foci were significantly increased by JQE at 30,000 ppm, with non-significant increases evident at 5000 ppm.	Phenobarbital	12-14	hematopoietic prostaglandin D synthase	Rattus norvegicus	56-81
17599282-3	2007	In particular, UGT1A1-dependent bilirubin conjugation plays a critical role in the detoxification of neurotoxic bilirubin and phenobarbital-mediated UGT1A1 induction therapy is commonly used in the treatment of unconjugated hyperbilirubinemic diseases such as Crigler-Najjar type II disease.	Phenobarbital	126-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	15-21
17599282-3	2007	In particular, UGT1A1-dependent bilirubin conjugation plays a critical role in the detoxification of neurotoxic bilirubin and phenobarbital-mediated UGT1A1 induction therapy is commonly used in the treatment of unconjugated hyperbilirubinemic diseases such as Crigler-Najjar type II disease.	Phenobarbital	126-139	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	149-155
17445763-3	2007	The present data, using the pig as model, demonstrate direct effects by phenobarbital on the expression of CYP27A1 and CYP2D25, two important 25-hydroxylases.	Phenobarbital	72-85	cytochrome P450 family 27 subfamily A member 1	Sus scrofa	107-114
17638512-2	2007	One of the less well-studied human cytochrome P450s is (CYP)2B6, a homologue of the rodent phenobarbital-inducible CYP2B enzymes.	Phenobarbital	91-104	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	56-63
17638512-2	2007	One of the less well-studied human cytochrome P450s is (CYP)2B6, a homologue of the rodent phenobarbital-inducible CYP2B enzymes.	Phenobarbital	91-104	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	115-120
17438330-6	2007	Striking abrogation of CCl(4)-induced hepatocellular proliferation and hepatotoxicity occurred in Pbp(DeltaLiv) mice pretreated with phenobarbital due to lack of expression of xenobiotic metabolizing enzymes necessary for CCl(4) activation.	Phenobarbital	133-146	mediator complex subunit 1	Mus musculus	98-101
17445763-3	2007	The present data, using the pig as model, demonstrate direct effects by phenobarbital on the expression of CYP27A1 and CYP2D25, two important 25-hydroxylases.	Phenobarbital	72-85	cytochrome P450 family 2 subfamily D member 6	Sus scrofa	119-126
17445763-4	2007	Treatment by phenobarbital markedly reduced the rate of 25-hydroxylation by primary hepatocytes and suppressed the cellular CYP27A1 mRNA levels.	Phenobarbital	13-26	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	124-131
17445763-5	2007	The rate of 25-hydroxylation by two different purified 25-hydroxylases, microsomal CYP2D25, and mitochondrial CYP27A1, respectively, was dose-dependently inhibited by phenobarbital.	Phenobarbital	167-180	cytochrome P450 family 2 subfamily D member 6	Sus scrofa	83-90
17445763-5	2007	The rate of 25-hydroxylation by two different purified 25-hydroxylases, microsomal CYP2D25, and mitochondrial CYP27A1, respectively, was dose-dependently inhibited by phenobarbital.	Phenobarbital	167-180	cytochrome P450 family 27 subfamily A member 1	Homo sapiens	110-117
17445763-7	2007	In addition, the data indicate that phenobarbital might affect the mRNA stability of CYP2D25.	Phenobarbital	36-49	cytochrome P450 family 2 subfamily D member 6	Sus scrofa	85-92
17437408-11	2007	Experiments with systemic administration of the Pgp substrate phenobarbital and the selective Pgp inhibitor tariquidar in TR(-) rats substantiated that Pgp is functional and compensates for the lack of MRP2 in the BBB.	Phenobarbital	62-75	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	48-51
17482559-4	2007	We have therefore investigated the regulation of Rfc1 by phenobarbital (PB)-type CYP450 inducers on the functional, transcriptional and translational level in a suitable in vitro model for rat liver.	Phenobarbital	57-70	replication factor C subunit 1	Rattus norvegicus	49-53
17482559-4	2007	We have therefore investigated the regulation of Rfc1 by phenobarbital (PB)-type CYP450 inducers on the functional, transcriptional and translational level in a suitable in vitro model for rat liver.	Phenobarbital	72-74	replication factor C subunit 1	Rattus norvegicus	49-53
17475251-5	2007	A smaller percentage of GluR2+ neurons (74%) was killed when status epilepticus was interrupted after 1-3.5 h with a single injection of phenobarbital, and the number of residual GluR2+ neurons varied among animals by a factor of 6.2.	Phenobarbital	137-150	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	24-29
17475251-7	2007	In rats administered phenobarbital, the extent of recurrent mossy fiber growth varied inversely and linearly with the number of GluR2+ hilar neurons that remained intact (P=0.0001).	Phenobarbital	21-34	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	128-133
17504224-5	2007	Addition of a PgP (e.g. verapamil and quinidine) or multi-drug resistance protein 1/2 (MRP1/2) inhibitor (e.g. probenecid and MK-571) in both luminal and abluminal sides attenuated the polarized transport.	Phenobarbital	142-149	phosphoglycolate phosphatase	Rattus norvegicus	14-17
17504224-5	2007	Addition of a PgP (e.g. verapamil and quinidine) or multi-drug resistance protein 1/2 (MRP1/2) inhibitor (e.g. probenecid and MK-571) in both luminal and abluminal sides attenuated the polarized transport.	Phenobarbital	142-149	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	52-85
17504224-5	2007	Addition of a PgP (e.g. verapamil and quinidine) or multi-drug resistance protein 1/2 (MRP1/2) inhibitor (e.g. probenecid and MK-571) in both luminal and abluminal sides attenuated the polarized transport.	Phenobarbital	142-149	ATP binding cassette subfamily C member 1	Rattus norvegicus	87-93
17314319-1	2007	The nuclear receptor constitutive active/androstane receptor (CAR) is sequestered in the cytoplasm of liver cells before its activation by therapeutic drugs and xenobiotics such as phenobarbital (PB) and 1,4-Bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) in mouse liver, the regulatory mechanism of which remains poorly understood.	Phenobarbital	181-194	nuclear receptor subfamily 1, group I, member 3	Mus musculus	21-60
17314319-1	2007	The nuclear receptor constitutive active/androstane receptor (CAR) is sequestered in the cytoplasm of liver cells before its activation by therapeutic drugs and xenobiotics such as phenobarbital (PB) and 1,4-Bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) in mouse liver, the regulatory mechanism of which remains poorly understood.	Phenobarbital	181-194	nuclear receptor subfamily 1, group I, member 3	Mus musculus	62-65
17314319-1	2007	The nuclear receptor constitutive active/androstane receptor (CAR) is sequestered in the cytoplasm of liver cells before its activation by therapeutic drugs and xenobiotics such as phenobarbital (PB) and 1,4-Bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) in mouse liver, the regulatory mechanism of which remains poorly understood.	Phenobarbital	196-198	nuclear receptor subfamily 1, group I, member 3	Mus musculus	21-60
17314319-1	2007	The nuclear receptor constitutive active/androstane receptor (CAR) is sequestered in the cytoplasm of liver cells before its activation by therapeutic drugs and xenobiotics such as phenobarbital (PB) and 1,4-Bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) in mouse liver, the regulatory mechanism of which remains poorly understood.	Phenobarbital	196-198	nuclear receptor subfamily 1, group I, member 3	Mus musculus	62-65
17314319-2	2007	Given the finding that epidermal growth factor repressed PB activation of CAR-mediated transcription (Mol Pharmacol 65:172-180, 2004), here we investigated the regulatory role of hepatocyte growth factor (HGF)-mediated signal in sequestering CAR in the cytoplasm of mouse primary hepatocytes.	Phenobarbital	57-59	nuclear receptor subfamily 1, group I, member 3	Mus musculus	74-77
17652830-11	2007	Phenobarbital (an inducer of CYP2B and other CYPs and a CYP2C11 inhibitor) moderately stimulated the metabolism of caffeine, but practically did not affect 7-N-demethylation.	Phenobarbital	0-13	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	56-63
17190925-2	2006	One concern, however, is the increased risk for OC failure with the use of cytochrome P450 3A4 enzyme-inducing AEDs, such as phenobarbital, carbamazepine, phenytoin, felbamate, topiramate, and oxcarbazepine.	Phenobarbital	125-138	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	75-94
17259171-8	2007	Gene mapping experiments including transfections of UGT1A1 reporter gene constructs into HepG2 cells coupled with functional analysis of Nrf2 expression and binding to anti-oxidant-response elements (ARE) resulted in identification of an ARE in the phenobarbital-response enhancer module region of the UGT1A1 gene.	Phenobarbital	249-262	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	52-58
17259171-8	2007	Gene mapping experiments including transfections of UGT1A1 reporter gene constructs into HepG2 cells coupled with functional analysis of Nrf2 expression and binding to anti-oxidant-response elements (ARE) resulted in identification of an ARE in the phenobarbital-response enhancer module region of the UGT1A1 gene.	Phenobarbital	249-262	NFE2 like bZIP transcription factor 2	Homo sapiens	137-141
17259171-8	2007	Gene mapping experiments including transfections of UGT1A1 reporter gene constructs into HepG2 cells coupled with functional analysis of Nrf2 expression and binding to anti-oxidant-response elements (ARE) resulted in identification of an ARE in the phenobarbital-response enhancer module region of the UGT1A1 gene.	Phenobarbital	249-262	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	302-308
17349291-7	2007	The activation of all three components of the UPR depends on the dissociation of the luminal chaperone BiP/GRP78 from the luminal part of these proteins.	Phenobarbital	85-92	heat shock protein family A (Hsp70) member 5	Homo sapiens	103-106
17349291-7	2007	The activation of all three components of the UPR depends on the dissociation of the luminal chaperone BiP/GRP78 from the luminal part of these proteins.	Phenobarbital	85-92	heat shock protein family A (Hsp70) member 5	Homo sapiens	107-112
17349291-7	2007	The activation of all three components of the UPR depends on the dissociation of the luminal chaperone BiP/GRP78 from the luminal part of these proteins.	Phenobarbital	122-129	heat shock protein family A (Hsp70) member 5	Homo sapiens	103-106
17349291-7	2007	The activation of all three components of the UPR depends on the dissociation of the luminal chaperone BiP/GRP78 from the luminal part of these proteins.	Phenobarbital	122-129	heat shock protein family A (Hsp70) member 5	Homo sapiens	107-112
17172636-0	2007	Orphan nuclear receptor constitutive active/androstane receptor-mediated alterations in DNA methylation during phenobarbital promotion of liver tumorigenesis.	Phenobarbital	111-124	nuclear receptor subfamily 1, group D, member 1	Mus musculus	0-23
17172636-2	2007	The constitutive active/androstane nuclear receptor (CAR) mediates half of the PB-induced hepatic gene expression changes and it is essential for liver tumor promotion in PB-treated mice.	Phenobarbital	79-81	nuclear receptor subfamily 1, group I, member 3	Mus musculus	4-51
17172636-2	2007	The constitutive active/androstane nuclear receptor (CAR) mediates half of the PB-induced hepatic gene expression changes and it is essential for liver tumor promotion in PB-treated mice.	Phenobarbital	79-81	nuclear receptor subfamily 1, group I, member 3	Mus musculus	53-56
17172636-2	2007	The constitutive active/androstane nuclear receptor (CAR) mediates half of the PB-induced hepatic gene expression changes and it is essential for liver tumor promotion in PB-treated mice.	Phenobarbital	171-173	nuclear receptor subfamily 1, group I, member 3	Mus musculus	4-51
17172636-2	2007	The constitutive active/androstane nuclear receptor (CAR) mediates half of the PB-induced hepatic gene expression changes and it is essential for liver tumor promotion in PB-treated mice.	Phenobarbital	171-173	nuclear receptor subfamily 1, group I, member 3	Mus musculus	53-56
17172636-3	2007	Here, a technique involving methylation-sensitive restriction digestion, arbitrarily primed PCR, and capillary electrophoresis was utilized to detect PB-induced regions of altered DNA methylation (RAMs) in CAR wildtype (WT) mice that are sensitive to promotion by PB and resistant CAR knockout (KO) mice.	Phenobarbital	150-152	nuclear receptor subfamily 1, group I, member 3	Mus musculus	206-209
17172636-3	2007	Here, a technique involving methylation-sensitive restriction digestion, arbitrarily primed PCR, and capillary electrophoresis was utilized to detect PB-induced regions of altered DNA methylation (RAMs) in CAR wildtype (WT) mice that are sensitive to promotion by PB and resistant CAR knockout (KO) mice.	Phenobarbital	150-152	nuclear receptor subfamily 1, group I, member 3	Mus musculus	281-284
17172636-4	2007	The CAR WT mice developed preneoplastic lesions after 23 weeks of PB treatment (precancerous) and liver tumors after 32 weeks, while the CAR KO mice did not develop tumors (Y. Yamamoto, et al., 2004, Cancer Res.	Phenobarbital	66-68	nuclear receptor subfamily 1, group I, member 3	Mus musculus	4-7
17161434-0	2007	Expression, microsomal and mitochondrial activities of cytochrome P450 enzymes in brain regions from control and phenobarbital-treated rabbits.	Phenobarbital	113-126	cytochrome P-450	Oryctolagus cuniculus	55-70
17161434-5	2007	NADPH cytochrome c reductase and some other enzymatic activities markers of CYP 2A, 2B, 3A and 4B activities were studied in liver microsomes as well as in microsomes and mitochondria of brain cortex, midbrain and cerebellum of control and phenobarbital-treated rabbits.	Phenobarbital	240-253	cytochrome P-450	Oryctolagus cuniculus	76-79
17161434-7	2007	However, we cannot exclude that a longer phenobarbital treatment may lead to a significant induction of CYP activities in brain.	Phenobarbital	41-54	cytochrome P-450	Oryctolagus cuniculus	104-107
17011741-3	2007	This study utilized precision-cut rat liver slices in dynamic organ culture to assess the effects of various media on the viability of rat liver slices and the expression of CYP2B and CYP2E1 when the slices are exposed to phenobarbital and isoniazid, which are drugs capable of inducing these respective CYPs.	Phenobarbital	222-235	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	184-190
17304159-0	2007	Population estimation of the effects of cytochrome P450 2C9 and 2C19 polymorphisms on phenobarbital clearance in Japanese.	Phenobarbital	86-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	40-59
17304159-1	2007	A nonlinear mixed-effect modeling (NONMEM) program was used to evaluate the effects of cytochrome P450 (CYP) 2C9 and CYP2C19 polymorphisms on the phenobarbital (PB) population clearance for Japanese epileptics.	Phenobarbital	146-159	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	87-112
17304159-5	2007	The total clearance of PB decreased by 48% in patients with CYP2C9*1/*3 genotype in comparison with those with CYP2C9*1/*1 genotype (P &lt; 0.001).	Phenobarbital	23-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	60-66
17304159-5	2007	The total clearance of PB decreased by 48% in patients with CYP2C9*1/*3 genotype in comparison with those with CYP2C9*1/*1 genotype (P &lt; 0.001).	Phenobarbital	23-25	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	111-117
17304159-7	2007	To our knowledge, this is the first report to demonstrate that the CYP2C9 genotype affects the PB metabolism in routine care, but the results should be further verified in other ethnic populations.	Phenobarbital	95-97	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	67-73
17213310-0	2007	In the regulation of cytochrome P450 genes, phenobarbital targets LKB1 for necessary activation of AMP-activated protein kinase.	Phenobarbital	44-57	serine/threonine kinase 11	Gallus gallus	66-70
17213310-6	2007	The activation of LKB1 adds a proximal target to the so far elusive sequence of events by which PB and other drugs induce the transcription of multiple genes.	Phenobarbital	96-98	serine/threonine kinase 11	Gallus gallus	18-22
17188729-4	2007	As a positive control, rats were also fed diets containing 1200-1558 ppm sodium Phenobarbital (NaPB) for 7 and 14 days.	Phenobarbital	73-93	NSF attachment protein beta	Rattus norvegicus	95-99
17032173-3	2007	It has been reported recently that AMPK (AMP-activated protein kinase) is involved in phenobarbital-mediated CYP2B induction in a particular culture system.	Phenobarbital	86-99	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	35-39
17032173-3	2007	It has been reported recently that AMPK (AMP-activated protein kinase) is involved in phenobarbital-mediated CYP2B induction in a particular culture system.	Phenobarbital	86-99	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	109-114
17032173-5	2007	Immunoblot analysis using an antibody which recognizes Thr-172-phosphorylated AMPKalpha1/2 revealed phenobarbital-induced AMPK activation in rat and mouse livers as well.	Phenobarbital	100-113	protein kinase AMP-activated catalytic subunit alpha 1	Rattus norvegicus	78-88
17032173-5	2007	Immunoblot analysis using an antibody which recognizes Thr-172-phosphorylated AMPKalpha1/2 revealed phenobarbital-induced AMPK activation in rat and mouse livers as well.	Phenobarbital	100-113	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	78-82
17032173-7	2007	In in vivo reporter gene assays employing PBREM (phenobarbital-responsive enhancer module) from CYP2B1, an AMPK inhibitor 8-bromo-AMP abolished phenobarbital-induced transactivation.	Phenobarbital	49-62	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	107-111
17032173-7	2007	In in vivo reporter gene assays employing PBREM (phenobarbital-responsive enhancer module) from CYP2B1, an AMPK inhibitor 8-bromo-AMP abolished phenobarbital-induced transactivation.	Phenobarbital	144-157	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	107-111
17032173-9	2007	Forced expression of a dominant-negative mutant and the wild-type of AMPKalpha2 in the mouse liver suppressed and further enhanced phenobarbital-induced PBREM-reporter activity respectively.	Phenobarbital	131-144	protein kinase, AMP-activated, alpha 2 catalytic subunit	Mus musculus	69-79
17032173-12	2007	These observations suggest that AMPK is at least partly involved in phenobarbital-originated signalling, but the kinase activation by itself is not sufficient for CYP2B induction in vivo.	Phenobarbital	68-81	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	32-36
17456340-15	2007	(3) For immature rats, concentration of plasma NSE was increased even after short-term treatment with PB [(8.84 +/- 2.10) nmol/L] compared with control group [(6.27 +/- 1.27) nmol/L] (P &lt; 0.01).	Phenobarbital	102-104	enolase 2	Rattus norvegicus	47-50
17456340-19	2007	In contrast, expression of Bax protein in the frontal lobe was increased significantly in immature rats receiving CZP and PB for long period compared with control.	Phenobarbital	122-124	BCL2 associated X, apoptosis regulator	Rattus norvegicus	27-30
17375979-10	2007	The minor contribution of CYP2C19 to the metabolism of phenobarbital (phenobarbitone) can be overlooked.	Phenobarbital	55-68	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
17375979-10	2007	The minor contribution of CYP2C19 to the metabolism of phenobarbital (phenobarbitone) can be overlooked.	Phenobarbital	70-84	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	26-33
17375984-5	2007	Recently, a new form of treatment based on porphobilinogen deaminase enzyme replacement therapy has been shown to be effective in an acute intermittent porphyria mouse model which, during phenobarbital (phenobarbitone) induction of haem biosynthesis, mimics the biochemical pattern of acute porphyric attacks.	Phenobarbital	188-201	hydroxymethylbilane synthase	Mus musculus	43-68
17375984-5	2007	Recently, a new form of treatment based on porphobilinogen deaminase enzyme replacement therapy has been shown to be effective in an acute intermittent porphyria mouse model which, during phenobarbital (phenobarbitone) induction of haem biosynthesis, mimics the biochemical pattern of acute porphyric attacks.	Phenobarbital	203-217	hydroxymethylbilane synthase	Mus musculus	43-68
17020958-8	2007	When PXR knockout mice were challenged with the CAR activator phenobarbital, a significant up-regulation of male CYP3A44 levels was observed, whereas levels in females remained unchanged.	Phenobarbital	62-75	nuclear receptor subfamily 1, group I, member 2	Mus musculus	5-8
17020958-8	2007	When PXR knockout mice were challenged with the CAR activator phenobarbital, a significant up-regulation of male CYP3A44 levels was observed, whereas levels in females remained unchanged.	Phenobarbital	62-75	nuclear receptor subfamily 1, group I, member 3	Mus musculus	48-51
17020958-8	2007	When PXR knockout mice were challenged with the CAR activator phenobarbital, a significant up-regulation of male CYP3A44 levels was observed, whereas levels in females remained unchanged.	Phenobarbital	62-75	cytochrome P450, family 3, subfamily a, polypeptide 44	Mus musculus	113-120
17786642-3	2007	Serum iron was approximately doubled within 6 h when HO-1 was induced by phenobarbital treatment of selenium-deficient mice.	Phenobarbital	73-86	heme oxygenase 1	Mus musculus	53-57
18330007-5	2007	In addition to AED target alterations, SE-induced overexpression of drug efflux transporters, such as P-glycoprotein (Pgp), in the brain may be involved in the resistance to AEDs (including phenytoin and phenobarbital) that are Pgp substrates.	Phenobarbital	204-217	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	102-116
18330007-5	2007	In addition to AED target alterations, SE-induced overexpression of drug efflux transporters, such as P-glycoprotein (Pgp), in the brain may be involved in the resistance to AEDs (including phenytoin and phenobarbital) that are Pgp substrates.	Phenobarbital	204-217	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	118-121
17536229-12	2007	However, the concentration of phenobarbital 100 mg tablets produced in Lao PDR (mean concentration 94.7 mg) was significantly lower (p = 0.005) than the imported equivalent (mean concentration 99.7 mg).	Phenobarbital	30-43	interleukin 4 induced 1	Homo sapiens	71-74
17341620-0	2006	Effects of TK promotor and hepatocyte nuclear factor-4 in CAR-mediated transcriptional activity of phenobarbital responsive unit of CYP2B gene in monkey kidney epithelial-derived cell line COS-7.	Phenobarbital	99-112	nuclear receptor subfamily 1 group I member 3	Homo sapiens	58-61
16815962-5	2006	In contrast, baseline and PB-treated expressions of CYP2E1 mRNA were reduced in HF-fed rats.	Phenobarbital	26-28	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	52-58
16936065-4	2006	In the present study, we report that murine CYP2C37 mRNA is induced by phenobarbital and phenytoin.	Phenobarbital	71-84	cytochrome P450, family 2. subfamily c, polypeptide 37	Mus musculus	44-51
16936065-6	2006	The induction of CYP2C37 mRNA by phenobarbital and phenytoin is essentially abolished in CAR-null mice; thus, induction of Cyp2c37 by these xenobiotics is CAR-dependent.	Phenobarbital	33-46	cytochrome P450, family 2. subfamily c, polypeptide 37	Mus musculus	17-24
16936065-6	2006	The induction of CYP2C37 mRNA by phenobarbital and phenytoin is essentially abolished in CAR-null mice; thus, induction of Cyp2c37 by these xenobiotics is CAR-dependent.	Phenobarbital	33-46	nuclear receptor subfamily 1, group I, member 3	Mus musculus	89-92
16936065-6	2006	The induction of CYP2C37 mRNA by phenobarbital and phenytoin is essentially abolished in CAR-null mice; thus, induction of Cyp2c37 by these xenobiotics is CAR-dependent.	Phenobarbital	33-46	cytochrome P450, family 2. subfamily c, polypeptide 37	Mus musculus	123-130
16936065-6	2006	The induction of CYP2C37 mRNA by phenobarbital and phenytoin is essentially abolished in CAR-null mice; thus, induction of Cyp2c37 by these xenobiotics is CAR-dependent.	Phenobarbital	33-46	nuclear receptor subfamily 1, group I, member 3	Mus musculus	155-158
17150334-8	2006	Systemic phenobarbital caused an acute and dose-dependent behavioral and EEGraphic anticonvulsant effect both in WARs.	Phenobarbital	9-22	tryptophanyl-tRNA synthetase 1	Rattus norvegicus	113-117
16988011-1	2006	Our previous studies have suggested a role for AMP-activated protein kinase (AMPK) in the induction of CYP2B6 by phenobarbital (PB) in hepatoma-derived cells (Rencurel et al., 2005).	Phenobarbital	113-126	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	103-109
16988011-1	2006	Our previous studies have suggested a role for AMP-activated protein kinase (AMPK) in the induction of CYP2B6 by phenobarbital (PB) in hepatoma-derived cells (Rencurel et al., 2005).	Phenobarbital	128-130	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	103-109
17148020-2	2006	Pgp is also expressed on the luminal surface of brain capillary endothelial cells wherein Pgp functionally comprises a major component of the blood-brain barrier by limiting central nervous system penetration of various therapeutic agents.	Phenobarbital	29-36	ATP binding cassette subfamily B member 1	Homo sapiens	0-3
17148020-2	2006	Pgp is also expressed on the luminal surface of brain capillary endothelial cells wherein Pgp functionally comprises a major component of the blood-brain barrier by limiting central nervous system penetration of various therapeutic agents.	Phenobarbital	29-36	ATP binding cassette subfamily B member 1	Homo sapiens	90-93
17167544-1	2006	Retinal dehydrogenase type 1 (RALDH1) catalyzes the oxidation of all-trans and 9-cis retinal to the respective retinoic acids (RAs), whereas another member of the aldehyde dehydrogenase (ALDH) family, the phenobarbital-induced aldehyde dehydrogenase (PB-ALDH), is very poorly active.	Phenobarbital	205-218	aldehyde dehydrogenase 1 family member A1	Homo sapiens	0-28
17167544-1	2006	Retinal dehydrogenase type 1 (RALDH1) catalyzes the oxidation of all-trans and 9-cis retinal to the respective retinoic acids (RAs), whereas another member of the aldehyde dehydrogenase (ALDH) family, the phenobarbital-induced aldehyde dehydrogenase (PB-ALDH), is very poorly active.	Phenobarbital	205-218	aldehyde dehydrogenase 1 family member A1	Homo sapiens	30-36
17167544-1	2006	Retinal dehydrogenase type 1 (RALDH1) catalyzes the oxidation of all-trans and 9-cis retinal to the respective retinoic acids (RAs), whereas another member of the aldehyde dehydrogenase (ALDH) family, the phenobarbital-induced aldehyde dehydrogenase (PB-ALDH), is very poorly active.	Phenobarbital	205-218	aldehyde dehydrogenase 1 family member A1	Homo sapiens	31-35
16837569-4	2006	With a threshold corresponding to a 1.5-fold factor change in mRNA levels, observed in at least three of seven independent human hepatocyte cultures, efflux transporters such as MDR1, MRP2 and BCRP were up-regulated by PB, RIF, and OPZ, whereas MRP3 was induced by OPZ and RIF.	Phenobarbital	219-221	ATP binding cassette subfamily B member 1	Homo sapiens	178-182
16837569-4	2006	With a threshold corresponding to a 1.5-fold factor change in mRNA levels, observed in at least three of seven independent human hepatocyte cultures, efflux transporters such as MDR1, MRP2 and BCRP were up-regulated by PB, RIF, and OPZ, whereas MRP3 was induced by OPZ and RIF.	Phenobarbital	219-221	ATP binding cassette subfamily C member 2	Homo sapiens	184-188
16837569-4	2006	With a threshold corresponding to a 1.5-fold factor change in mRNA levels, observed in at least three of seven independent human hepatocyte cultures, efflux transporters such as MDR1, MRP2 and BCRP were up-regulated by PB, RIF, and OPZ, whereas MRP3 was induced by OPZ and RIF.	Phenobarbital	219-221	BCR pseudogene 1	Homo sapiens	193-197
16815962-6	2006	The induction of P450s in response to PB was affected by the nutritional status of the rats; mRNA levels of CYP2B1 and CYP3A1 after PB treatment, as assessed by quantitative real-time polymerase chain reaction analysis were reduced in the inulin-supplemented HF (HF+I) group, compared with those in the HF group.	Phenobarbital	38-40	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	108-114
16837569-4	2006	With a threshold corresponding to a 1.5-fold factor change in mRNA levels, observed in at least three of seven independent human hepatocyte cultures, efflux transporters such as MDR1, MRP2 and BCRP were up-regulated by PB, RIF, and OPZ, whereas MRP3 was induced by OPZ and RIF.	Phenobarbital	219-221	ATP binding cassette subfamily C member 3	Homo sapiens	245-249
16837569-7	2006	Influx transporters such as OCT1, OATP-B, and OATP8 were repressed by PB and TCDD.	Phenobarbital	70-72	POU class 2 homeobox 1	Homo sapiens	28-32
16837569-7	2006	Influx transporters such as OCT1, OATP-B, and OATP8 were repressed by PB and TCDD.	Phenobarbital	70-72	solute carrier organic anion transporter family member 2B1	Homo sapiens	34-40
16837569-7	2006	Influx transporters such as OCT1, OATP-B, and OATP8 were repressed by PB and TCDD.	Phenobarbital	70-72	solute carrier organic anion transporter family member 1B3	Homo sapiens	46-51
16837569-8	2006	PB also decreased MRP6 expression, whereas mRNA levels of OCT1 and OATP8 were down-regulated by RIF and OPZ, respectively.	Phenobarbital	0-2	ATP binding cassette subfamily C member 6	Homo sapiens	18-22
16868070-9	2006	Although the expression of CYP2B1 could be detected in subcultured SHs treated with PB, it was not detected in cryopreserved SHs.	Phenobarbital	84-86	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	27-33
17069428-7	2006	The result that PTS metabolism was enhanced by PB and inhibited by Ket treatments suggested liver CYP was attributed to PTS metabolism.	Phenobarbital	47-49	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	98-101
16782779-2	2006	Since we have previously shown that tumor promotion by PB leads to clonal outgrowth of beta-catenin (Catnb)-mutated but not Ha-ras-mutated mouse liver tumors, we were interested to know whether the non-dioxin-like tumor promoter 2,2",4,4",5,5"-hexachlorobiphenyl (PCB 153) shows the same selective pressure during tumor promotion.	Phenobarbital	55-57	catenin (cadherin associated protein), beta 1	Mus musculus	87-99
16782779-2	2006	Since we have previously shown that tumor promotion by PB leads to clonal outgrowth of beta-catenin (Catnb)-mutated but not Ha-ras-mutated mouse liver tumors, we were interested to know whether the non-dioxin-like tumor promoter 2,2",4,4",5,5"-hexachlorobiphenyl (PCB 153) shows the same selective pressure during tumor promotion.	Phenobarbital	55-57	catenin (cadherin associated protein), beta 1	Mus musculus	101-106
16876710-1	2006	The effect of xenobiotics (phenobarbital and atrazine) on the expression of Drosophila melanogaster CYP genes encoding cytochromes P450, a gene family generally associated with detoxification, was analyzed by DNA microarray hybridization and verified by real-time RT-PCR in adults of both sexes.	Phenobarbital	27-40	disembodied	Drosophila melanogaster	100-103
16876710-1	2006	The effect of xenobiotics (phenobarbital and atrazine) on the expression of Drosophila melanogaster CYP genes encoding cytochromes P450, a gene family generally associated with detoxification, was analyzed by DNA microarray hybridization and verified by real-time RT-PCR in adults of both sexes.	Phenobarbital	27-40	Cytochrome P450-6a8	Drosophila melanogaster	131-135
16876710-3	2006	Eleven CYP genes and three glutathione S-transferases (GST) genes were significantly induced by phenobarbital, seven CYP and one GST gene were induced by atrazine.	Phenobarbital	96-109	disembodied	Drosophila melanogaster	7-10
16626768-4	2006	As a positive control, rats were also fed diets containing 1200-1558 ppm sodium Phenobarbital (NaPB) for 7 and 14 days.	Phenobarbital	73-93	NSF attachment protein beta	Rattus norvegicus	95-99
16542693-5	2006	Treatment of mice with 1000 ppm phenobarbital elicited the same effects as treatment of mice with 1300 ppm fenbuconazole, except that phenobarbital was more effective than fenbuconazole at inducing PROD activity, even though fenbuconazole induced CYP2B10 to the same extent as did phenobarbital.	Phenobarbital	32-45	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	247-254
16814731-5	2006	A DHR96 null mutant displays increased sensitivity to the sedative effects of phenobarbital and the pesticide DDT as well as defects in the expression of many phenobarbital-regulated genes.	Phenobarbital	78-91	Hormone receptor-like in 96	Drosophila melanogaster	2-7
16814731-5	2006	A DHR96 null mutant displays increased sensitivity to the sedative effects of phenobarbital and the pesticide DDT as well as defects in the expression of many phenobarbital-regulated genes.	Phenobarbital	159-172	Hormone receptor-like in 96	Drosophila melanogaster	2-7
16517146-0	2006	n-6 and n-3 polyunsaturated fatty acids down-regulate cytochrome P-450 2B1 gene expression induced by phenobarbital in primary rat hepatocytes.	Phenobarbital	102-115	cytochrome P450 2B1	Rattus norvegicus	54-74
16517146-3	2006	The objective of the present study was to determine whether individual n-6 and n-3 PUFAs affect cytochrome P-450 2B1 (CYP 2B1) expression induced by phenobarbital (PB) in primary rat hepatocytes.	Phenobarbital	149-162	cytochrome P450 2B1	Rattus norvegicus	96-116
16517146-3	2006	The objective of the present study was to determine whether individual n-6 and n-3 PUFAs affect cytochrome P-450 2B1 (CYP 2B1) expression induced by phenobarbital (PB) in primary rat hepatocytes.	Phenobarbital	149-162	cytochrome P450 2B1	Rattus norvegicus	118-125
16517146-3	2006	The objective of the present study was to determine whether individual n-6 and n-3 PUFAs affect cytochrome P-450 2B1 (CYP 2B1) expression induced by phenobarbital (PB) in primary rat hepatocytes.	Phenobarbital	164-166	cytochrome P450 2B1	Rattus norvegicus	96-116
16517146-3	2006	The objective of the present study was to determine whether individual n-6 and n-3 PUFAs affect cytochrome P-450 2B1 (CYP 2B1) expression induced by phenobarbital (PB) in primary rat hepatocytes.	Phenobarbital	164-166	cytochrome P450 2B1	Rattus norvegicus	118-125
16517146-5	2006	Phenobarbital-induced CYP 2B1 expression was down-regulated by n-6 and n-3 PUFAs, especially AA and DHA.	Phenobarbital	0-13	cytochrome P450 2B1	Rattus norvegicus	22-29
16517146-6	2006	Prostaglandin (PG) E2 but not PGE3 was found to down-regulate PB-induced CYP 2B1 expression.	Phenobarbital	62-64	cytochrome P450 2B1	Rattus norvegicus	73-80
16517146-7	2006	The cyclooxygenase inhibitor indomethacin (20 microM) attenuated the down-regulation of CYP 2B1 gene expression by n-6 and n-3 PUFAs induced by PB, and maximal attenuation was found in the AA-treated group.	Phenobarbital	144-146	cytochrome P450 2B1	Rattus norvegicus	88-95
16517146-10	2006	These results suggest that PB-induced CYP 2B1 expression is down-regulated by n-6 and n-3 PUFAs through different pathways.	Phenobarbital	27-29	cytochrome P450 2B1	Rattus norvegicus	38-45
16828057-1	2006	The constitutive androstane receptor (CAR) regulates transcription of phenobarbital-inducible genes that encode xenobiotic-metabolizing enzymes in liver.	Phenobarbital	70-83	nuclear receptor subfamily 1, group I, member 3	Mus musculus	4-36
16828057-1	2006	The constitutive androstane receptor (CAR) regulates transcription of phenobarbital-inducible genes that encode xenobiotic-metabolizing enzymes in liver.	Phenobarbital	70-83	nuclear receptor subfamily 1, group I, member 3	Mus musculus	38-41
16828057-2	2006	CAR is localized to the hepatocyte cytoplasm but to be functional, it translocates into the nucleus in the presence of phenobarbital-like CAR ligands.	Phenobarbital	119-132	nuclear receptor subfamily 1, group I, member 3	Mus musculus	0-3
16828057-2	2006	CAR is localized to the hepatocyte cytoplasm but to be functional, it translocates into the nucleus in the presence of phenobarbital-like CAR ligands.	Phenobarbital	119-132	nuclear receptor subfamily 1, group I, member 3	Mus musculus	138-141
16828057-3	2006	We now demonstrate that adenovirally driven EGFP-CAR, as expected, translocates into the nucleus of normal wild-type hepatocytes following phenobarbital treatment under both in vivo and in vitro conditions.	Phenobarbital	139-152	nuclear receptor subfamily 1, group I, member 3	Mus musculus	49-52
16828057-6	2006	Adenoviral expression of both PBP and EGFP-CAR restored phenobarbital-mediated nuclear translocation of exogenously expressed CAR in PBP null livers in vivo and in PBP null primary hepatocytes in vitro.	Phenobarbital	56-69	mediator complex subunit 1	Mus musculus	30-33
16828057-6	2006	Adenoviral expression of both PBP and EGFP-CAR restored phenobarbital-mediated nuclear translocation of exogenously expressed CAR in PBP null livers in vivo and in PBP null primary hepatocytes in vitro.	Phenobarbital	56-69	nuclear receptor subfamily 1, group I, member 3	Mus musculus	43-46
16828057-6	2006	Adenoviral expression of both PBP and EGFP-CAR restored phenobarbital-mediated nuclear translocation of exogenously expressed CAR in PBP null livers in vivo and in PBP null primary hepatocytes in vitro.	Phenobarbital	56-69	nuclear receptor subfamily 1, group I, member 3	Mus musculus	126-129
16828057-6	2006	Adenoviral expression of both PBP and EGFP-CAR restored phenobarbital-mediated nuclear translocation of exogenously expressed CAR in PBP null livers in vivo and in PBP null primary hepatocytes in vitro.	Phenobarbital	56-69	mediator complex subunit 1	Mus musculus	133-136
16828057-6	2006	Adenoviral expression of both PBP and EGFP-CAR restored phenobarbital-mediated nuclear translocation of exogenously expressed CAR in PBP null livers in vivo and in PBP null primary hepatocytes in vitro.	Phenobarbital	56-69	mediator complex subunit 1	Mus musculus	133-136
16623664-1	2006	CAR (constitutive active/androstane receptor) regulates both the distal enhancer PBREM (phenobarbital-responsive enhancer module) and the proximal element OARE [OA (okadaic acid) response element] to synergistically up-regulate the endogenous CYP2B6 (where CYP is cytochrome P450) gene in HepG2 cells.	Phenobarbital	88-101	nuclear receptor subfamily 1 group I member 3	Homo sapiens	0-3
16623664-1	2006	CAR (constitutive active/androstane receptor) regulates both the distal enhancer PBREM (phenobarbital-responsive enhancer module) and the proximal element OARE [OA (okadaic acid) response element] to synergistically up-regulate the endogenous CYP2B6 (where CYP is cytochrome P450) gene in HepG2 cells.	Phenobarbital	88-101	nuclear receptor subfamily 1 group I member 3	Homo sapiens	5-44
16623664-1	2006	CAR (constitutive active/androstane receptor) regulates both the distal enhancer PBREM (phenobarbital-responsive enhancer module) and the proximal element OARE [OA (okadaic acid) response element] to synergistically up-regulate the endogenous CYP2B6 (where CYP is cytochrome P450) gene in HepG2 cells.	Phenobarbital	88-101	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	243-249
16623664-1	2006	CAR (constitutive active/androstane receptor) regulates both the distal enhancer PBREM (phenobarbital-responsive enhancer module) and the proximal element OARE [OA (okadaic acid) response element] to synergistically up-regulate the endogenous CYP2B6 (where CYP is cytochrome P450) gene in HepG2 cells.	Phenobarbital	88-101	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	275-279
16867264-0	2006	Influences of 3-methylcholanthrene, phenobarbital and dexamethasone on xenobiotic metabolizing-related cytochrome P450 enzymes and steroidogenesis in human fetal adrenal cortical cells.	Phenobarbital	36-49	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	103-118
16867264-11	2006	CONCLUSION: 3-Methylcholanthrene, phenobarbital or dexamethasone could interfere with the synthesis of cortisol, aldosterone and progesterone in primary human fetal adrenal cortical cells, which likely act through xenobiotic metabolizing-related cytochrome P450 isoform activation.	Phenobarbital	34-47	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	246-261
16725103-0	2006	Analysis of multiple nuclear receptor binding sites for CAR/RXR in the phenobarbital responsive unit of CYP2B2.	Phenobarbital	71-84	nuclear receptor subfamily 1 group I member 3	Homo sapiens	56-59
16725103-0	2006	Analysis of multiple nuclear receptor binding sites for CAR/RXR in the phenobarbital responsive unit of CYP2B2.	Phenobarbital	71-84	retinoid X receptor alpha	Homo sapiens	60-63
16725103-1	2006	The phenobarbital (PB) responsive enhancers in CYP2B genes contain a core of two direct repeat-4 nuclear receptor binding sites, NR-1 and NR-2, which flank an NF-1 site and appear to be most important for PB responsiveness.	Phenobarbital	4-17	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	47-52
16725103-1	2006	The phenobarbital (PB) responsive enhancers in CYP2B genes contain a core of two direct repeat-4 nuclear receptor binding sites, NR-1 and NR-2, which flank an NF-1 site and appear to be most important for PB responsiveness.	Phenobarbital	4-17	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	129-142
16725103-1	2006	The phenobarbital (PB) responsive enhancers in CYP2B genes contain a core of two direct repeat-4 nuclear receptor binding sites, NR-1 and NR-2, which flank an NF-1 site and appear to be most important for PB responsiveness.	Phenobarbital	19-21	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	47-52
16725103-1	2006	The phenobarbital (PB) responsive enhancers in CYP2B genes contain a core of two direct repeat-4 nuclear receptor binding sites, NR-1 and NR-2, which flank an NF-1 site and appear to be most important for PB responsiveness.	Phenobarbital	19-21	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	129-142
16725103-1	2006	The phenobarbital (PB) responsive enhancers in CYP2B genes contain a core of two direct repeat-4 nuclear receptor binding sites, NR-1 and NR-2, which flank an NF-1 site and appear to be most important for PB responsiveness.	Phenobarbital	205-207	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	47-52
16725103-1	2006	The phenobarbital (PB) responsive enhancers in CYP2B genes contain a core of two direct repeat-4 nuclear receptor binding sites, NR-1 and NR-2, which flank an NF-1 site and appear to be most important for PB responsiveness.	Phenobarbital	205-207	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	129-142
16725103-3	2006	The PB response is mediated by constitutive androstane receptor (CAR) which binds as a CAR/RXR heterodimer to the NR sites.	Phenobarbital	4-6	nuclear receptor subfamily 1 group I member 3	Homo sapiens	31-63
16725103-3	2006	The PB response is mediated by constitutive androstane receptor (CAR) which binds as a CAR/RXR heterodimer to the NR sites.	Phenobarbital	4-6	nuclear receptor subfamily 1 group I member 3	Homo sapiens	65-68
16725103-3	2006	The PB response is mediated by constitutive androstane receptor (CAR) which binds as a CAR/RXR heterodimer to the NR sites.	Phenobarbital	4-6	nuclear receptor subfamily 1 group I member 3	Homo sapiens	87-90
16725103-3	2006	The PB response is mediated by constitutive androstane receptor (CAR) which binds as a CAR/RXR heterodimer to the NR sites.	Phenobarbital	4-6	retinoid X receptor alpha	Homo sapiens	91-94
16581946-2	2006	Recently, we reported that lipophilic cytochrome P450 inducers, beta-naphthoflavone (BNF), phenobarbital, and dexamethasone, induced CYP1, CYP2B, and CYP3A enzymes, respectively, in rat epididymal white adipose tissue (WAT) at both mRNA and protein levels.	Phenobarbital	91-104	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	133-137
16581946-2	2006	Recently, we reported that lipophilic cytochrome P450 inducers, beta-naphthoflavone (BNF), phenobarbital, and dexamethasone, induced CYP1, CYP2B, and CYP3A enzymes, respectively, in rat epididymal white adipose tissue (WAT) at both mRNA and protein levels.	Phenobarbital	91-104	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	150-155
16799975-2	2006	The constitutive androstane receptor (CAR; NR1I3) and to a lesser extent the pregnane X receptor (PXR; NR1I2) are responsible for mediating induction of many phenobarbital-responsive genes.	Phenobarbital	158-171	nuclear receptor subfamily 1, group I, member 3	Mus musculus	38-41
16799975-2	2006	The constitutive androstane receptor (CAR; NR1I3) and to a lesser extent the pregnane X receptor (PXR; NR1I2) are responsible for mediating induction of many phenobarbital-responsive genes.	Phenobarbital	158-171	nuclear receptor subfamily 1, group I, member 3	Mus musculus	43-48
16799975-2	2006	The constitutive androstane receptor (CAR; NR1I3) and to a lesser extent the pregnane X receptor (PXR; NR1I2) are responsible for mediating induction of many phenobarbital-responsive genes.	Phenobarbital	158-171	nuclear receptor subfamily 1, group I, member 2	Mus musculus	77-96
16799975-2	2006	The constitutive androstane receptor (CAR; NR1I3) and to a lesser extent the pregnane X receptor (PXR; NR1I2) are responsible for mediating induction of many phenobarbital-responsive genes.	Phenobarbital	158-171	nuclear receptor subfamily 1, group I, member 2	Mus musculus	98-101
16799975-2	2006	The constitutive androstane receptor (CAR; NR1I3) and to a lesser extent the pregnane X receptor (PXR; NR1I2) are responsible for mediating induction of many phenobarbital-responsive genes.	Phenobarbital	158-171	nuclear receptor subfamily 1, group I, member 2	Mus musculus	103-108
16799975-4	2006	We studied the effects of phenobarbital on HNF-4alpha expression in hepatocytes and provide evidence that HNF-4alpha nuclear expression is regulated in response to phenobarbital.	Phenobarbital	26-39	hepatic nuclear factor 4, alpha	Mus musculus	43-53
16799975-4	2006	We studied the effects of phenobarbital on HNF-4alpha expression in hepatocytes and provide evidence that HNF-4alpha nuclear expression is regulated in response to phenobarbital.	Phenobarbital	26-39	hepatic nuclear factor 4, alpha	Mus musculus	106-116
16799975-4	2006	We studied the effects of phenobarbital on HNF-4alpha expression in hepatocytes and provide evidence that HNF-4alpha nuclear expression is regulated in response to phenobarbital.	Phenobarbital	164-177	hepatic nuclear factor 4, alpha	Mus musculus	106-116
16799975-5	2006	Real-time polymerase chain reaction analyses revealed that HNF-4alpha mRNA is modestly up-regulated by phenobarbital.	Phenobarbital	103-116	hepatic nuclear factor 4, alpha	Mus musculus	59-69
16799975-6	2006	In addition, nuclear expression of HNF-4alpha protein is significantly elevated 3 hours after the administration of phenobarbital in wild-type, CAR-/-, and CAR-/-/PXR-/- mice.	Phenobarbital	116-129	hepatic nuclear factor 4, alpha	Mus musculus	35-45
16799975-6	2006	In addition, nuclear expression of HNF-4alpha protein is significantly elevated 3 hours after the administration of phenobarbital in wild-type, CAR-/-, and CAR-/-/PXR-/- mice.	Phenobarbital	116-129	nuclear receptor subfamily 1, group I, member 3	Mus musculus	144-147
16799975-6	2006	In addition, nuclear expression of HNF-4alpha protein is significantly elevated 3 hours after the administration of phenobarbital in wild-type, CAR-/-, and CAR-/-/PXR-/- mice.	Phenobarbital	116-129	nuclear receptor subfamily 1, group I, member 3	Mus musculus	156-159
16799975-6	2006	In addition, nuclear expression of HNF-4alpha protein is significantly elevated 3 hours after the administration of phenobarbital in wild-type, CAR-/-, and CAR-/-/PXR-/- mice.	Phenobarbital	116-129	nuclear receptor subfamily 1, group I, member 2	Mus musculus	163-166
16799975-7	2006	In vitro analysis revealed that phenobarbital-induced HNF-4alpha expression is both time- and dose dependent.	Phenobarbital	32-45	hepatic nuclear factor 4, alpha	Mus musculus	54-64
16815962-6	2006	The induction of P450s in response to PB was affected by the nutritional status of the rats; mRNA levels of CYP2B1 and CYP3A1 after PB treatment, as assessed by quantitative real-time polymerase chain reaction analysis were reduced in the inulin-supplemented HF (HF+I) group, compared with those in the HF group.	Phenobarbital	38-40	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	119-125
16799975-8	2006	In addition, the phosphatase inhibitor okadaic acid and the Ca2+/calmodulin-dependent protein kinase II inhibitor KN62 block nuclear induction of HNF-4alpha by phenobarbital.	Phenobarbital	160-173	hepatic nuclear factor 4, alpha	Mus musculus	146-156
16799975-10	2006	In conclusion, induced nuclear expression of HNF-4alpha and CAR is an integral part of the phenobarbital response, aimed at coordinated regulation of genes involved in drug metabolism and detoxification as well as maintenance of liver function.	Phenobarbital	91-104	hepatic nuclear factor 4, alpha	Mus musculus	45-55
16799975-10	2006	In conclusion, induced nuclear expression of HNF-4alpha and CAR is an integral part of the phenobarbital response, aimed at coordinated regulation of genes involved in drug metabolism and detoxification as well as maintenance of liver function.	Phenobarbital	91-104	nuclear receptor subfamily 1, group I, member 3	Mus musculus	60-63
16815962-6	2006	The induction of P450s in response to PB was affected by the nutritional status of the rats; mRNA levels of CYP2B1 and CYP3A1 after PB treatment, as assessed by quantitative real-time polymerase chain reaction analysis were reduced in the inulin-supplemented HF (HF+I) group, compared with those in the HF group.	Phenobarbital	132-134	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	108-114
16815962-6	2006	The induction of P450s in response to PB was affected by the nutritional status of the rats; mRNA levels of CYP2B1 and CYP3A1 after PB treatment, as assessed by quantitative real-time polymerase chain reaction analysis were reduced in the inulin-supplemented HF (HF+I) group, compared with those in the HF group.	Phenobarbital	132-134	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	119-125
16815962-10	2006	Taken together, these results indicate that inulin intake ameliorates PB-induced liver injury, associated with a decline in lipid accumulation and PB-induced expression of CYP2B and CYP3A, which may be related by a reduction in the nuclear expression of HNF4alpha.	Phenobarbital	147-149	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	182-187
16815962-10	2006	Taken together, these results indicate that inulin intake ameliorates PB-induced liver injury, associated with a decline in lipid accumulation and PB-induced expression of CYP2B and CYP3A, which may be related by a reduction in the nuclear expression of HNF4alpha.	Phenobarbital	147-149	hepatocyte nuclear factor 4, alpha	Rattus norvegicus	254-263
16608922-5	2006	TPA, 3-MC, BHA, and PB reduced HNF1alpha mRNA levels in preconfluent and confluent cells and caused marked reductions in luciferase activity in pGSTA1-1591-luc transfectants.	Phenobarbital	20-22	HNF1 homeobox A	Homo sapiens	31-40
16608922-8	2006	Immunoblot analysis of DNA binding studies indicate that variant (v)HNF1-C binding to HRE is increased in preconfluent cells treated with 3-MC, BHA, and PB.	Phenobarbital	153-155	HNF1 homeobox A	Homo sapiens	68-72
16608922-10	2006	Finally, treatment with 3-MC, BHA, and PB increased vHNF1-C mRNA levels in preconfluent cells.	Phenobarbital	39-41	HNF1 homeobox B	Homo sapiens	52-57
16492670-7	2006	Treatment of mice with phenobarbital or TCPOBOP resulted in decreased hepatic mRNA levels of the reported genes down-regulated by CAR, including Cyp7a1 and Pepck.	Phenobarbital	23-36	nuclear receptor subfamily 1, group I, member 3	Mus musculus	130-133
16531474-7	2006	The maximum fold induction of mRNA varied: 2500-fold for CYP1A1 with BNF, 680-fold for CYP2B1 with PB, 59-fold for CYP3A23 with DEX, and 16-fold for CYP4A1 with CLO.	Phenobarbital	99-101	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	87-93
16789993-0	2006	Effect of CYP2C19 genetic polymorphism on pharmacokinetics of phenytoin and phenobarbital in Japanese epileptic patients using Non-linear Mixed Effects Model approach.	Phenobarbital	76-89	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	10-17
16789993-1	2006	OBJECTIVE: To clarify the effect of genetic polymorphism of CYP2C19 on pharmacokinetics of phenytoin and phenobarbital using a Non-linear Mixed Effects Modelling analysis in Japanese epileptic patients.	Phenobarbital	105-118	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	60-67
16789993-5	2006	The total body clearance of phenobarbital decreased by 19.3% in patients with CYP2C19*1/*3 or the poor metabolizers of CYP2C19 compared with patients with normal CYP2C19 or with CYP2C19*1/*2.	Phenobarbital	28-41	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	78-85
16789993-5	2006	The total body clearance of phenobarbital decreased by 19.3% in patients with CYP2C19*1/*3 or the poor metabolizers of CYP2C19 compared with patients with normal CYP2C19 or with CYP2C19*1/*2.	Phenobarbital	28-41	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	119-126
16789993-5	2006	The total body clearance of phenobarbital decreased by 19.3% in patients with CYP2C19*1/*3 or the poor metabolizers of CYP2C19 compared with patients with normal CYP2C19 or with CYP2C19*1/*2.	Phenobarbital	28-41	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	119-126
16789993-5	2006	The total body clearance of phenobarbital decreased by 19.3% in patients with CYP2C19*1/*3 or the poor metabolizers of CYP2C19 compared with patients with normal CYP2C19 or with CYP2C19*1/*2.	Phenobarbital	28-41	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	119-126
16789993-6	2006	CONCLUSION: These findings indicated that the genetic polymorphisms of CYP2C19 contribute to the pharmacokinetic variability of phenytoin and phenobarbital, the poor metabolizers of CYP2C19, which are relatively common in Asian groups.	Phenobarbital	142-155	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
16789993-6	2006	CONCLUSION: These findings indicated that the genetic polymorphisms of CYP2C19 contribute to the pharmacokinetic variability of phenytoin and phenobarbital, the poor metabolizers of CYP2C19, which are relatively common in Asian groups.	Phenobarbital	142-155	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	182-189
16799975-0	2006	Phenobarbital regulates nuclear expression of HNF-4alpha in mouse and rat hepatocytes independent of CAR and PXR.	Phenobarbital	0-13	hepatic nuclear factor 4, alpha	Mus musculus	46-56
16799975-2	2006	The constitutive androstane receptor (CAR; NR1I3) and to a lesser extent the pregnane X receptor (PXR; NR1I2) are responsible for mediating induction of many phenobarbital-responsive genes.	Phenobarbital	158-171	nuclear receptor subfamily 1, group I, member 3	Mus musculus	4-36
16492670-8	2006	In vivo recruitment of endogenous CAR to the promoters of Cyp7a1 and Pepck was detected in mouse liver after phenobarbital treatment, whereas association of HNF-4 and coactivators, GRIP-1, p300, and PGC-1alpha, with these promoters was significantly decreased.	Phenobarbital	109-122	nuclear receptor subfamily 1, group I, member 3	Mus musculus	34-37
16492670-8	2006	In vivo recruitment of endogenous CAR to the promoters of Cyp7a1 and Pepck was detected in mouse liver after phenobarbital treatment, whereas association of HNF-4 and coactivators, GRIP-1, p300, and PGC-1alpha, with these promoters was significantly decreased.	Phenobarbital	109-122	cytochrome P450, family 7, subfamily a, polypeptide 1	Mus musculus	58-64
16492670-8	2006	In vivo recruitment of endogenous CAR to the promoters of Cyp7a1 and Pepck was detected in mouse liver after phenobarbital treatment, whereas association of HNF-4 and coactivators, GRIP-1, p300, and PGC-1alpha, with these promoters was significantly decreased.	Phenobarbital	109-122	phosphoenolpyruvate carboxykinase 1, cytosolic	Mus musculus	69-74
16492670-7	2006	Treatment of mice with phenobarbital or TCPOBOP resulted in decreased hepatic mRNA levels of the reported genes down-regulated by CAR, including Cyp7a1 and Pepck.	Phenobarbital	23-36	cytochrome P450, family 7, subfamily a, polypeptide 1	Mus musculus	145-151
16492670-7	2006	Treatment of mice with phenobarbital or TCPOBOP resulted in decreased hepatic mRNA levels of the reported genes down-regulated by CAR, including Cyp7a1 and Pepck.	Phenobarbital	23-36	phosphoenolpyruvate carboxykinase 1, cytosolic	Mus musculus	156-161
16749864-7	2006	Similarly, when animals were cotransfected with the pCMX-CAR plasmid, phenobarbital and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene enhanced luciferase gene expression by 10- and 57-fold, respectively.	Phenobarbital	70-83	nuclear receptor subfamily 1, group I, member 3	Mus musculus	57-60
16635107-7	2006	The CYP2A activity was significantly increased by exposure to phenobarbital, an indirect activator of constitutive androstane receptor, and the human constitutive androstane receptor-ligand CITCO.	Phenobarbital	62-75	cytochrome P450 family 2 subfamily A member 13	Homo sapiens	4-9
16635107-7	2006	The CYP2A activity was significantly increased by exposure to phenobarbital, an indirect activator of constitutive androstane receptor, and the human constitutive androstane receptor-ligand CITCO.	Phenobarbital	62-75	nuclear receptor subfamily 1 group I member 3	Homo sapiens	102-134
21783661-5	2006	Phenobarbital, an inducer of hepatic UGT1A1, only slightly increased BPD UGT activity, whereas UGT1A7 inducers more potently increased the activity.	Phenobarbital	0-13	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	37-43
16449384-2	2006	TSO is considered a phenobarbital-like compound because it induces Cyp2B mRNA expression in liver.	Phenobarbital	20-33	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	67-72
16488578-5	2006	In addition, expression of canalicular transporters in HepaRG cells was found to be up-regulated by known inducers of transporters such as rifampicin, phenobarbital and chenodeoxycholate acting on P-glycoprotein, MRP2 and BSEP, respectively.	Phenobarbital	151-164	ATP binding cassette subfamily B member 1	Homo sapiens	197-211
16488578-5	2006	In addition, expression of canalicular transporters in HepaRG cells was found to be up-regulated by known inducers of transporters such as rifampicin, phenobarbital and chenodeoxycholate acting on P-glycoprotein, MRP2 and BSEP, respectively.	Phenobarbital	151-164	ATP binding cassette subfamily C member 2	Homo sapiens	213-217
16488578-5	2006	In addition, expression of canalicular transporters in HepaRG cells was found to be up-regulated by known inducers of transporters such as rifampicin, phenobarbital and chenodeoxycholate acting on P-glycoprotein, MRP2 and BSEP, respectively.	Phenobarbital	151-164	ATP binding cassette subfamily B member 11	Homo sapiens	222-226
16724577-4	2006	METHODS: Effects of CSA and TAC were examined on CYP mediated oxidase functions by stimulated lipid peroxidation (LPO), H2O2 production, and lucigenin (LC) or luminol (LM) amplified chemiluminescence (CL) in liver microsomes of either untreated rats or of rats treated with beta-naphthoflavone (BNF), phenobarbital (PB) or dexamethasone (DEX) and in human liver microsomes.	Phenobarbital	301-314	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	49-52
16724577-4	2006	METHODS: Effects of CSA and TAC were examined on CYP mediated oxidase functions by stimulated lipid peroxidation (LPO), H2O2 production, and lucigenin (LC) or luminol (LM) amplified chemiluminescence (CL) in liver microsomes of either untreated rats or of rats treated with beta-naphthoflavone (BNF), phenobarbital (PB) or dexamethasone (DEX) and in human liver microsomes.	Phenobarbital	316-318	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	49-52
16421288-9	2006	Cotreatment of animals with PB and E(2) increased activities of NAD(P)H:quinone oxidoreductase and glutathione S-transferase to a greater extent than either compound alone.	Phenobarbital	28-30	hematopoietic prostaglandin D synthase	Rattus norvegicus	99-124
16839222-8	2006	In conclusion, PB at high dose enhances DEN-induced hepatocarcinogenesis in TGF-alpha transgenic mice, but low doses lack any significant effects.	Phenobarbital	15-17	transforming growth factor alpha	Mus musculus	76-85
16260000-6	2006	The MEIs polychlorinated biphenyl (PCB)126, phenobarbital, and PCB99 slightly repressed Mrp5, but no single class of receptor agonists induced or repressed Mrp5.	Phenobarbital	44-57	ATP binding cassette subfamily C member 5	Rattus norvegicus	88-92
16260000-9	2006	Mrp6 was slightly repressed by phenobarbital, dexamethasone, and isoniazid, but no one class of receptor agonists induced or repressed Mrp6, and expression was also unchanged bile-duct ligation.	Phenobarbital	31-44	ATP binding cassette subfamily C member 6	Rattus norvegicus	0-4
16377764-1	2006	The constitutive active receptor (CAR) in mouse primary hepatocytes undergoes okadaic acid (OA)-sensitive nuclear translocation after activation by xenobiotics such as phenobarbital (PB) and 1,4 bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP).	Phenobarbital	168-181	coxsackie virus and adenovirus receptor	Mus musculus	34-37
16597362-4	2006	In rats pretreated with 3-methylcholanthrene and phenobarbital (main inducers of CYP1A1/2 and 2B1/2 in rats, respectively), the CL values were significantly higher (153 and 67.2% increases, respectively).	Phenobarbital	49-62	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	81-99
16449384-3	2006	Phenobarbital increases Cyp2B expression in liver via activation of the constitutive androstane receptor (CAR).	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	24-29
16449384-3	2006	Phenobarbital increases Cyp2B expression in liver via activation of the constitutive androstane receptor (CAR).	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	72-104
16449384-3	2006	Phenobarbital increases Cyp2B expression in liver via activation of the constitutive androstane receptor (CAR).	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	106-109
16377764-1	2006	The constitutive active receptor (CAR) in mouse primary hepatocytes undergoes okadaic acid (OA)-sensitive nuclear translocation after activation by xenobiotics such as phenobarbital (PB) and 1,4 bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP).	Phenobarbital	183-185	coxsackie virus and adenovirus receptor	Mus musculus	34-37
16487217-4	2006	Carbamazepine, phenytoin, phenobarbital and primidone induce many cytochrome P450 (CYP) and glucuronyl transferase (GT) enzymes, and can reduce drastically the serum concentration of associated drugs which are substrates of the same enzymes.	Phenobarbital	26-39	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	66-81
16487217-4	2006	Carbamazepine, phenytoin, phenobarbital and primidone induce many cytochrome P450 (CYP) and glucuronyl transferase (GT) enzymes, and can reduce drastically the serum concentration of associated drugs which are substrates of the same enzymes.	Phenobarbital	26-39	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	83-86
16291874-5	2006	CYP3A4 was markedly elevated by the xenobiotic receptor activator phenobarbital in both male and female livers, demonstrating drug induction of the CYP3A4 transgene in this mouse model.	Phenobarbital	66-79	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
16291874-5	2006	CYP3A4 was markedly elevated by the xenobiotic receptor activator phenobarbital in both male and female livers, demonstrating drug induction of the CYP3A4 transgene in this mouse model.	Phenobarbital	66-79	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	148-154
16777703-7	2006	Interestingly, pretreatment with PB prior to itraconazole reduced the ALT and gamma-GT activities and the liver weight of rats.	Phenobarbital	33-35	gamma-glutamyltransferase 1	Rattus norvegicus	78-86
16525862-7	2006	The CYP2C11 activity was rapidly reduced by PB treatment.	Phenobarbital	44-46	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	4-11
16479536-6	2006	Tagging technology is shown to supersede conventional methods for P450 profiling in terms of discriminatory power and throughput, exemplified by the simultaneous detection of distinct induction profiles for cyp2c subfamily members in response to phenobarbitone: cyp2c29 expression, but not cyp2c40 or cyp2c50, was induced threefold by treatment.	Phenobarbital	246-260	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	207-212
16424820-0	2006	Study of the genetic determinants of UGT1A1 inducibility by phenobarbital in cultured human hepatocytes.	Phenobarbital	60-73	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	37-43
16424820-1	2006	UGT1A1 is induced by phenobarbital.	Phenobarbital	21-34	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
16424820-6	2006	Significant induction of UGT1A1 catalytic activity was observed in 82% and 100% of the cultures treated with phenobarbital for 2 days (median fold-induction = 1.6, range 1.3-2.8; n = 28) and 6 days (median fold-induction = 2.8, range 1.6-6.4; n = 16), respectively.	Phenobarbital	109-122	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	25-31
16354159-10	2006	Human CYP 1A1 and 2Cs mRNAs were induced 3-fold after 48 h of treatment with phenobarbital.	Phenobarbital	77-90	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	6-19
16154717-1	2006	Phenobarbital (PB) alters expression of numerous hepatic genes, including genes of cytochrome P450 2B1 and 2B2 (CYP2B).	Phenobarbital	0-13	cytochrome P450 2B1	Rattus norvegicus	83-110
16154717-1	2006	Phenobarbital (PB) alters expression of numerous hepatic genes, including genes of cytochrome P450 2B1 and 2B2 (CYP2B).	Phenobarbital	15-17	cytochrome P450 2B1	Rattus norvegicus	83-110
16154717-4	2006	We showed that PB induced an early, dose-dependent activation of ERK (extracellular signal-regulated kinase), JNK (c-Jun N-terminal kinase) and p38 MAPKs.	Phenobarbital	15-17	Eph receptor B1	Rattus norvegicus	65-68
16154717-4	2006	We showed that PB induced an early, dose-dependent activation of ERK (extracellular signal-regulated kinase), JNK (c-Jun N-terminal kinase) and p38 MAPKs.	Phenobarbital	15-17	Eph receptor B1	Rattus norvegicus	70-107
16154717-4	2006	We showed that PB induced an early, dose-dependent activation of ERK (extracellular signal-regulated kinase), JNK (c-Jun N-terminal kinase) and p38 MAPKs.	Phenobarbital	15-17	mitogen-activated protein kinase 8	Rattus norvegicus	110-113
16154717-4	2006	We showed that PB induced an early, dose-dependent activation of ERK (extracellular signal-regulated kinase), JNK (c-Jun N-terminal kinase) and p38 MAPKs.	Phenobarbital	15-17	mitogen-activated protein kinase 8	Rattus norvegicus	115-138
16154717-4	2006	We showed that PB induced an early, dose-dependent activation of ERK (extracellular signal-regulated kinase), JNK (c-Jun N-terminal kinase) and p38 MAPKs.	Phenobarbital	15-17	mitogen activated protein kinase 14	Rattus norvegicus	144-147
32288695-6	2006	Levels of ACE2 were surprisingly higher than ACE, which may reflect preferential targeting of the enzyme to the luminal surface of the renal epithelium.	Phenobarbital	112-119	angiotensin converting enzyme 2	Homo sapiens	10-14
32288695-6	2006	Levels of ACE2 were surprisingly higher than ACE, which may reflect preferential targeting of the enzyme to the luminal surface of the renal epithelium.	Phenobarbital	112-119	angiotensin I converting enzyme	Homo sapiens	10-13
16615094-5	2006	PB treatment, but not RIF treatment, caused maximal induction of CYP2B11 mRNA (149-fold) after 48 h of treatment.	Phenobarbital	0-2	cytochrome P450 2B11	Canis lupus familiaris	65-72
16684649-0	2006	Phenobarbital confers its diverse effects by activating the orphan nuclear receptor car.	Phenobarbital	0-13	CXADR pseudogene 1	Homo sapiens	84-87
16615094-6	2006	CYP3A12 and CYP3A26 mRNA levels were increased maximally after 72 h of treatment with PB and RIF (CYP3A12, 35-fold and 18-fold, and CYP3A26, 72-fold and 22-fold with PB and RIF treatment, respectively).	Phenobarbital	86-88	cytochrome P450 3A12	Canis lupus familiaris	0-7
16684649-3	2006	Upon activation by PB and numerous PB-type inducers, the nuclear receptor CAR mediates those pleiotropic actions by regulating various hepatic genes, utilizing multiple regulatory mechanisms.	Phenobarbital	19-21	CXADR pseudogene 1	Homo sapiens	74-77
16615094-6	2006	CYP3A12 and CYP3A26 mRNA levels were increased maximally after 72 h of treatment with PB and RIF (CYP3A12, 35-fold and 18-fold, and CYP3A26, 72-fold and 22-fold with PB and RIF treatment, respectively).	Phenobarbital	86-88	cytochrome P450 3A26	Canis lupus familiaris	12-19
16615094-6	2006	CYP3A12 and CYP3A26 mRNA levels were increased maximally after 72 h of treatment with PB and RIF (CYP3A12, 35-fold and 18-fold, and CYP3A26, 72-fold and 22-fold with PB and RIF treatment, respectively).	Phenobarbital	86-88	cytochrome P450 3A12	Canis lupus familiaris	98-105
16615094-6	2006	CYP3A12 and CYP3A26 mRNA levels were increased maximally after 72 h of treatment with PB and RIF (CYP3A12, 35-fold and 18-fold, and CYP3A26, 72-fold and 22-fold with PB and RIF treatment, respectively).	Phenobarbital	86-88	cytochrome P450 3A26	Canis lupus familiaris	132-139
16615094-6	2006	CYP3A12 and CYP3A26 mRNA levels were increased maximally after 72 h of treatment with PB and RIF (CYP3A12, 35-fold and 18-fold, and CYP3A26, 72-fold and 22-fold with PB and RIF treatment, respectively).	Phenobarbital	166-168	cytochrome P450 3A12	Canis lupus familiaris	0-7
16615094-6	2006	CYP3A12 and CYP3A26 mRNA levels were increased maximally after 72 h of treatment with PB and RIF (CYP3A12, 35-fold and 18-fold, and CYP3A26, 72-fold and 22-fold with PB and RIF treatment, respectively).	Phenobarbital	166-168	cytochrome P450 3A26	Canis lupus familiaris	12-19
16615094-6	2006	CYP3A12 and CYP3A26 mRNA levels were increased maximally after 72 h of treatment with PB and RIF (CYP3A12, 35-fold and 18-fold, and CYP3A26, 72-fold and 22-fold with PB and RIF treatment, respectively).	Phenobarbital	166-168	cytochrome P450 3A12	Canis lupus familiaris	98-105
16615094-6	2006	CYP3A12 and CYP3A26 mRNA levels were increased maximally after 72 h of treatment with PB and RIF (CYP3A12, 35-fold and 18-fold, and CYP3A26, 72-fold and 22-fold with PB and RIF treatment, respectively).	Phenobarbital	166-168	cytochrome P450 3A26	Canis lupus familiaris	132-139
16153763-0	2005	CAR expression and inducibility of CYP2B genes in liver of rats treated with PB-like inducers.	Phenobarbital	77-79	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	0-3
16326433-4	2005	Among others, phenobarbital (PB)-induced microsomes produced the metabolites paraoxon and p-nitrophenol to the greatest extent, indicating the involvement of CYP 2B in parathion metabolism.	Phenobarbital	14-27	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	158-164
16326433-4	2005	Among others, phenobarbital (PB)-induced microsomes produced the metabolites paraoxon and p-nitrophenol to the greatest extent, indicating the involvement of CYP 2B in parathion metabolism.	Phenobarbital	29-31	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	158-164
16033334-4	2005	We investigated the effects on the avian ALAS-1 gene promoter of a phenobarbital-like chemical, Glut (glutethimide), and a haem synthesis inhibitor, DHA (4,6-dioxoheptanoic acid), using a reporter gene assay in transiently transfected LMH (Leghorn male hepatoma) hepatoma cells.	Phenobarbital	67-80	5'-aminolevulinate synthase 1	Gallus gallus	41-47
16049124-5	2005	Furthermore, significant decrease in the activity of hepatic type I iodothyronine deiodinase, which mediates the deiodination of T4 and T3, by PB treatment was observed in both Wistar and Gunn rats.	Phenobarbital	143-145	iodothyronine deiodinase 1	Rattus norvegicus	61-92
16615094-3	2006	The purpose of this study was (1) to determine the temporal kinetics of drug-induced changes in canine CYP1A, CYP2B, and CYP3A mRNA and enzymatic activity, and (2) to characterize concentration-response relationships for CYP1A2, CYP2B11, and CYP3A12 using primary cultures of canine hepatocytes treated with beta-naphthoflavone (BNF), phenobarbital (PB), and rifampin (RIF), respectively.	Phenobarbital	335-348	cytochrome P450 family 1 subfamily A member 2	Canis lupus familiaris	221-227
16615094-3	2006	The purpose of this study was (1) to determine the temporal kinetics of drug-induced changes in canine CYP1A, CYP2B, and CYP3A mRNA and enzymatic activity, and (2) to characterize concentration-response relationships for CYP1A2, CYP2B11, and CYP3A12 using primary cultures of canine hepatocytes treated with beta-naphthoflavone (BNF), phenobarbital (PB), and rifampin (RIF), respectively.	Phenobarbital	350-352	cytochrome P450 family 1 subfamily A member 2	Canis lupus familiaris	221-227
16310787-2	2005	Upon activation by various drugs such as phenobarbital (PB), CAR translocates from the cytoplasm into the nucleus to regulate the genes that encode enzymes and proteins involved in hepatic metabolism.	Phenobarbital	41-54	nuclear receptor subfamily 1, group I, member 3	Mus musculus	61-64
16310787-2	2005	Upon activation by various drugs such as phenobarbital (PB), CAR translocates from the cytoplasm into the nucleus to regulate the genes that encode enzymes and proteins involved in hepatic metabolism.	Phenobarbital	56-58	nuclear receptor subfamily 1, group I, member 3	Mus musculus	61-64
16310787-4	2005	Levels of the cell membrane CAR increased after PB treatment.	Phenobarbital	48-50	nuclear receptor subfamily 1, group I, member 3	Mus musculus	28-31
16310787-6	2005	Thus, CAR undergoes PB-induced translocation to the cell membrane, indicating that CAR may exert a non-genomic action.	Phenobarbital	20-22	nuclear receptor subfamily 1, group I, member 3	Mus musculus	6-9
16310787-6	2005	Thus, CAR undergoes PB-induced translocation to the cell membrane, indicating that CAR may exert a non-genomic action.	Phenobarbital	20-22	nuclear receptor subfamily 1, group I, member 3	Mus musculus	83-86
16153763-1	2005	The expression of the CAR gene and inducibility of CYP2B protein in the liver of male Wistar rats treated with phenobarbital (PB) and triphenyldioxane (TPD) were investigated.	Phenobarbital	111-124	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	22-25
16153763-1	2005	The expression of the CAR gene and inducibility of CYP2B protein in the liver of male Wistar rats treated with phenobarbital (PB) and triphenyldioxane (TPD) were investigated.	Phenobarbital	126-128	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	22-25
16135659-7	2005	All 23 single assays were validated by assessing the effects (induction or repression) of known inducers (ethanol, 3-methylcholanthrene, rifampicin, dexamethasone, phenobarbital) on P450 expression in human primary hepatocytes.	Phenobarbital	164-177	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	182-186
15926192-1	2005	In order to find what types of hepatic microsomal cytochrome P450 (CYP) isozymes are involved in the metabolism of DA-8159 and in the formation of DA-8164 in rats, enzyme inducers, such as dexamethasone, phenobarbital, 3-methylcholanthrene and isoniazid, and enzyme inhibitors, such as troleandomycin and quinine, were pretreated in rats.	Phenobarbital	204-217	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	50-65
15885732-1	2005	Previously we reported a tendency for reduction of the development of glutathione-S-transferase placental form (GST-P) positive foci, recognized as preneoplastic changes in rat liver, by a low dose of 1,1-bis(p-chlorophenyl)-2,2,2-trichloroethane (DDT), which belongs to the same group of hepatic cytochrome P-450 inducers as phenobarbital and is itself a non-genotoxic hepatocarcinogen.	Phenobarbital	326-339	glutathione S-transferase pi 1	Rattus norvegicus	70-117
16203246-6	2005	PB induced hepatic uridine diphosphate-glucuronyltransferase (UDPGT) activity almost 2-fold, whereas PTU reduced hepatic 5 -deiodinase I (5 -DI) activity to &lt; 10% of control in support of previous reports regarding the mechanism of action of each chemical.	Phenobarbital	0-2	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	19-60
16203246-6	2005	PB induced hepatic uridine diphosphate-glucuronyltransferase (UDPGT) activity almost 2-fold, whereas PTU reduced hepatic 5 -deiodinase I (5 -DI) activity to &lt; 10% of control in support of previous reports regarding the mechanism of action of each chemical.	Phenobarbital	0-2	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	62-67
16239972-4	2005	P-glycoprotein (Pgp) is highly expressed on the luminal surface of brain capillary endothelial cells and contributes to the BBB.	Phenobarbital	48-55	phosphoglycolate phosphatase	Mus musculus	0-14
16239972-4	2005	P-glycoprotein (Pgp) is highly expressed on the luminal surface of brain capillary endothelial cells and contributes to the BBB.	Phenobarbital	48-55	phosphoglycolate phosphatase	Mus musculus	16-19
15926192-1	2005	In order to find what types of hepatic microsomal cytochrome P450 (CYP) isozymes are involved in the metabolism of DA-8159 and in the formation of DA-8164 in rats, enzyme inducers, such as dexamethasone, phenobarbital, 3-methylcholanthrene and isoniazid, and enzyme inhibitors, such as troleandomycin and quinine, were pretreated in rats.	Phenobarbital	204-217	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	67-70
15919853-8	2005	CAR activators [phenobarbital, 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene, and diallyl sulfide] decreased Oatp1a1 mRNA expression.	Phenobarbital	16-29	nuclear receptor subfamily 1, group I, member 3	Mus musculus	0-3
15919853-8	2005	CAR activators [phenobarbital, 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene, and diallyl sulfide] decreased Oatp1a1 mRNA expression.	Phenobarbital	16-29	solute carrier organic anion transporter family, member 1a1	Mus musculus	106-113
16125621-6	2005	RESULTS: Exposure of liver slices to the known CYP2B inducers phenobarbital, benzoyl-pyridine, cabarmazepine, metyrapone, RU486 and dexamethasone caused elevation of CYP2B1/2 expression 10- to 40-fold compared to the control values.	Phenobarbital	62-75	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	166-172
16276979-10	2005	These results indicate that CMT inhibits the OMP metabolism due to both decreased hepatic blood flow and inhibited enzyme activity of CYP2C19 and 3A4 and that PB increases the OMP metabolism due to stimulation of the liver blood flow and/or bile flow, due not to induction of the enzyme activity of CYP3A4.	Phenobarbital	159-161	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	299-305
15930522-0	2005	LXR deficiency and cholesterol feeding affect the expression and phenobarbital-mediated induction of cytochromes P450 in mouse liver.	Phenobarbital	65-78	nuclear receptor subfamily 1, group H, member 2	Mus musculus	0-3
16259607-3	2005	In general, the optimal heat shock exposure time was between 2 and 3 h. BROD activity (induced by sodium phenobarbital) increased approximately 6-fold in hepatocytes heat shocked for 3 h in comparison with hepatocytes maintained at 37 degrees C. EROD activity (induced by 3-methylcholanthrene) increased 2-fold on exposure to heat shock for 2 h. The expression of inducible heat shock proteins Hsp70 and Hsp32 was verified by Western immunoblot analyses.	Phenobarbital	98-118	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	394-399
16259607-3	2005	In general, the optimal heat shock exposure time was between 2 and 3 h. BROD activity (induced by sodium phenobarbital) increased approximately 6-fold in hepatocytes heat shocked for 3 h in comparison with hepatocytes maintained at 37 degrees C. EROD activity (induced by 3-methylcholanthrene) increased 2-fold on exposure to heat shock for 2 h. The expression of inducible heat shock proteins Hsp70 and Hsp32 was verified by Western immunoblot analyses.	Phenobarbital	98-118	heme oxygenase 1	Rattus norvegicus	404-409
15933229-6	2005	PB or PH also inhibited APAP glucuronidation in rat and human liver microsomes and expressed human UGT1A6, 1A9, and 2B15.	Phenobarbital	0-2	UDP glucuronosyltransferase family 1 member A6	Homo sapiens	99-105
16109766-3	2005	Here, we report that targeted deletion of PBP in liver parenchymal cells (PBP(Liv-/-)) results in the abrogation of hypertrophic and hyperplastic influences in liver mediated by constitutive androstane receptor (CAR) ligands phenobarbital (PB) and 1,4-bis-[2-(3,5-dichloropyridyloxy)]benzene, and of acetaminophen-induced hepatotoxicity.	Phenobarbital	225-238	mediator complex subunit 1	Mus musculus	42-45
16109766-3	2005	Here, we report that targeted deletion of PBP in liver parenchymal cells (PBP(Liv-/-)) results in the abrogation of hypertrophic and hyperplastic influences in liver mediated by constitutive androstane receptor (CAR) ligands phenobarbital (PB) and 1,4-bis-[2-(3,5-dichloropyridyloxy)]benzene, and of acetaminophen-induced hepatotoxicity.	Phenobarbital	225-238	mediator complex subunit 1	Mus musculus	74-77
16109766-3	2005	Here, we report that targeted deletion of PBP in liver parenchymal cells (PBP(Liv-/-)) results in the abrogation of hypertrophic and hyperplastic influences in liver mediated by constitutive androstane receptor (CAR) ligands phenobarbital (PB) and 1,4-bis-[2-(3,5-dichloropyridyloxy)]benzene, and of acetaminophen-induced hepatotoxicity.	Phenobarbital	42-44	mediator complex subunit 1	Mus musculus	74-77
16109766-3	2005	Here, we report that targeted deletion of PBP in liver parenchymal cells (PBP(Liv-/-)) results in the abrogation of hypertrophic and hyperplastic influences in liver mediated by constitutive androstane receptor (CAR) ligands phenobarbital (PB) and 1,4-bis-[2-(3,5-dichloropyridyloxy)]benzene, and of acetaminophen-induced hepatotoxicity.	Phenobarbital	42-44	nuclear receptor subfamily 1, group I, member 3	Mus musculus	178-210
16109766-3	2005	Here, we report that targeted deletion of PBP in liver parenchymal cells (PBP(Liv-/-)) results in the abrogation of hypertrophic and hyperplastic influences in liver mediated by constitutive androstane receptor (CAR) ligands phenobarbital (PB) and 1,4-bis-[2-(3,5-dichloropyridyloxy)]benzene, and of acetaminophen-induced hepatotoxicity.	Phenobarbital	42-44	nuclear receptor subfamily 1, group I, member 3	Mus musculus	212-215
16109766-9	2005	Adenoviral reconstitution of PBP in PBP(Liv-/-) mouse livers restored PB-mediated nuclear translocation of CAR as well as inducibility of CYP1A2, CYP2B10, CYP3A11, and CYP7A1 expression.	Phenobarbital	29-31	mediator complex subunit 1	Mus musculus	36-39
16109766-9	2005	Adenoviral reconstitution of PBP in PBP(Liv-/-) mouse livers restored PB-mediated nuclear translocation of CAR as well as inducibility of CYP1A2, CYP2B10, CYP3A11, and CYP7A1 expression.	Phenobarbital	29-31	nuclear receptor subfamily 1, group I, member 3	Mus musculus	107-110
16109766-9	2005	Adenoviral reconstitution of PBP in PBP(Liv-/-) mouse livers restored PB-mediated nuclear translocation of CAR as well as inducibility of CYP1A2, CYP2B10, CYP3A11, and CYP7A1 expression.	Phenobarbital	29-31	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	138-144
16109766-9	2005	Adenoviral reconstitution of PBP in PBP(Liv-/-) mouse livers restored PB-mediated nuclear translocation of CAR as well as inducibility of CYP1A2, CYP2B10, CYP3A11, and CYP7A1 expression.	Phenobarbital	29-31	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	155-162
16109766-9	2005	Adenoviral reconstitution of PBP in PBP(Liv-/-) mouse livers restored PB-mediated nuclear translocation of CAR as well as inducibility of CYP1A2, CYP2B10, CYP3A11, and CYP7A1 expression.	Phenobarbital	29-31	cytochrome P450, family 7, subfamily a, polypeptide 1	Mus musculus	168-174
16092956-6	2005	METHODS: Antisense in situ hybridization technique was used here to characterize the type(s) of foci in which IGF II mRNA had expressed during the development of hepatocarcinogenesis-induced by diethylnitrosamine and promoted by phenobarbital in rats.	Phenobarbital	229-242	insulin-like growth factor 2	Rattus norvegicus	110-116
16101572-3	2005	CAR is highly expressed in the liver and the small intestine, two key tissues expressing xenobiotic metabolizing enzymes, and mediates the induction of their expression by the widely used antiepileptic drug, phenobarbital (PB) and the potent synthetic inducer 1, 4-bis-(2-(3, 5, -dichloropyridyloxy)) benzene (TCPOBOP).	Phenobarbital	208-221	nuclear receptor subfamily 1 group I member 3	Homo sapiens	0-3
16101572-3	2005	CAR is highly expressed in the liver and the small intestine, two key tissues expressing xenobiotic metabolizing enzymes, and mediates the induction of their expression by the widely used antiepileptic drug, phenobarbital (PB) and the potent synthetic inducer 1, 4-bis-(2-(3, 5, -dichloropyridyloxy)) benzene (TCPOBOP).	Phenobarbital	223-225	nuclear receptor subfamily 1 group I member 3	Homo sapiens	0-3
16101572-5	2005	PB induces its nuclear translocation, which results in increased expression of CAR target genes since, unlike the classical, ligand-dependent nuclear receptors, CAR is an apparently constitutive transactivator.	Phenobarbital	0-2	nuclear receptor subfamily 1 group I member 3	Homo sapiens	79-82
16101572-5	2005	PB induces its nuclear translocation, which results in increased expression of CAR target genes since, unlike the classical, ligand-dependent nuclear receptors, CAR is an apparently constitutive transactivator.	Phenobarbital	0-2	nuclear receptor subfamily 1 group I member 3	Homo sapiens	161-164
23923552-3	2005	Phenobarbitone (PB) treatment elevated CYP activity by about 2.2-folds in controls, while CPF exposure to PB-treated rats did not cause further elevation in CYP levels.	Phenobarbital	0-14	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-42
23923552-3	2005	Phenobarbitone (PB) treatment elevated CYP activity by about 2.2-folds in controls, while CPF exposure to PB-treated rats did not cause further elevation in CYP levels.	Phenobarbital	16-18	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-42
15930522-5	2005	In particular, in vitro data suggest that oxysterols via the liver X receptor (LXR) inhibit phenobarbital (PB)-mediated induction of CYPs.	Phenobarbital	92-105	nuclear receptor subfamily 1, group H, member 2	Mus musculus	61-77
15930522-5	2005	In particular, in vitro data suggest that oxysterols via the liver X receptor (LXR) inhibit phenobarbital (PB)-mediated induction of CYPs.	Phenobarbital	92-105	nuclear receptor subfamily 1, group H, member 2	Mus musculus	79-82
15930522-5	2005	In particular, in vitro data suggest that oxysterols via the liver X receptor (LXR) inhibit phenobarbital (PB)-mediated induction of CYPs.	Phenobarbital	107-109	nuclear receptor subfamily 1, group H, member 2	Mus musculus	61-77
15930522-5	2005	In particular, in vitro data suggest that oxysterols via the liver X receptor (LXR) inhibit phenobarbital (PB)-mediated induction of CYPs.	Phenobarbital	107-109	nuclear receptor subfamily 1, group H, member 2	Mus musculus	79-82
15930522-8	2005	Our results suggest that, in the mouse, liver cholesterol status significantly alters the pattern of expression of Cyp3a11, whereas the absence of LXR leads to an increase in PB-mediated activation of Cyp2b10.	Phenobarbital	175-177	nuclear receptor subfamily 1, group H, member 2	Mus musculus	147-150
15930522-8	2005	Our results suggest that, in the mouse, liver cholesterol status significantly alters the pattern of expression of Cyp3a11, whereas the absence of LXR leads to an increase in PB-mediated activation of Cyp2b10.	Phenobarbital	175-177	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	201-208
15803482-1	2005	A 22-year-old man, with a past history of generalized tonic-clonic seizures treated with phenobarbital, presented with spinocerebellar ataxia.	Phenobarbital	89-102	immunoglobulin kappa variable 3-25 (pseudogene)	Homo sapiens	0-4
15751032-0	2005	Effect of the tumor promoter phenobarbital on the pattern of global gene expression in liver of connexin32-wild-type and connexin32-deficient mice.	Phenobarbital	29-42	gap junction protein, beta 1	Mus musculus	96-106
15751032-5	2005	We have used oligonucleotide microarrays to identify genes differentially modulated in expression by PB in liver of Cx32-wild-type and Cx32-null mice.	Phenobarbital	101-103	gap junction protein, beta 1	Mus musculus	116-120
15751032-5	2005	We have used oligonucleotide microarrays to identify genes differentially modulated in expression by PB in liver of Cx32-wild-type and Cx32-null mice.	Phenobarbital	101-103	gap junction protein, beta 1	Mus musculus	135-139
15751032-9	2005	PB affected the expression of 53 genes, of which 13 code for members of Phase-I/II of drug metabolism, and 12 genes were differentially affected in expression by PB in Cx32-null as compared to Cx32-wild-type mice.	Phenobarbital	162-164	gap junction protein, beta 1	Mus musculus	168-172
15953603-0	2005	Impaired nuclear translocation of CAR in hepatic preneoplastic lesions: association with an attenuated CYP2B induction by phenobarbital.	Phenobarbital	122-135	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	34-37
15953603-1	2005	Phenobarbital (PB) induction of CYP2B, a representative target gene of constitutive androstane receptor (CAR), has been observed to be attenuated in preneoplastic lesions of rat liver; however, molecular basis for this attenuation is poorly understood.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	71-103
15953603-1	2005	Phenobarbital (PB) induction of CYP2B, a representative target gene of constitutive androstane receptor (CAR), has been observed to be attenuated in preneoplastic lesions of rat liver; however, molecular basis for this attenuation is poorly understood.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	105-108
15953603-1	2005	Phenobarbital (PB) induction of CYP2B, a representative target gene of constitutive androstane receptor (CAR), has been observed to be attenuated in preneoplastic lesions of rat liver; however, molecular basis for this attenuation is poorly understood.	Phenobarbital	15-17	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	71-103
15953603-1	2005	Phenobarbital (PB) induction of CYP2B, a representative target gene of constitutive androstane receptor (CAR), has been observed to be attenuated in preneoplastic lesions of rat liver; however, molecular basis for this attenuation is poorly understood.	Phenobarbital	15-17	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	105-108
15953603-2	2005	In this report, we provide evidence indicating that the CAR expressed in the hepatic preneoplastic lesions of rats and mice was resistant to nuclear translocation and transactivation of the PB-responsive enhancer module upon PB treatment.	Phenobarbital	190-192	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	56-59
15802384-5	2005	Among them, HMG-CoA reductase inhibitors (cerivastatin, simvastatin, fluvastatin, and atorvastatin) enhanced the hCAR-mediated transcriptional activation of phenobarbital-responsive enhancer module reporter gene by up to 3-fold.	Phenobarbital	157-170	CXADR Ig-like cell adhesion molecule	Homo sapiens	113-117
15833926-8	2005	Treatment with arsenite in the presence of CYP3A4 inducers, rifampicin (Rif) or phenobarbital, caused major decreases in CYP3A4 mRNA, protein, and activity.	Phenobarbital	80-93	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	43-49
15802384-1	2005	Constitutive active (or androstane) receptor (CAR, NR1I3), a member of the nuclear receptor family, is a major regulator for induction of cytochrome P450 2B (CYP2B) genes by phenobarbital.	Phenobarbital	174-187	CXADR Ig-like cell adhesion molecule	Homo sapiens	46-49
15802384-1	2005	Constitutive active (or androstane) receptor (CAR, NR1I3), a member of the nuclear receptor family, is a major regulator for induction of cytochrome P450 2B (CYP2B) genes by phenobarbital.	Phenobarbital	174-187	nuclear receptor subfamily 1 group I member 3	Homo sapiens	51-56
15802384-1	2005	Constitutive active (or androstane) receptor (CAR, NR1I3), a member of the nuclear receptor family, is a major regulator for induction of cytochrome P450 2B (CYP2B) genes by phenobarbital.	Phenobarbital	174-187	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	138-156
15802384-1	2005	Constitutive active (or androstane) receptor (CAR, NR1I3), a member of the nuclear receptor family, is a major regulator for induction of cytochrome P450 2B (CYP2B) genes by phenobarbital.	Phenobarbital	174-187	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	158-163
15802384-2	2005	Phenobarbital-like inducer, 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene is a potent mouse CAR ligand that has been used to study CAR target genes in mice but does not activate human CAR (hCAR) or rat CAR (rCAR).	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	89-92
15802384-2	2005	Phenobarbital-like inducer, 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene is a potent mouse CAR ligand that has been used to study CAR target genes in mice but does not activate human CAR (hCAR) or rat CAR (rCAR).	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	128-131
15802384-2	2005	Phenobarbital-like inducer, 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene is a potent mouse CAR ligand that has been used to study CAR target genes in mice but does not activate human CAR (hCAR) or rat CAR (rCAR).	Phenobarbital	0-13	CXADR Ig-like cell adhesion molecule	Homo sapiens	128-131
15802384-2	2005	Phenobarbital-like inducer, 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene is a potent mouse CAR ligand that has been used to study CAR target genes in mice but does not activate human CAR (hCAR) or rat CAR (rCAR).	Phenobarbital	0-13	CXADR Ig-like cell adhesion molecule	Homo sapiens	186-190
15802384-2	2005	Phenobarbital-like inducer, 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene is a potent mouse CAR ligand that has been used to study CAR target genes in mice but does not activate human CAR (hCAR) or rat CAR (rCAR).	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	128-131
15833926-8	2005	Treatment with arsenite in the presence of CYP3A4 inducers, rifampicin (Rif) or phenobarbital, caused major decreases in CYP3A4 mRNA, protein, and activity.	Phenobarbital	80-93	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	121-127
15843486-1	2005	Recently, two new classes of reversible inhibitors, the benzbromarones (BZBRs) and the N-3 substituted phenobarbitals (PBs), were used to study the active site characteristics of CYP2C9 and 2C19, respectively.	Phenobarbital	119-122	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	179-185
15833929-8	2005	Mrp3 was also induced by two other CAR activators phenobarbital and diallyl sulfide, two PXR ligands, pregnenalone-16alpha-carbonitrile and spironolactone, and the PPARalpha ligands clofibrate, ciprofibrate, and diethylhexylphthalate.	Phenobarbital	50-63	prolactin family 2, subfamily c, member 4	Mus musculus	0-4
15833929-8	2005	Mrp3 was also induced by two other CAR activators phenobarbital and diallyl sulfide, two PXR ligands, pregnenalone-16alpha-carbonitrile and spironolactone, and the PPARalpha ligands clofibrate, ciprofibrate, and diethylhexylphthalate.	Phenobarbital	50-63	nuclear receptor subfamily 1, group I, member 3	Mus musculus	35-38
15936348-7	2005	In PB-and Dex-treated mouse liver microsomes, the demethylation activity was inhibited by both anti-CYP3A and anti-CYP2B.	Phenobarbital	3-5	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	100-105
15769864-1	2005	The role of heme in the phenobarbital-mediated induction of CYP2B1/2 was reexamined in rat hepatocytes in monolayer culture, acutely depleted of heme by treatment with either 3,5-dicarbethoxy-2,6-dimethyl-4-ethyl-1,4-dihydropyridine (DDEP) or N-methylprotoporphyrins (NMPP).	Phenobarbital	24-37	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	60-66
15936348-7	2005	In PB-and Dex-treated mouse liver microsomes, the demethylation activity was inhibited by both anti-CYP3A and anti-CYP2B.	Phenobarbital	3-5	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	115-120
15936348-12	2005	Both CYP3A and CYP2B were involved in this demethylation in PB- and Dex-treated mice.	Phenobarbital	60-62	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	5-10
15936348-12	2005	Both CYP3A and CYP2B were involved in this demethylation in PB- and Dex-treated mice.	Phenobarbital	60-62	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	15-20
15610065-1	2005	The mouse nuclear receptor CAR (constitutively active receptor) is a transcription factor that is activated by phenobarbital-type inducers such as TCPOBOP {1,4 bis[2-(3,5-dichloropyridyloxy)]benzene} in liver in vivo.	Phenobarbital	111-124	nuclear receptor subfamily 1, group I, member 3	Mus musculus	27-30
15921992-2	2005	The reductase activity was enhanced in liver microsomes of phenobarbital-treated rats, and inhibited by diphenyliodonium chloride, a NADPH-cytochrome P450 reductase (P450 reductase) inhibitor, but was not inhibited by SKF 525-A or carbon monoxide.	Phenobarbital	59-72	cytochrome p450 oxidoreductase	Rattus norvegicus	133-164
15941388-0	2005	Correlation between alterations in nucleosomal organization of LINEs in the promoter of cytochrome P450 2B1/2 gene and induction of CYP 2B1/2B2 mRNA expression by phenobarbitone in rat liver.	Phenobarbital	163-177	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	88-109
15941388-0	2005	Correlation between alterations in nucleosomal organization of LINEs in the promoter of cytochrome P450 2B1/2 gene and induction of CYP 2B1/2B2 mRNA expression by phenobarbitone in rat liver.	Phenobarbital	163-177	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	132-143
15941388-6	2005	Phenobarbitone (PB), a prototype xenobiotic drug, strongly induced CYP 2B1/2 mRNA expression in the rat liver.	Phenobarbital	0-14	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	67-76
15941388-6	2005	Phenobarbitone (PB), a prototype xenobiotic drug, strongly induced CYP 2B1/2 mRNA expression in the rat liver.	Phenobarbital	16-18	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	67-76
15941388-7	2005	3P and 5P LINE sequences showed an alteration in the nucleosomal organization in the CYP 2B1/2 promoter after 2, 4, and 6 h of PB induction, and the promoter was mostly devoid of nucleosomes during the induction.	Phenobarbital	127-129	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	85-92
15946133-8	2005	CYP1A1/2, CYP2B1, CYP3A2, CYP4A1, and CYP2E1 were induced by the addition of 3-methylcholanthrene, phenobarbital, pregnenolone-16alpha-carbonitrile, clofibric acid, and ethanol, respectively.	Phenobarbital	99-112	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	0-6
15946133-8	2005	CYP1A1/2, CYP2B1, CYP3A2, CYP4A1, and CYP2E1 were induced by the addition of 3-methylcholanthrene, phenobarbital, pregnenolone-16alpha-carbonitrile, clofibric acid, and ethanol, respectively.	Phenobarbital	99-112	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	10-16
15946133-8	2005	CYP1A1/2, CYP2B1, CYP3A2, CYP4A1, and CYP2E1 were induced by the addition of 3-methylcholanthrene, phenobarbital, pregnenolone-16alpha-carbonitrile, clofibric acid, and ethanol, respectively.	Phenobarbital	99-112	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	18-24
15946133-8	2005	CYP1A1/2, CYP2B1, CYP3A2, CYP4A1, and CYP2E1 were induced by the addition of 3-methylcholanthrene, phenobarbital, pregnenolone-16alpha-carbonitrile, clofibric acid, and ethanol, respectively.	Phenobarbital	99-112	cytochrome P450, family 4, subfamily a, polypeptide 1	Rattus norvegicus	26-32
15946133-8	2005	CYP1A1/2, CYP2B1, CYP3A2, CYP4A1, and CYP2E1 were induced by the addition of 3-methylcholanthrene, phenobarbital, pregnenolone-16alpha-carbonitrile, clofibric acid, and ethanol, respectively.	Phenobarbital	99-112	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	38-44
15864128-2	2005	MRP2 is expressed on the luminal side of hepatocytes and renal proximal tubular cells, indicating an important role in drug elimination.	Phenobarbital	25-32	ATP binding cassette subfamily C member 2	Homo sapiens	0-4
16012075-8	2005	Phenobarbital-mediated responsiveness of cytochrome P450 2B6, a potential indicator of hepatocyte differentiation status, was markedly higher in overlaid relative to non-overlaid hepatocytes.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	41-60
15713442-0	2005	Induction of cytochrome P450 isozymes by phenobarbital in pregnant rat and fetal livers and placenta.	Phenobarbital	41-54	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-28
15713442-4	2005	In this study, we examined the changes in the expression of CYP proteins in the pregnant rat and fetal livers and placenta after treatment with phenobarbital (PB), one of the antiepileptic drugs which is well known to induce several phase I and phase II drug metabolizing enzymes in the liver.	Phenobarbital	144-157	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	60-63
15713442-4	2005	In this study, we examined the changes in the expression of CYP proteins in the pregnant rat and fetal livers and placenta after treatment with phenobarbital (PB), one of the antiepileptic drugs which is well known to induce several phase I and phase II drug metabolizing enzymes in the liver.	Phenobarbital	159-161	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	60-63
15713442-8	2005	Western blot analysis revealed that CYP3A1 protein was significantly induced, CYP2B1 protein was detected, and CYP2D1 protein was significantly decreased in the dam"s liver after PB-treatment.	Phenobarbital	179-181	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	36-42
15713442-8	2005	Western blot analysis revealed that CYP3A1 protein was significantly induced, CYP2B1 protein was detected, and CYP2D1 protein was significantly decreased in the dam"s liver after PB-treatment.	Phenobarbital	179-181	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	78-84
15713442-8	2005	Western blot analysis revealed that CYP3A1 protein was significantly induced, CYP2B1 protein was detected, and CYP2D1 protein was significantly decreased in the dam"s liver after PB-treatment.	Phenobarbital	179-181	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	111-117
15713442-11	2005	In the fetal liver, CYP3A1 and CYP2C6 proteins were significantly induced after the PB-treatment, but their immunostainability was not prominent.	Phenobarbital	84-86	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	20-26
15713442-11	2005	In the fetal liver, CYP3A1 and CYP2C6 proteins were significantly induced after the PB-treatment, but their immunostainability was not prominent.	Phenobarbital	84-86	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	31-37
15703377-5	2005	To further validate S. cerevisiae as a model for exploring mammalian P450 turnover, the degradation of phenobarbital-inducible liver CYP2B1, an enzyme reportedly degraded via the rat hepatic autophagic-lysosomal pathway, was examined in a yeast strain (pep4delta) deficient in vacuolar degradation and its isogenic wild-type control (PEP4).	Phenobarbital	103-116	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	69-73
15703377-5	2005	To further validate S. cerevisiae as a model for exploring mammalian P450 turnover, the degradation of phenobarbital-inducible liver CYP2B1, an enzyme reportedly degraded via the rat hepatic autophagic-lysosomal pathway, was examined in a yeast strain (pep4delta) deficient in vacuolar degradation and its isogenic wild-type control (PEP4).	Phenobarbital	103-116	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	133-139
15703377-5	2005	To further validate S. cerevisiae as a model for exploring mammalian P450 turnover, the degradation of phenobarbital-inducible liver CYP2B1, an enzyme reportedly degraded via the rat hepatic autophagic-lysosomal pathway, was examined in a yeast strain (pep4delta) deficient in vacuolar degradation and its isogenic wild-type control (PEP4).	Phenobarbital	103-116	proteinase A	Saccharomyces cerevisiae S288C	334-338
15610065-1	2005	The mouse nuclear receptor CAR (constitutively active receptor) is a transcription factor that is activated by phenobarbital-type inducers such as TCPOBOP {1,4 bis[2-(3,5-dichloropyridyloxy)]benzene} in liver in vivo.	Phenobarbital	111-124	nuclear receptor subfamily 1, group I, member 3	Mus musculus	32-62
15656786-0	2005	The CYP2B2 phenobarbital response unit contains binding sites for hepatocyte nuclear factor 4, PBX-PREP1, the thyroid hormone receptor beta and the liver X receptor.	Phenobarbital	11-24	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	4-10
15656786-0	2005	The CYP2B2 phenobarbital response unit contains binding sites for hepatocyte nuclear factor 4, PBX-PREP1, the thyroid hormone receptor beta and the liver X receptor.	Phenobarbital	11-24	hepatocyte nuclear factor 4, alpha	Rattus norvegicus	66-93
15656786-0	2005	The CYP2B2 phenobarbital response unit contains binding sites for hepatocyte nuclear factor 4, PBX-PREP1, the thyroid hormone receptor beta and the liver X receptor.	Phenobarbital	11-24	thyroid hormone receptor beta	Rattus norvegicus	110-139
15656786-1	2005	A 163 bp enhancer in the CYP2B2 5" flank confers PB (phenobarbital) inducibility and constitutes a PBRU (PB response unit).	Phenobarbital	49-51	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	25-31
15656786-1	2005	A 163 bp enhancer in the CYP2B2 5" flank confers PB (phenobarbital) inducibility and constitutes a PBRU (PB response unit).	Phenobarbital	53-66	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	25-31
15656786-8	2005	A mutation described previously, GRE1m1, which decreases PB responsiveness, increased the affinity of this site for HNF-4.	Phenobarbital	57-59	hepatocyte nuclear factor 4, alpha	Rattus norvegicus	116-121
15656786-12	2005	This parallels the functional differences in conferring PB responsiveness between NR1 and NR3 on the one hand, and NR2 on the other.	Phenobarbital	56-58	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	82-85
15656786-12	2005	This parallels the functional differences in conferring PB responsiveness between NR1 and NR3 on the one hand, and NR2 on the other.	Phenobarbital	56-58	glutamate ionotropic receptor NMDA type subunit 3A	Rattus norvegicus	90-93
15771689-3	2005	Recently, it was reported that the -3263T &gt; G mutation in the phenobarbital response enhancer module in UGT1A1 was associated with the majority of cases of Gilbert syndrome.	Phenobarbital	65-78	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	107-113
16019954-11	2005	These results suggest that PB-inducible CYP forms, especially guinea pig CYP2B18, rat CYP2B1 and hamster CYP2B, are important in CB187 metabolism and that CB187 metabolism in guinea pigs may proceed via the formation of 3,4- or 3",4"-oxide and subsequent NIH-shift or dechlorination.	Phenobarbital	27-29	cytochrome P450 3A14	Cavia porcellus	40-43
16019954-11	2005	These results suggest that PB-inducible CYP forms, especially guinea pig CYP2B18, rat CYP2B1 and hamster CYP2B, are important in CB187 metabolism and that CB187 metabolism in guinea pigs may proceed via the formation of 3,4- or 3",4"-oxide and subsequent NIH-shift or dechlorination.	Phenobarbital	27-29	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	73-79
15832810-6	2005	Similarly, the steroid family of orphan nuclear receptors, the constitutive androstane receptor (CAR) and pregnane X receptor (PXR), both heterodimerize with the retinoid X receptor (RXR), are shown to transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	301-314	nuclear receptor subfamily 1 group I member 3	Homo sapiens	63-95
15832810-6	2005	Similarly, the steroid family of orphan nuclear receptors, the constitutive androstane receptor (CAR) and pregnane X receptor (PXR), both heterodimerize with the retinoid X receptor (RXR), are shown to transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	301-314	nuclear receptor subfamily 1 group I member 3	Homo sapiens	97-100
15832810-6	2005	Similarly, the steroid family of orphan nuclear receptors, the constitutive androstane receptor (CAR) and pregnane X receptor (PXR), both heterodimerize with the retinoid X receptor (RXR), are shown to transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	301-314	nuclear receptor subfamily 1 group I member 2	Homo sapiens	106-125
15832810-6	2005	Similarly, the steroid family of orphan nuclear receptors, the constitutive androstane receptor (CAR) and pregnane X receptor (PXR), both heterodimerize with the retinoid X receptor (RXR), are shown to transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	301-314	nuclear receptor subfamily 1 group I member 2	Homo sapiens	127-130
15832810-6	2005	Similarly, the steroid family of orphan nuclear receptors, the constitutive androstane receptor (CAR) and pregnane X receptor (PXR), both heterodimerize with the retinoid X receptor (RXR), are shown to transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	301-314	retinoid X receptor alpha	Homo sapiens	162-181
15832810-6	2005	Similarly, the steroid family of orphan nuclear receptors, the constitutive androstane receptor (CAR) and pregnane X receptor (PXR), both heterodimerize with the retinoid X receptor (RXR), are shown to transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	301-314	retinoid X receptor alpha	Homo sapiens	183-186
15832810-6	2005	Similarly, the steroid family of orphan nuclear receptors, the constitutive androstane receptor (CAR) and pregnane X receptor (PXR), both heterodimerize with the retinoid X receptor (RXR), are shown to transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	301-314	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	256-261
15832810-6	2005	Similarly, the steroid family of orphan nuclear receptors, the constitutive androstane receptor (CAR) and pregnane X receptor (PXR), both heterodimerize with the retinoid X receptor (RXR), are shown to transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	301-314	nuclear receptor subfamily 1 group I member 3	Homo sapiens	331-334
15832810-6	2005	Similarly, the steroid family of orphan nuclear receptors, the constitutive androstane receptor (CAR) and pregnane X receptor (PXR), both heterodimerize with the retinoid X receptor (RXR), are shown to transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	301-314	nuclear receptor subfamily 1 group I member 2	Homo sapiens	383-386
15564320-2	2005	The xenobiotic receptor constitutive androstane receptor (CAR) (NR1I3) mediates the well-studied induction of CYP2B genes and other drug-metabolizing enzymes by phenobarbital (PB), an antiepileptic drug that has been shown to alter thyroid hormone (TH) levels.	Phenobarbital	161-174	nuclear receptor subfamily 1, group I, member 3	Mus musculus	24-56
15564320-2	2005	The xenobiotic receptor constitutive androstane receptor (CAR) (NR1I3) mediates the well-studied induction of CYP2B genes and other drug-metabolizing enzymes by phenobarbital (PB), an antiepileptic drug that has been shown to alter thyroid hormone (TH) levels.	Phenobarbital	161-174	nuclear receptor subfamily 1, group I, member 3	Mus musculus	58-61
15564320-2	2005	The xenobiotic receptor constitutive androstane receptor (CAR) (NR1I3) mediates the well-studied induction of CYP2B genes and other drug-metabolizing enzymes by phenobarbital (PB), an antiepileptic drug that has been shown to alter thyroid hormone (TH) levels.	Phenobarbital	161-174	nuclear receptor subfamily 1, group I, member 3	Mus musculus	64-69
15564320-2	2005	The xenobiotic receptor constitutive androstane receptor (CAR) (NR1I3) mediates the well-studied induction of CYP2B genes and other drug-metabolizing enzymes by phenobarbital (PB), an antiepileptic drug that has been shown to alter thyroid hormone (TH) levels.	Phenobarbital	176-178	nuclear receptor subfamily 1, group I, member 3	Mus musculus	24-56
15564320-2	2005	The xenobiotic receptor constitutive androstane receptor (CAR) (NR1I3) mediates the well-studied induction of CYP2B genes and other drug-metabolizing enzymes by phenobarbital (PB), an antiepileptic drug that has been shown to alter thyroid hormone (TH) levels.	Phenobarbital	176-178	nuclear receptor subfamily 1, group I, member 3	Mus musculus	58-61
15564320-2	2005	The xenobiotic receptor constitutive androstane receptor (CAR) (NR1I3) mediates the well-studied induction of CYP2B genes and other drug-metabolizing enzymes by phenobarbital (PB), an antiepileptic drug that has been shown to alter thyroid hormone (TH) levels.	Phenobarbital	176-178	nuclear receptor subfamily 1, group I, member 3	Mus musculus	64-69
15564320-3	2005	Here we show that CAR is required for PB-mediated disruption of TH homeostasis and the induction of thyroid follicular cell proliferation.	Phenobarbital	38-40	nuclear receptor subfamily 1, group I, member 3	Mus musculus	18-21
15564320-4	2005	Treatment with PB or the more potent and more effective CAR ligand 1, 4-bis-[2-(3, 5,-dichloropyridyloxy)] benzene resulted in universal induction of thyroid hormone glucuronidation and sulfation pathways in a CAR-dependent manner.	Phenobarbital	15-17	nuclear receptor subfamily 1, group I, member 3	Mus musculus	56-59
15564320-4	2005	Treatment with PB or the more potent and more effective CAR ligand 1, 4-bis-[2-(3, 5,-dichloropyridyloxy)] benzene resulted in universal induction of thyroid hormone glucuronidation and sulfation pathways in a CAR-dependent manner.	Phenobarbital	15-17	nuclear receptor subfamily 1, group I, member 3	Mus musculus	210-213
15634872-5	2005	At 2 yr of age, in agreement with an overexpression of hepatic CYP2C6 and CYP2C7, both in vitro and in vivo drug metabolism was more rapid in the phenobarbital-imprinted male and female animals.	Phenobarbital	146-159	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	63-69
15634872-5	2005	At 2 yr of age, in agreement with an overexpression of hepatic CYP2C6 and CYP2C7, both in vitro and in vivo drug metabolism was more rapid in the phenobarbital-imprinted male and female animals.	Phenobarbital	146-159	cytochrome P450, family 2, subfamily c, polypeptide 7	Rattus norvegicus	74-80
15744758-2	2005	Hepatic cytochrome P450 1A1 and principally P450 2B1/2 were induced by beta-naphthoflavone and phenobarbital, respectively.	Phenobarbital	95-108	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	8-27
15849716-3	2005	Concentration-dependent changes in UGT1A1 response were evaluated in hepatocyte cultures after treatment with 3-methylchloranthrene, beta-napthoflavone, rifampicin, or phenobarbital.	Phenobarbital	168-181	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	35-41
15666291-8	2005	Purified CYP450 reductase from phenobarbital-treated rabbit or untreated human livers metabolized MGd suggesting involvement of CYP450 reductase.	Phenobarbital	31-44	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	9-15
15666291-8	2005	Purified CYP450 reductase from phenobarbital-treated rabbit or untreated human livers metabolized MGd suggesting involvement of CYP450 reductase.	Phenobarbital	31-44	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	128-134
15557560-2	2005	In a previous article, we described the phenobarbital response activity to a 290-base pair (bp) distal enhancer sequence (-3499/-3210) of the human UGT1A1 gene that is activated by the constitutive androstane receptor (CAR).	Phenobarbital	40-53	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	148-154
15557560-2	2005	In a previous article, we described the phenobarbital response activity to a 290-base pair (bp) distal enhancer sequence (-3499/-3210) of the human UGT1A1 gene that is activated by the constitutive androstane receptor (CAR).	Phenobarbital	40-53	nuclear receptor subfamily 1 group I member 3	Homo sapiens	185-217
15557560-2	2005	In a previous article, we described the phenobarbital response activity to a 290-base pair (bp) distal enhancer sequence (-3499/-3210) of the human UGT1A1 gene that is activated by the constitutive androstane receptor (CAR).	Phenobarbital	40-53	nuclear receptor subfamily 1 group I member 3	Homo sapiens	219-222
15591315-1	2005	Nuclear translocation of constitutive androstane receptor (CAR) is a primary mechanism for the induction of cytochrome P450 genes by phenobarbital (PB).	Phenobarbital	133-146	nuclear receptor subfamily 1 group I member 3	Homo sapiens	25-57
15591315-1	2005	Nuclear translocation of constitutive androstane receptor (CAR) is a primary mechanism for the induction of cytochrome P450 genes by phenobarbital (PB).	Phenobarbital	133-146	nuclear receptor subfamily 1 group I member 3	Homo sapiens	59-62
15591315-1	2005	Nuclear translocation of constitutive androstane receptor (CAR) is a primary mechanism for the induction of cytochrome P450 genes by phenobarbital (PB).	Phenobarbital	148-150	nuclear receptor subfamily 1 group I member 3	Homo sapiens	25-57
15591315-1	2005	Nuclear translocation of constitutive androstane receptor (CAR) is a primary mechanism for the induction of cytochrome P450 genes by phenobarbital (PB).	Phenobarbital	148-150	nuclear receptor subfamily 1 group I member 3	Homo sapiens	59-62
15591315-2	2005	We have shown that exogenous expression of the p160 coactivator glucocorticoid receptor interacting protein-1 (GRIP1) in hepatocytes in vivo can mediate PB-independent nuclear accumulation of murine CAR (mCAR).	Phenobarbital	153-155	nuclear receptor coactivator 2	Homo sapiens	64-109
15591315-2	2005	We have shown that exogenous expression of the p160 coactivator glucocorticoid receptor interacting protein-1 (GRIP1) in hepatocytes in vivo can mediate PB-independent nuclear accumulation of murine CAR (mCAR).	Phenobarbital	153-155	glutamate receptor interacting protein 1	Mus musculus	111-116
15591315-4	2005	Mutations of the xenobiotic response sequence (XRS), which had been shown to block PB-dependent nuclear translocation of human CAR in mouse hepatocytes in vivo, also blocked GRIP1-mediated nuclear accumulation of mCAR in mouse hepatocytes in vivo and further blocked nuclear localization in cultured HepG2 cells.	Phenobarbital	83-85	nuclear receptor subfamily 1 group I member 3	Homo sapiens	127-130
15591315-4	2005	Mutations of the xenobiotic response sequence (XRS), which had been shown to block PB-dependent nuclear translocation of human CAR in mouse hepatocytes in vivo, also blocked GRIP1-mediated nuclear accumulation of mCAR in mouse hepatocytes in vivo and further blocked nuclear localization in cultured HepG2 cells.	Phenobarbital	83-85	glutamate receptor interacting protein 1	Mus musculus	174-179
15591315-4	2005	Mutations of the xenobiotic response sequence (XRS), which had been shown to block PB-dependent nuclear translocation of human CAR in mouse hepatocytes in vivo, also blocked GRIP1-mediated nuclear accumulation of mCAR in mouse hepatocytes in vivo and further blocked nuclear localization in cultured HepG2 cells.	Phenobarbital	83-85	coxsackie virus and adenovirus receptor	Mus musculus	213-217
15680401-2	2005	Mice deficient in Cx32 demonstrate enhanced liver tumor formation, but are resistant to promotion of hepatocarcinogenesis by the model tumor promoter phenobarbital (PB).	Phenobarbital	150-163	gap junction protein, beta 1	Mus musculus	18-22
15680401-2	2005	Mice deficient in Cx32 demonstrate enhanced liver tumor formation, but are resistant to promotion of hepatocarcinogenesis by the model tumor promoter phenobarbital (PB).	Phenobarbital	165-167	gap junction protein, beta 1	Mus musculus	18-22
15572372-0	2005	AMP-activated protein kinase mediates phenobarbital induction of CYP2B gene expression in hepatocytes and a newly derived human hepatoma cell line.	Phenobarbital	38-51	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	65-70
15572372-9	2005	Expression of a constitutively active form of AMPK mimics the PB induction of CYP2B6 and CYP2B1 gene expression.	Phenobarbital	62-64	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	78-84
15572372-9	2005	Expression of a constitutively active form of AMPK mimics the PB induction of CYP2B6 and CYP2B1 gene expression.	Phenobarbital	62-64	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	89-95
15572372-12	2005	Our data strongly support a role for AMPK in the PB induction of CYP2B gene expression and provide new insights into the regulation of gene expression by barbiturate drugs.	Phenobarbital	49-51	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	65-70
15596261-5	2005	Treatment of rats with okadaic acid (OA), an inhibitor of protein phosphatases PP1 and PP2A, caused considerable decreases in PROD activity during the induction by TPD and PB (8- and 2.5-fold, respectively).	Phenobarbital	172-174	neuropeptide Y receptor Y4	Rattus norvegicus	79-82
15629132-0	2005	Prostaglandin E2 down-regulation of cytochrome P-450 2B1 expression induced by phenobarbital is through EP2 receptor in rat hepatocytes.	Phenobarbital	79-92	cytochrome P450 2B1	Rattus norvegicus	36-56
15629132-3	2005	We showed previously that prostaglandin E(2) (PGE(2)), a fatty acid metabolite, down-regulates cytochrome P-450 2B1 (CYP 2B1) expression induced by phenobarbital.	Phenobarbital	148-161	cytochrome P450 2B1	Rattus norvegicus	95-115
15629132-3	2005	We showed previously that prostaglandin E(2) (PGE(2)), a fatty acid metabolite, down-regulates cytochrome P-450 2B1 (CYP 2B1) expression induced by phenobarbital.	Phenobarbital	148-161	cytochrome P450 2B1	Rattus norvegicus	117-124
15629132-10	2005	These results suggest that EP(2) and the downstream pathways of cAMP and protein kinase A are involved in the down-regulation of CYP 2B1 expression by PGE(2) in the presence of phenobarbital.	Phenobarbital	177-190	cytochrome P450 2B1	Rattus norvegicus	129-136
15563456-1	2005	The constitutive active receptor (CAR) regulates the induction of the cytochrome P450 2B6 (CYP2B6) gene by phenobarbital-type inducers, such as 1,4 bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) via the distal phenobarbital-responsive enhancer module (PBREM, at -1732/-1685 bp).	Phenobarbital	107-120	nuclear receptor subfamily 1, group I, member 3	Mus musculus	34-37
15563456-1	2005	The constitutive active receptor (CAR) regulates the induction of the cytochrome P450 2B6 (CYP2B6) gene by phenobarbital-type inducers, such as 1,4 bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) via the distal phenobarbital-responsive enhancer module (PBREM, at -1732/-1685 bp).	Phenobarbital	107-120	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	70-89
15563456-1	2005	The constitutive active receptor (CAR) regulates the induction of the cytochrome P450 2B6 (CYP2B6) gene by phenobarbital-type inducers, such as 1,4 bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) via the distal phenobarbital-responsive enhancer module (PBREM, at -1732/-1685 bp).	Phenobarbital	107-120	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	91-97
15563456-1	2005	The constitutive active receptor (CAR) regulates the induction of the cytochrome P450 2B6 (CYP2B6) gene by phenobarbital-type inducers, such as 1,4 bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) via the distal phenobarbital-responsive enhancer module (PBREM, at -1732/-1685 bp).	Phenobarbital	212-225	nuclear receptor subfamily 1, group I, member 3	Mus musculus	34-37
15563456-1	2005	The constitutive active receptor (CAR) regulates the induction of the cytochrome P450 2B6 (CYP2B6) gene by phenobarbital-type inducers, such as 1,4 bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) via the distal phenobarbital-responsive enhancer module (PBREM, at -1732/-1685 bp).	Phenobarbital	212-225	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	70-89
15563456-1	2005	The constitutive active receptor (CAR) regulates the induction of the cytochrome P450 2B6 (CYP2B6) gene by phenobarbital-type inducers, such as 1,4 bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) via the distal phenobarbital-responsive enhancer module (PBREM, at -1732/-1685 bp).	Phenobarbital	212-225	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	91-97
15588932-9	2005	PB enhanced CYP2B1 and 3A2 expression, and DEX and PCN increased CYP3A2 immunostaining.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	12-18
15596064-7	2005	Being common to dam"s and fetal livers, the gene expression of Cyp3A1 (CYP3A subfamily) and cytochrome P-450e (CYP2B subfamily) increased in both PCN and PB groups.	Phenobarbital	154-156	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	63-69
15596064-8	2005	In placenta, the expression of Cyp3A1 gene was significantly induced in PB group, and it also showed a tendency to increase in PCN group.	Phenobarbital	72-74	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	31-37
15471898-2	2005	In the mouse, the promotional effect of PB results from a selective stimulation of clonal outgrowth of hepatocytes harboring activating mutations in the beta-catenin (catnb) gene.	Phenobarbital	40-42	catenin (cadherin associated protein), beta 1	Mus musculus	153-173
15881424-5	2005	After 2 weeks phenobarbitone was added to promote the enzymatic activity of UDPGT of the transplanted hepatocytes.	Phenobarbital	14-28	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-81
15881424-10	2005	However, the introduction of phenobarbitone was followed by a drop of tacrolimus level with increase of alanine aminotransferase (ALT) and increase of bilirubin.	Phenobarbital	29-43	glutamic--pyruvic transaminase	Homo sapiens	104-128
15740176-5	2005	The use of the liver enzyme-inducing AEDs phenobarbital, phenytoin and carbamazepine increases serum sex hormone-binding globulin (SHBG) concentrations in both men and women with epilepsy.	Phenobarbital	42-55	sex hormone binding globulin	Homo sapiens	101-129
15740176-5	2005	The use of the liver enzyme-inducing AEDs phenobarbital, phenytoin and carbamazepine increases serum sex hormone-binding globulin (SHBG) concentrations in both men and women with epilepsy.	Phenobarbital	42-55	sex hormone binding globulin	Homo sapiens	131-135
15466162-5	2005	In contrast, results from positive control experiments indicated that phenobarbital increased CYP2B1 mRNA and BROD activity, dexamethasone increased CYP3A23 mRNA, and beta-naphthoflavone increased CYP1A2 mRNA and EROD activity levels.	Phenobarbital	70-83	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	94-100
15747502-9	2005	Some drugs such as anticonvulsants (phenobarbital, phenytoin, and carbamazepine) and halothane are suggested to induce hepatitis with anti-CYP3A and anti-CYP2E1, respectively.	Phenobarbital	36-49	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	139-144
15747502-9	2005	Some drugs such as anticonvulsants (phenobarbital, phenytoin, and carbamazepine) and halothane are suggested to induce hepatitis with anti-CYP3A and anti-CYP2E1, respectively.	Phenobarbital	36-49	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	154-160
16302890-14	2005	In our hands, patients with refractory IGEs may respond to combinations of levetiracetam with valproate, lamotrigine, and phenobarbital, and adverse effects when they occur are usually limited to tiredness.	Phenobarbital	122-135	IGES	Homo sapiens	39-43
16421897-8	2005	Notably, phenobarbital resulted in significant induction of CYP2B1, CYP2B2, CYP2C6, CYP2C13, CYP2E1, CYP3A1, and CYP3A2.	Phenobarbital	9-22	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	60-66
16421897-8	2005	Notably, phenobarbital resulted in significant induction of CYP2B1, CYP2B2, CYP2C6, CYP2C13, CYP2E1, CYP3A1, and CYP3A2.	Phenobarbital	9-22	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	68-74
16421897-8	2005	Notably, phenobarbital resulted in significant induction of CYP2B1, CYP2B2, CYP2C6, CYP2C13, CYP2E1, CYP3A1, and CYP3A2.	Phenobarbital	9-22	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	76-82
16421897-8	2005	Notably, phenobarbital resulted in significant induction of CYP2B1, CYP2B2, CYP2C6, CYP2C13, CYP2E1, CYP3A1, and CYP3A2.	Phenobarbital	9-22	cytochrome P450, family 2, subfamily c, polypeptide 13	Rattus norvegicus	84-91
15849716-7	2005	UGT1A1 was most responsive to the pregnane-X-receptor-agonists rifampicin, ritonavir, and clotrimazole at the mRNA level and, to a lesser extent, the constitutive androstane receptor-activators, phenobarbital and phenytoin.	Phenobarbital	195-208	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
16421897-8	2005	Notably, phenobarbital resulted in significant induction of CYP2B1, CYP2B2, CYP2C6, CYP2C13, CYP2E1, CYP3A1, and CYP3A2.	Phenobarbital	9-22	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	93-99
16421897-8	2005	Notably, phenobarbital resulted in significant induction of CYP2B1, CYP2B2, CYP2C6, CYP2C13, CYP2E1, CYP3A1, and CYP3A2.	Phenobarbital	9-22	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	101-107
16421897-8	2005	Notably, phenobarbital resulted in significant induction of CYP2B1, CYP2B2, CYP2C6, CYP2C13, CYP2E1, CYP3A1, and CYP3A2.	Phenobarbital	9-22	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	113-119
15849716-7	2005	UGT1A1 was most responsive to the pregnane-X-receptor-agonists rifampicin, ritonavir, and clotrimazole at the mRNA level and, to a lesser extent, the constitutive androstane receptor-activators, phenobarbital and phenytoin.	Phenobarbital	195-208	nuclear receptor subfamily 1 group I member 2	Homo sapiens	34-53
15167984-4	2004	Following the administration of phenobarbital (24 mg/egg) on day 21, enzyme activities of ECOD, EROD, ALD, EH and GLUT, but not of GST, were increased by two-fold or higher levels by day 22.	Phenobarbital	32-45	LOW QUALITY PROTEIN: glutathione S-transferase	Meleagris gallopavo	131-134
15496940-2	2005	In our previous studies, we identified deficits in hippocampal muscarinic cholinergic receptor-induced membrane translocation of protein kinase C (PKC)gamma as the likely mechanism responsible for adverse behavioral effects of prenatal phenobarbital exposure.	Phenobarbital	236-249	protein kinase C, gamma	Mus musculus	147-156
15864124-0	2005	Genetic polymorphism in the phenobarbital-responsive enhancer module of the UDP-glucuronosyltransferase 1A1 gene and irinotecan toxicity.	Phenobarbital	28-41	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	76-107
15864124-2	2005	The phenobarbital-responsive enhancer module (PBREM) of the UGT1A1 promoter region has been reportedly associated with the transcriptional activity of the gene.	Phenobarbital	4-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	60-66
20021072-7	2005	In contrast, CYP2B6, the human orthologue of the rodent phenobarbital-inducible P450 2B, is known to be inducible by a range of substances, but our recent studies also show a high degree of genetic polymorphism.	Phenobarbital	56-69	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	13-19
16243774-6	2005	In addition, we investigated the promotional effect of phenobarbital (PB) on Cx32Delta Tg-High rats pretreated with DEN and found enhanced formation of GST-P positive lesions, in contrast to the lack of promoting effects reported for Cx32 deficient mice.	Phenobarbital	70-72	gap junction protein, beta 1	Rattus norvegicus	77-81
15557548-8	2004	Phenytoin and phenobarbital are metabolized by cytochrome P450 isozymes, with activity dependent on genetic polymorphism (CYP2C9, CYP2C19).	Phenobarbital	14-27	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	122-128
15557548-8	2004	Phenytoin and phenobarbital are metabolized by cytochrome P450 isozymes, with activity dependent on genetic polymorphism (CYP2C9, CYP2C19).	Phenobarbital	14-27	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	130-137
15569486-8	2004	Phenytoin, phenobarbital, carbamazepine, and valproic acid induced the overexpression of Pgp in astrocytes in a dose- and time-dependent manner.	Phenobarbital	11-24	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	89-92
15569486-9	2004	Significantly higher levels of Pgp staining were detected at therapeutic concentrations of certain antiepileptic drugs (20 microg/ml phenobarbital, 40 microg/ml phenobarbital, and 20 microg/ml phenytoin) on day 30.	Phenobarbital	133-146	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	31-34
15569486-9	2004	Significantly higher levels of Pgp staining were detected at therapeutic concentrations of certain antiepileptic drugs (20 microg/ml phenobarbital, 40 microg/ml phenobarbital, and 20 microg/ml phenytoin) on day 30.	Phenobarbital	161-174	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	31-34
15569486-10	2004	Upregulation of Pgp was detected when using higher concentrations of phenytoin, phenobarbital, and valproic acid on day 20 and when using higher concentrations of any of the four antiepileptic drugs on day 30.	Phenobarbital	80-93	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	16-19
15607757-9	2004	PB significantly induced CYP2B1.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	25-31
15607757-10	2004	In liver slices a minor induction of CYP1A1 and CYP3A1 by PB was observed, whereas DEX significantly induced CYP3A1, CYP2B1 and CYP1A2 mRNA levels.	Phenobarbital	58-60	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	37-43
15607757-10	2004	In liver slices a minor induction of CYP1A1 and CYP3A1 by PB was observed, whereas DEX significantly induced CYP3A1, CYP2B1 and CYP1A2 mRNA levels.	Phenobarbital	58-60	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	48-54
15495087-14	2004	Painter 1999 showed that both of the two most commonly used anticonvulsants (phenobarbital and phenytoin) were similarly effective (RR 1.03 95% CI 0.96 to 1.62), controlling seizures in less than fifty percent of infants.	Phenobarbital	77-90	ribonucleotide reductase catalytic subunit M1	Homo sapiens	132-136
15345328-0	2004	GABA(A)/central benzodiazepine receptor and peripheral benzodiazepine receptor ligands as inducers of phenobarbital-inducible CYP2B and CYP3A.	Phenobarbital	102-115	translocator protein	Rattus norvegicus	44-78
15345328-0	2004	GABA(A)/central benzodiazepine receptor and peripheral benzodiazepine receptor ligands as inducers of phenobarbital-inducible CYP2B and CYP3A.	Phenobarbital	102-115	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	136-141
15345328-1	2004	A sequence critical for phenobarbital (PB) induction, the PB response unit (PBRU), situated upstream of the rat CYP2B1 and CYP2B2 genes, includes two nuclear receptor binding sites, NR1 and NR2.	Phenobarbital	24-37	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	112-118
15345328-1	2004	A sequence critical for phenobarbital (PB) induction, the PB response unit (PBRU), situated upstream of the rat CYP2B1 and CYP2B2 genes, includes two nuclear receptor binding sites, NR1 and NR2.	Phenobarbital	24-37	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	123-129
15345328-1	2004	A sequence critical for phenobarbital (PB) induction, the PB response unit (PBRU), situated upstream of the rat CYP2B1 and CYP2B2 genes, includes two nuclear receptor binding sites, NR1 and NR2.	Phenobarbital	24-37	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	182-185
15345328-1	2004	A sequence critical for phenobarbital (PB) induction, the PB response unit (PBRU), situated upstream of the rat CYP2B1 and CYP2B2 genes, includes two nuclear receptor binding sites, NR1 and NR2.	Phenobarbital	39-41	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	112-118
15345328-1	2004	A sequence critical for phenobarbital (PB) induction, the PB response unit (PBRU), situated upstream of the rat CYP2B1 and CYP2B2 genes, includes two nuclear receptor binding sites, NR1 and NR2.	Phenobarbital	39-41	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	123-129
15345328-1	2004	A sequence critical for phenobarbital (PB) induction, the PB response unit (PBRU), situated upstream of the rat CYP2B1 and CYP2B2 genes, includes two nuclear receptor binding sites, NR1 and NR2.	Phenobarbital	39-41	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	182-185
15345328-2	2004	When NR1 and NR2 are mutated PB responsiveness is abolished.	Phenobarbital	29-31	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	5-8
15345328-3	2004	While no nuclear receptor for which PB is an agonist ligand has yet been identified, PB is a ligand of GABA(A) receptors and it can displace [(3)H] 1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinolinecarboxamide (PK 11195) from its binding site on the peripheral benzodiazepine receptor (PBR).	Phenobarbital	85-87	translocator protein	Rattus norvegicus	261-295
15345328-3	2004	While no nuclear receptor for which PB is an agonist ligand has yet been identified, PB is a ligand of GABA(A) receptors and it can displace [(3)H] 1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinolinecarboxamide (PK 11195) from its binding site on the peripheral benzodiazepine receptor (PBR).	Phenobarbital	85-87	translocator protein	Rattus norvegicus	297-300
15382119-2	2004	At the hepatic level, the orphan nuclear constitutive androstane receptor (CAR) (NR1I3) controls phase I (cytochrome P450 [CYP] 2B and CYP3A), phase II (UGT1A1), and transporter (SLC21A6, MRP2) genes involved in drug metabolism and bilirubin clearance in response to xenobiotics such as phenobarbital or endobiotics such as bilirubin.	Phenobarbital	287-300	nuclear receptor subfamily 1 group I member 3	Homo sapiens	41-73
15382119-2	2004	At the hepatic level, the orphan nuclear constitutive androstane receptor (CAR) (NR1I3) controls phase I (cytochrome P450 [CYP] 2B and CYP3A), phase II (UGT1A1), and transporter (SLC21A6, MRP2) genes involved in drug metabolism and bilirubin clearance in response to xenobiotics such as phenobarbital or endobiotics such as bilirubin.	Phenobarbital	287-300	nuclear receptor subfamily 1 group I member 3	Homo sapiens	75-78
15382119-2	2004	At the hepatic level, the orphan nuclear constitutive androstane receptor (CAR) (NR1I3) controls phase I (cytochrome P450 [CYP] 2B and CYP3A), phase II (UGT1A1), and transporter (SLC21A6, MRP2) genes involved in drug metabolism and bilirubin clearance in response to xenobiotics such as phenobarbital or endobiotics such as bilirubin.	Phenobarbital	287-300	nuclear receptor subfamily 1 group I member 3	Homo sapiens	81-86
15382119-2	2004	At the hepatic level, the orphan nuclear constitutive androstane receptor (CAR) (NR1I3) controls phase I (cytochrome P450 [CYP] 2B and CYP3A), phase II (UGT1A1), and transporter (SLC21A6, MRP2) genes involved in drug metabolism and bilirubin clearance in response to xenobiotics such as phenobarbital or endobiotics such as bilirubin.	Phenobarbital	287-300	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	106-130
15382119-4	2004	We show that IL-1beta decreases CAR expression and decreases phenobarbital- or bilirubin-mediated induction of CYP2B6, CYP2C9, CYP3A4, UGT1A1, GSTA1, GSTA2, and SLC21A6 messenger RNA.	Phenobarbital	61-74	interleukin 1 beta	Homo sapiens	13-21
15382119-4	2004	We show that IL-1beta decreases CAR expression and decreases phenobarbital- or bilirubin-mediated induction of CYP2B6, CYP2C9, CYP3A4, UGT1A1, GSTA1, GSTA2, and SLC21A6 messenger RNA.	Phenobarbital	61-74	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	111-117
15382119-4	2004	We show that IL-1beta decreases CAR expression and decreases phenobarbital- or bilirubin-mediated induction of CYP2B6, CYP2C9, CYP3A4, UGT1A1, GSTA1, GSTA2, and SLC21A6 messenger RNA.	Phenobarbital	61-74	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	119-125
15382119-4	2004	We show that IL-1beta decreases CAR expression and decreases phenobarbital- or bilirubin-mediated induction of CYP2B6, CYP2C9, CYP3A4, UGT1A1, GSTA1, GSTA2, and SLC21A6 messenger RNA.	Phenobarbital	61-74	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	127-133
15382119-4	2004	We show that IL-1beta decreases CAR expression and decreases phenobarbital- or bilirubin-mediated induction of CYP2B6, CYP2C9, CYP3A4, UGT1A1, GSTA1, GSTA2, and SLC21A6 messenger RNA.	Phenobarbital	61-74	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	135-141
15382119-4	2004	We show that IL-1beta decreases CAR expression and decreases phenobarbital- or bilirubin-mediated induction of CYP2B6, CYP2C9, CYP3A4, UGT1A1, GSTA1, GSTA2, and SLC21A6 messenger RNA.	Phenobarbital	61-74	glutathione S-transferase alpha 1	Homo sapiens	143-148
15382119-4	2004	We show that IL-1beta decreases CAR expression and decreases phenobarbital- or bilirubin-mediated induction of CYP2B6, CYP2C9, CYP3A4, UGT1A1, GSTA1, GSTA2, and SLC21A6 messenger RNA.	Phenobarbital	61-74	glutathione S-transferase alpha 2	Homo sapiens	150-155
15382119-4	2004	We show that IL-1beta decreases CAR expression and decreases phenobarbital- or bilirubin-mediated induction of CYP2B6, CYP2C9, CYP3A4, UGT1A1, GSTA1, GSTA2, and SLC21A6 messenger RNA.	Phenobarbital	61-74	solute carrier organic anion transporter family member 1B1	Homo sapiens	161-168
15272053-7	2004	In contrast, meclizine suppresses hCAR transactivation and inhibits the phenobarbital-induced expression of the CAR target genes, cytochrome p450 monooxygenase (CYP)2B10, CYP3A11, and CYP1A2, in primary hepatocytes derived from mice expressing hCAR, but not mCAR.	Phenobarbital	72-85	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	130-169
15272053-7	2004	In contrast, meclizine suppresses hCAR transactivation and inhibits the phenobarbital-induced expression of the CAR target genes, cytochrome p450 monooxygenase (CYP)2B10, CYP3A11, and CYP1A2, in primary hepatocytes derived from mice expressing hCAR, but not mCAR.	Phenobarbital	72-85	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	171-178
15272053-7	2004	In contrast, meclizine suppresses hCAR transactivation and inhibits the phenobarbital-induced expression of the CAR target genes, cytochrome p450 monooxygenase (CYP)2B10, CYP3A11, and CYP1A2, in primary hepatocytes derived from mice expressing hCAR, but not mCAR.	Phenobarbital	72-85	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	184-190
15272053-7	2004	In contrast, meclizine suppresses hCAR transactivation and inhibits the phenobarbital-induced expression of the CAR target genes, cytochrome p450 monooxygenase (CYP)2B10, CYP3A11, and CYP1A2, in primary hepatocytes derived from mice expressing hCAR, but not mCAR.	Phenobarbital	72-85	CXADR Ig-like cell adhesion molecule	Homo sapiens	244-248
15272053-7	2004	In contrast, meclizine suppresses hCAR transactivation and inhibits the phenobarbital-induced expression of the CAR target genes, cytochrome p450 monooxygenase (CYP)2B10, CYP3A11, and CYP1A2, in primary hepatocytes derived from mice expressing hCAR, but not mCAR.	Phenobarbital	72-85	coxsackie virus and adenovirus receptor	Mus musculus	258-262
15288127-3	2004	PB significantly increased P450 levels (200% of control levels) and the activities (300-400% of control) of the specific isoforms (CYP), CYP3A2 and CYP2B1, in male rats.	Phenobarbital	0-2	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	137-143
15288127-3	2004	PB significantly increased P450 levels (200% of control levels) and the activities (300-400% of control) of the specific isoforms (CYP), CYP3A2 and CYP2B1, in male rats.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	148-154
15288127-5	2004	Furthermore, either troleandomycin or ketoconazole, specific CYP3A inhibitors, significantly inhibited LPS-induced liver injury in control and PB-treated male rats.	Phenobarbital	143-145	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	61-66
15317825-4	2004	The serum activity of ChE was determined in a group of 90 adult epileptic patients (56 male and 34 female) treated with phenobarbital, phenytoin, and carbamazepine.	Phenobarbital	120-133	butyrylcholinesterase	Homo sapiens	22-25
15365254-11	2004	The number of AFB1-induced GST-P positive foci was increased 5-10 fold in the presence of PB in both groups.	Phenobarbital	90-92	glutathione S-transferase pi 1	Rattus norvegicus	27-32
14742323-0	2004	Activation of beta-catenin provides proliferative and invasive advantages in c-myc/TGF-alpha hepatocarcinogenesis promoted by phenobarbital.	Phenobarbital	126-139	catenin (cadherin associated protein), beta 1	Mus musculus	14-26
15492232-0	2004	The orphan nuclear receptor constitutive active/androstane receptor is essential for liver tumor promotion by phenobarbital in mice.	Phenobarbital	110-123	nuclear receptor subfamily 1, group I, member 3	Mus musculus	28-67
15492232-4	2004	The nuclear receptor constitutive active/androstane receptor (CAR) is activated by PB as well as by various other xenobiotics such as therapeutic drugs and environmental pollutants.	Phenobarbital	83-85	nuclear receptor subfamily 1, group I, member 3	Mus musculus	21-60
15492232-4	2004	The nuclear receptor constitutive active/androstane receptor (CAR) is activated by PB as well as by various other xenobiotics such as therapeutic drugs and environmental pollutants.	Phenobarbital	83-85	nuclear receptor subfamily 1, group I, member 3	Mus musculus	62-65
15107969-5	2004	Transcript content of glycolytic genes was decreased by PB treatments, while that of lipoprotein lipase was continuously increased, suggesting a notion that repetitive PB treatments impaired glycolysis and stimulated lipolysis in the liver.	Phenobarbital	168-170	lipoprotein lipase	Rattus norvegicus	85-103
15107969-9	2004	Although ketogenesis would normally occur under such cellular conditions, it was only weakly observed after the repeated PB treatments, presumably owing to a decrease in HMG-CoA synthase mRNA content.	Phenobarbital	121-123	3-hydroxy-3-methylglutaryl-CoA synthase 2	Rattus norvegicus	170-186
15558951-1	2004	Succinate-cytochrome c reductase was inhibited in vitro and in vivo by phenobarbitone, aminophylline and neostigmine using both 2,6-dichlorophenolindophenol (DCIP) and cytochrome c (cyt c) as substrates.	Phenobarbital	71-85	cytochrome c, somatic	Homo sapiens	10-22
15558951-1	2004	Succinate-cytochrome c reductase was inhibited in vitro and in vivo by phenobarbitone, aminophylline and neostigmine using both 2,6-dichlorophenolindophenol (DCIP) and cytochrome c (cyt c) as substrates.	Phenobarbital	71-85	cytochrome c, somatic	Homo sapiens	168-180
15558951-1	2004	Succinate-cytochrome c reductase was inhibited in vitro and in vivo by phenobarbitone, aminophylline and neostigmine using both 2,6-dichlorophenolindophenol (DCIP) and cytochrome c (cyt c) as substrates.	Phenobarbital	71-85	cytochrome c, somatic	Homo sapiens	182-187
15558951-3	2004	In vitro, phenobarbitone and aminophylline inhibited the enzyme with respect to the reduction of DCIP and cyt c in a non-competitive manner with Ki values of 1.5 x 10(-5) and 5.7 x 10(-5)M, respectively.	Phenobarbital	10-24	cytochrome c, somatic	Homo sapiens	106-111
15178021-1	2004	Constitutive androstane receptor (CAR) plays a key role in the transcriptional regulation of CYP2B, 2C and 3A genes in response to phenobarbital, ortho-chlorine substituted polychlorinated biphenyls (PCBs) and sex steroids in rodents and human.	Phenobarbital	131-144	nuclear receptor subfamily 1 group I member 3	Homo sapiens	0-32
15178021-1	2004	Constitutive androstane receptor (CAR) plays a key role in the transcriptional regulation of CYP2B, 2C and 3A genes in response to phenobarbital, ortho-chlorine substituted polychlorinated biphenyls (PCBs) and sex steroids in rodents and human.	Phenobarbital	131-144	nuclear receptor subfamily 1 group I member 3	Homo sapiens	34-37
14749302-8	2004	The steady-state levels of FSHR mRNA increased from estrus (Day 1) to reach a peak on proestrus (Day 4) noon; however, significant attenuation was noted following the gonadotropin surge, which was blocked by phenobarbital.	Phenobarbital	208-221	follicle stimulating hormone receptor	Mus musculus	27-31
15690761-13	2004	In phenobarbital (PB)-induced fractions CYP2B1-mediated AD 16beta-hydroxylation was inhibited potently in a reversible fashion by parathion (Ki = 0.37 microM; Km/Ki ratio about 73).	Phenobarbital	3-16	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	40-46
15690761-13	2004	In phenobarbital (PB)-induced fractions CYP2B1-mediated AD 16beta-hydroxylation was inhibited potently in a reversible fashion by parathion (Ki = 0.37 microM; Km/Ki ratio about 73).	Phenobarbital	18-20	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	40-46
15690761-21	2004	Potent reversible inhibition of CYP2B1 occurred in PB-induced fractions and DEX-inducible CYPs 3A were more susceptible to mechanism-based inactivation than the corresponding constitutive CYPs from the same subfamily.	Phenobarbital	51-53	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	32-38
15123723-4	2004	In primary human hepatocytes, expression of CYP2B6 reporter genes containing phenobarbital-responsive enhancer module (PBREM) or PBREM/xenobiotic-responsive enhancer module (XREM) response elements were activated up to 14- and 28-fold, respectively, by 50 microm PHY.	Phenobarbital	77-90	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	44-50
15183191-10	2004	Allopurinol and diphenyleneiodonium chloride pretreatment also attenuated the repressive effects of LPS on dexamethasone-, rifampicin-, mifepristone-, and phenobarbital-inducible CYP3A11 mRNA expression and ERND catalytic activity in mouse liver.	Phenobarbital	155-168	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	179-186
15183191-13	2004	These antioxidants also prevented the repressive effects of LPS on dexamethasone-, rifampicin-, mifepristone-, and phenobarbital-inducible CYP3A11 mRNA expression and ERND catalytic activity in mouse liver.	Phenobarbital	115-128	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	139-146
15208357-3	2004	Fidelity of expression in the methacarn-fixed PET sections, with reference to dose-dependent induction of cytochrome P450 2B1 in the phenobarbital-treated rat liver, was high in comparison with the unfixed frozen tissue case, even after hematoxylin staining.	Phenobarbital	133-146	cytochrome P450 2B1	Rattus norvegicus	106-125
14742323-0	2004	Activation of beta-catenin provides proliferative and invasive advantages in c-myc/TGF-alpha hepatocarcinogenesis promoted by phenobarbital.	Phenobarbital	126-139	transforming growth factor alpha	Mus musculus	83-92
14742323-2	2004	Given that PB selectively promoted initiated cells harboring beta-catenin mutations during chemically induced hepatocarcinogenesis and that Wnt/beta-catenin signaling is involved in both anti-apoptotic and proliferative processes, we now have extended our analysis to investigate whether promotion by PB affects the occurrence of beta-catenin mutations in c-myc/TGF-alpha-driven tumors.	Phenobarbital	11-13	catenin (cadherin associated protein), beta 1	Mus musculus	61-73
14742323-2	2004	Given that PB selectively promoted initiated cells harboring beta-catenin mutations during chemically induced hepatocarcinogenesis and that Wnt/beta-catenin signaling is involved in both anti-apoptotic and proliferative processes, we now have extended our analysis to investigate whether promotion by PB affects the occurrence of beta-catenin mutations in c-myc/TGF-alpha-driven tumors.	Phenobarbital	11-13	transforming growth factor alpha	Mus musculus	362-371
14742323-3	2004	The frequency of beta-catenin activation as judged by somatic mutations and/or nuclear localization was significantly increased in hepatocellular carcinomas (HCCs) from c-myc/TGF-alpha mice treated with PB (15/28; 53.6%) as compared with that in control HCCs (2/28; 7.1%).	Phenobarbital	203-205	catenin (cadherin associated protein), beta 1	Mus musculus	17-29
14742323-3	2004	The frequency of beta-catenin activation as judged by somatic mutations and/or nuclear localization was significantly increased in hepatocellular carcinomas (HCCs) from c-myc/TGF-alpha mice treated with PB (15/28; 53.6%) as compared with that in control HCCs (2/28; 7.1%).	Phenobarbital	203-205	transforming growth factor alpha	Mus musculus	175-184
14742323-4	2004	Furthermore, an intact beta-catenin locus was detected in all neoplasms following PB treatment, whereas 57.1% (16/28) of malignant tumors from c-myc/TGF-alpha untreated mice displayed loss of heterozygosity at the beta-catenin locus.	Phenobarbital	82-84	catenin (cadherin associated protein), beta 1	Mus musculus	23-35
14742323-5	2004	Strikingly, in the majority of PB-treated HCCs beta-catenin nuclear localization was limited to small cells with high nuclear/cytoplasmic ratio forming an invasion front (NAinv).	Phenobarbital	31-33	catenin (cadherin associated protein), beta 1	Mus musculus	47-59
14742323-8	2004	These findings show that PB treatment positively selects for a cell population displaying activation of beta-catenin in c-myc/TGF-alpha HCCs.	Phenobarbital	25-27	catenin (cadherin associated protein), beta 1	Mus musculus	104-116
14742323-8	2004	These findings show that PB treatment positively selects for a cell population displaying activation of beta-catenin in c-myc/TGF-alpha HCCs.	Phenobarbital	25-27	transforming growth factor alpha	Mus musculus	126-135
15151625-7	2004	RESULTS: It was observed that in the DEN-treated and PB-promoted group (group A) the expression of the numbers and areas of the placental form of glutathione S-transferase (GST-P)-positive altered hepatic foci (AHF) was maximum.	Phenobarbital	53-55	hematopoietic prostaglandin D synthase	Rattus norvegicus	146-171
15151625-7	2004	RESULTS: It was observed that in the DEN-treated and PB-promoted group (group A) the expression of the numbers and areas of the placental form of glutathione S-transferase (GST-P)-positive altered hepatic foci (AHF) was maximum.	Phenobarbital	53-55	glutathione S-transferase pi 1	Rattus norvegicus	173-178
15100175-8	2004	Finally, the role of these sites was examined in activation of CYP3A4 expression by rifampicin, metyrapone, clotrimazole, and phenobarbital.	Phenobarbital	126-139	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	63-69
15341071-3	2004	It was established that the 10-day treatment with PB inhibits the proliferative activity in concanavalin A stimulated lymphocytes of rat thymus, decreases the ACE activity, and increases the CA content in the nerve fibers.	Phenobarbital	50-52	angiotensin I converting enzyme	Rattus norvegicus	159-162
15082532-3	2004	Conditionally deleted Foxm1b mouse hepatocytes fail to proliferate and are highly resistant to developing HCC in response to a Diethylnitrosamine (DEN)/Phenobarbital (PB) liver tumor-induction protocol.	Phenobarbital	152-165	forkhead box M1	Mus musculus	22-28
15135080-7	2004	The barbiturate phenobarbital and the environmental toxicant 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE) are among the well characterized inducers for the CYP 2B and 3A enzymes and selected conjugation enzymes.	Phenobarbital	16-29	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	162-165
15082532-3	2004	Conditionally deleted Foxm1b mouse hepatocytes fail to proliferate and are highly resistant to developing HCC in response to a Diethylnitrosamine (DEN)/Phenobarbital (PB) liver tumor-induction protocol.	Phenobarbital	167-169	forkhead box M1	Mus musculus	22-28
14977870-7	2004	EC50 values for CYP2B6 and CYP3A4 induction by clotrimazole, phenobarbital, phenytoin, and rifampin were strongly correlated (r2 = 0.99) and were statistically indistinguishable for clotrimazole, phenytoin, and rifampin.	Phenobarbital	61-74	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	16-22
15043764-1	2004	BACKGROUND: The constitutive androstane receptor (CAR) plays a key role in the control of drug metabolism and transport by mediating the phenobarbital-type induction of many phase I and II drug metabolizing enzymes and drug transporters.	Phenobarbital	137-150	nuclear receptor subfamily 1 group I member 3	Homo sapiens	16-48
15043764-1	2004	BACKGROUND: The constitutive androstane receptor (CAR) plays a key role in the control of drug metabolism and transport by mediating the phenobarbital-type induction of many phase I and II drug metabolizing enzymes and drug transporters.	Phenobarbital	137-150	nuclear receptor subfamily 1 group I member 3	Homo sapiens	50-53
14977870-7	2004	EC50 values for CYP2B6 and CYP3A4 induction by clotrimazole, phenobarbital, phenytoin, and rifampin were strongly correlated (r2 = 0.99) and were statistically indistinguishable for clotrimazole, phenytoin, and rifampin.	Phenobarbital	61-74	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	27-33
14978227-7	2004	In the reporter gene assays employing the phenobarbital-responsible enhancer module (PBREM) from CYP2B6 and UGT1A1 genes, the splice variants, except for SV1, were inactive, whereas SV1 transactivated the CYP2B6 PBREM but not the UGT1A1 PBREM reporter.	Phenobarbital	42-55	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	97-103
15003996-6	2004	GABA and the GABA(A) receptor agonists phenobarbital and melatonin also protect neurons against Abeta-induced neurotoxicity.	Phenobarbital	39-52	gamma-aminobutyric acid type A receptor gamma3 subunit	Gallus gallus	13-29
14978227-7	2004	In the reporter gene assays employing the phenobarbital-responsible enhancer module (PBREM) from CYP2B6 and UGT1A1 genes, the splice variants, except for SV1, were inactive, whereas SV1 transactivated the CYP2B6 PBREM but not the UGT1A1 PBREM reporter.	Phenobarbital	42-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	108-114
14978227-7	2004	In the reporter gene assays employing the phenobarbital-responsible enhancer module (PBREM) from CYP2B6 and UGT1A1 genes, the splice variants, except for SV1, were inactive, whereas SV1 transactivated the CYP2B6 PBREM but not the UGT1A1 PBREM reporter.	Phenobarbital	42-55	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	205-211
14978227-7	2004	In the reporter gene assays employing the phenobarbital-responsible enhancer module (PBREM) from CYP2B6 and UGT1A1 genes, the splice variants, except for SV1, were inactive, whereas SV1 transactivated the CYP2B6 PBREM but not the UGT1A1 PBREM reporter.	Phenobarbital	42-55	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	230-236
15038401-3	2004	Potent inductors of CYP isoenzymes are carbamazepine, phenobarbital, phenytoin, and primidone, thereby decreasing not only their own plasma levels and efficacy but also that of other antiepileptics and other drugs.	Phenobarbital	54-67	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	20-23
14600250-0	2004	Induction of human CYP2C9 by rifampicin, hyperforin, and phenobarbital is mediated by the pregnane X receptor.	Phenobarbital	57-70	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	19-25
15000748-1	2004	The induction of CYP2B gene expression by phenobarbital (PB) is mediated by the translocation of the constitutive androstane receptor (CAR) from the cytoplasm to the nucleus.	Phenobarbital	42-55	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	17-22
15000748-1	2004	The induction of CYP2B gene expression by phenobarbital (PB) is mediated by the translocation of the constitutive androstane receptor (CAR) from the cytoplasm to the nucleus.	Phenobarbital	42-55	nuclear receptor subfamily 1 group I member 3	Homo sapiens	101-133
15000748-1	2004	The induction of CYP2B gene expression by phenobarbital (PB) is mediated by the translocation of the constitutive androstane receptor (CAR) from the cytoplasm to the nucleus.	Phenobarbital	42-55	nuclear receptor subfamily 1 group I member 3	Homo sapiens	135-138
15000748-1	2004	The induction of CYP2B gene expression by phenobarbital (PB) is mediated by the translocation of the constitutive androstane receptor (CAR) from the cytoplasm to the nucleus.	Phenobarbital	57-59	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	17-22
15000748-1	2004	The induction of CYP2B gene expression by phenobarbital (PB) is mediated by the translocation of the constitutive androstane receptor (CAR) from the cytoplasm to the nucleus.	Phenobarbital	57-59	nuclear receptor subfamily 1 group I member 3	Homo sapiens	101-133
15000748-1	2004	The induction of CYP2B gene expression by phenobarbital (PB) is mediated by the translocation of the constitutive androstane receptor (CAR) from the cytoplasm to the nucleus.	Phenobarbital	57-59	nuclear receptor subfamily 1 group I member 3	Homo sapiens	135-138
15000748-2	2004	The CAR/RXR heterodimer binds to two DR-4 sites in a complex phenobarbital responsive unit (PBRU) in the CYP2B gene.	Phenobarbital	61-74	nuclear receptor subfamily 1 group I member 3	Homo sapiens	4-7
15000748-2	2004	The CAR/RXR heterodimer binds to two DR-4 sites in a complex phenobarbital responsive unit (PBRU) in the CYP2B gene.	Phenobarbital	61-74	retinoid X receptor alpha	Homo sapiens	8-11
15000748-2	2004	The CAR/RXR heterodimer binds to two DR-4 sites in a complex phenobarbital responsive unit (PBRU) in the CYP2B gene.	Phenobarbital	61-74	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	105-110
14600250-0	2004	Induction of human CYP2C9 by rifampicin, hyperforin, and phenobarbital is mediated by the pregnane X receptor.	Phenobarbital	57-70	nuclear receptor subfamily 1 group I member 2	Homo sapiens	90-109
14600250-2	2004	Several studies have reported that certain drugs such as rifampicin and phenobarbital induce CYP2C9, but the molecular basis for this induction remains unknown.	Phenobarbital	72-85	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	93-99
14600250-3	2004	In the present study, we demonstrate that the human pregnane X receptor (hPXR) mediates induction of CYP2C9 by the prototype drugs rifampicin, hyperforin (found in St. John"s Wart), and phenobarbital.	Phenobarbital	186-199	nuclear receptor subfamily 1 group I member 2	Homo sapiens	52-71
14600250-3	2004	In the present study, we demonstrate that the human pregnane X receptor (hPXR) mediates induction of CYP2C9 by the prototype drugs rifampicin, hyperforin (found in St. John"s Wart), and phenobarbital.	Phenobarbital	186-199	nuclear receptor subfamily 1 group I member 2	Homo sapiens	73-77
14600250-3	2004	In the present study, we demonstrate that the human pregnane X receptor (hPXR) mediates induction of CYP2C9 by the prototype drugs rifampicin, hyperforin (found in St. John"s Wart), and phenobarbital.	Phenobarbital	186-199	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
14600250-8	2004	This is the first report to demonstrate that the nuclear receptor PXR mediates induction of CYP2C9 with rifampicin, phenobarbital, and hyperforin.	Phenobarbital	116-129	nuclear receptor subfamily 1 group I member 2	Homo sapiens	66-69
14600250-8	2004	This is the first report to demonstrate that the nuclear receptor PXR mediates induction of CYP2C9 with rifampicin, phenobarbital, and hyperforin.	Phenobarbital	116-129	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	92-98
14732219-5	2004	Phenobarbital (PB) which is a typical inducer of CYP2B1 and 3A2 induced production of hydroxyl radicals by rat liver and ketoconazole, an inhibitor of P450, inhibited production of hydroxyl radicals in vitro.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	49-55
14711988-2	2004	DYT1 dystonia is a form of primary dystonia caused by an in-frame GAG deletion (DeltaE302/3) in the TOR1A gene that encodes the endoplasmic reticulum luminal protein torsinA.	Phenobarbital	150-157	torsin family 1 member A	Homo sapiens	0-4
14711988-2	2004	DYT1 dystonia is a form of primary dystonia caused by an in-frame GAG deletion (DeltaE302/3) in the TOR1A gene that encodes the endoplasmic reticulum luminal protein torsinA.	Phenobarbital	150-157	torsin family 1 member A	Homo sapiens	100-105
14711988-2	2004	DYT1 dystonia is a form of primary dystonia caused by an in-frame GAG deletion (DeltaE302/3) in the TOR1A gene that encodes the endoplasmic reticulum luminal protein torsinA.	Phenobarbital	150-157	torsin family 1 member A	Homo sapiens	166-173
15646366-5	2004	Compound 4 exhibited a slightly lower activity than the reference drug phenobarbital (CAS 50-06-6).	Phenobarbital	71-84	BCAR1 scaffold protein, Cas family member	Homo sapiens	86-89
14732219-5	2004	Phenobarbital (PB) which is a typical inducer of CYP2B1 and 3A2 induced production of hydroxyl radicals by rat liver and ketoconazole, an inhibitor of P450, inhibited production of hydroxyl radicals in vitro.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	49-55
14709631-7	2004	UGT1A9-mediated propofol glucuronidation was induced by phenobarbital (up to 2.2-fold) and rifampicin (up to 1.7-fold).	Phenobarbital	56-69	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	0-6
15188805-9	2004	RESULTS: CSF levels of MDA, SOD, GPx and blood levels of vitamins A and E were significantly lower in the Phenobarbital group (p&lt;0.001).	Phenobarbital	106-119	colony stimulating factor 2	Homo sapiens	9-12
15252867-8	2004	We hypothesize that the compromised phenobarbital inducibility of CYP2B18A stems from its lack of a functional phenobarbital responsive enhancer module.	Phenobarbital	36-49	cytochrome P450IIB	Cavia porcellus	66-74
15252867-8	2004	We hypothesize that the compromised phenobarbital inducibility of CYP2B18A stems from its lack of a functional phenobarbital responsive enhancer module.	Phenobarbital	111-124	cytochrome P450IIB	Cavia porcellus	66-74
14722249-2	2004	Phenobarbital-dependent induction of cytochrome P-450 2B1 (CYP2B1) is subject to regulation by cytokines [e.g., by epidermal growth factor (EGF)], hormones [e.g., by growth hormone (GH)], or the cellular redox status.	Phenobarbital	0-13	gonadotropin releasing hormone receptor	Rattus norvegicus	182-184
14722249-4	2004	The 2679-bp native 5"-flanking region of the CYP2B1 gene conferred reporter gene activation by PB and the potent PB-like inducer permethrin (PM).	Phenobarbital	95-97	cytochrome P450 2B1	Rattus norvegicus	45-51
14722249-8	2004	Mutational analyses of the region at -2230 to -2170 suggested that the mechanisms of PB-dependent induction of CYP2B1 and the modulating effects by EGF or NAC are closely related.	Phenobarbital	85-87	cytochrome P450 2B1	Rattus norvegicus	111-117
14770174-7	2004	Phenobarbital and TCPOBOP induce CYP3A11 expression only in the presence of CAR, but have no effect on CYP3A41 expression.	Phenobarbital	0-13	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	33-40
14722249-2	2004	Phenobarbital-dependent induction of cytochrome P-450 2B1 (CYP2B1) is subject to regulation by cytokines [e.g., by epidermal growth factor (EGF)], hormones [e.g., by growth hormone (GH)], or the cellular redox status.	Phenobarbital	0-13	cytochrome P450 2B1	Rattus norvegicus	37-57
14722249-2	2004	Phenobarbital-dependent induction of cytochrome P-450 2B1 (CYP2B1) is subject to regulation by cytokines [e.g., by epidermal growth factor (EGF)], hormones [e.g., by growth hormone (GH)], or the cellular redox status.	Phenobarbital	0-13	cytochrome P450 2B1	Rattus norvegicus	59-65
14722249-2	2004	Phenobarbital-dependent induction of cytochrome P-450 2B1 (CYP2B1) is subject to regulation by cytokines [e.g., by epidermal growth factor (EGF)], hormones [e.g., by growth hormone (GH)], or the cellular redox status.	Phenobarbital	0-13	gonadotropin releasing hormone receptor	Rattus norvegicus	166-180
14770174-7	2004	Phenobarbital and TCPOBOP induce CYP3A11 expression only in the presence of CAR, but have no effect on CYP3A41 expression.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	76-79
14642740-8	2003	For example, PCB 47, 52, and 54 bind preferentially to CYP2B and to a lesser extent to CYP3A enzymes in microsomes from PB-treated male rats; PCB 52 binds primarily to CYP3A enzymes in microsomes from DEX-treated female rats; and PCB 54 binds to CYP3A and to CYP2C enzymes in microsomes from control male rats.	Phenobarbital	120-122	pyruvate carboxylase	Rattus norvegicus	142-145
12923173-5	2003	A role for CAR in protection against bile acid toxicity was confirmed by a marked reduction of serum bile acid and bilirubin concentrations, with an elevation of the expression of the hepatic genes involved in bile acid and/or bilirubin metabolism and excretion (CYP2B, CYP3A, MRP2, MRP3, UGT1A, and glutathione S-transferase alpha), following pretreatment with phenobarbital or TCPOBOP.	Phenobarbital	362-375	nuclear receptor subfamily 1, group I, member 3	Mus musculus	11-14
14683479-1	2003	Cytochrome p450 2B genes have been used extensively as prototypical models to study phenobarbital induction of p450 enzymes.	Phenobarbital	84-97	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	11-15
14683479-1	2003	Cytochrome p450 2B genes have been used extensively as prototypical models to study phenobarbital induction of p450 enzymes.	Phenobarbital	84-97	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	111-115
14561525-11	2003	In an in vivo study, pretreatment of female rats with SKF525A, an inhibitor of CYPs including CYP3A1, significantly (p &lt; 0.05) enhanced MPA-induced hypercoagulation, whereas pretreatment with phenobarbital, an inducer of CYPs including CYP3A1, reduced it.	Phenobarbital	195-208	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	94-100
14570762-7	2003	Mrp3, however, was induced by PB, diallyl sulfide, trans-stilbene oxide and oltipraz in both wild-type and RXRalpha-/- mice.	Phenobarbital	30-32	prolactin family 2, subfamily c, member 4	Mus musculus	0-4
14570762-1	2003	We previously demonstrated that multidrug resistance protein 3 (Mrp3/ABCC3) is induced in rat liver by phenobarbital (PB) and several other microsomal enzyme inducers that induce cytochrome P450 2B (CYP2B).	Phenobarbital	103-116	ATP binding cassette subfamily C member 3	Rattus norvegicus	32-62
14570762-1	2003	We previously demonstrated that multidrug resistance protein 3 (Mrp3/ABCC3) is induced in rat liver by phenobarbital (PB) and several other microsomal enzyme inducers that induce cytochrome P450 2B (CYP2B).	Phenobarbital	103-116	ATP binding cassette subfamily C member 3	Rattus norvegicus	64-68
14570762-1	2003	We previously demonstrated that multidrug resistance protein 3 (Mrp3/ABCC3) is induced in rat liver by phenobarbital (PB) and several other microsomal enzyme inducers that induce cytochrome P450 2B (CYP2B).	Phenobarbital	103-116	ATP binding cassette subfamily C member 3	Rattus norvegicus	69-74
14570762-1	2003	We previously demonstrated that multidrug resistance protein 3 (Mrp3/ABCC3) is induced in rat liver by phenobarbital (PB) and several other microsomal enzyme inducers that induce cytochrome P450 2B (CYP2B).	Phenobarbital	103-116	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	199-204
14570762-1	2003	We previously demonstrated that multidrug resistance protein 3 (Mrp3/ABCC3) is induced in rat liver by phenobarbital (PB) and several other microsomal enzyme inducers that induce cytochrome P450 2B (CYP2B).	Phenobarbital	118-120	ATP binding cassette subfamily C member 3	Rattus norvegicus	32-62
14570762-1	2003	We previously demonstrated that multidrug resistance protein 3 (Mrp3/ABCC3) is induced in rat liver by phenobarbital (PB) and several other microsomal enzyme inducers that induce cytochrome P450 2B (CYP2B).	Phenobarbital	118-120	ATP binding cassette subfamily C member 3	Rattus norvegicus	64-68
14570762-1	2003	We previously demonstrated that multidrug resistance protein 3 (Mrp3/ABCC3) is induced in rat liver by phenobarbital (PB) and several other microsomal enzyme inducers that induce cytochrome P450 2B (CYP2B).	Phenobarbital	118-120	ATP binding cassette subfamily C member 3	Rattus norvegicus	69-74
14570762-1	2003	We previously demonstrated that multidrug resistance protein 3 (Mrp3/ABCC3) is induced in rat liver by phenobarbital (PB) and several other microsomal enzyme inducers that induce cytochrome P450 2B (CYP2B).	Phenobarbital	118-120	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	199-204
14570762-2	2003	CYP2B is induced by constitutive androstane receptor (CAR)-retinoid X receptor (RXR) heterodimer binding to a phenobarbital-responsive promoter element in the CYP2B promoter.	Phenobarbital	110-123	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	0-5
14570762-2	2003	CYP2B is induced by constitutive androstane receptor (CAR)-retinoid X receptor (RXR) heterodimer binding to a phenobarbital-responsive promoter element in the CYP2B promoter.	Phenobarbital	110-123	nuclear receptor subfamily 1, group I, member 3	Mus musculus	20-52
14570762-2	2003	CYP2B is induced by constitutive androstane receptor (CAR)-retinoid X receptor (RXR) heterodimer binding to a phenobarbital-responsive promoter element in the CYP2B promoter.	Phenobarbital	110-123	nuclear receptor subfamily 1, group I, member 3	Mus musculus	54-57
14570762-2	2003	CYP2B is induced by constitutive androstane receptor (CAR)-retinoid X receptor (RXR) heterodimer binding to a phenobarbital-responsive promoter element in the CYP2B promoter.	Phenobarbital	110-123	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	159-164
14570762-4	2003	In Wistar Kyoto rats, where males express higher CAR protein levels than females, the induction of CYP2B1/2 was significantly higher in males than in females by PB, diallyl sulfide, and trans-stilbene oxide but not oltipraz.	Phenobarbital	161-163	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	99-105
14570762-6	2003	In male hepatocyte-specific RXRalpha-/- mice, CYP2B10 was not induced by diallyl sulfide or oltipraz but remained inducible by PB and trans-stilbene oxide after considering the decrease in basal CYP2B10 expression.	Phenobarbital	127-129	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	46-53
14573755-1	2003	The nuclear constitutive active receptor (CAR) is a key transcription factor regulating phenobarbital (PB)-inducible transcription of various hepatic genes that encode xenobiotic/steroid-metabolizing enzymes.	Phenobarbital	88-101	nuclear receptor subfamily 1 group I member 3	Homo sapiens	42-45
14573755-1	2003	The nuclear constitutive active receptor (CAR) is a key transcription factor regulating phenobarbital (PB)-inducible transcription of various hepatic genes that encode xenobiotic/steroid-metabolizing enzymes.	Phenobarbital	103-105	nuclear receptor subfamily 1 group I member 3	Homo sapiens	42-45
14573755-2	2003	CAR is retained in the cytoplasm of noninduced livers and translocates into the nucleus after PB induction.	Phenobarbital	94-96	nuclear receptor subfamily 1 group I member 3	Homo sapiens	0-3
12896978-3	2003	Clusters of CAR REs, referred to as phenobarbital response enhancer modules (PBREMs), have been identified in several CAR target genes.	Phenobarbital	36-49	nuclear receptor subfamily 1 group I member 3	Homo sapiens	12-15
12896978-3	2003	Clusters of CAR REs, referred to as phenobarbital response enhancer modules (PBREMs), have been identified in several CAR target genes.	Phenobarbital	36-49	nuclear receptor subfamily 1 group I member 3	Homo sapiens	118-121
14522368-7	2003	Cytochrome P450 3A4 inducing anti-epileptic drugs like phenytoin, carbamazepine and phenobarbital may significantly increase the metabolism of many chemotherapeutic agents like CPT11 and paclitaxel (but also of newer biological agents like many tyrosine kinase inhibitors).	Phenobarbital	84-97	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-19
12905009-10	2003	Two hundred micrograms of TGF-beta1/kg stimulated apoptoses in NL as well as in neoplastic lesions (significant increase in NL, HCA, and HCC); the most pronounced proapoptotic action of TGF-ss1 was observed in lesions of NDEA+PB pretreated mice (about 1.7%).	Phenobarbital	226-228	transforming growth factor, beta 1	Mus musculus	26-35
12905009-10	2003	Two hundred micrograms of TGF-beta1/kg stimulated apoptoses in NL as well as in neoplastic lesions (significant increase in NL, HCA, and HCC); the most pronounced proapoptotic action of TGF-ss1 was observed in lesions of NDEA+PB pretreated mice (about 1.7%).	Phenobarbital	226-228	transforming growth factor, beta 1	Mus musculus	26-29
14531464-4	2003	The sleeping time of the phenobarbital group (80 mg/kg daily ip injection for 4 days) was shortened at 24 h after the last injection with increased P450 content of hepatic microsome, but it showed no difference at 48 h. The zoxazolamine-paralysis times of mice treated with p-amino-2",4"-dichlorodiphenyl ether were longer than those of the control mice, while the same dose of zoxazolamine did not lead to paralysis in mice pretreated with BNF.	Phenobarbital	25-38	natriuretic peptide type B	Mus musculus	441-444
12807726-9	2003	Suppression of 8-OHdG formation by PB at low dose might be related to the enhanced mRNA expression of 8-OHdG repair enzyme, oxoguanine glycosylase 1 (Ogg1).	Phenobarbital	35-37	8-oxoguanine DNA glycosylase	Rattus norvegicus	124-148
12807726-9	2003	Suppression of 8-OHdG formation by PB at low dose might be related to the enhanced mRNA expression of 8-OHdG repair enzyme, oxoguanine glycosylase 1 (Ogg1).	Phenobarbital	35-37	8-oxoguanine DNA glycosylase	Rattus norvegicus	150-154
12807726-10	2003	Moreover, as detected by cDNA microarray analysis, PB treatment at low dose enhanced mRNA expression of glutamic acid decarboxylase (GAD65), an enzyme involved in the synthesis of gamma-aminobutyric acid (GABA), and suppressed MAP kinase p38 and other intracellular kinases gene expression.	Phenobarbital	51-53	glutamate decarboxylase 2	Rattus norvegicus	133-138
12807726-10	2003	Moreover, as detected by cDNA microarray analysis, PB treatment at low dose enhanced mRNA expression of glutamic acid decarboxylase (GAD65), an enzyme involved in the synthesis of gamma-aminobutyric acid (GABA), and suppressed MAP kinase p38 and other intracellular kinases gene expression.	Phenobarbital	51-53	mitogen activated protein kinase 14	Rattus norvegicus	238-241
12807726-11	2003	On the contrary, when PB was applied at a high dose, GST-P positive foci numbers and areas, tumor multiplicity, hydroxyl radicals and 8-OHdG levels were greatly elevated with the increase in CYP2B1/2 and CYP3A2 mRNA, protein, activity and gene expression of GST, nuclear tyrosine phosphatase, NADPH- cytochrome P-450 reductase and guanine nucleotide binding protein G(O) alpha subunit.	Phenobarbital	22-24	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	191-197
12807726-11	2003	On the contrary, when PB was applied at a high dose, GST-P positive foci numbers and areas, tumor multiplicity, hydroxyl radicals and 8-OHdG levels were greatly elevated with the increase in CYP2B1/2 and CYP3A2 mRNA, protein, activity and gene expression of GST, nuclear tyrosine phosphatase, NADPH- cytochrome P-450 reductase and guanine nucleotide binding protein G(O) alpha subunit.	Phenobarbital	22-24	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	204-210
12807726-11	2003	On the contrary, when PB was applied at a high dose, GST-P positive foci numbers and areas, tumor multiplicity, hydroxyl radicals and 8-OHdG levels were greatly elevated with the increase in CYP2B1/2 and CYP3A2 mRNA, protein, activity and gene expression of GST, nuclear tyrosine phosphatase, NADPH- cytochrome P-450 reductase and guanine nucleotide binding protein G(O) alpha subunit.	Phenobarbital	22-24	cytochrome p450 oxidoreductase	Rattus norvegicus	293-326
12867494-8	2003	Male-specific CYP2C11 was a major enzyme in (-)-verbenone 10-hydroxylation by untreated rat livers, and CYP2B1 catalyzed this reaction in liver microsomes of phenobarbital-treated rats.	Phenobarbital	158-171	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	14-21
12867494-8	2003	Male-specific CYP2C11 was a major enzyme in (-)-verbenone 10-hydroxylation by untreated rat livers, and CYP2B1 catalyzed this reaction in liver microsomes of phenobarbital-treated rats.	Phenobarbital	158-171	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	104-110
14642740-8	2003	For example, PCB 47, 52, and 54 bind preferentially to CYP2B and to a lesser extent to CYP3A enzymes in microsomes from PB-treated male rats; PCB 52 binds primarily to CYP3A enzymes in microsomes from DEX-treated female rats; and PCB 54 binds to CYP3A and to CYP2C enzymes in microsomes from control male rats.	Phenobarbital	120-122	pyruvate carboxylase	Rattus norvegicus	13-16
14642740-8	2003	For example, PCB 47, 52, and 54 bind preferentially to CYP2B and to a lesser extent to CYP3A enzymes in microsomes from PB-treated male rats; PCB 52 binds primarily to CYP3A enzymes in microsomes from DEX-treated female rats; and PCB 54 binds to CYP3A and to CYP2C enzymes in microsomes from control male rats.	Phenobarbital	120-122	pyruvate carboxylase	Rattus norvegicus	142-145
14705859-3	2003	Constitutive androstane receptor (CAR) is activated by xenobiotics, such as phenobarbital, but also by toxic endogenous compounds such as bilirubin metabolite(s).	Phenobarbital	76-89	nuclear receptor subfamily 1 group I member 3	Homo sapiens	0-32
14705859-3	2003	Constitutive androstane receptor (CAR) is activated by xenobiotics, such as phenobarbital, but also by toxic endogenous compounds such as bilirubin metabolite(s).	Phenobarbital	76-89	nuclear receptor subfamily 1 group I member 3	Homo sapiens	34-37
14705859-10	2003	As expected, we observed that these molecules inhibit both CAR gene expression and phenobarbital-mediated CYP gene expression in human hepatocytes.	Phenobarbital	83-96	peptidylprolyl isomerase G	Homo sapiens	106-109
14705863-6	2003	This explains the risk for drug interactions that is inherent to pharmacotherapy with PXR ligands such as rifampin, phenobarbital, statins, and St. John"s wort.	Phenobarbital	116-129	nuclear receptor subfamily 1 group I member 2	Homo sapiens	86-89
14566026-6	2003	The hepatic CYP2A5 inducers pyrazole and phenobarbital neither changed the CYP2A5 expression pattern nor damaged the olfactory mucosa.	Phenobarbital	41-54	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	12-18
14566026-6	2003	The hepatic CYP2A5 inducers pyrazole and phenobarbital neither changed the CYP2A5 expression pattern nor damaged the olfactory mucosa.	Phenobarbital	41-54	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	75-81
14642999-5	2003	The significant correlations (P&lt;0.01) between ceruloplasmin and the urinary excretion of D-glucaric acid, serum gamma-glutamyltransferase (GGT) and drug score in the patients group, would suggest that phenobarbital-type enzyme-inducing agents may increase the hepatic synthesis of ceruloplasmin.	Phenobarbital	204-217	ceruloplasmin	Homo sapiens	49-62
14642999-7	2003	The values obtained for the specific oxidase activity of ceruloplasmin (activity per unit mass of enzyme protein) suggest that in the most of the cases, chronic administration of phenobarbital, phenytoin, carbamazepine or valproic acid, does not produce marginal or moderate copper deficiency.	Phenobarbital	179-192	ceruloplasmin	Homo sapiens	57-70
13679865-2	2003	To investigate the influence of FoxM1B on liver tumor formation, we examined the effect of sustained enrichment of FoxM1B in the hepatocytes of mice treated with a diethylnitrosamine (DEN)/phenobarbital tumor induction protocol.	Phenobarbital	189-202	forkhead box M1	Mus musculus	115-121
12920159-4	2003	CYP2B2 expression was limited to the livers of PB-treated male and female rats and was not detected in spleen.	Phenobarbital	47-49	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	0-6
12920159-5	2003	Low constitutive levels of CYP2B1 mRNA were markedly induced approximately 7- to 17-fold in the livers of PB-treated male and female rats, respectively.	Phenobarbital	106-108	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	27-33
12920159-7	2003	Putative splenic CYP2B1 mRNA was significantly elevated by the PB treatment, although not as profoundly as the hepatic response.	Phenobarbital	63-65	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	17-23
15208740-0	2003	Biochemical characterization of porphobilinogen deaminase-deficient mice during phenobarbital induction of heme synthesis and the effect of enzyme replacement.	Phenobarbital	80-93	hydroxymethylbilane synthase	Mus musculus	32-57
12788952-6	2003	Taken together, the data suggest an unanticipated role for PITP alpha in with glucose homeostasis and in mammalian endoplasmic reticulum functions that interface with transport of specific luminal lipid cargoes.	Phenobarbital	189-196	phosphatidylinositol transfer protein alpha	Homo sapiens	59-69
14570762-9	2003	In CAR-/- mice, the robust induction of CYP2B10 by PB was completely absent.	Phenobarbital	51-53	nuclear receptor subfamily 1, group I, member 3	Mus musculus	3-6
14570762-9	2003	In CAR-/- mice, the robust induction of CYP2B10 by PB was completely absent.	Phenobarbital	51-53	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	40-47
14570762-10	2003	However, Mrp3 was equally induced both in wild-type and CAR-/- mice by PB.	Phenobarbital	71-73	prolactin family 2, subfamily c, member 4	Mus musculus	9-13
14570762-11	2003	These data clearly demonstrate that induction of hepatic Mrp3 by PB and other microsomal enzyme inducers is CAR-independent and implies a role for RXRalpha in the constitutive expression of Mrp3.	Phenobarbital	65-67	prolactin family 2, subfamily c, member 4	Mus musculus	57-61
14570762-11	2003	These data clearly demonstrate that induction of hepatic Mrp3 by PB and other microsomal enzyme inducers is CAR-independent and implies a role for RXRalpha in the constitutive expression of Mrp3.	Phenobarbital	65-67	nuclear receptor subfamily 1, group I, member 3	Mus musculus	108-111
14570766-6	2003	Phenobarbital (PB) induced CYP2B9, CYP2B10, and CYP2B20 mRNAs and suppressed CYP2B19 mRNA levels.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	27-33
14570766-6	2003	Phenobarbital (PB) induced CYP2B9, CYP2B10, and CYP2B20 mRNAs and suppressed CYP2B19 mRNA levels.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	35-42
14570766-6	2003	Phenobarbital (PB) induced CYP2B9, CYP2B10, and CYP2B20 mRNAs and suppressed CYP2B19 mRNA levels.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	48-55
14570766-6	2003	Phenobarbital (PB) induced CYP2B9, CYP2B10, and CYP2B20 mRNAs and suppressed CYP2B19 mRNA levels.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 19	Mus musculus	77-84
14570766-6	2003	Phenobarbital (PB) induced CYP2B9, CYP2B10, and CYP2B20 mRNAs and suppressed CYP2B19 mRNA levels.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	27-33
14570766-6	2003	Phenobarbital (PB) induced CYP2B9, CYP2B10, and CYP2B20 mRNAs and suppressed CYP2B19 mRNA levels.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	35-42
14570766-6	2003	Phenobarbital (PB) induced CYP2B9, CYP2B10, and CYP2B20 mRNAs and suppressed CYP2B19 mRNA levels.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	48-55
14570766-6	2003	Phenobarbital (PB) induced CYP2B9, CYP2B10, and CYP2B20 mRNAs and suppressed CYP2B19 mRNA levels.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 19	Mus musculus	77-84
14570766-7	2003	PB also induced CYP2C29 and CYP2C40, but not CYP2C38 mRNA.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	16-23
14570766-7	2003	PB also induced CYP2C29 and CYP2C40, but not CYP2C38 mRNA.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily c, polypeptide 40	Mus musculus	28-35
14570766-9	2003	CYP1A1 was inducible by beta-naphthoflavone (BNF), CYP2B and CYP2C by PB, and CYP3A by DEX.	Phenobarbital	70-72	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	0-6
14570766-9	2003	CYP1A1 was inducible by beta-naphthoflavone (BNF), CYP2B and CYP2C by PB, and CYP3A by DEX.	Phenobarbital	70-72	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	51-56
12869653-8	2003	Nuclear accumulation of CAR, but not PXR, was observed in the liver tissue following DDE and PB treatment.	Phenobarbital	93-95	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	24-27
12933323-4	2003	Phenobarbital induces hepatic cytochrome P450s CYP2B1/2 and CYP3A1/2 and thyroxine (T(4))-UDP-glucuronosyltransferase (T(4)-UGT), which enhances thyroxine clearance and thus indirectly increases thyroid gland activity.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	47-53
12869653-3	2003	The induction of CYP 2B and 3A by PB is known to be regulated through the nuclear receptors constitutive androstane receptor (CAR) and pregnane X receptor (PXR), respectively.	Phenobarbital	34-36	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	92-124
12869653-3	2003	The induction of CYP 2B and 3A by PB is known to be regulated through the nuclear receptors constitutive androstane receptor (CAR) and pregnane X receptor (PXR), respectively.	Phenobarbital	34-36	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	126-129
12869653-3	2003	The induction of CYP 2B and 3A by PB is known to be regulated through the nuclear receptors constitutive androstane receptor (CAR) and pregnane X receptor (PXR), respectively.	Phenobarbital	34-36	nuclear receptor subfamily 1, group I, member 2	Rattus norvegicus	135-154
12869653-3	2003	The induction of CYP 2B and 3A by PB is known to be regulated through the nuclear receptors constitutive androstane receptor (CAR) and pregnane X receptor (PXR), respectively.	Phenobarbital	34-36	nuclear receptor subfamily 1, group I, member 2	Rattus norvegicus	156-159
12837975-0	2003	Phenobarbital-imprinted overinduction of adult constituent CYP isoforms.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	59-62
12837975-4	2003	The major female-specific CYP2C12 and male-specific CYP2C13 were unresponsive to induction, whereas the major male-specific CYP2C11 responded to phenobarbital administration with a 100% increase in transcript levels that were not translated into new protein.	Phenobarbital	145-158	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	124-131
12837975-5	2003	The expression of the other isoforms was significantly elevated by both doses of phenobarbital (10 mg &gt;1 mg), though CYP2C6, CYP3A1, and CYP3A2 levels were increased an additional 30-50% when the animals were neonatally exposed to the barbiturate, demonstrating for the first time that mechanisms regulating induction of constitutive CYPs in adults are imprintable at birth.	Phenobarbital	81-94	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	120-126
12837975-5	2003	The expression of the other isoforms was significantly elevated by both doses of phenobarbital (10 mg &gt;1 mg), though CYP2C6, CYP3A1, and CYP3A2 levels were increased an additional 30-50% when the animals were neonatally exposed to the barbiturate, demonstrating for the first time that mechanisms regulating induction of constitutive CYPs in adults are imprintable at birth.	Phenobarbital	81-94	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	128-134
12837975-5	2003	The expression of the other isoforms was significantly elevated by both doses of phenobarbital (10 mg &gt;1 mg), though CYP2C6, CYP3A1, and CYP3A2 levels were increased an additional 30-50% when the animals were neonatally exposed to the barbiturate, demonstrating for the first time that mechanisms regulating induction of constitutive CYPs in adults are imprintable at birth.	Phenobarbital	81-94	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	140-146
12885400-1	2003	The nuclear receptor CAR, a phenobarbital (PB)-responsive transcription factor, translocates into the nucleus of hepatocytes after PB induction.	Phenobarbital	28-41	nuclear receptor subfamily 1, group I, member 3	Mus musculus	21-24
12885400-1	2003	The nuclear receptor CAR, a phenobarbital (PB)-responsive transcription factor, translocates into the nucleus of hepatocytes after PB induction.	Phenobarbital	43-45	nuclear receptor subfamily 1, group I, member 3	Mus musculus	21-24
12885400-1	2003	The nuclear receptor CAR, a phenobarbital (PB)-responsive transcription factor, translocates into the nucleus of hepatocytes after PB induction.	Phenobarbital	131-133	nuclear receptor subfamily 1, group I, member 3	Mus musculus	21-24
12885400-3	2003	In response to PB induction, protein phosphatase 2A is recruited to the CAR:HSP90 complex.	Phenobarbital	15-17	nuclear receptor subfamily 1, group I, member 3	Mus musculus	72-75
12885400-3	2003	In response to PB induction, protein phosphatase 2A is recruited to the CAR:HSP90 complex.	Phenobarbital	15-17	heat shock protein, 2	Mus musculus	76-81
12885400-4	2003	This recruitment may lead CAR to translocate into the nucleus, consistent with the inhibitions of nuclear CAR accumulation in PB-induced mouse primary hepatocytes by okadaic acid as well as by geldanamycin.	Phenobarbital	126-128	nuclear receptor subfamily 1, group I, member 3	Mus musculus	26-29
12885400-4	2003	This recruitment may lead CAR to translocate into the nucleus, consistent with the inhibitions of nuclear CAR accumulation in PB-induced mouse primary hepatocytes by okadaic acid as well as by geldanamycin.	Phenobarbital	126-128	nuclear receptor subfamily 1, group I, member 3	Mus musculus	106-109
12848774-7	2003	After administration of phenobarbitone dosed to steady-state, the pharmacokinetics of retigabine at steady-state were similar (AUC of 4433 ng x ml(-1) x h and t1/2 of 8.5 h) to those of retigabine alone.	Phenobarbital	24-38	CD5 molecule	Homo sapiens	159-172
12933323-4	2003	Phenobarbital induces hepatic cytochrome P450s CYP2B1/2 and CYP3A1/2 and thyroxine (T(4))-UDP-glucuronosyltransferase (T(4)-UGT), which enhances thyroxine clearance and thus indirectly increases thyroid gland activity.	Phenobarbital	0-13	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	60-66
12815171-0	2003	Phenobarbital alters hepatic Mrp2 function by direct and indirect interactions.	Phenobarbital	0-13	ATP binding cassette subfamily C member 2	Rattus norvegicus	29-33
12815171-4	2003	The role of multidrug resistance-associated protein 2 (Mrp2) in the biliary excretion of PB and metabolites was studied using isolated perfused livers (IPLs) from Wistar and Mrp2-deficient TR- rats.	Phenobarbital	89-91	ATP binding cassette subfamily C member 2	Rattus norvegicus	12-53
12815171-4	2003	The role of multidrug resistance-associated protein 2 (Mrp2) in the biliary excretion of PB and metabolites was studied using isolated perfused livers (IPLs) from Wistar and Mrp2-deficient TR- rats.	Phenobarbital	89-91	ATP binding cassette subfamily C member 2	Rattus norvegicus	55-59
12815171-7	2003	Mrp2 message was increased (2.3-fold) by PB pretreatment (80 mg/kg i.p.	Phenobarbital	41-43	ATP binding cassette subfamily C member 2	Rattus norvegicus	0-4
12815171-9	2003	Mrp2 protein was increased slightly in PB-treated livers and remained slightly elevated after a 24-h washout, but it was decreased significantly to 62 +/-7% of control values after a 48-h washout.	Phenobarbital	39-41	ATP binding cassette subfamily C member 2	Rattus norvegicus	0-4
12815171-11	2003	These data support two mechanisms for impaired biliary excretion of some organic anions by PB treatment: 1) PBOH-glucuronide is a substrate for Mrp2 and may compete with other organic anions for biliary excretion and 2) Mrp2 protein expression and functional capacity is decreased 48 h after PB treatment.	Phenobarbital	91-93	ATP binding cassette subfamily C member 2	Rattus norvegicus	144-148
12815171-11	2003	These data support two mechanisms for impaired biliary excretion of some organic anions by PB treatment: 1) PBOH-glucuronide is a substrate for Mrp2 and may compete with other organic anions for biliary excretion and 2) Mrp2 protein expression and functional capacity is decreased 48 h after PB treatment.	Phenobarbital	91-93	ATP binding cassette subfamily C member 2	Rattus norvegicus	220-224
12815171-11	2003	These data support two mechanisms for impaired biliary excretion of some organic anions by PB treatment: 1) PBOH-glucuronide is a substrate for Mrp2 and may compete with other organic anions for biliary excretion and 2) Mrp2 protein expression and functional capacity is decreased 48 h after PB treatment.	Phenobarbital	108-110	ATP binding cassette subfamily C member 2	Rattus norvegicus	144-148
12815171-11	2003	These data support two mechanisms for impaired biliary excretion of some organic anions by PB treatment: 1) PBOH-glucuronide is a substrate for Mrp2 and may compete with other organic anions for biliary excretion and 2) Mrp2 protein expression and functional capacity is decreased 48 h after PB treatment.	Phenobarbital	108-110	ATP binding cassette subfamily C member 2	Rattus norvegicus	220-224
12815172-4	2003	Colchicine (COL) decreased both basal and rifampicin- and phenobarbital-inducible expression of CYP2B6, CYP2C8/9, and CYP3A4.	Phenobarbital	58-71	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	96-102
12815172-4	2003	Colchicine (COL) decreased both basal and rifampicin- and phenobarbital-inducible expression of CYP2B6, CYP2C8/9, and CYP3A4.	Phenobarbital	58-71	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	104-110
12815172-4	2003	Colchicine (COL) decreased both basal and rifampicin- and phenobarbital-inducible expression of CYP2B6, CYP2C8/9, and CYP3A4.	Phenobarbital	58-71	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	118-124
12877362-5	2003	Following 24 h culture of rat liver slices in the presence of phenobarbital, the level of UGT2B12-mRNA increased about twofold, which corresponds to the inducibility in vivo.	Phenobarbital	62-75	UDP glucuronosyltransferase 2 family, polypeptide B35	Rattus norvegicus	90-97
12948624-0	2003	Phenytoin and phenobarbital inhibit human HERG potassium channels.	Phenobarbital	14-27	potassium voltage-gated channel subfamily H member 2	Homo sapiens	42-46
12948624-4	2003	Tail currents, which are purely related to HERG, were blocked with an IC50 (the concentration when 50% inhibition was obtained compared to control values) of 240 microM for PHT and 3 mM for PB.	Phenobarbital	190-192	potassium voltage-gated channel subfamily H member 2	Homo sapiens	43-47
12870655-7	2003	Additional experiments showed that phenobarbital increased CYP2B6 mRNA expression and that pregnane X receptor (PXR) but not constitutive androstane receptor (CAR) was detected in HL-60 cells.	Phenobarbital	35-48	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	59-65
12695338-6	2003	Additionally, phenobarbital (PB)-inducible Oatp2 and Mrp3 gene expression was significantly increased in the PXR-KO mice when compared with wild-type PB-treated mice.	Phenobarbital	14-27	solute carrier organic anion transporter family, member 1a4	Mus musculus	43-48
12695338-6	2003	Additionally, phenobarbital (PB)-inducible Oatp2 and Mrp3 gene expression was significantly increased in the PXR-KO mice when compared with wild-type PB-treated mice.	Phenobarbital	14-27	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	53-57
12695338-6	2003	Additionally, phenobarbital (PB)-inducible Oatp2 and Mrp3 gene expression was significantly increased in the PXR-KO mice when compared with wild-type PB-treated mice.	Phenobarbital	14-27	nuclear receptor subfamily 1, group I, member 2	Mus musculus	109-115
12695338-6	2003	Additionally, phenobarbital (PB)-inducible Oatp2 and Mrp3 gene expression was significantly increased in the PXR-KO mice when compared with wild-type PB-treated mice.	Phenobarbital	29-31	solute carrier organic anion transporter family, member 1a4	Mus musculus	43-48
12695338-6	2003	Additionally, phenobarbital (PB)-inducible Oatp2 and Mrp3 gene expression was significantly increased in the PXR-KO mice when compared with wild-type PB-treated mice.	Phenobarbital	29-31	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	53-57
12695338-6	2003	Additionally, phenobarbital (PB)-inducible Oatp2 and Mrp3 gene expression was significantly increased in the PXR-KO mice when compared with wild-type PB-treated mice.	Phenobarbital	29-31	nuclear receptor subfamily 1, group I, member 2	Mus musculus	109-115
12695338-6	2003	Additionally, phenobarbital (PB)-inducible Oatp2 and Mrp3 gene expression was significantly increased in the PXR-KO mice when compared with wild-type PB-treated mice.	Phenobarbital	150-152	solute carrier organic anion transporter family, member 1a4	Mus musculus	43-48
12695338-6	2003	Additionally, phenobarbital (PB)-inducible Oatp2 and Mrp3 gene expression was significantly increased in the PXR-KO mice when compared with wild-type PB-treated mice.	Phenobarbital	150-152	ATP-binding cassette, sub-family C (CFTR/MRP), member 3	Mus musculus	53-57
12695338-6	2003	Additionally, phenobarbital (PB)-inducible Oatp2 and Mrp3 gene expression was significantly increased in the PXR-KO mice when compared with wild-type PB-treated mice.	Phenobarbital	150-152	nuclear receptor subfamily 1, group I, member 2	Mus musculus	109-115
12695338-7	2003	We also examined the effect of PXR ablation on PB-inducible hepatic CYP3A activity in vivo.	Phenobarbital	47-49	nuclear receptor subfamily 1, group I, member 2	Mus musculus	31-34
12695338-8	2003	Microsomes isolated from PB-treated PXR-KO mice exhibited a significantly elevated rate of testosterone 6 beta-hydroxylation when compared with microsomes isolated from wild-type PB-treated mice.	Phenobarbital	25-27	nuclear receptor subfamily 1, group I, member 2	Mus musculus	36-42
12695338-9	2003	PB treatment produced significantly increased levels of hepatomegaly in PXR-KO mice when compared with wild-type PB-treated mice.	Phenobarbital	0-2	nuclear receptor subfamily 1, group I, member 2	Mus musculus	72-78
12872719-6	2003	In hamsters, the concentration of M-4 was increased to 1.8-fold of untreated animals by PB treatment and 2.6-fold by MC treatment.	Phenobarbital	88-90	cholinergic receptor, muscarinic 4	Rattus norvegicus	34-37
12673034-3	2003	In this study, we demonstrated the inductive effects of phenobarbital, rifampicin, carbamazepine, phenytoin, prednisolone, ciclosporin and clotrimazole on CYP3A4, CYP3A5 and CYP3A7 mRNA expression, and established the relationship between the expression of human glucocorticoid receptor alpha (hGR) mRNA and the induction of CYP3A4 mRNA in cultured HepG2 cells by reverse transcription polymerase chain reaction (RT-PCR).	Phenobarbital	56-69	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	155-161
12695351-4	2003	In contrast, treatment with 0.1 microM DEX enhanced CYP2B6 induction by different pregnane X receptor (PXR) activators, including rifampin, phenytoin, clotrimazole, and phenobarbital.	Phenobarbital	169-182	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	52-58
12695351-5	2003	In Huh7 cells, cotransfection of human (h)GR and hPXR with CYP2B6-phenobarbital-responsive enhancer module (PBREM) reporter constructs revealed that all hPXR ligands induce CYP2B6 reporter gene activity, and this ligand-dependent activation is greatly enhanced by activated hGR.	Phenobarbital	66-79	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	59-65
12571232-2	2003	Previous studies have shown that the nuclear receptors constitutive androstane receptor (CAR) and pregnane X receptor (PXR) are involved in the transcriptional regulation of CYP2B genes through the phenobarbital-responsive enhancer module (PBREM).	Phenobarbital	198-211	nuclear receptor subfamily 1 group I member 3	Homo sapiens	89-92
12571232-2	2003	Previous studies have shown that the nuclear receptors constitutive androstane receptor (CAR) and pregnane X receptor (PXR) are involved in the transcriptional regulation of CYP2B genes through the phenobarbital-responsive enhancer module (PBREM).	Phenobarbital	198-211	nuclear receptor subfamily 1 group I member 2	Homo sapiens	98-117
12571232-2	2003	Previous studies have shown that the nuclear receptors constitutive androstane receptor (CAR) and pregnane X receptor (PXR) are involved in the transcriptional regulation of CYP2B genes through the phenobarbital-responsive enhancer module (PBREM).	Phenobarbital	198-211	nuclear receptor subfamily 1 group I member 2	Homo sapiens	119-122
12659874-5	2003	This effect was mimicked by the PXR ligands clotrimazole and phenobarbital, but not by Wy14,643 or rosiglitazone, which are ligands for PPAR alpha and -gamma, respectively.	Phenobarbital	61-74	nuclear receptor subfamily 1 group I member 2	Homo sapiens	32-35
12751798-7	2003	Phenobarbital treatment sharply increased HO-1 mRNA and protein expression in selenium-deficient liver and HO activity in hepatocytes, but had no effect in control liver or in the Kupffer cell/endothelial cell fraction of selenium-deficient liver.	Phenobarbital	0-13	heme oxygenase 1	Rattus norvegicus	42-46
12751798-8	2003	Electrophoretic mobility shift assays showed increased AP-1 binding activity, suggesting an involvement of this redox-sensitive transcription factor in the induction by phenobarbital of HO-1 in selenium deficiency.	Phenobarbital	169-182	heme oxygenase 1	Rattus norvegicus	186-190
12673034-3	2003	In this study, we demonstrated the inductive effects of phenobarbital, rifampicin, carbamazepine, phenytoin, prednisolone, ciclosporin and clotrimazole on CYP3A4, CYP3A5 and CYP3A7 mRNA expression, and established the relationship between the expression of human glucocorticoid receptor alpha (hGR) mRNA and the induction of CYP3A4 mRNA in cultured HepG2 cells by reverse transcription polymerase chain reaction (RT-PCR).	Phenobarbital	56-69	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	163-169
12673034-3	2003	In this study, we demonstrated the inductive effects of phenobarbital, rifampicin, carbamazepine, phenytoin, prednisolone, ciclosporin and clotrimazole on CYP3A4, CYP3A5 and CYP3A7 mRNA expression, and established the relationship between the expression of human glucocorticoid receptor alpha (hGR) mRNA and the induction of CYP3A4 mRNA in cultured HepG2 cells by reverse transcription polymerase chain reaction (RT-PCR).	Phenobarbital	56-69	cytochrome P450 family 3 subfamily A member 7	Homo sapiens	174-180
12673034-3	2003	In this study, we demonstrated the inductive effects of phenobarbital, rifampicin, carbamazepine, phenytoin, prednisolone, ciclosporin and clotrimazole on CYP3A4, CYP3A5 and CYP3A7 mRNA expression, and established the relationship between the expression of human glucocorticoid receptor alpha (hGR) mRNA and the induction of CYP3A4 mRNA in cultured HepG2 cells by reverse transcription polymerase chain reaction (RT-PCR).	Phenobarbital	56-69	nuclear receptor subfamily 3 group C member 1	Homo sapiens	263-286
12673034-3	2003	In this study, we demonstrated the inductive effects of phenobarbital, rifampicin, carbamazepine, phenytoin, prednisolone, ciclosporin and clotrimazole on CYP3A4, CYP3A5 and CYP3A7 mRNA expression, and established the relationship between the expression of human glucocorticoid receptor alpha (hGR) mRNA and the induction of CYP3A4 mRNA in cultured HepG2 cells by reverse transcription polymerase chain reaction (RT-PCR).	Phenobarbital	56-69	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	325-331
12642458-8	2003	We have found that CYP2A10 previously reported only in rabbit olfactory and respiratory nasal mucosa is present in phenobarbital (PB)-induced rabbit liver microsomes.	Phenobarbital	115-128	cytochrome P450 2A10	Oryctolagus cuniculus	19-26
12642458-8	2003	We have found that CYP2A10 previously reported only in rabbit olfactory and respiratory nasal mucosa is present in phenobarbital (PB)-induced rabbit liver microsomes.	Phenobarbital	130-132	cytochrome P450 2A10	Oryctolagus cuniculus	19-26
12739762-0	2003	Induction of cytochrome P450 2B6 and 3A4 expression by phenobarbital and cyclophosphamide in cultured human liver slices.	Phenobarbital	55-68	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	13-32
12739762-4	2003	Then we tested the effects of phenobarbital and cyclophosphamide on CYP expression in both models.	Phenobarbital	30-43	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	68-71
12739762-8	2003	CYP2B6 and 3A4 mRNA, apoprotein, and enzyme-related activities were induced by phenobarbital and cyclophosphamide, whereas CYP2C9 apoprotein was not.	Phenobarbital	79-92	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-6
12712632-2	2003	Pretreatment with phenobarbital (PB) or dexamethasone (DEX) resulted in a significant increase in 4 beta-hydroxymethyl-4 beta-demethylterritrem A (MA1) production.	Phenobarbital	18-31	Activity QTL 1	Rattus norvegicus	147-150
12712632-2	2003	Pretreatment with phenobarbital (PB) or dexamethasone (DEX) resulted in a significant increase in 4 beta-hydroxymethyl-4 beta-demethylterritrem A (MA1) production.	Phenobarbital	33-35	Activity QTL 1	Rattus norvegicus	147-150
12712632-3	2003	SKF 525A (0.025 and 0.05 mM), a general cytochrome P-450 (CYP450) inhibitor, blocked MA1 formation in liver microsomes from PB-pretreated female rats.	Phenobarbital	124-126	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	58-64
12712632-3	2003	SKF 525A (0.025 and 0.05 mM), a general cytochrome P-450 (CYP450) inhibitor, blocked MA1 formation in liver microsomes from PB-pretreated female rats.	Phenobarbital	124-126	Activity QTL 1	Rattus norvegicus	85-88
12712632-4	2003	Anti-CYP2B antibody had no marked effect on MA1 formation, although orphenadrine (0.5 mM), which inhibits CYP2B, blocked MA1 formation in liver microsomes from PB-treated female rats.	Phenobarbital	160-162	Activity QTL 1	Rattus norvegicus	121-124
12712632-5	2003	An immunoinhibition study showed that anti-CYP3A2 antibody reduced MA1 formation to nondetectable levels in liver microsomes from PB-treated female rats.	Phenobarbital	130-132	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	43-49
12712632-5	2003	An immunoinhibition study showed that anti-CYP3A2 antibody reduced MA1 formation to nondetectable levels in liver microsomes from PB-treated female rats.	Phenobarbital	130-132	Activity QTL 1	Rattus norvegicus	67-70
12573483-0	2003	Phenobarbital induction of drug/steroid-metabolizing enzymes and nuclear receptor CAR.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	82-85
12573483-3	2003	In response to PB, CAR forms a heterodimer with the retinoid X receptor (RXR), binds to a PB response element (typified by DR-4 motif), and activates transcription of the gene.	Phenobarbital	15-17	nuclear receptor subfamily 1, group I, member 3	Mus musculus	19-22
12573483-3	2003	In response to PB, CAR forms a heterodimer with the retinoid X receptor (RXR), binds to a PB response element (typified by DR-4 motif), and activates transcription of the gene.	Phenobarbital	90-92	nuclear receptor subfamily 1, group I, member 3	Mus musculus	19-22
12573483-4	2003	In the CAR-null mouse, PB does not only induce the Cyp2b10 gene, but also induces genes encoding various metabolizing enzymes.	Phenobarbital	23-25	nuclear receptor subfamily 1, group I, member 3	Mus musculus	7-10
12573483-4	2003	In the CAR-null mouse, PB does not only induce the Cyp2b10 gene, but also induces genes encoding various metabolizing enzymes.	Phenobarbital	23-25	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	51-58
12573483-5	2003	Thus, CAR is a general nuclear receptor that is essential for PB induction of drug/steroid metabolizing enzymes.	Phenobarbital	62-64	nuclear receptor subfamily 1, group I, member 3	Mus musculus	6-9
12573483-6	2003	PB also induces amino levulinate synthase 1 (ALAS-1), the rate-limiting enzyme in heme biosynthesis, to increase heme supply.	Phenobarbital	0-2	aminolevulinic acid synthase 1	Mus musculus	16-43
12573483-6	2003	PB also induces amino levulinate synthase 1 (ALAS-1), the rate-limiting enzyme in heme biosynthesis, to increase heme supply.	Phenobarbital	0-2	aminolevulinic acid synthase 1	Mus musculus	45-51
12573485-2	2003	The core of the PBRU contains two nuclear receptor sites, NR-1 and NR-2, and a nuclear factor-1 (NF 1) binding site, which are required for PB responsiveness, but the importance of sequences flanking the core is not clear.	Phenobarbital	16-18	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	58-71
12573485-2	2003	The core of the PBRU contains two nuclear receptor sites, NR-1 and NR-2, and a nuclear factor-1 (NF 1) binding site, which are required for PB responsiveness, but the importance of sequences flanking the core is not clear.	Phenobarbital	16-18	neurofibromin 1	Mus musculus	97-101
12573485-4	2003	In this assay PB treatment increased transactivation by the Cyp2b10 PBRU about 100-fold, which is similar to the increase in the expression of the endogenous gene while the Cyp2b9 PBRU was unresponsive.	Phenobarbital	14-16	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	60-67
12573485-10	2003	These results indicate that changes in the NR sites which eliminate CAR/RXR binding are sufficient for the non-responsiveness to PB of Cyp2b9, but changes in sequences flanking the core independently eliminate PB responsiveness.	Phenobarbital	129-131	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	135-141
12167560-6	2002	Uptake of AG by Mrp2 and Mrp3, and inhibition of Mrp2- and Mrp3-mediated transport by PB and major PB metabolites, were investigated with rat Mrp2- or Mrp3-expressing Sf9 cell plasma membrane vesicles (Sf9-PMVs).	Phenobarbital	86-88	ATP binding cassette subfamily C member 3	Rattus norvegicus	59-63
12604189-9	2003	Additionally, ALDH3A1, CRP, and HPT were induced by BaP subacute treatment, whereas another type of ALDH inducer, phenobarbital, did not affect the levels of APPs or ALDH3A1, but did increase ALDH1A3 activity.	Phenobarbital	114-127	aldehyde dehydrogenase 1 family, member A3	Rattus norvegicus	192-199
12464260-1	2003	The nuclear receptor CAR (constitutive active receptor) mediates the induction of transcription of cytochrome P450 (CYP) genes by phenobarbital (PB) and PB-type inducers.	Phenobarbital	130-143	nuclear receptor subfamily 1, group I, member 3	Mus musculus	21-24
12464260-1	2003	The nuclear receptor CAR (constitutive active receptor) mediates the induction of transcription of cytochrome P450 (CYP) genes by phenobarbital (PB) and PB-type inducers.	Phenobarbital	130-143	nuclear receptor subfamily 1, group I, member 3	Mus musculus	26-54
12464260-1	2003	The nuclear receptor CAR (constitutive active receptor) mediates the induction of transcription of cytochrome P450 (CYP) genes by phenobarbital (PB) and PB-type inducers.	Phenobarbital	145-147	nuclear receptor subfamily 1, group I, member 3	Mus musculus	21-24
12464260-1	2003	The nuclear receptor CAR (constitutive active receptor) mediates the induction of transcription of cytochrome P450 (CYP) genes by phenobarbital (PB) and PB-type inducers.	Phenobarbital	145-147	nuclear receptor subfamily 1, group I, member 3	Mus musculus	26-54
12464260-1	2003	The nuclear receptor CAR (constitutive active receptor) mediates the induction of transcription of cytochrome P450 (CYP) genes by phenobarbital (PB) and PB-type inducers.	Phenobarbital	153-155	nuclear receptor subfamily 1, group I, member 3	Mus musculus	21-24
12464260-1	2003	The nuclear receptor CAR (constitutive active receptor) mediates the induction of transcription of cytochrome P450 (CYP) genes by phenobarbital (PB) and PB-type inducers.	Phenobarbital	153-155	nuclear receptor subfamily 1, group I, member 3	Mus musculus	26-54
14569871-4	2003	CYP2B, CYP2C and CYP3A activities in the CP sensitive tumor were comparable to those in liver, and CYP2B, CYP2C were induced by phenobarbital and dexamethasone.	Phenobarbital	128-141	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	0-5
14569871-4	2003	CYP2B, CYP2C and CYP3A activities in the CP sensitive tumor were comparable to those in liver, and CYP2B, CYP2C were induced by phenobarbital and dexamethasone.	Phenobarbital	128-141	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	99-104
14569871-4	2003	CYP2B, CYP2C and CYP3A activities in the CP sensitive tumor were comparable to those in liver, and CYP2B, CYP2C were induced by phenobarbital and dexamethasone.	Phenobarbital	128-141	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	106-111
14569871-8	2003	LS insignificantly influenced liver CYP2B, CYP2C and CYP3A activities and their inducibility by phenobarbital and dexamethasone was similar to that obtained in liver of mice without tumor.	Phenobarbital	96-109	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	53-58
14569871-9	2003	At the same time, CYP2B and CYP2C activity in liver of RLS-bearing mice were essentially reduced, the activity CYP3A remained unchanged, and inducibility of CYP2B, CYP2C and CYP3A by phenobarbital and dexamethasone was similar to that in liver of mice without tumor.	Phenobarbital	183-196	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	157-162
14569871-9	2003	At the same time, CYP2B and CYP2C activity in liver of RLS-bearing mice were essentially reduced, the activity CYP3A remained unchanged, and inducibility of CYP2B, CYP2C and CYP3A by phenobarbital and dexamethasone was similar to that in liver of mice without tumor.	Phenobarbital	183-196	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	164-169
14569871-9	2003	At the same time, CYP2B and CYP2C activity in liver of RLS-bearing mice were essentially reduced, the activity CYP3A remained unchanged, and inducibility of CYP2B, CYP2C and CYP3A by phenobarbital and dexamethasone was similar to that in liver of mice without tumor.	Phenobarbital	183-196	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	174-179
12949661-1	2003	Ultralow doses of antibodies to phenobarbital and their mixture (1:1) with ultralow doses of antibodies to cholecystokinin reduced the severity of structural and metabolic disturbances in the liver of rats with acute CCl4-induced hepatitis.	Phenobarbital	32-45	C-C motif chemokine ligand 4	Rattus norvegicus	217-221
12511605-1	2003	The constitutive androstane receptor (CAR, NR1I3) transcriptionally activates cytochrome P450 2B6, 2C9, and 3A4 when activated by xenobiotics, such as phenobarbital.	Phenobarbital	151-164	nuclear receptor subfamily 1 group I member 3	Homo sapiens	4-36
12511605-1	2003	The constitutive androstane receptor (CAR, NR1I3) transcriptionally activates cytochrome P450 2B6, 2C9, and 3A4 when activated by xenobiotics, such as phenobarbital.	Phenobarbital	151-164	nuclear receptor subfamily 1 group I member 3	Homo sapiens	38-41
12511605-1	2003	The constitutive androstane receptor (CAR, NR1I3) transcriptionally activates cytochrome P450 2B6, 2C9, and 3A4 when activated by xenobiotics, such as phenobarbital.	Phenobarbital	151-164	nuclear receptor subfamily 1 group I member 3	Homo sapiens	43-48
12511605-1	2003	The constitutive androstane receptor (CAR, NR1I3) transcriptionally activates cytochrome P450 2B6, 2C9, and 3A4 when activated by xenobiotics, such as phenobarbital.	Phenobarbital	151-164	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	78-102
12445859-3	2002	The current study was designed to examine the NO dependencies of the down-regulation of phenobarbital-induced CYP2B mRNAs and proteins by bacterial endotoxin (lipopolysaccharide, LPS) treatment in vivo, using an NOS2-null mouse model.	Phenobarbital	88-101	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	110-115
12445859-3	2002	The current study was designed to examine the NO dependencies of the down-regulation of phenobarbital-induced CYP2B mRNAs and proteins by bacterial endotoxin (lipopolysaccharide, LPS) treatment in vivo, using an NOS2-null mouse model.	Phenobarbital	88-101	nitric oxide synthase 2, inducible	Mus musculus	212-216
12445859-4	2002	Treatment of C57/BL6 mice with 0.3 mg/kg of LPS maximally suppressed phenobarbital-induced CYP2B9 and 2B10 mRNAs measured 12 hr after injection, whereas 1-10 mg/kg of LPS was required to elevate NO production.	Phenobarbital	69-82	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	91-97
12464801-2	2002	UGT1A1 basal transcription is affected by a polymorphic (TA)n repeat, and another important regulatory element is the phenobarbital-responsive enhancer module (PBREM) which might contain variants affecting inducible gene expression.	Phenobarbital	118-131	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
12423659-9	2002	Phenobarbital caused an enhanced CYP2B1 and 3A2 and dexamethasone and pregnenolone 16 alpha-carbonitrile an increased CYP3A2 immunostaining.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	33-39
12423659-9	2002	Phenobarbital caused an enhanced CYP2B1 and 3A2 and dexamethasone and pregnenolone 16 alpha-carbonitrile an increased CYP3A2 immunostaining.	Phenobarbital	0-13	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	118-124
12384525-0	2002	Overexpression of glutamine synthetase is associated with beta-catenin-mutations in mouse liver tumors during promotion of hepatocarcinogenesis by phenobarbital.	Phenobarbital	147-160	glutamate-ammonia ligase (glutamine synthetase)	Mus musculus	18-38
12384525-2	2002	In the mouse, the promotional effect of PB on liver tumor development results from a selective stimulation of clonal outgrowth of hepatocytes harboring activating mutations in the beta-catenin gene.	Phenobarbital	40-42	catenin (cadherin associated protein), beta 1	Mus musculus	180-192
12384525-8	2002	We have previously shown that beta-catenin mutations are present in approximately 80% of liver tumors from PB-treated mice but are absent in liver tumors from mice treated with DEN only.	Phenobarbital	107-109	catenin (cadherin associated protein), beta 1	Mus musculus	30-42
12384525-11	2002	These data suggest that promotion of hepatocarcinogenesis by PB confers beta-catenin-mutated tumor cells with a selective advantage by up-regulation of GS expression.	Phenobarbital	61-63	catenin (cadherin associated protein), beta 1	Mus musculus	72-84
12231384-0	2002	Lack of effects of prolonged treatment with phenobarbital or phenytoin on the expression of P-glycoprotein in various rat brain regions.	Phenobarbital	44-57	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	92-106
12231384-4	2002	Two antiepileptic drugs, phenobarbital and phenytoin, have been reported to up-regulate P-glycoprotein in cell cultures, so that chronic treatment with antiepileptic drugs may enhance P-glycoprotein expression in the blood-brain barrier.	Phenobarbital	25-38	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	88-102
12231384-4	2002	Two antiepileptic drugs, phenobarbital and phenytoin, have been reported to up-regulate P-glycoprotein in cell cultures, so that chronic treatment with antiepileptic drugs may enhance P-glycoprotein expression in the blood-brain barrier.	Phenobarbital	25-38	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	184-198
12231384-6	2002	Except for a moderate increase in the intensity of P-glycoprotein expression in the piriform/parietal cortex and cerebellum of phenobarbital-treated rats, no significant P-glycoprotein increases were seen after prolonged treatment with phenobarbital or phenytoin in any brain region examined.	Phenobarbital	127-140	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	51-65
12167560-3	2002	It was hypothesized that inhibition of Mrp2-mediated AG transport by PB or PB metabolites, and PB induction of Mrp3, may contribute to the impaired biliary excretion of AG by PB.	Phenobarbital	69-71	ATP binding cassette subfamily C member 2	Rattus norvegicus	39-43
12167560-3	2002	It was hypothesized that inhibition of Mrp2-mediated AG transport by PB or PB metabolites, and PB induction of Mrp3, may contribute to the impaired biliary excretion of AG by PB.	Phenobarbital	75-77	ATP binding cassette subfamily C member 2	Rattus norvegicus	39-43
12167560-3	2002	It was hypothesized that inhibition of Mrp2-mediated AG transport by PB or PB metabolites, and PB induction of Mrp3, may contribute to the impaired biliary excretion of AG by PB.	Phenobarbital	75-77	ATP binding cassette subfamily C member 2	Rattus norvegicus	39-43
12167560-3	2002	It was hypothesized that inhibition of Mrp2-mediated AG transport by PB or PB metabolites, and PB induction of Mrp3, may contribute to the impaired biliary excretion of AG by PB.	Phenobarbital	75-77	ATP binding cassette subfamily C member 2	Rattus norvegicus	39-43
12167560-6	2002	Uptake of AG by Mrp2 and Mrp3, and inhibition of Mrp2- and Mrp3-mediated transport by PB and major PB metabolites, were investigated with rat Mrp2- or Mrp3-expressing Sf9 cell plasma membrane vesicles (Sf9-PMVs).	Phenobarbital	86-88	ATP binding cassette subfamily C member 3	Rattus norvegicus	59-63
12673034-5	2003	However, phenytoin and phenobarbital gradually induced CYP3A4 mRNA level by 3 to 4-fold.	Phenobarbital	23-36	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	55-61
12488538-1	2003	We have previously identified an upstream 556-bp enhancer domain for the chicken CYP2H1 gene that responds to phenobarbital and binds several transcription factors, including the orphan chicken xenobiotic receptor (CXR).	Phenobarbital	110-123	cytochrome P450 2H1	Gallus gallus	81-87
12488538-1	2003	We have previously identified an upstream 556-bp enhancer domain for the chicken CYP2H1 gene that responds to phenobarbital and binds several transcription factors, including the orphan chicken xenobiotic receptor (CXR).	Phenobarbital	110-123	nuclear receptor subfamily 1 group I member 3	Gallus gallus	215-218
12488538-8	2003	The work provides evidence for the first time for the involvement of the coactivators CBP and p/CAF in the phenobarbital-mediated induction of the CYP2H1 gene.	Phenobarbital	107-120	lysine acetyltransferase 2B	Gallus gallus	94-99
12488538-8	2003	The work provides evidence for the first time for the involvement of the coactivators CBP and p/CAF in the phenobarbital-mediated induction of the CYP2H1 gene.	Phenobarbital	107-120	cytochrome P450 2H1	Gallus gallus	147-153
12515593-4	2002	Although PB treatment resulted in a significant elevation in CYP2B, CYP2C11, and CYP3A levels, only CYP3A levels were significantly increased by DEX treatment.	Phenobarbital	9-11	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	68-75
12515593-4	2002	Although PB treatment resulted in a significant elevation in CYP2B, CYP2C11, and CYP3A levels, only CYP3A levels were significantly increased by DEX treatment.	Phenobarbital	9-11	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	81-86
12515593-8	2002	Furthermore, an immunoinhibition study demonstrated that anti-CYP3A2 antibody reduced MA(1), MAX, and MA(2) formation to nondetectable levels in liver microsomes from 2- and 7-wk-old rats, whereas anti-CYP2C11 or anti-CYP2B antibody, respectively, had no marked effect on MA(1), MAX, and MA(2) formation in liver microsomes from 7-wk-old untreated or PB-treated rats.	Phenobarbital	351-353	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	62-68
12470631-1	2002	Multidrug resistance-associated protein 3 (Mrp3/ABCC3), which can mediate the cellular extrusion of bile acids, is induced on the hepatic sinusoidal membrane of Mrp2/ABCC2-deficient rats (Eisai hyperbilirubinemic rats; EHBRs) and phenobarbital-treated Sprague-Dawley rats.	Phenobarbital	230-243	ATP binding cassette subfamily C member 3	Rattus norvegicus	0-41
12470631-1	2002	Multidrug resistance-associated protein 3 (Mrp3/ABCC3), which can mediate the cellular extrusion of bile acids, is induced on the hepatic sinusoidal membrane of Mrp2/ABCC2-deficient rats (Eisai hyperbilirubinemic rats; EHBRs) and phenobarbital-treated Sprague-Dawley rats.	Phenobarbital	230-243	ATP binding cassette subfamily C member 3	Rattus norvegicus	43-47
12470631-1	2002	Multidrug resistance-associated protein 3 (Mrp3/ABCC3), which can mediate the cellular extrusion of bile acids, is induced on the hepatic sinusoidal membrane of Mrp2/ABCC2-deficient rats (Eisai hyperbilirubinemic rats; EHBRs) and phenobarbital-treated Sprague-Dawley rats.	Phenobarbital	230-243	ATP binding cassette subfamily C member 3	Rattus norvegicus	48-53
12470631-1	2002	Multidrug resistance-associated protein 3 (Mrp3/ABCC3), which can mediate the cellular extrusion of bile acids, is induced on the hepatic sinusoidal membrane of Mrp2/ABCC2-deficient rats (Eisai hyperbilirubinemic rats; EHBRs) and phenobarbital-treated Sprague-Dawley rats.	Phenobarbital	230-243	ATP binding cassette subfamily C member 2	Rattus norvegicus	161-165
12367775-10	2002	The activities of glutamine synthase and biotinidase were decreased significantly in the livers of ethanol/phenobarbital-treated rats as well as the ethanol-treated rats as compared with the controls.	Phenobarbital	107-120	biotinidase	Rattus norvegicus	41-52
12367775-12	2002	In the plasma of ethanol/phenobarbital-treated rats as well as the ethanol-treated rats total thiol, albumin and the activity of biotinidase were decreased significantly as compared with the controls.	Phenobarbital	25-38	biotinidase	Rattus norvegicus	129-140
12386126-5	2002	Phenobarbital caused a 13-fold increase in 7-benzyloxyresorufin O-dealkylase (CYP2B11) activity in vitro and up to a 9.9-fold increase in vivo.	Phenobarbital	0-13	cytochrome P450 2B11	Canis lupus familiaris	78-85
12413652-9	2002	PB treatment significantly inhibited changes of NPY in terms of both immunoreactivity and mRNA expression; however, the same treatment failed to affect changes in SOM expression.	Phenobarbital	0-2	neuropeptide Y	Rattus norvegicus	48-51
12167560-10	2002	p-Hydroxyphenobarbital glucuronide (p-OHPBG), but not PB or p-hydroxyphenobarbital, significantly inhibited Mrp2-mediated CDF transport.	Phenobarbital	40-42	ATP binding cassette subfamily C member 2	Rattus norvegicus	108-112
12167560-12	2002	PB treatment (80 mg/kg/day x 4 days) markedly increased hepatic Mrp3 expression in Wistar rats.	Phenobarbital	0-2	ATP binding cassette subfamily C member 3	Rattus norvegicus	64-68
12167560-13	2002	In conclusion, inhibition of Mrp2-mediated AG transport by p-OHPBG provided one possible explanation for the impaired biliary excretion of AG after acute PB treatment.	Phenobarbital	63-65	ATP binding cassette subfamily C member 2	Rattus norvegicus	29-33
12167560-14	2002	However, impaired biliary excretion of AG after PB pretreatment may be attributed primarily to the induction of hepatic Mrp3 by PB.	Phenobarbital	128-130	ATP binding cassette subfamily C member 3	Rattus norvegicus	120-124
12130704-2	2002	We used primary cultures of human hepatocytes from 15 subjects to assess the inducibility of CYP2C enzyme expression by prototypical inducer agents, including rifampicin, dexamethasone, and phenobarbital.	Phenobarbital	190-203	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	93-98
12181452-3	2002	This report examines the regulation of CYP2C9 with respect to two specific receptors thought to be involved in phenobarbital (PB) induction, the constitutive androstane receptor (CAR) and pregnane X receptor (PXR).	Phenobarbital	111-124	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
12181452-3	2002	This report examines the regulation of CYP2C9 with respect to two specific receptors thought to be involved in phenobarbital (PB) induction, the constitutive androstane receptor (CAR) and pregnane X receptor (PXR).	Phenobarbital	111-124	nuclear receptor subfamily 1 group I member 3	Homo sapiens	145-177
12181452-3	2002	This report examines the regulation of CYP2C9 with respect to two specific receptors thought to be involved in phenobarbital (PB) induction, the constitutive androstane receptor (CAR) and pregnane X receptor (PXR).	Phenobarbital	111-124	nuclear receptor subfamily 1 group I member 3	Homo sapiens	179-182
12181452-3	2002	This report examines the regulation of CYP2C9 with respect to two specific receptors thought to be involved in phenobarbital (PB) induction, the constitutive androstane receptor (CAR) and pregnane X receptor (PXR).	Phenobarbital	126-128	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
12181452-3	2002	This report examines the regulation of CYP2C9 with respect to two specific receptors thought to be involved in phenobarbital (PB) induction, the constitutive androstane receptor (CAR) and pregnane X receptor (PXR).	Phenobarbital	126-128	nuclear receptor subfamily 1 group I member 3	Homo sapiens	145-177
12181452-11	2002	In summary, a new CAR/PXR binding site was identified in the CYP2C9 promoter, and this site seems to constitutively regulate transcription via a CAR-dependent mechanism; however, it could not be shown to account for PB inducibility of the gene.	Phenobarbital	216-218	coxsackie virus and adenovirus receptor	Mus musculus	18-21
12181452-11	2002	In summary, a new CAR/PXR binding site was identified in the CYP2C9 promoter, and this site seems to constitutively regulate transcription via a CAR-dependent mechanism; however, it could not be shown to account for PB inducibility of the gene.	Phenobarbital	216-218	nuclear receptor subfamily 1 group I member 2	Homo sapiens	22-25
12181452-11	2002	In summary, a new CAR/PXR binding site was identified in the CYP2C9 promoter, and this site seems to constitutively regulate transcription via a CAR-dependent mechanism; however, it could not be shown to account for PB inducibility of the gene.	Phenobarbital	216-218	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	61-67
12124310-0	2002	Role of constitutive androstane receptor in the in vivo induction of Mrp3 and CYP2B1/2 by phenobarbital.	Phenobarbital	90-103	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	8-40
12124310-0	2002	Role of constitutive androstane receptor in the in vivo induction of Mrp3 and CYP2B1/2 by phenobarbital.	Phenobarbital	90-103	ATP binding cassette subfamily C member 3	Rattus norvegicus	69-73
12124310-0	2002	Role of constitutive androstane receptor in the in vivo induction of Mrp3 and CYP2B1/2 by phenobarbital.	Phenobarbital	90-103	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	78-84
12124310-1	2002	Phenobarbital (PB) induces the hepatic organic anion transporter, Mrp3.	Phenobarbital	0-13	ATP binding cassette subfamily C member 3	Rattus norvegicus	66-70
12124310-1	2002	Phenobarbital (PB) induces the hepatic organic anion transporter, Mrp3.	Phenobarbital	15-17	ATP binding cassette subfamily C member 3	Rattus norvegicus	66-70
12124310-2	2002	The present study tested the hypothesis that Mrp3 induction by PB is mediated by the constitutive androstane receptor (CAR).	Phenobarbital	63-65	ATP binding cassette subfamily C member 3	Rattus norvegicus	45-49
12124310-2	2002	The present study tested the hypothesis that Mrp3 induction by PB is mediated by the constitutive androstane receptor (CAR).	Phenobarbital	63-65	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	85-117
12124310-2	2002	The present study tested the hypothesis that Mrp3 induction by PB is mediated by the constitutive androstane receptor (CAR).	Phenobarbital	63-65	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	119-122
12124310-3	2002	PB induction of Mrp3 and CYP2B was examined in lean and obese Zucker rats, male and female Wistar Kyoto (WKY) rats, HepG2 and mouse CAR-expressing HepG2 (g2car-3) cells; HepG2 and g2car-3 cells also were treated with 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP).	Phenobarbital	0-2	ATP binding cassette subfamily C member 3	Rattus norvegicus	16-20
12124310-3	2002	PB induction of Mrp3 and CYP2B was examined in lean and obese Zucker rats, male and female Wistar Kyoto (WKY) rats, HepG2 and mouse CAR-expressing HepG2 (g2car-3) cells; HepG2 and g2car-3 cells also were treated with 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP).	Phenobarbital	0-2	nuclear receptor subfamily 1, group I, member 3	Mus musculus	132-135
12124310-4	2002	In obese Zucker rat livers, total and nuclear CAR levels were markedly lower compared with lean rat livers, which correlated with the poor induction of CYP2B1/2 by PB in obese Zucker rats.	Phenobarbital	164-166	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	46-49
12124310-4	2002	In obese Zucker rat livers, total and nuclear CAR levels were markedly lower compared with lean rat livers, which correlated with the poor induction of CYP2B1/2 by PB in obese Zucker rats.	Phenobarbital	164-166	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	152-158
12124310-5	2002	Mrp3 induction by PB also was impaired in obese Zucker rat livers.	Phenobarbital	18-20	ATP binding cassette subfamily C member 3	Rattus norvegicus	0-4
12124310-6	2002	Induction of Mrp3 by PB was similar in male and female WKY rat livers, despite the fact that CAR protein levels were significantly lower in female relative to male WKY rat livers.	Phenobarbital	21-23	ATP binding cassette subfamily C member 3	Rattus norvegicus	13-17
12124310-7	2002	MRP3 levels in both HepG2 and g2car-3 cells were induced to a similar extent in the two cell lines by PB but not by TCPOBOP.	Phenobarbital	102-104	ATP binding cassette subfamily C member 3	Homo sapiens	0-4
12124310-10	2002	Impaired induction of Mrp3 by PB in obese Zucker rats is not due solely to CAR deficiency.	Phenobarbital	30-32	ATP binding cassette subfamily C member 3	Rattus norvegicus	22-26
12130704-8	2002	Our results show that CYP2C enzyme expression in human hepatocytes is highly inducible by rifampicin, dexamethasone, and phenobarbital.	Phenobarbital	121-134	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	22-27
12130704-7	2002	Phenobarbital (100 microM) was a powerful inducer of CYP2C9 (850%) and CYP2C19 (735%) mRNA content, and also increased CYP2C8 (610%) and CYP3A4 (205%) transcripts.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	53-59
12130704-7	2002	Phenobarbital (100 microM) was a powerful inducer of CYP2C9 (850%) and CYP2C19 (735%) mRNA content, and also increased CYP2C8 (610%) and CYP3A4 (205%) transcripts.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	71-78
12130704-7	2002	Phenobarbital (100 microM) was a powerful inducer of CYP2C9 (850%) and CYP2C19 (735%) mRNA content, and also increased CYP2C8 (610%) and CYP3A4 (205%) transcripts.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	119-125
12130704-7	2002	Phenobarbital (100 microM) was a powerful inducer of CYP2C9 (850%) and CYP2C19 (735%) mRNA content, and also increased CYP2C8 (610%) and CYP3A4 (205%) transcripts.	Phenobarbital	0-13	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	137-143
12130690-1	2002	The constitutive androstane receptor (CAR) regulates mouse and human CYP2B genes through binding to the direct repeat-4 (DR4) motifs present in the phenobarbital-responsive enhancer module (PBREM).	Phenobarbital	148-161	nuclear receptor subfamily 1, group I, member 3	Mus musculus	4-36
12130690-1	2002	The constitutive androstane receptor (CAR) regulates mouse and human CYP2B genes through binding to the direct repeat-4 (DR4) motifs present in the phenobarbital-responsive enhancer module (PBREM).	Phenobarbital	148-161	nuclear receptor subfamily 1, group I, member 3	Mus musculus	38-41
12130690-1	2002	The constitutive androstane receptor (CAR) regulates mouse and human CYP2B genes through binding to the direct repeat-4 (DR4) motifs present in the phenobarbital-responsive enhancer module (PBREM).	Phenobarbital	148-161	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	69-74
12296987-5	2002	The induction factor of phenobarbital (PB)-induced formation of 16beta-hydroxytestosterone (OHT), a testosterone biotransformation product predominantly formed by CYP2B1, is increased 18-fold by the addition of 32 nM DEX to the culture medium.	Phenobarbital	24-37	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	163-169
12110287-1	2002	Triphenyldioxane (TPD) is a potent phenobarbital-type (PB) inducer of the CYP2B cytochrome isoforms, the inducing effect of which is one order of magnitude higher than PB.	Phenobarbital	35-48	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	74-79
12296987-5	2002	The induction factor of phenobarbital (PB)-induced formation of 16beta-hydroxytestosterone (OHT), a testosterone biotransformation product predominantly formed by CYP2B1, is increased 18-fold by the addition of 32 nM DEX to the culture medium.	Phenobarbital	39-41	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	163-169
12296987-9	2002	Qualitatively similar but smaller permissive and suppressive effects of DEX were observed for PB-induced CYP3A1 activity as evidenced by formation of 2beta-, 6beta- and 15beta-OHT.	Phenobarbital	94-96	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	105-111
12113905-0	2002	P-Glycoprotein-mediated efflux of phenobarbital, lamotrigine, and felbamate at the blood-brain barrier: evidence from microdialysis experiments in rats.	Phenobarbital	34-47	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	0-14
12000748-1	2002	Phenobarbital (PB) induction of CYP2B genes is mediated by translocation of the constitutively active androstane receptor (CAR) to the nucleus.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	32-37
12369894-10	2002	Similarly, the steroid family of orphan receptors, the constitutive androstane receptor (CAR) and pregnane X receptors (PXR), heterodimerize with the retinoid X receptor (RXR), transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	276-289	nuclear receptor subfamily 1 group I member 3	Homo sapiens	55-87
12369894-10	2002	Similarly, the steroid family of orphan receptors, the constitutive androstane receptor (CAR) and pregnane X receptors (PXR), heterodimerize with the retinoid X receptor (RXR), transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	276-289	nuclear receptor subfamily 1 group I member 3	Homo sapiens	89-92
12369894-10	2002	Similarly, the steroid family of orphan receptors, the constitutive androstane receptor (CAR) and pregnane X receptors (PXR), heterodimerize with the retinoid X receptor (RXR), transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	276-289	nuclear receptor subfamily 1 group I member 2	Homo sapiens	98-118
12369894-10	2002	Similarly, the steroid family of orphan receptors, the constitutive androstane receptor (CAR) and pregnane X receptors (PXR), heterodimerize with the retinoid X receptor (RXR), transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	276-289	nuclear receptor subfamily 1 group I member 2	Homo sapiens	120-123
12369894-10	2002	Similarly, the steroid family of orphan receptors, the constitutive androstane receptor (CAR) and pregnane X receptors (PXR), heterodimerize with the retinoid X receptor (RXR), transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	276-289	retinoid X receptor alpha	Homo sapiens	150-169
12369894-10	2002	Similarly, the steroid family of orphan receptors, the constitutive androstane receptor (CAR) and pregnane X receptors (PXR), heterodimerize with the retinoid X receptor (RXR), transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	276-289	retinoid X receptor alpha	Homo sapiens	171-174
12369894-10	2002	Similarly, the steroid family of orphan receptors, the constitutive androstane receptor (CAR) and pregnane X receptors (PXR), heterodimerize with the retinoid X receptor (RXR), transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	276-289	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	231-236
12369894-10	2002	Similarly, the steroid family of orphan receptors, the constitutive androstane receptor (CAR) and pregnane X receptors (PXR), heterodimerize with the retinoid X receptor (RXR), transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	276-289	nuclear receptor subfamily 1 group I member 3	Homo sapiens	306-309
12369894-10	2002	Similarly, the steroid family of orphan receptors, the constitutive androstane receptor (CAR) and pregnane X receptors (PXR), heterodimerize with the retinoid X receptor (RXR), transcriptionally activate the promoters of CYP2B and CYP3A gene expression by xenobiotics such as phenobarbital-like compounds (CAR) and dexamethasone and rifampin-type of agents (PXR).	Phenobarbital	276-289	nuclear receptor subfamily 1 group I member 2	Homo sapiens	358-361
12000748-1	2002	Phenobarbital (PB) induction of CYP2B genes is mediated by translocation of the constitutively active androstane receptor (CAR) to the nucleus.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	123-126
12000748-1	2002	Phenobarbital (PB) induction of CYP2B genes is mediated by translocation of the constitutively active androstane receptor (CAR) to the nucleus.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	32-37
12000748-1	2002	Phenobarbital (PB) induction of CYP2B genes is mediated by translocation of the constitutively active androstane receptor (CAR) to the nucleus.	Phenobarbital	15-17	nuclear receptor subfamily 1, group I, member 3	Mus musculus	123-126
12000748-9	2002	Remarkably, CAR and GRIP1 together synergistically transactivated the enhancer about 150-fold, which is approximately equal to activation by PB treatment.	Phenobarbital	141-143	nuclear receptor subfamily 1, group I, member 3	Mus musculus	12-15
12000748-9	2002	Remarkably, CAR and GRIP1 together synergistically transactivated the enhancer about 150-fold, which is approximately equal to activation by PB treatment.	Phenobarbital	141-143	glutamate receptor interacting protein 1	Mus musculus	20-25
12000748-10	2002	In PB-treated mice, expression of exogenous CAR alone had little effect, expression of GRIP1 increased transactivation about 2-fold, and with CAR and GRIP, a 4-fold activation was observed.	Phenobarbital	3-5	glutamate receptor interacting protein 1	Mus musculus	87-92
12000748-10	2002	In PB-treated mice, expression of exogenous CAR alone had little effect, expression of GRIP1 increased transactivation about 2-fold, and with CAR and GRIP, a 4-fold activation was observed.	Phenobarbital	3-5	nuclear receptor subfamily 1, group I, member 3	Mus musculus	142-145
12000748-10	2002	In PB-treated mice, expression of exogenous CAR alone had little effect, expression of GRIP1 increased transactivation about 2-fold, and with CAR and GRIP, a 4-fold activation was observed.	Phenobarbital	3-5	glutamate receptor interacting protein 1	Mus musculus	87-91
12000748-12	2002	These results strongly suggest that a p160 coactivator functions in CAR-mediated transactivation in vivo in response to PB treatment and that the synergistic activation of CAR by GRIP in untreated animals results from both nuclear translocation and activation of CAR.	Phenobarbital	120-122	MYB binding protein (P160) 1a	Mus musculus	38-42
12000748-12	2002	These results strongly suggest that a p160 coactivator functions in CAR-mediated transactivation in vivo in response to PB treatment and that the synergistic activation of CAR by GRIP in untreated animals results from both nuclear translocation and activation of CAR.	Phenobarbital	120-122	nuclear receptor subfamily 1, group I, member 3	Mus musculus	68-71
12105905-7	2002	In the present study, we found that liver microsomes from phenobarbital pretreated rats (which contain CYP2B1 as the predominant isozyme) oxidize [1"-(13)C, 1"-(14)C]-2a efficiently (80% consumption in 90 min).	Phenobarbital	58-71	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	103-109
12093615-4	2002	Exposure to 100 microM phenobarbital caused a more than 20-fold increase in CYP2B1-mRNA expression within 24 h, reaching concentrations comparable with those of PB-exposed fresh rat liver slices.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	76-82
12051692-4	2002	Phenobarbital induced CYP2B and rifampicin induced CYP3A, respectively, in addition to NADPH-cytochrome P450 reductase.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	22-27
12065438-7	2002	Clotrimazole, phenobarbital, rifampin, and sulfinpyrazone highly activated PXR and increased CYP3A4 activity; carbamazepine, dexamethasone, dexamethasone-t-butylacetate, phenytoin, sulfadimidine, and taxol weakly activated PXR and induced CYP3A4 activity, and methotrexate and probenecid showed no marked activation in either system.	Phenobarbital	14-27	nuclear receptor subfamily 1 group I member 2	Homo sapiens	75-78
12065438-7	2002	Clotrimazole, phenobarbital, rifampin, and sulfinpyrazone highly activated PXR and increased CYP3A4 activity; carbamazepine, dexamethasone, dexamethasone-t-butylacetate, phenytoin, sulfadimidine, and taxol weakly activated PXR and induced CYP3A4 activity, and methotrexate and probenecid showed no marked activation in either system.	Phenobarbital	14-27	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	93-99
12065438-7	2002	Clotrimazole, phenobarbital, rifampin, and sulfinpyrazone highly activated PXR and increased CYP3A4 activity; carbamazepine, dexamethasone, dexamethasone-t-butylacetate, phenytoin, sulfadimidine, and taxol weakly activated PXR and induced CYP3A4 activity, and methotrexate and probenecid showed no marked activation in either system.	Phenobarbital	14-27	nuclear receptor subfamily 1 group I member 2	Homo sapiens	223-226
12065438-7	2002	Clotrimazole, phenobarbital, rifampin, and sulfinpyrazone highly activated PXR and increased CYP3A4 activity; carbamazepine, dexamethasone, dexamethasone-t-butylacetate, phenytoin, sulfadimidine, and taxol weakly activated PXR and induced CYP3A4 activity, and methotrexate and probenecid showed no marked activation in either system.	Phenobarbital	14-27	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	239-245
12193254-5	2002	Dioxins and polychlorinated biphenyls bind to the aryl hydrocarbon receptor, phenobarbital binds to the constitutive androstane receptor and peroxisome proliferators act via the their activated receptor alpha.	Phenobarbital	77-90	aryl-hydrocarbon receptor	Mus musculus	50-75
12193254-5	2002	Dioxins and polychlorinated biphenyls bind to the aryl hydrocarbon receptor, phenobarbital binds to the constitutive androstane receptor and peroxisome proliferators act via the their activated receptor alpha.	Phenobarbital	77-90	nuclear receptor subfamily 1, group I, member 3	Mus musculus	104-136
12051692-4	2002	Phenobarbital induced CYP2B and rifampicin induced CYP3A, respectively, in addition to NADPH-cytochrome P450 reductase.	Phenobarbital	0-13	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	51-56
12051692-4	2002	Phenobarbital induced CYP2B and rifampicin induced CYP3A, respectively, in addition to NADPH-cytochrome P450 reductase.	Phenobarbital	0-13	cytochrome p450 oxidoreductase	Mus musculus	87-118
12112853-4	2002	Both 1-DE and 2-DE showed that phenobarbital induces not only cytochromes P450 2B1and 2B2 but such stress related endoplasmic reticulum proteins as protein disulfide isomerase A(3) and A(6) and 78 kDa glucose regulated protein.	Phenobarbital	31-44	protein disulfide isomerase family A, member 3	Rattus norvegicus	148-226
12113905-5	2002	In the present study, the effect of PGP inhibition by verapamil on brain access of the AEDs phenobarbital, lamotrigine, and felbamate was investigated by in vivo microdialysis in rats.	Phenobarbital	92-105	phosphoglycolate phosphatase	Rattus norvegicus	36-39
12113905-7	2002	The data indicate that overexpression of PGP in epileptic tissue is likely to limit brain access of the AEDs phenobarbital, lamotrigine, and felbamate, thus favoring the hypothesis that multidrug transporters play a crucial role in the phenomenon of drug-refractory epilepsy.	Phenobarbital	109-122	ATP binding cassette subfamily B member 1	Homo sapiens	41-44
11976065-1	2002	The mammalian constitutively active receptor (CAR) is a novel ligand-activated transcription factor that participates in controlling the expression of cytochrome P450 2B (CYP2B) genes in response to pharmaceutical agents (phenobarbital) and halogenated aromatic hydrocarbons (ortho-substituted PCBs).	Phenobarbital	222-235	nuclear receptor subfamily 1 group I member 3	Homo sapiens	14-44
11867618-0	2002	Transcriptional activation of cytochrome P450 CYP2C45 by drugs is mediated by the chicken xenobiotic receptor (CXR) interacting with a phenobarbital response enhancer unit.	Phenobarbital	135-148	cytochrome P450 family 2 subfamily C member 18	Gallus gallus	46-53
11867618-0	2002	Transcriptional activation of cytochrome P450 CYP2C45 by drugs is mediated by the chicken xenobiotic receptor (CXR) interacting with a phenobarbital response enhancer unit.	Phenobarbital	135-148	nuclear receptor subfamily 1 group I member 3	Gallus gallus	90-109
11867618-0	2002	Transcriptional activation of cytochrome P450 CYP2C45 by drugs is mediated by the chicken xenobiotic receptor (CXR) interacting with a phenobarbital response enhancer unit.	Phenobarbital	135-148	nuclear receptor subfamily 1 group I member 3	Gallus gallus	111-114
11867618-7	2002	Exposure of LMH cells to phenobarbital or metyrapone led to a 95- or 210-fold increase in CYP2C45 mRNA and a 140- or 290-fold increase in reporter gene expression, respectively.	Phenobarbital	25-38	cytochrome P450 family 2 subfamily C member 18	Gallus gallus	90-97
12076846-5	2002	Pre-treatment with PB (80 mg/kg; once daily for 4 days) significantly increased CYP(450) content and activity in mouse liver.	Phenobarbital	19-21	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	80-88
11948501-9	2002	Furthermore, since CYP3A2 protein expression appears to be important for the effects of phenobarbital and the alpha-isomer of benzene hexachloride, mRNAs for IL-1 receptor type 1 (IL-1R1) and TNF-alpha receptor type 1 (TNFR1) whose ligands have roles not only in downregulating CYP3A2 expression but also in inducing antiproliferative effect or apoptosis in hepatocyte were examined.	Phenobarbital	88-101	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	19-25
11948501-9	2002	Furthermore, since CYP3A2 protein expression appears to be important for the effects of phenobarbital and the alpha-isomer of benzene hexachloride, mRNAs for IL-1 receptor type 1 (IL-1R1) and TNF-alpha receptor type 1 (TNFR1) whose ligands have roles not only in downregulating CYP3A2 expression but also in inducing antiproliferative effect or apoptosis in hepatocyte were examined.	Phenobarbital	88-101	TNF receptor superfamily member 1A	Rattus norvegicus	219-224
11948501-9	2002	Furthermore, since CYP3A2 protein expression appears to be important for the effects of phenobarbital and the alpha-isomer of benzene hexachloride, mRNAs for IL-1 receptor type 1 (IL-1R1) and TNF-alpha receptor type 1 (TNFR1) whose ligands have roles not only in downregulating CYP3A2 expression but also in inducing antiproliferative effect or apoptosis in hepatocyte were examined.	Phenobarbital	88-101	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	278-284
11976065-1	2002	The mammalian constitutively active receptor (CAR) is a novel ligand-activated transcription factor that participates in controlling the expression of cytochrome P450 2B (CYP2B) genes in response to pharmaceutical agents (phenobarbital) and halogenated aromatic hydrocarbons (ortho-substituted PCBs).	Phenobarbital	222-235	nuclear receptor subfamily 1 group I member 3	Homo sapiens	46-49
11976065-1	2002	The mammalian constitutively active receptor (CAR) is a novel ligand-activated transcription factor that participates in controlling the expression of cytochrome P450 2B (CYP2B) genes in response to pharmaceutical agents (phenobarbital) and halogenated aromatic hydrocarbons (ortho-substituted PCBs).	Phenobarbital	222-235	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	151-169
11976065-1	2002	The mammalian constitutively active receptor (CAR) is a novel ligand-activated transcription factor that participates in controlling the expression of cytochrome P450 2B (CYP2B) genes in response to pharmaceutical agents (phenobarbital) and halogenated aromatic hydrocarbons (ortho-substituted PCBs).	Phenobarbital	222-235	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	171-176
11906189-2	2002	We identified a polymorphism that results in a T to G substitution at nucleotide number -3263 of the phenobarbital-responsive enhancer module of the UGT1A1 gene, thereby significantly decreasing transcriptional activity as indicated by the luciferase-reporter assay.	Phenobarbital	101-114	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	149-155
11967242-5	2002	The inhibitory effects of estradiol on VSMCs were enhanced by cytochrome-P450 (CYP450) inducers 3-methylcholanthrene and phenobarbital.	Phenobarbital	121-134	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	62-77
11967242-5	2002	The inhibitory effects of estradiol on VSMCs were enhanced by cytochrome-P450 (CYP450) inducers 3-methylcholanthrene and phenobarbital.	Phenobarbital	121-134	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	79-85
12000532-1	2002	In dogs effects of phenobarbital (PB) on hepatic cytochrome P450 (CYP) activities and on concentrations of plasma alpha 1-acid glycoprotein (AGP) were examined.	Phenobarbital	34-36	Cytochrome P450 1A1	Canis lupus familiaris	49-64
12000532-3	2002	Cl(B) of antipyrine, which reflects hepatic CYP activities, gradually increased and was maintained at about threefold concentrations compared with that before treatment, suggesting that PB induced CYP activities at a large extent even in a therapeutic dose, necessary for an antiepileptic effect.	Phenobarbital	186-188	Cytochrome P450 1A1	Canis lupus familiaris	44-47
12000532-3	2002	Cl(B) of antipyrine, which reflects hepatic CYP activities, gradually increased and was maintained at about threefold concentrations compared with that before treatment, suggesting that PB induced CYP activities at a large extent even in a therapeutic dose, necessary for an antiepileptic effect.	Phenobarbital	186-188	Cytochrome P450 1A1	Canis lupus familiaris	197-200
12028663-7	2002	The major phenobarbital (PB)-inducible forms of P450, CYP2B1, CYP2B2, CYP3A2 and CYP2C6, were substantially induced by 3-MeSO(2)-TetraBrB, but CYP1A1 and CYP1A2 were not.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	54-60
12028663-7	2002	The major phenobarbital (PB)-inducible forms of P450, CYP2B1, CYP2B2, CYP3A2 and CYP2C6, were substantially induced by 3-MeSO(2)-TetraBrB, but CYP1A1 and CYP1A2 were not.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	62-68
12028663-7	2002	The major phenobarbital (PB)-inducible forms of P450, CYP2B1, CYP2B2, CYP3A2 and CYP2C6, were substantially induced by 3-MeSO(2)-TetraBrB, but CYP1A1 and CYP1A2 were not.	Phenobarbital	10-23	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	70-76
12028663-7	2002	The major phenobarbital (PB)-inducible forms of P450, CYP2B1, CYP2B2, CYP3A2 and CYP2C6, were substantially induced by 3-MeSO(2)-TetraBrB, but CYP1A1 and CYP1A2 were not.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	81-87
12028663-7	2002	The major phenobarbital (PB)-inducible forms of P450, CYP2B1, CYP2B2, CYP3A2 and CYP2C6, were substantially induced by 3-MeSO(2)-TetraBrB, but CYP1A1 and CYP1A2 were not.	Phenobarbital	10-23	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	143-149
12028663-7	2002	The major phenobarbital (PB)-inducible forms of P450, CYP2B1, CYP2B2, CYP3A2 and CYP2C6, were substantially induced by 3-MeSO(2)-TetraBrB, but CYP1A1 and CYP1A2 were not.	Phenobarbital	10-23	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	154-160
12028663-7	2002	The major phenobarbital (PB)-inducible forms of P450, CYP2B1, CYP2B2, CYP3A2 and CYP2C6, were substantially induced by 3-MeSO(2)-TetraBrB, but CYP1A1 and CYP1A2 were not.	Phenobarbital	25-27	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	54-60
12028663-7	2002	The major phenobarbital (PB)-inducible forms of P450, CYP2B1, CYP2B2, CYP3A2 and CYP2C6, were substantially induced by 3-MeSO(2)-TetraBrB, but CYP1A1 and CYP1A2 were not.	Phenobarbital	25-27	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	62-68
12028663-7	2002	The major phenobarbital (PB)-inducible forms of P450, CYP2B1, CYP2B2, CYP3A2 and CYP2C6, were substantially induced by 3-MeSO(2)-TetraBrB, but CYP1A1 and CYP1A2 were not.	Phenobarbital	25-27	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	70-76
12028663-7	2002	The major phenobarbital (PB)-inducible forms of P450, CYP2B1, CYP2B2, CYP3A2 and CYP2C6, were substantially induced by 3-MeSO(2)-TetraBrB, but CYP1A1 and CYP1A2 were not.	Phenobarbital	25-27	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	81-87
12028663-7	2002	The major phenobarbital (PB)-inducible forms of P450, CYP2B1, CYP2B2, CYP3A2 and CYP2C6, were substantially induced by 3-MeSO(2)-TetraBrB, but CYP1A1 and CYP1A2 were not.	Phenobarbital	25-27	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	143-149
12028663-7	2002	The major phenobarbital (PB)-inducible forms of P450, CYP2B1, CYP2B2, CYP3A2 and CYP2C6, were substantially induced by 3-MeSO(2)-TetraBrB, but CYP1A1 and CYP1A2 were not.	Phenobarbital	25-27	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	154-160
11891097-5	2002	The PKC gamma staining intensity in hippocampal CA1-2 region of training group was significant greater than that of the control and PB group.	Phenobarbital	132-134	protein kinase C, gamma	Rattus norvegicus	4-13
11891097-5	2002	The PKC gamma staining intensity in hippocampal CA1-2 region of training group was significant greater than that of the control and PB group.	Phenobarbital	132-134	carbonic anhydrase 1	Rattus norvegicus	48-51
11891097-12	2002	PB and VPA likely adversely affect learning and memory by interfering with PKC gamma activation, whereas CBZ may act by a different mechanism, possibly in the post-translocation process or by a PKC gamma independent pathway.	Phenobarbital	0-2	protein kinase C, gamma	Rattus norvegicus	75-84
11854139-2	2002	In the present study, N-3-benzyl derivatives of nirvanol and phenobarbital were synthesized, their respective (+)- and (-)-enantiomers resolved chromatographically, and inhibitor potencies determined for these compounds toward CYP2C19 and other human liver cytochromes P450 (P450s).	Phenobarbital	61-74	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	227-234
11854139-2	2002	In the present study, N-3-benzyl derivatives of nirvanol and phenobarbital were synthesized, their respective (+)- and (-)-enantiomers resolved chromatographically, and inhibitor potencies determined for these compounds toward CYP2C19 and other human liver cytochromes P450 (P450s).	Phenobarbital	61-74	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	269-273
11861787-0	2002	Enhanced induction of cytochrome P450 enzymes and CAR binding in TNF (p55(-/-)/p75(-/-)) double receptor knockout mice following phenobarbital treatment.	Phenobarbital	129-142	nuclear receptor subfamily 1, group I, member 3	Mus musculus	50-53
11861787-0	2002	Enhanced induction of cytochrome P450 enzymes and CAR binding in TNF (p55(-/-)/p75(-/-)) double receptor knockout mice following phenobarbital treatment.	Phenobarbital	129-142	tumor necrosis factor	Mus musculus	65-68
11861969-9	2002	PB and PCN also increased Mrp2 protein levels, but 3MC and BaP did not.	Phenobarbital	0-2	ATP binding cassette subfamily B member 4	Rattus norvegicus	26-30
11861787-0	2002	Enhanced induction of cytochrome P450 enzymes and CAR binding in TNF (p55(-/-)/p75(-/-)) double receptor knockout mice following phenobarbital treatment.	Phenobarbital	129-142	tumor necrosis factor receptor superfamily, member 1b	Mus musculus	79-104
11992629-7	2002	An antibody raised against CYP2B1 markedly inhibited the PCB-dependent bilirubin degradation and PROD activities of phenobarbital-induced microsomes with similar dose-response curves for the two effects.	Phenobarbital	116-129	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	27-33
11846416-4	2002	Bile acids also reduced the phenobarbital induction of CYP2H1 but not of CYP3A37 mRNA.	Phenobarbital	28-41	cytochrome P450 2H1	Gallus gallus	55-61
11846416-5	2002	The effects of SQ1 and its reversal by 25-hydroxycholesterol and the effects of bile acids were reproduced in reporter gene assays with a phenobarbital-responsive enhancer unit of CYP2H1.	Phenobarbital	138-151	cytochrome P450 2H1	Gallus gallus	180-186
11992629-7	2002	An antibody raised against CYP2B1 markedly inhibited the PCB-dependent bilirubin degradation and PROD activities of phenobarbital-induced microsomes with similar dose-response curves for the two effects.	Phenobarbital	116-129	pyruvate carboxylase	Rattus norvegicus	57-60
11872643-2	2002	Significant increase of hydroxyl radical levels by day 4 of PB exposure accompanied the accumulation of 8-OHdG in the nucleus and P-450 isoenzymes CYP2B1/2 and CYP3A2 in the cytoplasm of hepatocytes.	Phenobarbital	60-62	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	147-153
11861787-7	2002	In parallel with enhanced CYP2B induction, an apparent elevation in the nuclear accumulation of the principal regulatory protein for transcription of CYP2B genes, the constitutively activated receptor (CAR), was detected in ko-TNF nuclear extracts following PB treatment.	Phenobarbital	258-260	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	26-31
11872643-2	2002	Significant increase of hydroxyl radical levels by day 4 of PB exposure accompanied the accumulation of 8-OHdG in the nucleus and P-450 isoenzymes CYP2B1/2 and CYP3A2 in the cytoplasm of hepatocytes.	Phenobarbital	60-62	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	160-166
11861787-7	2002	In parallel with enhanced CYP2B induction, an apparent elevation in the nuclear accumulation of the principal regulatory protein for transcription of CYP2B genes, the constitutively activated receptor (CAR), was detected in ko-TNF nuclear extracts following PB treatment.	Phenobarbital	258-260	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	150-155
11861787-7	2002	In parallel with enhanced CYP2B induction, an apparent elevation in the nuclear accumulation of the principal regulatory protein for transcription of CYP2B genes, the constitutively activated receptor (CAR), was detected in ko-TNF nuclear extracts following PB treatment.	Phenobarbital	258-260	nuclear receptor subfamily 1, group I, member 3	Mus musculus	202-205
11872643-3	2002	Conspicuous elevation of 8-OHdG and apoptosis in the liver tissue were associated with reduction of the proliferating cell nuclear antigen (PCNA) index after 8 days of PB application.	Phenobarbital	168-170	proliferating cell nuclear antigen	Rattus norvegicus	104-138
11861787-7	2002	In parallel with enhanced CYP2B induction, an apparent elevation in the nuclear accumulation of the principal regulatory protein for transcription of CYP2B genes, the constitutively activated receptor (CAR), was detected in ko-TNF nuclear extracts following PB treatment.	Phenobarbital	258-260	tumor necrosis factor	Mus musculus	227-230
11861787-8	2002	Additionally, nuclear factor kappa-B binding was induced by PB in wt-TNF mice, but not in ko-TNF mice, indicating that the hepatic inflammatory response following PB treatment differed between wt-TNF and ko-TNF mice.	Phenobarbital	60-62	tumor necrosis factor	Mus musculus	69-72
11861787-9	2002	These data demonstrate that endogenous TNFalpha signaling modulates PB induction of hepatic CYP2B and CYP3A isoforms in vivo.	Phenobarbital	68-70	tumor necrosis factor	Mus musculus	39-47
11861787-9	2002	These data demonstrate that endogenous TNFalpha signaling modulates PB induction of hepatic CYP2B and CYP3A isoforms in vivo.	Phenobarbital	68-70	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	92-97
11861787-9	2002	These data demonstrate that endogenous TNFalpha signaling modulates PB induction of hepatic CYP2B and CYP3A isoforms in vivo.	Phenobarbital	68-70	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	102-107
11861787-10	2002	Further, the data presented herein suggest that endogenous TNFalpha signaling influences PB induction of CYP2B through inhibition of CAR nuclear accumulation.	Phenobarbital	89-91	tumor necrosis factor	Mus musculus	59-67
11861787-10	2002	Further, the data presented herein suggest that endogenous TNFalpha signaling influences PB induction of CYP2B through inhibition of CAR nuclear accumulation.	Phenobarbital	89-91	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	105-110
11861787-10	2002	Further, the data presented herein suggest that endogenous TNFalpha signaling influences PB induction of CYP2B through inhibition of CAR nuclear accumulation.	Phenobarbital	89-91	nuclear receptor subfamily 1, group I, member 3	Mus musculus	133-136
11872643-0	2002	Formation of 8-hydroxydeoxyguanosine and cell-cycle arrest in the rat liver via generation of oxidative stress by phenobarbital: association with expression profiles of p21(WAF1/Cip1), cyclin D1 and Ogg1.	Phenobarbital	114-127	KRAS proto-oncogene, GTPase	Rattus norvegicus	169-172
11872643-3	2002	Conspicuous elevation of 8-OHdG and apoptosis in the liver tissue were associated with reduction of the proliferating cell nuclear antigen (PCNA) index after 8 days of PB application.	Phenobarbital	168-170	proliferating cell nuclear antigen	Rattus norvegicus	140-144
11872643-0	2002	Formation of 8-hydroxydeoxyguanosine and cell-cycle arrest in the rat liver via generation of oxidative stress by phenobarbital: association with expression profiles of p21(WAF1/Cip1), cyclin D1 and Ogg1.	Phenobarbital	114-127	cyclin-dependent kinase inhibitor 1A	Rattus norvegicus	173-177
11841808-0	2002	Differential regulation of multidrug resistance-associated protein 2 (MRP2) and cytochromes P450 2B1/2 and 3A1/2 in phenobarbital-treated hepatocytes.	Phenobarbital	116-129	ATP binding cassette subfamily C member 2	Rattus norvegicus	27-68
11872643-0	2002	Formation of 8-hydroxydeoxyguanosine and cell-cycle arrest in the rat liver via generation of oxidative stress by phenobarbital: association with expression profiles of p21(WAF1/Cip1), cyclin D1 and Ogg1.	Phenobarbital	114-127	cyclin D1	Rattus norvegicus	185-194
11872643-0	2002	Formation of 8-hydroxydeoxyguanosine and cell-cycle arrest in the rat liver via generation of oxidative stress by phenobarbital: association with expression profiles of p21(WAF1/Cip1), cyclin D1 and Ogg1.	Phenobarbital	114-127	8-oxoguanine DNA glycosylase	Rattus norvegicus	199-203
11792692-1	2002	The nuclear orphan receptor constitutive active receptor (CAR) can be activated to induce CYP2B genes by the potent phenobarbital-type inducer 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) in which the receptor forms a heterodimer with the retinoid X receptor (RXR) and binds to a conserved enhancer element NR1.	Phenobarbital	116-129	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	90-95
11792692-1	2002	The nuclear orphan receptor constitutive active receptor (CAR) can be activated to induce CYP2B genes by the potent phenobarbital-type inducer 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) in which the receptor forms a heterodimer with the retinoid X receptor (RXR) and binds to a conserved enhancer element NR1.	Phenobarbital	116-129	retinoid X receptor alpha	Homo sapiens	268-271
11792692-1	2002	The nuclear orphan receptor constitutive active receptor (CAR) can be activated to induce CYP2B genes by the potent phenobarbital-type inducer 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) in which the receptor forms a heterodimer with the retinoid X receptor (RXR) and binds to a conserved enhancer element NR1.	Phenobarbital	116-129	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	315-318
11706036-7	2002	In contrast, induction of MRP2 by phenobarbital, an activator of CAR, was comparable in wild-type and PXR null mice.	Phenobarbital	34-47	ATP-binding cassette, sub-family C (CFTR/MRP), member 2	Mus musculus	26-30
11706036-7	2002	In contrast, induction of MRP2 by phenobarbital, an activator of CAR, was comparable in wild-type and PXR null mice.	Phenobarbital	34-47	nuclear receptor subfamily 1, group I, member 3	Mus musculus	65-68
11841808-0	2002	Differential regulation of multidrug resistance-associated protein 2 (MRP2) and cytochromes P450 2B1/2 and 3A1/2 in phenobarbital-treated hepatocytes.	Phenobarbital	116-129	ATP binding cassette subfamily C member 2	Rattus norvegicus	70-74
11841808-2	2002	In the present study, we have investigated its expression in response to phenobarbital, a liver tumor promoter known to up-regulate hepatic cytochromes P450 (CYPs), such as CYP2B1/2 and CYP3A1/2.	Phenobarbital	73-86	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	173-179
11841808-2	2002	In the present study, we have investigated its expression in response to phenobarbital, a liver tumor promoter known to up-regulate hepatic cytochromes P450 (CYPs), such as CYP2B1/2 and CYP3A1/2.	Phenobarbital	73-86	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	186-194
11841808-3	2002	MRP2 mRNA and protein levels were found to be markedly increased in both primary rat and human hepatocytes exposed to phenobarbital.	Phenobarbital	118-131	ATP binding cassette subfamily C member 2	Rattus norvegicus	0-4
11841808-5	2002	In addition, hepatic MRP2 expression remained unaltered in rats treated by phenobarbital that, by contrast, increased CYP2B1/2 and CYP3A1/2 gene expression in the liver.	Phenobarbital	75-88	ATP binding cassette subfamily C member 2	Rattus norvegicus	21-25
11841808-5	2002	In addition, hepatic MRP2 expression remained unaltered in rats treated by phenobarbital that, by contrast, increased CYP2B1/2 and CYP3A1/2 gene expression in the liver.	Phenobarbital	75-88	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	118-124
11841808-5	2002	In addition, hepatic MRP2 expression remained unaltered in rats treated by phenobarbital that, by contrast, increased CYP2B1/2 and CYP3A1/2 gene expression in the liver.	Phenobarbital	75-88	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	131-139
11841808-6	2002	Therefore, MRP2 and CYPs appeared differently regulated in response to phenobarbital in both in vivo and in vitro situations, suggesting that cellular and molecular mechanisms underlying up-regulation of MRP2 are, at least in part, unrelated to those operating for CYPs.	Phenobarbital	71-84	ATP binding cassette subfamily C member 2	Rattus norvegicus	11-15
11841808-6	2002	Therefore, MRP2 and CYPs appeared differently regulated in response to phenobarbital in both in vivo and in vitro situations, suggesting that cellular and molecular mechanisms underlying up-regulation of MRP2 are, at least in part, unrelated to those operating for CYPs.	Phenobarbital	71-84	ATP binding cassette subfamily C member 2	Rattus norvegicus	204-208
11841808-7	2002	Phenobarbital-related MRP2 induction in primary rat hepatocytes was associated with some phenotypic effects of the barbiturate, such as prolonged cell survival and inhibition of cell proliferation.	Phenobarbital	0-13	ATP binding cassette subfamily C member 2	Rattus norvegicus	22-26
11841808-8	2002	Phenobarbital also inhibited growth of human hepatoma HepG(2) cells and increased their level of MRP2 gene expression.	Phenobarbital	0-13	ATP binding cassette subfamily C member 2	Homo sapiens	97-101
11841808-9	2002	Such results may favor a putative relationship between phenobarbital-mediated MRP2 regulation in cultured liver parenchymal cells and alteration of cell cycle and survival.	Phenobarbital	55-68	ATP binding cassette subfamily C member 2	Rattus norvegicus	78-82
11679585-3	2002	In previous work, we have shown that CYP2C9 is inducible in primary human hepatocytes by xenobiotics including dexamethasone, rifampicin, and phenobarbital.	Phenobarbital	142-155	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	37-43
11679585-8	2002	Identification of these functional elements provides rational mechanistic basis for CYP2C9 induction by dexamethasone (submicromolar concentrations), and by phenobarbital and rifampicin, respectively.	Phenobarbital	157-170	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	84-90
11860347-6	2002	The inhibitory potency of (-)-deprenyl on MAO-B activity was markedly influenced by pre-treatment of rats with an inducer (phenobarbitone), or an inhibitor (SKF-525A) of cytochrome P-450 mono-oxygenases in the liver.	Phenobarbital	123-137	monoamine oxidase B	Rattus norvegicus	42-47
12206135-3	2002	In addition, MRP2 levels are altered in hepatocytes in response to hormones such as glucocorticoids and to structurally unrelated drugs such as rifampicin, phenobarbital, ritonavir, and cisplatin.	Phenobarbital	156-169	ATP binding cassette subfamily C member 2	Homo sapiens	13-17
12405865-13	2002	Rifampicin (rifampin), phenobarbital, phenytoin, carbamazepine, nevirapine, and efavirenz decrease methadone blood concentrations, probably by induction of CYP3A4 activity, which can result in severe withdrawal symptoms.	Phenobarbital	23-36	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	156-162
11752199-0	2002	Diverse roles of the nuclear orphan receptor CAR in regulating hepatic genes in response to phenobarbital.	Phenobarbital	92-105	nuclear receptor subfamily 1, group I, member 3	Mus musculus	45-48
11752118-4	2002	Levels of rat hepatic oatp2 protein and mRNA are regulated by PCN and phenobarbital treatment; however, the effects of other microsomal enzyme inducers on oatp2 have not been investigated.	Phenobarbital	70-83	solute carrier organic anion transporter family, member 1a4	Rattus norvegicus	22-27
11752199-4	2002	The results show that a total of 138 genes were detected to be either induced or repressed in response to PB treatment, of which about half were under CAR regulation.	Phenobarbital	106-108	nuclear receptor subfamily 1, group I, member 3	Mus musculus	151-154
11752199-5	2002	Including CYP2B10, CYP3A11, and NADPH-CYP reductase, CAR regulated a group of the PB-induced drug/steroid-metabolizing enzymes.	Phenobarbital	82-84	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	10-17
11752199-5	2002	Including CYP2B10, CYP3A11, and NADPH-CYP reductase, CAR regulated a group of the PB-induced drug/steroid-metabolizing enzymes.	Phenobarbital	82-84	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	19-26
11752199-5	2002	Including CYP2B10, CYP3A11, and NADPH-CYP reductase, CAR regulated a group of the PB-induced drug/steroid-metabolizing enzymes.	Phenobarbital	82-84	nuclear receptor subfamily 1, group I, member 3	Mus musculus	53-56
11752199-6	2002	Enzymes such as amino levulinate synthase 1 and squalene epoxidase displayed CAR-independent induction by PB.	Phenobarbital	106-108	nuclear receptor subfamily 1, group I, member 3	Mus musculus	77-80
11752199-7	2002	Cyp4a10 and Cyp4a14 represented the group of genes induced by PB only in CAR-null mice, indicating that CAR may be a transcription blocker that prevents these genes from being induced by PB.	Phenobarbital	62-64	cytochrome P450, family 4, subfamily a, polypeptide 10	Mus musculus	0-7
11752199-7	2002	Cyp4a10 and Cyp4a14 represented the group of genes induced by PB only in CAR-null mice, indicating that CAR may be a transcription blocker that prevents these genes from being induced by PB.	Phenobarbital	62-64	cytochrome P450, family 4, subfamily a, polypeptide 14	Mus musculus	12-19
11752199-7	2002	Cyp4a10 and Cyp4a14 represented the group of genes induced by PB only in CAR-null mice, indicating that CAR may be a transcription blocker that prevents these genes from being induced by PB.	Phenobarbital	62-64	nuclear receptor subfamily 1, group I, member 3	Mus musculus	73-76
11752199-7	2002	Cyp4a10 and Cyp4a14 represented the group of genes induced by PB only in CAR-null mice, indicating that CAR may be a transcription blocker that prevents these genes from being induced by PB.	Phenobarbital	62-64	nuclear receptor subfamily 1, group I, member 3	Mus musculus	104-107
11752199-7	2002	Cyp4a10 and Cyp4a14 represented the group of genes induced by PB only in CAR-null mice, indicating that CAR may be a transcription blocker that prevents these genes from being induced by PB.	Phenobarbital	187-189	cytochrome P450, family 4, subfamily a, polypeptide 10	Mus musculus	0-7
11752199-7	2002	Cyp4a10 and Cyp4a14 represented the group of genes induced by PB only in CAR-null mice, indicating that CAR may be a transcription blocker that prevents these genes from being induced by PB.	Phenobarbital	187-189	cytochrome P450, family 4, subfamily a, polypeptide 14	Mus musculus	12-19
11752199-7	2002	Cyp4a10 and Cyp4a14 represented the group of genes induced by PB only in CAR-null mice, indicating that CAR may be a transcription blocker that prevents these genes from being induced by PB.	Phenobarbital	187-189	nuclear receptor subfamily 1, group I, member 3	Mus musculus	73-76
11752199-7	2002	Cyp4a10 and Cyp4a14 represented the group of genes induced by PB only in CAR-null mice, indicating that CAR may be a transcription blocker that prevents these genes from being induced by PB.	Phenobarbital	187-189	nuclear receptor subfamily 1, group I, member 3	Mus musculus	104-107
11752199-9	2002	Thus, CAR seems to have diverse roles, both as a positive and negative regulator, in the regulation of hepatic genes in response to PB beyond drug/steroid metabolism.	Phenobarbital	132-134	nuclear receptor subfamily 1, group I, member 3	Mus musculus	6-9
11868391-5	2002	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR (the NR-constitutive active receptor) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates the PB-responsive enhancer module (PBREM) in the PB-inducible CYP2B genes.	Phenobarbital	15-28	nuclear receptor subfamily 1 group I member 3	Homo sapiens	83-86
11868391-5	2002	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR (the NR-constitutive active receptor) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates the PB-responsive enhancer module (PBREM) in the PB-inducible CYP2B genes.	Phenobarbital	15-28	nuclear receptor subfamily 1 group I member 3	Homo sapiens	92-123
11868391-5	2002	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR (the NR-constitutive active receptor) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates the PB-responsive enhancer module (PBREM) in the PB-inducible CYP2B genes.	Phenobarbital	15-28	retinoid X receptor alpha	Homo sapiens	177-196
11868391-5	2002	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR (the NR-constitutive active receptor) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates the PB-responsive enhancer module (PBREM) in the PB-inducible CYP2B genes.	Phenobarbital	15-28	retinoid X receptor alpha	Homo sapiens	198-201
11868391-5	2002	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR (the NR-constitutive active receptor) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates the PB-responsive enhancer module (PBREM) in the PB-inducible CYP2B genes.	Phenobarbital	30-32	nuclear receptor subfamily 1 group I member 3	Homo sapiens	83-86
11868391-5	2002	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR (the NR-constitutive active receptor) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates the PB-responsive enhancer module (PBREM) in the PB-inducible CYP2B genes.	Phenobarbital	30-32	nuclear receptor subfamily 1 group I member 3	Homo sapiens	92-123
11868391-5	2002	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR (the NR-constitutive active receptor) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates the PB-responsive enhancer module (PBREM) in the PB-inducible CYP2B genes.	Phenobarbital	30-32	retinoid X receptor alpha	Homo sapiens	177-196
11868391-5	2002	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR (the NR-constitutive active receptor) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates the PB-responsive enhancer module (PBREM) in the PB-inducible CYP2B genes.	Phenobarbital	30-32	retinoid X receptor alpha	Homo sapiens	198-201
11868391-5	2002	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR (the NR-constitutive active receptor) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates the PB-responsive enhancer module (PBREM) in the PB-inducible CYP2B genes.	Phenobarbital	44-46	nuclear receptor subfamily 1 group I member 3	Homo sapiens	83-86
11868391-5	2002	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR (the NR-constitutive active receptor) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates the PB-responsive enhancer module (PBREM) in the PB-inducible CYP2B genes.	Phenobarbital	44-46	nuclear receptor subfamily 1 group I member 3	Homo sapiens	92-123
11868391-5	2002	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR (the NR-constitutive active receptor) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates the PB-responsive enhancer module (PBREM) in the PB-inducible CYP2B genes.	Phenobarbital	44-46	retinoid X receptor alpha	Homo sapiens	177-196
11868391-5	2002	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR (the NR-constitutive active receptor) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates the PB-responsive enhancer module (PBREM) in the PB-inducible CYP2B genes.	Phenobarbital	44-46	retinoid X receptor alpha	Homo sapiens	198-201
11868391-5	2002	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR (the NR-constitutive active receptor) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates the PB-responsive enhancer module (PBREM) in the PB-inducible CYP2B genes.	Phenobarbital	44-46	nuclear receptor subfamily 1 group I member 3	Homo sapiens	83-86
11868391-5	2002	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR (the NR-constitutive active receptor) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates the PB-responsive enhancer module (PBREM) in the PB-inducible CYP2B genes.	Phenobarbital	44-46	nuclear receptor subfamily 1 group I member 3	Homo sapiens	92-123
11868391-5	2002	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR (the NR-constitutive active receptor) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates the PB-responsive enhancer module (PBREM) in the PB-inducible CYP2B genes.	Phenobarbital	44-46	retinoid X receptor alpha	Homo sapiens	177-196
11868391-5	2002	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR (the NR-constitutive active receptor) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates the PB-responsive enhancer module (PBREM) in the PB-inducible CYP2B genes.	Phenobarbital	44-46	retinoid X receptor alpha	Homo sapiens	198-201
12664659-6	2002	Unexpectedly, it has been shown that SXR, which regulates CYP3A, can also regulate CYP2B via recognition of the phenobarbital response element (PBRE).	Phenobarbital	112-125	nuclear receptor subfamily 1 group I member 2	Homo sapiens	37-40
12049174-2	2002	We have previously shown that the nuclear hormone receptor CAR (Constitutive Androstane Receptor, NR113) mediates the well studied induction of CYP2B10 gene expression by phenobarbital (PB) and 1, 4-bis-[2-(3, 5,-dichloropyridyloxy)] benzene (TCPOBOP).	Phenobarbital	171-184	nuclear receptor subfamily 1, group I, member 3	Mus musculus	59-62
12049174-2	2002	We have previously shown that the nuclear hormone receptor CAR (Constitutive Androstane Receptor, NR113) mediates the well studied induction of CYP2B10 gene expression by phenobarbital (PB) and 1, 4-bis-[2-(3, 5,-dichloropyridyloxy)] benzene (TCPOBOP).	Phenobarbital	171-184	nuclear receptor subfamily 1, group I, member 3	Mus musculus	64-96
12049174-2	2002	We have previously shown that the nuclear hormone receptor CAR (Constitutive Androstane Receptor, NR113) mediates the well studied induction of CYP2B10 gene expression by phenobarbital (PB) and 1, 4-bis-[2-(3, 5,-dichloropyridyloxy)] benzene (TCPOBOP).	Phenobarbital	171-184	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	144-151
12049174-2	2002	We have previously shown that the nuclear hormone receptor CAR (Constitutive Androstane Receptor, NR113) mediates the well studied induction of CYP2B10 gene expression by phenobarbital (PB) and 1, 4-bis-[2-(3, 5,-dichloropyridyloxy)] benzene (TCPOBOP).	Phenobarbital	186-188	nuclear receptor subfamily 1, group I, member 3	Mus musculus	59-62
12049174-2	2002	We have previously shown that the nuclear hormone receptor CAR (Constitutive Androstane Receptor, NR113) mediates the well studied induction of CYP2B10 gene expression by phenobarbital (PB) and 1, 4-bis-[2-(3, 5,-dichloropyridyloxy)] benzene (TCPOBOP).	Phenobarbital	186-188	nuclear receptor subfamily 1, group I, member 3	Mus musculus	64-96
12049174-2	2002	We have previously shown that the nuclear hormone receptor CAR (Constitutive Androstane Receptor, NR113) mediates the well studied induction of CYP2B10 gene expression by phenobarbital (PB) and 1, 4-bis-[2-(3, 5,-dichloropyridyloxy)] benzene (TCPOBOP).	Phenobarbital	186-188	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	144-151
12049174-4	2002	In addition to the liver, CAR is expressed in the epithelial cells of the villi in the small intestine, and this expression is required for CYP2B10 induction in response to PB and TCPOBOP in those cells.	Phenobarbital	173-175	nuclear receptor subfamily 1, group I, member 3	Mus musculus	26-29
12049174-4	2002	In addition to the liver, CAR is expressed in the epithelial cells of the villi in the small intestine, and this expression is required for CYP2B10 induction in response to PB and TCPOBOP in those cells.	Phenobarbital	173-175	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	140-147
12664659-6	2002	Unexpectedly, it has been shown that SXR, which regulates CYP3A, can also regulate CYP2B via recognition of the phenobarbital response element (PBRE).	Phenobarbital	112-125	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	83-88
11551824-0	2001	A duplicated HNF-3 binding site in the CYP2H2 promoter underlies the weak phenobarbital induction response.	Phenobarbital	74-87	cytochrome P450 family 2 subfamily C member 23b	Gallus gallus	39-45
11719063-7	2001	Phenobarbital is a well studied inducer of P450s in insects and it induced expression of CYP6D3 mRNA in both the CS (16-fold) and LPR (1.6 fold) strains.	Phenobarbital	0-13	cytochrome P450 6d3	Musca domestica	89-95
11714877-13	2001	We conclude that midazolam is a phenobarbital-like CYP inducer in rats.	Phenobarbital	32-45	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	51-54
11698173-9	2001	PB treatment induced CYP2A, CYP2C, CYP2B1/2 and CYP3A activities.	Phenobarbital	0-2	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	28-33
11698173-9	2001	PB treatment induced CYP2A, CYP2C, CYP2B1/2 and CYP3A activities.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	35-41
11698173-9	2001	PB treatment induced CYP2A, CYP2C, CYP2B1/2 and CYP3A activities.	Phenobarbital	0-2	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	48-53
11753661-7	2001	By contrast, Ha-ras mutations were undetectable in tumors from mice treated with DEN/PB (0/32), while approximately 80% (37/46) of tumors from this group showed beta-catenin mutations.	Phenobarbital	85-87	Harvey rat sarcoma virus oncogene	Mus musculus	13-19
11753661-0	2001	Selective pressure during tumor promotion by phenobarbital leads to clonal outgrowth of beta-catenin-mutated mouse liver tumors.	Phenobarbital	45-58	catenin (cadherin associated protein), beta 1	Mus musculus	88-100
11551824-10	2001	Hence, duplication of the HNF-3 site in the CYP2H2 promoter does not allow binding of HNF-3 in the promoter context and may be predominantly, if not exclusively, responsible for the poor response of the CYP2H2 gene to phenobarbital.	Phenobarbital	218-231	cytochrome P450 family 2 subfamily C member 23b	Gallus gallus	44-50
11551824-10	2001	Hence, duplication of the HNF-3 site in the CYP2H2 promoter does not allow binding of HNF-3 in the promoter context and may be predominantly, if not exclusively, responsible for the poor response of the CYP2H2 gene to phenobarbital.	Phenobarbital	218-231	cytochrome P450 family 2 subfamily C member 23b	Gallus gallus	203-209
11804372-0	2001	Postnatal phenobarbitone for preventing hyperbilirubinaemia in newborns with ABO incompatibility.	Phenobarbital	10-24	ABO, alpha 1-3-N-acetylgalactosaminyltransferase and alpha 1-3-galactosyltransferase	Homo sapiens	77-80
11502734-9	2001	Pretreatment with phenobarbital, a known inducer of CYP2A and CYP2B, increased VCH bioactivation in both species.	Phenobarbital	18-31	cytochrome P450, family 2, subfamily a	Mus musculus	52-57
11709545-11	2001	According to a four-transmembrane domain model, the mutations concentrated mostly in the myoplasmic and luminal loops linking, respectively, transmembrane domains T1 and T2 or T3 and T4 of RYR1.	Phenobarbital	104-111	ryanodine receptor 1	Homo sapiens	189-193
11557128-6	2001	2-Acetylaminofluorene also induces MRP2; in addition, expression of this transporter in liver cells is increased in response to various drugs, such as the barbiturate phenobarbital, the chemopreventive agent, oltipraz and the anticancer drug, cisplatin.	Phenobarbital	167-180	ATP binding cassette subfamily C member 2	Rattus norvegicus	35-39
11502734-9	2001	Pretreatment with phenobarbital, a known inducer of CYP2A and CYP2B, increased VCH bioactivation in both species.	Phenobarbital	18-31	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	62-67
11518807-4	2001	Thus, the phenobarbital-inducible enhancer units of the mouse Cyp2b10, rat CYP2B2, and human CYP2B6 genes were activated in reporter gene assays by the same compounds that activate the chicken CYP2H1 phenobarbital-inducible enhancer units.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	62-69
11562429-2	2001	In previous studies, a 264-base-pair (bp) phenobarbital-responsive enhancer unit (PBRU) located at -1671 to -1408 upstream of the chicken CYP2H1 transcriptional start-site increased gene expression when activated by the chicken xenobiotic-sensing orphan nuclear receptor CXR.	Phenobarbital	42-55	cytochrome P450 2H1	Gallus gallus	138-144
11562429-2	2001	In previous studies, a 264-base-pair (bp) phenobarbital-responsive enhancer unit (PBRU) located at -1671 to -1408 upstream of the chicken CYP2H1 transcriptional start-site increased gene expression when activated by the chicken xenobiotic-sensing orphan nuclear receptor CXR.	Phenobarbital	42-55	nuclear receptor subfamily 1 group I member 3	Gallus gallus	271-274
11502872-5	2001	PXR was shown to be capable of activating the phenobarbital-responsive enhancer module (PBREM) region of the CYP2B6 gene, a 51-base-pair enhancer element that mediates induction of CYP2B6 expression by CAR.	Phenobarbital	46-59	nuclear receptor subfamily 1 group I member 2	Homo sapiens	0-3
11502872-5	2001	PXR was shown to be capable of activating the phenobarbital-responsive enhancer module (PBREM) region of the CYP2B6 gene, a 51-base-pair enhancer element that mediates induction of CYP2B6 expression by CAR.	Phenobarbital	46-59	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	109-115
11502872-5	2001	PXR was shown to be capable of activating the phenobarbital-responsive enhancer module (PBREM) region of the CYP2B6 gene, a 51-base-pair enhancer element that mediates induction of CYP2B6 expression by CAR.	Phenobarbital	46-59	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	181-187
11502872-5	2001	PXR was shown to be capable of activating the phenobarbital-responsive enhancer module (PBREM) region of the CYP2B6 gene, a 51-base-pair enhancer element that mediates induction of CYP2B6 expression by CAR.	Phenobarbital	46-59	nuclear receptor subfamily 1 group I member 3	Homo sapiens	202-205
11518807-4	2001	Thus, the phenobarbital-inducible enhancer units of the mouse Cyp2b10, rat CYP2B2, and human CYP2B6 genes were activated in reporter gene assays by the same compounds that activate the chicken CYP2H1 phenobarbital-inducible enhancer units.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	75-81
11518807-4	2001	Thus, the phenobarbital-inducible enhancer units of the mouse Cyp2b10, rat CYP2B2, and human CYP2B6 genes were activated in reporter gene assays by the same compounds that activate the chicken CYP2H1 phenobarbital-inducible enhancer units.	Phenobarbital	10-23	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	93-99
11518807-4	2001	Thus, the phenobarbital-inducible enhancer units of the mouse Cyp2b10, rat CYP2B2, and human CYP2B6 genes were activated in reporter gene assays by the same compounds that activate the chicken CYP2H1 phenobarbital-inducible enhancer units.	Phenobarbital	10-23	cytochrome P450 2H1	Gallus gallus	193-199
11518807-4	2001	Thus, the phenobarbital-inducible enhancer units of the mouse Cyp2b10, rat CYP2B2, and human CYP2B6 genes were activated in reporter gene assays by the same compounds that activate the chicken CYP2H1 phenobarbital-inducible enhancer units.	Phenobarbital	200-213	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	62-69
11518807-4	2001	Thus, the phenobarbital-inducible enhancer units of the mouse Cyp2b10, rat CYP2B2, and human CYP2B6 genes were activated in reporter gene assays by the same compounds that activate the chicken CYP2H1 phenobarbital-inducible enhancer units.	Phenobarbital	200-213	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	75-81
11518807-4	2001	Thus, the phenobarbital-inducible enhancer units of the mouse Cyp2b10, rat CYP2B2, and human CYP2B6 genes were activated in reporter gene assays by the same compounds that activate the chicken CYP2H1 phenobarbital-inducible enhancer units.	Phenobarbital	200-213	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	93-99
11518807-4	2001	Thus, the phenobarbital-inducible enhancer units of the mouse Cyp2b10, rat CYP2B2, and human CYP2B6 genes were activated in reporter gene assays by the same compounds that activate the chicken CYP2H1 phenobarbital-inducible enhancer units.	Phenobarbital	200-213	cytochrome P450 2H1	Gallus gallus	193-199
11518807-5	2001	Chicken xenobiotic receptor, pregnane X receptor, and constitutive androstane receptor all bound to the CYP2H1 phenobarbital-inducible enhancer units in gel-shift experiments.	Phenobarbital	111-124	nuclear receptor subfamily 1 group I member 3	Gallus gallus	8-27
11518807-5	2001	Chicken xenobiotic receptor, pregnane X receptor, and constitutive androstane receptor all bound to the CYP2H1 phenobarbital-inducible enhancer units in gel-shift experiments.	Phenobarbital	111-124	nuclear receptor subfamily 1 group I member 3	Gallus gallus	54-86
11518807-5	2001	Chicken xenobiotic receptor, pregnane X receptor, and constitutive androstane receptor all bound to the CYP2H1 phenobarbital-inducible enhancer units in gel-shift experiments.	Phenobarbital	111-124	cytochrome P450 2H1	Gallus gallus	104-110
11589781-4	2001	Most importantly, a nuclear orphan receptor, the constitutive androstane receptor has been identified as a primary determinant of the transcriptional activation of CYP genes in response to phenobarbital-like inducers in mammals.	Phenobarbital	189-202	nuclear receptor subfamily 1, group I, member 3	Mus musculus	49-81
11589781-6	2001	The response of mammalian CYP2B genes to phenobarbital was abolished in the liver of mice carrying a null allele of the constitutive androstane receptor gene, whereas that of CYP3A genes was lost in pregnane X receptor knock-out mice.	Phenobarbital	41-54	nuclear receptor subfamily 1, group I, member 3	Mus musculus	120-152
11589781-6	2001	The response of mammalian CYP2B genes to phenobarbital was abolished in the liver of mice carrying a null allele of the constitutive androstane receptor gene, whereas that of CYP3A genes was lost in pregnane X receptor knock-out mice.	Phenobarbital	41-54	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	175-180
11434912-3	2001	In this study, we examined the induction of two heat shock proteins, heat shock protein 70 (HSP70) and heme oxygenase-1 (HO-1), in the livers of rats pretreated with or without phenobarbital, followed by exposure to isoflurane or halothane under hypoxic conditions.	Phenobarbital	177-190	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	69-90
11434912-3	2001	In this study, we examined the induction of two heat shock proteins, heat shock protein 70 (HSP70) and heme oxygenase-1 (HO-1), in the livers of rats pretreated with or without phenobarbital, followed by exposure to isoflurane or halothane under hypoxic conditions.	Phenobarbital	177-190	heme oxygenase 1	Rattus norvegicus	121-125
11434912-4	2001	In the phenobarbital-pretreated rats, the maximal induction of HSP70 was observed by halothane-hypoxia treatment, followed by a half-maximal induction by isoflurane-hypoxia treatment, and less than 30% induction by hypoxia treatment alone.	Phenobarbital	7-20	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	63-68
11437368-1	2001	Regioselective 7-demethylation of scoparone is regularly employed as an indicator of phenobarbital-like induction of rat liver cytochrome P450 isoform CYP2B1, e.g., by the antiepileptic drug phenytoin.	Phenobarbital	85-98	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	151-157
11489433-4	2001	In a reaction mixture of rat liver mitochondria and cytosol with NADPH, phenobarbital, a specific inhibitor of aldehyde reductase, and 4-nitrobenzaldehyde (4-NBA), a substrate inhibitor of aldehyde reductase, decreased the formation of PGL from NDP.	Phenobarbital	72-85	aldo-keto reductase family 1, member B7	Rattus norvegicus	111-129
11454735-5	2001	CYP2B1 activity was assessed by measuring depentylation of 7-pentoxyresorufin by liver microsomes obtained from phenobarbital-treated rats.	Phenobarbital	112-125	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	0-6
11455014-0	2001	The antiglucocorticoid RU486 inhibits phenobarbital induction of the chicken CYP2H1 gene in primary hepatocytes.	Phenobarbital	38-51	cytochrome P450 2H1	Gallus gallus	77-83
11455014-1	2001	The cytochrome P450 gene CYP2H1 is highly induced by phenobarbital in chick embryo hepatocytes.	Phenobarbital	53-66	cytochrome P450 2H1	Gallus gallus	25-31
11455014-3	2001	Here, we show that a high concentration of the potent glucocorticoid and progesterone receptor antagonist RU486 almost completely blocks phenobarbital-induced accumulation of CYP2H1 mRNA in hepatocytes yet has no effect on basal expression.	Phenobarbital	137-150	cytochrome P450 2H1	Gallus gallus	175-181
11455014-4	2001	In marked contrast, CYP2H1 mRNA induced by the phenobarbital-type inducers glutethimide and 2-allylisopropylacetamide is not affected by RU486.	Phenobarbital	47-60	cytochrome P450 2H1	Gallus gallus	20-26
11477212-10	2001	These data indicate that caffeine and phenobarbital have similar Glut1 inhibitory properties in these two subjects.	Phenobarbital	38-51	solute carrier family 2 member 1	Homo sapiens	65-70
11389874-5	2001	In the liver, PB, PCN, and DDT induced both CYP2B9 and CYP2B10 in both sexes to the same extent, whereas Dex induced only CYP2B10 and simultaneously suppressed CYP2B9.	Phenobarbital	14-16	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	44-50
11389874-5	2001	In the liver, PB, PCN, and DDT induced both CYP2B9 and CYP2B10 in both sexes to the same extent, whereas Dex induced only CYP2B10 and simultaneously suppressed CYP2B9.	Phenobarbital	14-16	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	55-62
11437368-2	2001	After induction with phenobarbital and phenytoin, a new reaction sequence catalyzed by Cyp2c29 was identified in mouse liver microsomes.	Phenobarbital	21-34	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	87-94
11377393-0	2001	Functional analysis of the phenobarbital-responsive unit in rat CYP2B2.	Phenobarbital	27-40	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	64-70
11377398-2	2001	In this project, we examined the influence of pyrethroids (permethrin, cypermethrin, and fenvalerate) on the expression and activity of the phenobarbital (PB)-inducible cytochrome P450 2B1 isoform (CYP2B1) in primary rat hepatocyte cultures.	Phenobarbital	140-153	cytochrome P450 2B1	Rattus norvegicus	169-188
11377398-2	2001	In this project, we examined the influence of pyrethroids (permethrin, cypermethrin, and fenvalerate) on the expression and activity of the phenobarbital (PB)-inducible cytochrome P450 2B1 isoform (CYP2B1) in primary rat hepatocyte cultures.	Phenobarbital	140-153	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	198-204
11377398-2	2001	In this project, we examined the influence of pyrethroids (permethrin, cypermethrin, and fenvalerate) on the expression and activity of the phenobarbital (PB)-inducible cytochrome P450 2B1 isoform (CYP2B1) in primary rat hepatocyte cultures.	Phenobarbital	155-157	cytochrome P450 2B1	Rattus norvegicus	169-188
11377398-2	2001	In this project, we examined the influence of pyrethroids (permethrin, cypermethrin, and fenvalerate) on the expression and activity of the phenobarbital (PB)-inducible cytochrome P450 2B1 isoform (CYP2B1) in primary rat hepatocyte cultures.	Phenobarbital	155-157	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	198-204
11377398-6	2001	Permethrin-dependent enhancement of CYP2B1 and CYP3A1 mRNA expression was repressed by the hepatotrophic cytokine epidermal growth factor, which is known to also inhibit PB-dependent induction of CYP2B1.	Phenobarbital	170-172	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	36-42
11377398-6	2001	Permethrin-dependent enhancement of CYP2B1 and CYP3A1 mRNA expression was repressed by the hepatotrophic cytokine epidermal growth factor, which is known to also inhibit PB-dependent induction of CYP2B1.	Phenobarbital	170-172	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	47-53
11377398-6	2001	Permethrin-dependent enhancement of CYP2B1 and CYP3A1 mRNA expression was repressed by the hepatotrophic cytokine epidermal growth factor, which is known to also inhibit PB-dependent induction of CYP2B1.	Phenobarbital	170-172	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	196-202
11377393-1	2001	An 163-bp fragment of the rat cytochrome P450 gene, CYP2B2 has been shown to contain sequences that mediate phenobarbital (PB) responsiveness of this gene.	Phenobarbital	108-121	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	52-58
11377393-1	2001	An 163-bp fragment of the rat cytochrome P450 gene, CYP2B2 has been shown to contain sequences that mediate phenobarbital (PB) responsiveness of this gene.	Phenobarbital	123-125	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	52-58
11377393-2	2001	In studies on this rat gene and the orthologous mouse gene, Cyp2b10, the minimal fragment required for near full PB responsiveness has varied from about 50 to 80 bp depending on the gene used and the number of copies of the PB responsive sequences assessed.	Phenobarbital	113-115	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	60-67
11377393-2	2001	In studies on this rat gene and the orthologous mouse gene, Cyp2b10, the minimal fragment required for near full PB responsiveness has varied from about 50 to 80 bp depending on the gene used and the number of copies of the PB responsive sequences assessed.	Phenobarbital	224-226	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	60-67
11377393-10	2001	These results indicate that sequences in addition to the NR-1 and -2 and the NF-1 sites are required for full responsiveness to PB and suggest that proteins which bind to these sites may interact.	Phenobarbital	128-130	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	57-68
21047472-2	2001	METHODS: The enhancing effect of combination of caffeine and phenobarbital on the cytotoxicity of DDP on SPC-A-1 was detected by MTT assay.	Phenobarbital	61-74	ATPase secretory pathway Ca2+ transporting 1	Homo sapiens	105-112
11560253-2	2001	In this study, we investigated immunohistochemically the association between expression of TGF-alpha and cell proliferation activity in mouse hepatoblastomas (HBs) and hepatocellular carcinomas (HCCs) induced in B6C3F1 mice by diethylnitrosamine and sodium phenobarbital.	Phenobarbital	250-270	transforming growth factor alpha	Mus musculus	91-100
11439219-0	2001	Phenobarbitone-induced liver response in wild type and in p53 deficient mice.	Phenobarbital	0-14	transformation related protein 53, pseudogene	Mus musculus	58-61
11406319-5	2001	Phenobarbital abolished not only seizures and aggression, but also the changes of neuropeptide expressions.	Phenobarbital	0-13	pyroglutamylated RFamide peptide	Rattus norvegicus	82-94
11399265-3	2001	Increased expression of HO-1 and HSP27 was observed in the hippocampus and the cerebral cortex of phenobarbital-withdrawn rats.	Phenobarbital	98-111	heme oxygenase 1	Rattus norvegicus	24-28
11399265-3	2001	Increased expression of HO-1 and HSP27 was observed in the hippocampus and the cerebral cortex of phenobarbital-withdrawn rats.	Phenobarbital	98-111	heat shock protein family B (small) member 1	Rattus norvegicus	33-38
11399265-7	2001	These findings suggest that the induction of HO-1 and HSP27 during withdrawal from phenobarbital dependence may play a role in protection against glutamate toxicity.	Phenobarbital	83-96	heme oxygenase 1	Rattus norvegicus	45-49
11353762-3	2001	An induction cocktail containing beta-naphthoflavone, phenobarbital, and dexamethasone induced immunoreactive homologs of 1A1, 1A2, 2B1, 2B2, 3A1, and 3A2.	Phenobarbital	54-67	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	132-135
11399265-7	2001	These findings suggest that the induction of HO-1 and HSP27 during withdrawal from phenobarbital dependence may play a role in protection against glutamate toxicity.	Phenobarbital	83-96	heat shock protein family B (small) member 1	Rattus norvegicus	54-59
11391536-12	2001	These results suggest that Oatp2, but not Oatp1, is inducible by PB and PCN, which imparts the increased capacity of the liver to extract cardiac glycosides from the plasma.	Phenobarbital	65-67	solute carrier organic anion transporter family, member 1a4	Rattus norvegicus	27-32
11344206-2	2001	There are 2 forms of PHA1: the autosomal recessive form with symptoms persisting into adulthood, caused by mutations in the amiloride-sensitive luminal sodium channel, and the autosomal dominant or sporadic form, which shows milder symptoms that remit with age.	Phenobarbital	144-151	sodium channel epithelial 1 subunit gamma	Homo sapiens	21-25
11391536-3	2001	We postulated that increased uptake of cardiac glycosides observed after pretreatment of animals with phenobarbital (PB) and pregnenolone-16alpha-carbonitrile (PCN) occurs via increased hepatic expression of Oatp1 and/or Oatp2.	Phenobarbital	102-115	solute carrier organic anion transporter family, member 1a1	Rattus norvegicus	208-213
11391536-3	2001	We postulated that increased uptake of cardiac glycosides observed after pretreatment of animals with phenobarbital (PB) and pregnenolone-16alpha-carbonitrile (PCN) occurs via increased hepatic expression of Oatp1 and/or Oatp2.	Phenobarbital	102-115	solute carrier organic anion transporter family, member 1a4	Rattus norvegicus	221-226
11391536-3	2001	We postulated that increased uptake of cardiac glycosides observed after pretreatment of animals with phenobarbital (PB) and pregnenolone-16alpha-carbonitrile (PCN) occurs via increased hepatic expression of Oatp1 and/or Oatp2.	Phenobarbital	117-119	solute carrier organic anion transporter family, member 1a1	Rattus norvegicus	208-213
11391536-3	2001	We postulated that increased uptake of cardiac glycosides observed after pretreatment of animals with phenobarbital (PB) and pregnenolone-16alpha-carbonitrile (PCN) occurs via increased hepatic expression of Oatp1 and/or Oatp2.	Phenobarbital	117-119	solute carrier organic anion transporter family, member 1a4	Rattus norvegicus	221-226
11391536-7	2001	Increases in Oatp2 expression were observed from livers of rats treated with PB and PCN, in which PCN caused a robust elevation of Oatp2 mRNA and protein.	Phenobarbital	77-79	solute carrier organic anion transporter family, member 1a4	Rattus norvegicus	13-18
11391536-7	2001	Increases in Oatp2 expression were observed from livers of rats treated with PB and PCN, in which PCN caused a robust elevation of Oatp2 mRNA and protein.	Phenobarbital	77-79	solute carrier organic anion transporter family, member 1a4	Rattus norvegicus	131-136
11391536-11	2001	The finding that Oatp2 expression increases in response to PB and PCN is consistent with our previous findings that PB and PCN enhance hepatic uptake of cardiac glycosides.	Phenobarbital	59-61	solute carrier organic anion transporter family, member 1a4	Rattus norvegicus	17-22
11391536-11	2001	The finding that Oatp2 expression increases in response to PB and PCN is consistent with our previous findings that PB and PCN enhance hepatic uptake of cardiac glycosides.	Phenobarbital	116-118	solute carrier organic anion transporter family, member 1a4	Rattus norvegicus	17-22
11353799-0	2001	Repression of phenobarbital-dependent CYP2B1 mRNA induction by reactive oxygen species in primary rat hepatocyte cultures.	Phenobarbital	14-27	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	38-44
11353799-4	2001	A primary rat hepatocyte culture system was used to investigate whether reactive oxygen species might modulate PB-dependent CYP2B1 induction.	Phenobarbital	111-113	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	124-130
11353799-5	2001	In cells cultivated for 3 days with 1.5 mM PB, substantial CYP2B1 mRNA induction was observed (100%).	Phenobarbital	43-45	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	59-65
11353799-9	2001	Furthermore, a 263-base pair CYP2B1 promoter fragment encompassing the phenobarbital-responsive enhancer module conferred suppression of PB-dependent luciferase expression by AT and activation by NAC in a heterologous SV40-promoter construct.	Phenobarbital	71-84	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	29-35
11353799-10	2001	In summary, these data demonstrate a regulatory mechanism that is dependent on the cellular redox status, which modulates CYP2B1 mRNA induction by PB on the transcriptional level, thus representing a feedback mechanism preventing further P-450-dependent production of reactive oxygen intermediates under oxidative stress.	Phenobarbital	147-149	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	122-128
11322933-2	2001	We found that EGF, added to basal culture medium or phenobarbital (3.2 mM) containing medium, provoked a moderate decrease of CYP1A1 and CYP2B1/2 activities.	Phenobarbital	52-65	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	126-132
11322933-2	2001	We found that EGF, added to basal culture medium or phenobarbital (3.2 mM) containing medium, provoked a moderate decrease of CYP1A1 and CYP2B1/2 activities.	Phenobarbital	52-65	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	137-143
11451172-5	2001	RESULTS: Compared to control rats, PB treatment increased expression of the organic anion transporting polypeptide 2 (Oatp2; Slc21aS) more than 2-fold on the RNA (P &lt; 0.05) and protein (P &lt; 0.001) levels.	Phenobarbital	35-37	solute carrier organic anion transporter family, member 1a4	Rattus norvegicus	76-116
11451172-5	2001	RESULTS: Compared to control rats, PB treatment increased expression of the organic anion transporting polypeptide 2 (Oatp2; Slc21aS) more than 2-fold on the RNA (P &lt; 0.05) and protein (P &lt; 0.001) levels.	Phenobarbital	35-37	solute carrier organic anion transporter family, member 1a4	Rattus norvegicus	118-123
11451172-9	2001	CONCLUSIONS: The induction of digoxin uptake by PB correlates with Oatp2 expression.	Phenobarbital	48-50	solute carrier organic anion transporter family, member 1a4	Rattus norvegicus	67-72
11343253-0	2001	The phenobarbital response enhancer module in the human bilirubin UDP-glucuronosyltransferase UGT1A1 gene and regulation by the nuclear receptor CAR.	Phenobarbital	4-17	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	94-100
11343253-0	2001	The phenobarbital response enhancer module in the human bilirubin UDP-glucuronosyltransferase UGT1A1 gene and regulation by the nuclear receptor CAR.	Phenobarbital	4-17	CXADR Ig-like cell adhesion molecule	Homo sapiens	145-148
11343253-2	2001	For decades, phenobarbital (PB) treatment for hyperbilirubinemia has been known to increase expression of the UGT1A1 gene in liver.	Phenobarbital	13-26	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
11343253-2	2001	For decades, phenobarbital (PB) treatment for hyperbilirubinemia has been known to increase expression of the UGT1A1 gene in liver.	Phenobarbital	28-30	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	110-116
11343253-3	2001	We have now delineated the PB response activity to a 290-bp distal enhancer sequence (-3483/-3194) of the UGT1A1 gene.	Phenobarbital	27-29	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112
11343253-7	2001	Moreover, the 290-bp DNA was effectively activated in mouse primary hepatocytes in response to PB, offering an excellent clinical test for the examination of the responsiveness of the UGT1A1 to PB in the human population, particularly individuals with hyperbilirubinemia.	Phenobarbital	95-97	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	184-190
11295255-10	2001	At the same sites, phenobarbital led to an increased CYP 2B1 and 3A2 expression and dexamethasone to an elevated CYP 3A2 immunostaining.	Phenobarbital	19-32	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	53-60
11256950-1	2001	The constitutive androstane receptor (CAR) activates the expression of a reporter gene attached to the phenobarbital-response element (PBRE) of the cytochrome P450 2B1 (CYP2B1) gene in response to the barbiturate phenobarbital and the plant product picrotoxin.	Phenobarbital	103-116	nuclear receptor subfamily 1 group I member 3	Homo sapiens	4-36
11256950-1	2001	The constitutive androstane receptor (CAR) activates the expression of a reporter gene attached to the phenobarbital-response element (PBRE) of the cytochrome P450 2B1 (CYP2B1) gene in response to the barbiturate phenobarbital and the plant product picrotoxin.	Phenobarbital	103-116	nuclear receptor subfamily 1 group I member 3	Homo sapiens	38-41
11256950-1	2001	The constitutive androstane receptor (CAR) activates the expression of a reporter gene attached to the phenobarbital-response element (PBRE) of the cytochrome P450 2B1 (CYP2B1) gene in response to the barbiturate phenobarbital and the plant product picrotoxin.	Phenobarbital	213-226	nuclear receptor subfamily 1 group I member 3	Homo sapiens	4-36
11256950-1	2001	The constitutive androstane receptor (CAR) activates the expression of a reporter gene attached to the phenobarbital-response element (PBRE) of the cytochrome P450 2B1 (CYP2B1) gene in response to the barbiturate phenobarbital and the plant product picrotoxin.	Phenobarbital	213-226	nuclear receptor subfamily 1 group I member 3	Homo sapiens	38-41
11294510-0	2001	P-hydroxylation of phenobarbital: relationship to (S)-mephenytoin hydroxylation (CYP2C19) polymorphism.	Phenobarbital	19-32	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	81-88
11294510-9	2001	These results indicated that the p-hydroxylation pathway of PB co-segregates with the CYP2C19 metabolic polymorphism.	Phenobarbital	60-62	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	86-93
11278292-5	2001	To exert their effect the receptors bind to the same direct repeat site (DR4) within the phenobarbital response element of the CYP2B1 promoter and to the same DR3 site in the pregnane X response element of CYP3A1.	Phenobarbital	89-102	major histocompatibility complex, class II, DR beta 4	Homo sapiens	73-76
11274859-13	2001	In addition, the method could determine the non-inducible, and 3-methylcholanthrene- and phenobarbital-inducible activities of UGT1A6 in rat liver microsomes under the same assay conditions.	Phenobarbital	89-102	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	127-133
11283262-1	2001	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR translocates to the mouse liver nucleus (T. Kawamoto et al., Mol.	Phenobarbital	15-28	nuclear receptor subfamily 1, group I, member 3	Mus musculus	83-86
11283262-1	2001	In response to phenobarbital (PB) and other PB-type inducers, the nuclear receptor CAR translocates to the mouse liver nucleus (T. Kawamoto et al., Mol.	Phenobarbital	30-32	nuclear receptor subfamily 1, group I, member 3	Mus musculus	83-86
11283262-6	2001	As in the wild-type hCAR, the truncated receptor lacking the C-terminal 10 residues (i.e., AF2 domain) translocated to the nucleus, indicating that the PB-inducible translocation is AF2 independent.	Phenobarbital	152-154	CXADR Ig-like cell adhesion molecule	Homo sapiens	20-24
11323161-3	2001	Similar to the rat mrp2 gene, human mrp2 is inducible by the chemical carcinogen 2-AAF, the chemotherapeutic drug cisplatin and the barbiturate phenobarbital, as demonstrated in Northern and Western Blots.	Phenobarbital	144-157	ATP binding cassette subfamily C member 2	Rattus norvegicus	19-23
11323161-3	2001	Similar to the rat mrp2 gene, human mrp2 is inducible by the chemical carcinogen 2-AAF, the chemotherapeutic drug cisplatin and the barbiturate phenobarbital, as demonstrated in Northern and Western Blots.	Phenobarbital	144-157	ATP binding cassette subfamily C member 2	Homo sapiens	36-40
11181490-4	2001	Compounds known to activate the pregnane X receptor (PXR) such as rifampicin, or the constitutively activated receptor (CAR) such as phenobarbital, induced CYP2C8, CYP2C9, and to a lesser extent CYP2C19 mRNAs and proteins.	Phenobarbital	133-146	nuclear receptor subfamily 1 group I member 3	Homo sapiens	120-123
11113125-0	2001	Chromatin assembly enhances binding to the CYP2B1 phenobarbital-responsive unit (PBRU) of nuclear factor-1, which binds simultaneously with constitutive androstane receptor (CAR)/retinoid X receptor (RXR) and enhances CAR/RXR-mediated activation of the PBRU.	Phenobarbital	50-63	carnation	Drosophila melanogaster	140-172
11113125-0	2001	Chromatin assembly enhances binding to the CYP2B1 phenobarbital-responsive unit (PBRU) of nuclear factor-1, which binds simultaneously with constitutive androstane receptor (CAR)/retinoid X receptor (RXR) and enhances CAR/RXR-mediated activation of the PBRU.	Phenobarbital	50-63	carnation	Drosophila melanogaster	174-177
11113125-0	2001	Chromatin assembly enhances binding to the CYP2B1 phenobarbital-responsive unit (PBRU) of nuclear factor-1, which binds simultaneously with constitutive androstane receptor (CAR)/retinoid X receptor (RXR) and enhances CAR/RXR-mediated activation of the PBRU.	Phenobarbital	50-63	carnation	Drosophila melanogaster	218-221
11113125-1	2001	Phenobarbital induction of CYP2B genes is mediated by a complex phenobarbital-responsive enhancer (PBRU), which contains a binding site for nuclear factor-1 (NF-1) flanked by two DR-4 nuclear receptor (NR) binding sites for a heterodimer of constitutive androstane receptor (CAR) and retinoid X receptor (RXR).	Phenobarbital	0-13	Neurofibromin 1	Drosophila melanogaster	158-162
11113125-1	2001	Phenobarbital induction of CYP2B genes is mediated by a complex phenobarbital-responsive enhancer (PBRU), which contains a binding site for nuclear factor-1 (NF-1) flanked by two DR-4 nuclear receptor (NR) binding sites for a heterodimer of constitutive androstane receptor (CAR) and retinoid X receptor (RXR).	Phenobarbital	0-13	carnation	Drosophila melanogaster	241-273
11113125-1	2001	Phenobarbital induction of CYP2B genes is mediated by a complex phenobarbital-responsive enhancer (PBRU), which contains a binding site for nuclear factor-1 (NF-1) flanked by two DR-4 nuclear receptor (NR) binding sites for a heterodimer of constitutive androstane receptor (CAR) and retinoid X receptor (RXR).	Phenobarbital	0-13	carnation	Drosophila melanogaster	275-278
11113125-1	2001	Phenobarbital induction of CYP2B genes is mediated by a complex phenobarbital-responsive enhancer (PBRU), which contains a binding site for nuclear factor-1 (NF-1) flanked by two DR-4 nuclear receptor (NR) binding sites for a heterodimer of constitutive androstane receptor (CAR) and retinoid X receptor (RXR).	Phenobarbital	64-77	Neurofibromin 1	Drosophila melanogaster	158-162
11113125-1	2001	Phenobarbital induction of CYP2B genes is mediated by a complex phenobarbital-responsive enhancer (PBRU), which contains a binding site for nuclear factor-1 (NF-1) flanked by two DR-4 nuclear receptor (NR) binding sites for a heterodimer of constitutive androstane receptor (CAR) and retinoid X receptor (RXR).	Phenobarbital	64-77	carnation	Drosophila melanogaster	241-273
11113125-1	2001	Phenobarbital induction of CYP2B genes is mediated by a complex phenobarbital-responsive enhancer (PBRU), which contains a binding site for nuclear factor-1 (NF-1) flanked by two DR-4 nuclear receptor (NR) binding sites for a heterodimer of constitutive androstane receptor (CAR) and retinoid X receptor (RXR).	Phenobarbital	64-77	carnation	Drosophila melanogaster	275-278
11113125-8	2001	These studies demonstrate that NF-1 and CAR/RXR can both bind to the PBRU at the same time and that chromatin assembly increases NF-1 binding, which is consistent with previous in vivo footprinting studies in which the NF-1 site was occupied in untreated animals and the NF-1 and flanking NR sites were occupied after phenobarbital treatment.	Phenobarbital	318-331	Neurofibromin 1	Drosophila melanogaster	31-47
11113125-8	2001	These studies demonstrate that NF-1 and CAR/RXR can both bind to the PBRU at the same time and that chromatin assembly increases NF-1 binding, which is consistent with previous in vivo footprinting studies in which the NF-1 site was occupied in untreated animals and the NF-1 and flanking NR sites were occupied after phenobarbital treatment.	Phenobarbital	318-331	Neurofibromin 1	Drosophila melanogaster	31-35
11113125-8	2001	These studies demonstrate that NF-1 and CAR/RXR can both bind to the PBRU at the same time and that chromatin assembly increases NF-1 binding, which is consistent with previous in vivo footprinting studies in which the NF-1 site was occupied in untreated animals and the NF-1 and flanking NR sites were occupied after phenobarbital treatment.	Phenobarbital	318-331	Neurofibromin 1	Drosophila melanogaster	129-133
11113125-8	2001	These studies demonstrate that NF-1 and CAR/RXR can both bind to the PBRU at the same time and that chromatin assembly increases NF-1 binding, which is consistent with previous in vivo footprinting studies in which the NF-1 site was occupied in untreated animals and the NF-1 and flanking NR sites were occupied after phenobarbital treatment.	Phenobarbital	318-331	Neurofibromin 1	Drosophila melanogaster	129-133
11113125-9	2001	CAR-mediated trans-activation of the PBRU was increased by NF-1, analogous to NF-1 effects on phenobarbital induction in previous transient transfection studies and consistent with mediation of phenobarbital induction by CAR.	Phenobarbital	94-107	carnation	Drosophila melanogaster	0-3
11113125-9	2001	CAR-mediated trans-activation of the PBRU was increased by NF-1, analogous to NF-1 effects on phenobarbital induction in previous transient transfection studies and consistent with mediation of phenobarbital induction by CAR.	Phenobarbital	94-107	Neurofibromin 1	Drosophila melanogaster	78-82
11113125-9	2001	CAR-mediated trans-activation of the PBRU was increased by NF-1, analogous to NF-1 effects on phenobarbital induction in previous transient transfection studies and consistent with mediation of phenobarbital induction by CAR.	Phenobarbital	194-207	carnation	Drosophila melanogaster	0-3
11113125-9	2001	CAR-mediated trans-activation of the PBRU was increased by NF-1, analogous to NF-1 effects on phenobarbital induction in previous transient transfection studies and consistent with mediation of phenobarbital induction by CAR.	Phenobarbital	194-207	carnation	Drosophila melanogaster	221-224
11262762-6	2001	Treatment with PB (3.2 mM) resulted in an increase in the CYP2B activity and a higher hydroxylation of testosterone in the 16alpha-position (CYP2B1/2 and CYP2C11), the 7alpha-position (CYP2A1/2), and the 6beta-position (CYP3A1).	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	141-147
11262762-6	2001	Treatment with PB (3.2 mM) resulted in an increase in the CYP2B activity and a higher hydroxylation of testosterone in the 16alpha-position (CYP2B1/2 and CYP2C11), the 7alpha-position (CYP2A1/2), and the 6beta-position (CYP3A1).	Phenobarbital	15-17	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	154-161
11262762-6	2001	Treatment with PB (3.2 mM) resulted in an increase in the CYP2B activity and a higher hydroxylation of testosterone in the 16alpha-position (CYP2B1/2 and CYP2C11), the 7alpha-position (CYP2A1/2), and the 6beta-position (CYP3A1).	Phenobarbital	15-17	cytochrome P450, family 2, subfamily a, polypeptide 1	Rattus norvegicus	185-191
11262762-6	2001	Treatment with PB (3.2 mM) resulted in an increase in the CYP2B activity and a higher hydroxylation of testosterone in the 16alpha-position (CYP2B1/2 and CYP2C11), the 7alpha-position (CYP2A1/2), and the 6beta-position (CYP3A1).	Phenobarbital	15-17	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	220-226
11181491-6	2001	LPS inhibited the mRNA expression of CYP2B10 and CYP2B9 at 6 and 12 h of treatment, with the inhibitory effect more profound at 12 h. LPS also suppressed the CYP2B9 mRNA level at 24 h. However, CYP2B10 mRNA levels in mice treated with PB alone had declined markedly by 24 h after the last PB injection; therefore, no effect of LPS could be discerned.	Phenobarbital	235-237	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	37-44
11181491-6	2001	LPS inhibited the mRNA expression of CYP2B10 and CYP2B9 at 6 and 12 h of treatment, with the inhibitory effect more profound at 12 h. LPS also suppressed the CYP2B9 mRNA level at 24 h. However, CYP2B10 mRNA levels in mice treated with PB alone had declined markedly by 24 h after the last PB injection; therefore, no effect of LPS could be discerned.	Phenobarbital	235-237	toll-like receptor 4	Mus musculus	134-137
11181491-6	2001	LPS inhibited the mRNA expression of CYP2B10 and CYP2B9 at 6 and 12 h of treatment, with the inhibitory effect more profound at 12 h. LPS also suppressed the CYP2B9 mRNA level at 24 h. However, CYP2B10 mRNA levels in mice treated with PB alone had declined markedly by 24 h after the last PB injection; therefore, no effect of LPS could be discerned.	Phenobarbital	235-237	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	158-164
11181491-6	2001	LPS inhibited the mRNA expression of CYP2B10 and CYP2B9 at 6 and 12 h of treatment, with the inhibitory effect more profound at 12 h. LPS also suppressed the CYP2B9 mRNA level at 24 h. However, CYP2B10 mRNA levels in mice treated with PB alone had declined markedly by 24 h after the last PB injection; therefore, no effect of LPS could be discerned.	Phenobarbital	235-237	toll-like receptor 4	Mus musculus	134-137
11181491-6	2001	LPS inhibited the mRNA expression of CYP2B10 and CYP2B9 at 6 and 12 h of treatment, with the inhibitory effect more profound at 12 h. LPS also suppressed the CYP2B9 mRNA level at 24 h. However, CYP2B10 mRNA levels in mice treated with PB alone had declined markedly by 24 h after the last PB injection; therefore, no effect of LPS could be discerned.	Phenobarbital	289-291	toll-like receptor 4	Mus musculus	0-3
11181491-6	2001	LPS inhibited the mRNA expression of CYP2B10 and CYP2B9 at 6 and 12 h of treatment, with the inhibitory effect more profound at 12 h. LPS also suppressed the CYP2B9 mRNA level at 24 h. However, CYP2B10 mRNA levels in mice treated with PB alone had declined markedly by 24 h after the last PB injection; therefore, no effect of LPS could be discerned.	Phenobarbital	289-291	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	37-44
11181491-6	2001	LPS inhibited the mRNA expression of CYP2B10 and CYP2B9 at 6 and 12 h of treatment, with the inhibitory effect more profound at 12 h. LPS also suppressed the CYP2B9 mRNA level at 24 h. However, CYP2B10 mRNA levels in mice treated with PB alone had declined markedly by 24 h after the last PB injection; therefore, no effect of LPS could be discerned.	Phenobarbital	289-291	toll-like receptor 4	Mus musculus	134-137
11181491-6	2001	LPS inhibited the mRNA expression of CYP2B10 and CYP2B9 at 6 and 12 h of treatment, with the inhibitory effect more profound at 12 h. LPS also suppressed the CYP2B9 mRNA level at 24 h. However, CYP2B10 mRNA levels in mice treated with PB alone had declined markedly by 24 h after the last PB injection; therefore, no effect of LPS could be discerned.	Phenobarbital	289-291	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	158-164
11181491-6	2001	LPS inhibited the mRNA expression of CYP2B10 and CYP2B9 at 6 and 12 h of treatment, with the inhibitory effect more profound at 12 h. LPS also suppressed the CYP2B9 mRNA level at 24 h. However, CYP2B10 mRNA levels in mice treated with PB alone had declined markedly by 24 h after the last PB injection; therefore, no effect of LPS could be discerned.	Phenobarbital	289-291	toll-like receptor 4	Mus musculus	134-137
11181491-7	2001	Further experiments showed that injections of 33 mg/kg PB every 8 h produced more stable CYP2B10 mRNA and enzymatic activity.	Phenobarbital	55-57	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	89-96
11181491-9	2001	This study suggests that LPS suppresses the expression of phenobarbital-induced CYP2B expression in mice, which resembles its effects in rats.	Phenobarbital	58-71	toll-like receptor 4	Mus musculus	25-28
11181491-9	2001	This study suggests that LPS suppresses the expression of phenobarbital-induced CYP2B expression in mice, which resembles its effects in rats.	Phenobarbital	58-71	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	80-85
11257517-5	2001	Treatment with phenobarbitone caused CYP2B, CYP2C-2 and CYP3A21 levels to increase, rifampicin caused increases in CYP2B and CYP2C-1 and a decrease in CYP3A21 levels, whereas dioxin caused CYP1A1 and CYP1A2 levels to increase and CYP2E1 levels to decrease.	Phenobarbital	15-29	cytochrome P450 3A21	Callithrix jacchus	56-63
11257517-5	2001	Treatment with phenobarbitone caused CYP2B, CYP2C-2 and CYP3A21 levels to increase, rifampicin caused increases in CYP2B and CYP2C-1 and a decrease in CYP3A21 levels, whereas dioxin caused CYP1A1 and CYP1A2 levels to increase and CYP2E1 levels to decrease.	Phenobarbital	15-29	cytochrome P450 family 1 subfamily A member 1	Callithrix jacchus	189-195
11257517-5	2001	Treatment with phenobarbitone caused CYP2B, CYP2C-2 and CYP3A21 levels to increase, rifampicin caused increases in CYP2B and CYP2C-1 and a decrease in CYP3A21 levels, whereas dioxin caused CYP1A1 and CYP1A2 levels to increase and CYP2E1 levels to decrease.	Phenobarbital	15-29	cytochrome P450 1A2	Callithrix jacchus	200-206
11257517-5	2001	Treatment with phenobarbitone caused CYP2B, CYP2C-2 and CYP3A21 levels to increase, rifampicin caused increases in CYP2B and CYP2C-1 and a decrease in CYP3A21 levels, whereas dioxin caused CYP1A1 and CYP1A2 levels to increase and CYP2E1 levels to decrease.	Phenobarbital	15-29	cytochrome P450 2E1	Callithrix jacchus	230-236
11257517-7	2001	P450 enzyme activities were assessed using 8 different substrates and increases were found after treatment with phenobarbitone, rifampicin, and dioxin.	Phenobarbital	112-126	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	0-4
11238185-8	2001	TGFbeta-induced apoptosis of FTO-2B cells was inhibited by dexamethasone, insulin, phenobarbital and dieldrin.	Phenobarbital	83-96	transforming growth factor, beta 1	Rattus norvegicus	0-7
11238185-8	2001	TGFbeta-induced apoptosis of FTO-2B cells was inhibited by dexamethasone, insulin, phenobarbital and dieldrin.	Phenobarbital	83-96	FTO, alpha-ketoglutarate dependent dioxygenase	Rattus norvegicus	29-32
11181490-4	2001	Compounds known to activate the pregnane X receptor (PXR) such as rifampicin, or the constitutively activated receptor (CAR) such as phenobarbital, induced CYP2C8, CYP2C9, and to a lesser extent CYP2C19 mRNAs and proteins.	Phenobarbital	133-146	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	156-162
11231298-5	2001	Methylcholanthrene induced an increase in CYP1A1/2 enzyme activity (eightfold), phenobarbital induced CYP2B6 activity (1.7-fold), and dexamethasone induced CYP3A4 activity (fivefold).	Phenobarbital	80-93	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	102-108
11181490-4	2001	Compounds known to activate the pregnane X receptor (PXR) such as rifampicin, or the constitutively activated receptor (CAR) such as phenobarbital, induced CYP2C8, CYP2C9, and to a lesser extent CYP2C19 mRNAs and proteins.	Phenobarbital	133-146	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	195-202
11181490-6	2001	The concentration dependence of CYP2C8 and CYP2C9 mRNAs in response to rifampicin and phenobarbital paralleled that of CYP3A4 and CYP2B6, the maximum accumulation being reached with 10 microM rifampicin and 100 microM phenobarbital.	Phenobarbital	86-99	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	32-38
11181490-6	2001	The concentration dependence of CYP2C8 and CYP2C9 mRNAs in response to rifampicin and phenobarbital paralleled that of CYP3A4 and CYP2B6, the maximum accumulation being reached with 10 microM rifampicin and 100 microM phenobarbital.	Phenobarbital	86-99	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
11181490-6	2001	The concentration dependence of CYP2C8 and CYP2C9 mRNAs in response to rifampicin and phenobarbital paralleled that of CYP3A4 and CYP2B6, the maximum accumulation being reached with 10 microM rifampicin and 100 microM phenobarbital.	Phenobarbital	86-99	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	130-136
11181490-6	2001	The concentration dependence of CYP2C8 and CYP2C9 mRNAs in response to rifampicin and phenobarbital paralleled that of CYP3A4 and CYP2B6, the maximum accumulation being reached with 10 microM rifampicin and 100 microM phenobarbital.	Phenobarbital	218-231	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	32-38
11181490-6	2001	The concentration dependence of CYP2C8 and CYP2C9 mRNAs in response to rifampicin and phenobarbital paralleled that of CYP3A4 and CYP2B6, the maximum accumulation being reached with 10 microM rifampicin and 100 microM phenobarbital.	Phenobarbital	218-231	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	43-49
11181490-6	2001	The concentration dependence of CYP2C8 and CYP2C9 mRNAs in response to rifampicin and phenobarbital paralleled that of CYP3A4 and CYP2B6, the maximum accumulation being reached with 10 microM rifampicin and 100 microM phenobarbital.	Phenobarbital	218-231	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	130-136
11181490-9	2001	Furthermore, dexamethasone, which has been recently shown to up-regulate PXR and CAR expression through the glucocorticoid receptor, potentiated CYP2C8 and CYP2C9 mRNA induction in response to rifampicin and phenobarbital.	Phenobarbital	208-221	nuclear receptor subfamily 1 group I member 2	Homo sapiens	73-76
11181490-9	2001	Furthermore, dexamethasone, which has been recently shown to up-regulate PXR and CAR expression through the glucocorticoid receptor, potentiated CYP2C8 and CYP2C9 mRNA induction in response to rifampicin and phenobarbital.	Phenobarbital	208-221	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	145-151
11181490-9	2001	Furthermore, dexamethasone, which has been recently shown to up-regulate PXR and CAR expression through the glucocorticoid receptor, potentiated CYP2C8 and CYP2C9 mRNA induction in response to rifampicin and phenobarbital.	Phenobarbital	208-221	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	156-162
11181491-0	2001	Effects of bacterial lipopolysaccharide on phenobarbital-induced CYP2B expression in mice.	Phenobarbital	43-56	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	65-70
11181491-2	2001	The effects of LPS on expression of phenobarbital (PB)-induced CYP2B1/2 in rats have been well characterized, but less is known about the effects of LPS on PB-induced CYP2B in mice.	Phenobarbital	36-49	toll-like receptor 4	Mus musculus	15-18
11181491-2	2001	The effects of LPS on expression of phenobarbital (PB)-induced CYP2B1/2 in rats have been well characterized, but less is known about the effects of LPS on PB-induced CYP2B in mice.	Phenobarbital	36-49	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	63-69
11181491-2	2001	The effects of LPS on expression of phenobarbital (PB)-induced CYP2B1/2 in rats have been well characterized, but less is known about the effects of LPS on PB-induced CYP2B in mice.	Phenobarbital	36-49	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	63-68
11181491-2	2001	The effects of LPS on expression of phenobarbital (PB)-induced CYP2B1/2 in rats have been well characterized, but less is known about the effects of LPS on PB-induced CYP2B in mice.	Phenobarbital	51-53	toll-like receptor 4	Mus musculus	15-18
11181491-2	2001	The effects of LPS on expression of phenobarbital (PB)-induced CYP2B1/2 in rats have been well characterized, but less is known about the effects of LPS on PB-induced CYP2B in mice.	Phenobarbital	51-53	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	63-69
11181491-2	2001	The effects of LPS on expression of phenobarbital (PB)-induced CYP2B1/2 in rats have been well characterized, but less is known about the effects of LPS on PB-induced CYP2B in mice.	Phenobarbital	51-53	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	63-68
11181491-3	2001	Since genetically manipulated mice represent an attractive model to study the mechanisms involved in the down-regulation of CYP2B expression by LPS, we investigated the effects of LPS on PB-induced CYP2B expression in mouse liver.	Phenobarbital	187-189	toll-like receptor 4	Mus musculus	180-183
11181491-3	2001	Since genetically manipulated mice represent an attractive model to study the mechanisms involved in the down-regulation of CYP2B expression by LPS, we investigated the effects of LPS on PB-induced CYP2B expression in mouse liver.	Phenobarbital	187-189	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	198-203
11181491-6	2001	LPS inhibited the mRNA expression of CYP2B10 and CYP2B9 at 6 and 12 h of treatment, with the inhibitory effect more profound at 12 h. LPS also suppressed the CYP2B9 mRNA level at 24 h. However, CYP2B10 mRNA levels in mice treated with PB alone had declined markedly by 24 h after the last PB injection; therefore, no effect of LPS could be discerned.	Phenobarbital	235-237	toll-like receptor 4	Mus musculus	0-3
11159809-7	2001	Hepatic microsomes prepared from mice and rats pretreated with CYP-inducing agents (phenobarbital and acetone) were also incubated with (R)-VCH or (S)-VCH.	Phenobarbital	84-97	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	63-66
11311572-3	2001	We have investigated the effect of p53 on sodium phenobarbitone (PB)-induced liver proliferation and polyploidisation.	Phenobarbital	42-63	transformation related protein 53, pseudogene	Mus musculus	35-38
11293546-2	2001	Rotational diffusion of cytochrome P450 in the microsomal membrane of phenobarbital-induced rabbit liver was measured by detecting the decay of absorption anisotropy after photolysis of the heme CO complex by a vertically polarized laser flash.	Phenobarbital	70-83	cytochrome P-450	Oryctolagus cuniculus	24-39
11158222-6	2001	The regulation of liver CYP450 by dexamethasone and phenobarbital was assessed in CRF rats.	Phenobarbital	52-65	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	24-30
11158222-14	2001	Although liver CYP450 was reduced in CRF, its induction by dexamethasone and phenobarbital was present.	Phenobarbital	77-90	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	15-21
11405283-4	2001	The luciferase expression in CAR-producing cells could be suppressed by androstanes and reactivated by structurally unrelated drugs chlorpromazine, metyrapone, phenobarbital, and clotrimazole.	Phenobarbital	160-173	nuclear receptor subfamily 1 group I member 3	Homo sapiens	29-32
11160864-0	2001	Nuclear receptor CAR as a regulatory factor for the sexually dimorphic induction of CYB2B1 gene by phenobarbital in rat livers.	Phenobarbital	99-112	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	17-20
11160864-1	2001	The nuclear receptor constitutive active receptor (CAR) translocates into liver nuclei after phenobarbital (PB) treatment, and activates the conserved enhancer called the PB-response element module (PBREM) found in CYP2B genes.	Phenobarbital	93-106	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	4-49
11160864-1	2001	The nuclear receptor constitutive active receptor (CAR) translocates into liver nuclei after phenobarbital (PB) treatment, and activates the conserved enhancer called the PB-response element module (PBREM) found in CYP2B genes.	Phenobarbital	93-106	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	51-54
11160864-1	2001	The nuclear receptor constitutive active receptor (CAR) translocates into liver nuclei after phenobarbital (PB) treatment, and activates the conserved enhancer called the PB-response element module (PBREM) found in CYP2B genes.	Phenobarbital	108-110	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	4-49
11160864-1	2001	The nuclear receptor constitutive active receptor (CAR) translocates into liver nuclei after phenobarbital (PB) treatment, and activates the conserved enhancer called the PB-response element module (PBREM) found in CYP2B genes.	Phenobarbital	108-110	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	51-54
11160864-2	2001	We have examined whether CAR regulates the dimorphic induction by PB of the CYP2B1 gene in Wistar Kyoto (WKY) rats.	Phenobarbital	66-68	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	25-28
11160864-2	2001	We have examined whether CAR regulates the dimorphic induction by PB of the CYP2B1 gene in Wistar Kyoto (WKY) rats.	Phenobarbital	66-68	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	76-82
11160864-3	2001	Northern blot analysis showed that PB induced CYP2B1 mRNA in male WKY rats but not female rats.	Phenobarbital	35-37	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	46-52
11160864-6	2001	CAR was accumulated in the liver nucleus of male rats in response to PB treatment, whereas the receptor was barely detectable in the liver nuclei of PB-induced females.	Phenobarbital	69-71	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	0-3
11161067-5	2001	NA and T induce expression of both CYP92A1 and CYP72A5 transcripts in older seedling shoots, whereas phenobarbital induces CYP92A1 expression in older seedling shoots and highly induces CYP72A5 expression in young and older seedling roots.	Phenobarbital	101-114	Trimethyltridecatetraene synthase	Zea mays	123-130
11306051-5	2001	In this study, we used two Wistar rat substrains which have been well-characterized for different inducibility of ALDH1A3 enzyme activity after treatment with phenobarbital.	Phenobarbital	159-172	aldehyde dehydrogenase 1 family, member A3	Rattus norvegicus	114-121
11306051-4	2001	Phenobarbital-type inducers increase the ALDH1A3, while polycyclic hydrocarbons (such as BaP and TCDD) increase the expression of the two members of ALDH3A subfamily (3A1 and 3A2).	Phenobarbital	0-13	aldehyde dehydrogenase 1 family, member A3	Rattus norvegicus	41-48
11306051-10	2001	Additionally, data concerning time- and dose-response induction of ALDH1A3 after phenobarbital and griseofulvin treatment are presented.	Phenobarbital	81-94	aldehyde dehydrogenase 1 family, member A3	Rattus norvegicus	67-74
11162586-4	2001	Phenobarbital (PB) elicited a 3-fold increase in CYP2A5 expression (catalytic activity and mRNA), while the cAMP and protein kinase A (PKA) stimulators dibutyryl-cAMP, forskolin and Sp-cAMPs caused up to 18-fold increases in the amount of CYP2A5 mRNA.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	49-55
11162586-4	2001	Phenobarbital (PB) elicited a 3-fold increase in CYP2A5 expression (catalytic activity and mRNA), while the cAMP and protein kinase A (PKA) stimulators dibutyryl-cAMP, forskolin and Sp-cAMPs caused up to 18-fold increases in the amount of CYP2A5 mRNA.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	239-245
11162586-4	2001	Phenobarbital (PB) elicited a 3-fold increase in CYP2A5 expression (catalytic activity and mRNA), while the cAMP and protein kinase A (PKA) stimulators dibutyryl-cAMP, forskolin and Sp-cAMPs caused up to 18-fold increases in the amount of CYP2A5 mRNA.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	49-55
11162586-4	2001	Phenobarbital (PB) elicited a 3-fold increase in CYP2A5 expression (catalytic activity and mRNA), while the cAMP and protein kinase A (PKA) stimulators dibutyryl-cAMP, forskolin and Sp-cAMPs caused up to 18-fold increases in the amount of CYP2A5 mRNA.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	239-245
11121869-8	2001	The induction of cell proliferation and GSTP foci in the rat liver by phenobarbital is consistent with its ability to promote tamoxifen-initiated liver tumours in the rat.	Phenobarbital	70-83	glutathione S-transferase pi 1	Rattus norvegicus	40-44
11174078-1	2001	Pretreatment of the rat with phenobarbital (PB) is known to increase gene expression of the canalicular multispecific organic anion transporter (cMOAT) and hepatobiliary transport of its substrates (glutathione, sulfobromophthalein).	Phenobarbital	29-42	ATP binding cassette subfamily C member 2	Rattus norvegicus	92-143
11174078-1	2001	Pretreatment of the rat with phenobarbital (PB) is known to increase gene expression of the canalicular multispecific organic anion transporter (cMOAT) and hepatobiliary transport of its substrates (glutathione, sulfobromophthalein).	Phenobarbital	29-42	ATP binding cassette subfamily C member 2	Rattus norvegicus	145-150
11174078-1	2001	Pretreatment of the rat with phenobarbital (PB) is known to increase gene expression of the canalicular multispecific organic anion transporter (cMOAT) and hepatobiliary transport of its substrates (glutathione, sulfobromophthalein).	Phenobarbital	44-46	ATP binding cassette subfamily C member 2	Rattus norvegicus	92-143
11174078-1	2001	Pretreatment of the rat with phenobarbital (PB) is known to increase gene expression of the canalicular multispecific organic anion transporter (cMOAT) and hepatobiliary transport of its substrates (glutathione, sulfobromophthalein).	Phenobarbital	44-46	ATP binding cassette subfamily C member 2	Rattus norvegicus	145-150
11174078-2	2001	To determine the effect of PB on the hepatobiliary transport of methotrexate (MTX, another substrate of cMOAT) and its metabolism to 7-hydroxymethotrexate (7-OHMTX) in the rat, we compared the steady-state pharmacokinetics of MTX in the isolated liver of either PB-pretreated (80 mg/day/kg bw for 4 days, i.p.)	Phenobarbital	27-29	ATP binding cassette subfamily C member 2	Rattus norvegicus	104-109
12094624-8	2001	Forskolin significantly increased intracellular cAMP level and inhibited cytochrome P-450 2B1 expression in the presence of phenobarbital.	Phenobarbital	124-137	cytochrome P450 2B1	Rattus norvegicus	73-93
11264453-3	2001	Responding to PB exposure in liver, the NR constitutive active receptor (CAR) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates PBREM via binding to DR-4 motifs.	Phenobarbital	14-16	retinoid X receptor alpha	Homo sapiens	130-149
11264453-3	2001	Responding to PB exposure in liver, the NR constitutive active receptor (CAR) translocates to the nucleus, forms a dimer with the retinoid X receptor (RXR), and activates PBREM via binding to DR-4 motifs.	Phenobarbital	14-16	retinoid X receptor alpha	Homo sapiens	151-154
11264453-6	2001	Pregnane X receptor (PXR) could bind to all of these sites and, upon PB induction, a PXR:RXR heterodimer could transactivate XREM.	Phenobarbital	69-71	nuclear receptor subfamily 1 group I member 2	Homo sapiens	0-19
11264453-6	2001	Pregnane X receptor (PXR) could bind to all of these sites and, upon PB induction, a PXR:RXR heterodimer could transactivate XREM.	Phenobarbital	69-71	nuclear receptor subfamily 1 group I member 2	Homo sapiens	21-24
11264453-6	2001	Pregnane X receptor (PXR) could bind to all of these sites and, upon PB induction, a PXR:RXR heterodimer could transactivate XREM.	Phenobarbital	69-71	nuclear receptor subfamily 1 group I member 2	Homo sapiens	85-88
11264453-6	2001	Pregnane X receptor (PXR) could bind to all of these sites and, upon PB induction, a PXR:RXR heterodimer could transactivate XREM.	Phenobarbital	69-71	retinoid X receptor alpha	Homo sapiens	89-92
11201247-13	2001	This method was applied to the head hair of two patients who orally took toxic amounts of PB and two volunteers who orally took 100 mg of PPH daily for 5 d. The hair concentrations of PB in the two patients were 16.2 and 14.7 ng/mg, and those of PPH in the two volunteers were 3.3 and 0.1 ng/mg.	Phenobarbital	184-186	enolase 1	Homo sapiens	138-141
11201247-13	2001	This method was applied to the head hair of two patients who orally took toxic amounts of PB and two volunteers who orally took 100 mg of PPH daily for 5 d. The hair concentrations of PB in the two patients were 16.2 and 14.7 ng/mg, and those of PPH in the two volunteers were 3.3 and 0.1 ng/mg.	Phenobarbital	184-186	enolase 1	Homo sapiens	246-249
11437078-3	2001	The constitutive expression in vivo of CYP2B1/2 is low but it is induced in the presence of various drugs such as phenobarbital (PB).	Phenobarbital	114-127	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	39-45
11437078-3	2001	The constitutive expression in vivo of CYP2B1/2 is low but it is induced in the presence of various drugs such as phenobarbital (PB).	Phenobarbital	129-131	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	39-45
11284048-0	2001	Localization of estradiol-responsive region in the phenobarbital-responsive enhancer module of mouse Cyp2b-10 gene.	Phenobarbital	51-64	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	101-109
11284048-1	2001	The mouse Cyp2b-10 gene is inducible by treatment with estradiol as well as so-called phenobarbital (PB)-like inducers.	Phenobarbital	86-99	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	10-18
11284048-1	2001	The mouse Cyp2b-10 gene is inducible by treatment with estradiol as well as so-called phenobarbital (PB)-like inducers.	Phenobarbital	101-103	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	10-18
11284048-6	2001	Several nucleotide mutations in the putative binding sites of the PBREM core element showed that the NR1 site was required for estradiol induction, and the same element was required for PB induction.	Phenobarbital	66-68	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	101-104
12094624-0	2001	Prostaglandin E2 is involved in the increase of cytochrome P-450 2B1 expression by alpha-tocopheryl succinate in primary rat hepatocytes in the presence of phenobarbital.	Phenobarbital	156-169	cytochrome P450 2B1	Rattus norvegicus	48-68
12094624-5	2001	alpha-Tocopheryl succinate inhibited prostaglandin E2 synthesis by hepatocytes and increased cytochrome P-450 2B1 expression in the presence of phenobarbital; however, it had little effect on intracellular cAMP level.	Phenobarbital	144-157	cytochrome P450 2B1	Rattus norvegicus	93-113
12094624-7	2001	High doses of exogenous prostaglandin E2 (100 and 1,000 nM) inhibited the cytochrome P-450 2B1 expression in the presence of phenobarbital compared with low doses (1 and 10 nM); however, the presence of high doses of prostaglandin E2 had no effect on intracellular cAMP level.	Phenobarbital	125-138	cytochrome P450 2B1	Rattus norvegicus	74-94
12094624-9	2001	The results of this study indicate that alpha-tocopheryl succinate increases cytochrome P-450 2B1 expression via its inhibition of prostaglandin E2 synthesis in the presence of phenobarbital; however, changes in intracellular cAMP level are not related to cytochrome P-450 2B1 expression.	Phenobarbital	177-190	cytochrome P450 2B1	Rattus norvegicus	77-97
11112454-2	2000	The expression of hepatic CYP2B mRNAs in B6 was lightly induced by beta-estradiol (ES), while that by phenobarbital (PB) or 1,1,1-trichloro-2, 2-bis(p-chlorophenyl) ethane (DDT) was prominent.	Phenobarbital	102-115	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	26-31
10993889-0	2000	Mutational analysis of the CYP2B2 phenobarbital response unit and inhibitory effect of the constitutive androstane receptor on phenobarbital responsiveness.	Phenobarbital	127-140	nuclear receptor subfamily 1 group I member 3	Homo sapiens	91-123
10993889-10	2000	The latter can be attributed to nuclear accumulation of CAR after PB exposure.	Phenobarbital	66-68	nuclear receptor subfamily 1 group I member 3	Homo sapiens	56-59
10993889-11	2000	Exogenous CAR increased both the basal and PB-induced response of betaRAREx2-tk but reduced PBRU-dependent PB response.	Phenobarbital	43-45	nuclear receptor subfamily 1 group I member 3	Homo sapiens	10-13
11112454-2	2000	The expression of hepatic CYP2B mRNAs in B6 was lightly induced by beta-estradiol (ES), while that by phenobarbital (PB) or 1,1,1-trichloro-2, 2-bis(p-chlorophenyl) ethane (DDT) was prominent.	Phenobarbital	117-119	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	26-31
10993889-11	2000	Exogenous CAR increased both the basal and PB-induced response of betaRAREx2-tk but reduced PBRU-dependent PB response.	Phenobarbital	92-94	nuclear receptor subfamily 1 group I member 3	Homo sapiens	10-13
11106424-0	2000	Limited heme synthesis in porphobilinogen deaminase-deficient mice impairs transcriptional activation of specific cytochrome P450 genes by phenobarbital.	Phenobarbital	139-152	hydroxymethylbilane synthase	Mus musculus	26-51
10993889-13	2000	Thus, CAR acts negatively on PB responsiveness mediated by the CYP2B2 PBRU just as it prevents maximal at-RA responsiveness mediated by betaRARE.	Phenobarbital	29-31	nuclear receptor subfamily 1 group I member 3	Homo sapiens	6-9
11106424-7	2000	The activity and mRNA level of this particular cytochrome P450 are significantly lower in the phenobarbital-induced porphobilinogen deaminase-deficient mice (55% and 43%, respectively), but its expression can be restored to normal values when exogenous heme is administered.	Phenobarbital	94-107	hydroxymethylbilane synthase	Mus musculus	116-141
11082433-0	2000	Sequence analyses of CYP2B genes and catalytic profiles for P450s in Qdj:Sprague-dawley rats that lack response to the phenobarbital-mediated induction of CYP2B2.	Phenobarbital	119-132	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	155-161
11114890-4	2000	Unexpectedly, we found that SXR can regulate CYP2B, both in cultured cells and in transgenic mice via adaptive recognition of the phenobarbital response element (PBRE).	Phenobarbital	130-143	nuclear receptor subfamily 1, group I, member 2	Mus musculus	28-31
11114890-4	2000	Unexpectedly, we found that SXR can regulate CYP2B, both in cultured cells and in transgenic mice via adaptive recognition of the phenobarbital response element (PBRE).	Phenobarbital	130-143	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	45-50
11082433-1	2000	The Qdj:Sprague-Dawley (SD) rat is a mutant strain lacking in phenobarbital (PB)-mediated induction of CYP2B2.	Phenobarbital	62-75	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	103-109
11082433-1	2000	The Qdj:Sprague-Dawley (SD) rat is a mutant strain lacking in phenobarbital (PB)-mediated induction of CYP2B2.	Phenobarbital	77-79	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	103-109
11082433-3	2000	Although PB-treated Qdj:SD (-/-) rats expressed CYP2B1 normally, testosterone 16beta-hydroxylase activity in these rats was quite low.	Phenobarbital	9-11	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	48-54
11093784-1	2000	The barbiturate phenobarbital induces the transcription of cytochromes P450 (CYPs) 2B through the constitutive androstane receptor (CAR; NR1I3).	Phenobarbital	16-29	nuclear receptor subfamily 1 group I member 3	Homo sapiens	98-130
11191639-5	2000	The expression of the number and area of altered hepatocyte foci (AHF) positive for placental glutathione S-transferase (GST-P) was maximum in DEN-treated and PB promoted group (Group A).	Phenobarbital	159-161	hematopoietic prostaglandin D synthase	Rattus norvegicus	94-119
11191639-5	2000	The expression of the number and area of altered hepatocyte foci (AHF) positive for placental glutathione S-transferase (GST-P) was maximum in DEN-treated and PB promoted group (Group A).	Phenobarbital	159-161	glutathione S-transferase pi 1	Rattus norvegicus	121-126
11093784-4	2000	We show that submicromolar concentrations of dexamethasone enhance phenobarbital-mediated induction of CYP3A4, CYP2B6, and CYP2C8 mRNA in cultured human hepatocytes.	Phenobarbital	67-80	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	111-117
11093784-1	2000	The barbiturate phenobarbital induces the transcription of cytochromes P450 (CYPs) 2B through the constitutive androstane receptor (CAR; NR1I3).	Phenobarbital	16-29	nuclear receptor subfamily 1 group I member 3	Homo sapiens	132-135
11093784-4	2000	We show that submicromolar concentrations of dexamethasone enhance phenobarbital-mediated induction of CYP3A4, CYP2B6, and CYP2C8 mRNA in cultured human hepatocytes.	Phenobarbital	67-80	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	123-129
11093784-1	2000	The barbiturate phenobarbital induces the transcription of cytochromes P450 (CYPs) 2B through the constitutive androstane receptor (CAR; NR1I3).	Phenobarbital	16-29	nuclear receptor subfamily 1 group I member 3	Homo sapiens	137-142
11093784-8	2000	Furthermore, dexamethasone increases both basal and phenobarbital-mediated nuclear translocation of CAR immunoreactive protein in human hepatocytes.	Phenobarbital	52-65	nuclear receptor subfamily 1 group I member 3	Homo sapiens	100-103
11093784-2	2000	CAR is a member of the nuclear receptor family (NR1) mostly expressed in the liver, which heterodimerizes with retinoid X receptor (RXR) and was shown to transactivate both the phenobarbital responsive element module of the human CYP2B6 gene and the CYP3A4 xenobiotic response element.	Phenobarbital	177-190	nuclear receptor subfamily 1 group I member 3	Homo sapiens	0-3
11093784-9	2000	The up-regulation of CAR mRNA and protein in response to dexamethasone explains the synergistic effect of this glucocorticoid on phenobarbital-mediated induction of CYP2B genes and the controversial role of the glucocorticoid receptor on phenobarbital-mediated CYP gene inductions.	Phenobarbital	129-142	nuclear receptor subfamily 1 group I member 3	Homo sapiens	21-24
11093784-9	2000	The up-regulation of CAR mRNA and protein in response to dexamethasone explains the synergistic effect of this glucocorticoid on phenobarbital-mediated induction of CYP2B genes and the controversial role of the glucocorticoid receptor on phenobarbital-mediated CYP gene inductions.	Phenobarbital	238-251	nuclear receptor subfamily 1 group I member 3	Homo sapiens	21-24
11093784-2	2000	CAR is a member of the nuclear receptor family (NR1) mostly expressed in the liver, which heterodimerizes with retinoid X receptor (RXR) and was shown to transactivate both the phenobarbital responsive element module of the human CYP2B6 gene and the CYP3A4 xenobiotic response element.	Phenobarbital	177-190	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	48-51
11093784-2	2000	CAR is a member of the nuclear receptor family (NR1) mostly expressed in the liver, which heterodimerizes with retinoid X receptor (RXR) and was shown to transactivate both the phenobarbital responsive element module of the human CYP2B6 gene and the CYP3A4 xenobiotic response element.	Phenobarbital	177-190	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	230-236
11093784-2	2000	CAR is a member of the nuclear receptor family (NR1) mostly expressed in the liver, which heterodimerizes with retinoid X receptor (RXR) and was shown to transactivate both the phenobarbital responsive element module of the human CYP2B6 gene and the CYP3A4 xenobiotic response element.	Phenobarbital	177-190	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	250-256
11152384-6	2000	GABAergic allosteric modulators (3 or 12 mg/kg diazepam and 50 mg/kg phenobarbital) blocked the appearance of seizure and reduced almost completely the death caused by BAL.	Phenobarbital	69-82	poly (ADP-ribose) polymerase family, member 9	Mus musculus	168-171
11093784-4	2000	We show that submicromolar concentrations of dexamethasone enhance phenobarbital-mediated induction of CYP3A4, CYP2B6, and CYP2C8 mRNA in cultured human hepatocytes.	Phenobarbital	67-80	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	103-109
11152384-12	2000	The results reported here demonstrate that GABAergic allosteric modulators (diazepam and phenobarbital) and carbamazepine, a compound that acts by prolonging the recovery of voltage-activated ion channels from inactivation, are able to abolish BAL-induced seizures, while the NMDA antagonist (MK-801) prolonged the latencies for onset of seizures suggesting that modulators of this subtype of glutamate receptor have a modest role on BAL-induced seizures.	Phenobarbital	89-102	poly (ADP-ribose) polymerase family, member 9	Mus musculus	244-247
11033061-4	2000	Treatment of cultures with various model inducers such as phenobarbital (PB), beta-naphthoflavone (NF) and clofibric acid (CLO) induced a strong increase in T(4)-UGT activity in rat hepatocyte monolayers.	Phenobarbital	58-71	solute carrier family 35 (UDP-galactose transporter), member A2	Mus musculus	162-165
11152384-12	2000	The results reported here demonstrate that GABAergic allosteric modulators (diazepam and phenobarbital) and carbamazepine, a compound that acts by prolonging the recovery of voltage-activated ion channels from inactivation, are able to abolish BAL-induced seizures, while the NMDA antagonist (MK-801) prolonged the latencies for onset of seizures suggesting that modulators of this subtype of glutamate receptor have a modest role on BAL-induced seizures.	Phenobarbital	89-102	poly (ADP-ribose) polymerase family, member 9	Mus musculus	434-437
11033061-4	2000	Treatment of cultures with various model inducers such as phenobarbital (PB), beta-naphthoflavone (NF) and clofibric acid (CLO) induced a strong increase in T(4)-UGT activity in rat hepatocyte monolayers.	Phenobarbital	73-75	solute carrier family 35 (UDP-galactose transporter), member A2	Mus musculus	162-165
11033061-5	2000	In addition, and as expected from available in vivo data, treatment of rat hepatocyte cultures with NF also increased p-nitrophenol (PNP)-UGT activity and treatment with PB or CLO increased bilirubin (Bili)-UGT activity.	Phenobarbital	170-172	solute carrier family 35 (UDP-galactose transporter), member A2	Mus musculus	207-210
11057673-4	2000	Here we show that the nuclear receptor CAR mediates the response evoked by a class of xenobiotics known as the "phenobarbital-like inducers".	Phenobarbital	112-125	nuclear receptor subfamily 1, group I, member 3	Mus musculus	39-42
11075820-1	2000	The nuclear orphan receptor CAR (constitutively active receptor or constitutive androstane receptor) can be activated in response to xenochemical exposure, such as activation by phenobarbital of a response element called NR1 found in the CYP2B gene.	Phenobarbital	178-191	nuclear receptor subfamily 1, group I, member 3	Mus musculus	28-31
11075820-1	2000	The nuclear orphan receptor CAR (constitutively active receptor or constitutive androstane receptor) can be activated in response to xenochemical exposure, such as activation by phenobarbital of a response element called NR1 found in the CYP2B gene.	Phenobarbital	178-191	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	221-224
11075820-1	2000	The nuclear orphan receptor CAR (constitutively active receptor or constitutive androstane receptor) can be activated in response to xenochemical exposure, such as activation by phenobarbital of a response element called NR1 found in the CYP2B gene.	Phenobarbital	178-191	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	238-243
11137894-7	2000	Although acute administration (16 hr) of PCB, 3-methylcholanthrene, and phenobarbital induced cytochrome P-450 gene expression in the liver, hepatic apo A-I gene expression was not increased by these xenobiotics.	Phenobarbital	72-85	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	94-110
11137894-7	2000	Although acute administration (16 hr) of PCB, 3-methylcholanthrene, and phenobarbital induced cytochrome P-450 gene expression in the liver, hepatic apo A-I gene expression was not increased by these xenobiotics.	Phenobarbital	72-85	apolipoprotein A1	Rattus norvegicus	149-156
11057673-5	2000	The strong activation of Cyp2b10 gene expression by phenobarbital, or by the more potent TCPOBOP, is absent in mice lacking the CAR gene.	Phenobarbital	52-65	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	25-32
11057673-5	2000	The strong activation of Cyp2b10 gene expression by phenobarbital, or by the more potent TCPOBOP, is absent in mice lacking the CAR gene.	Phenobarbital	52-65	nuclear receptor subfamily 1, group I, member 3	Mus musculus	128-131
11027641-2	2000	Two isomers of RA, 9-cis- and all-trans-RA, suppressed markedly the effect of PB on CYP2B1/2 expression, while ASE had no suppressive effect.	Phenobarbital	78-80	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	84-90
11129524-1	2000	Phenobarbital (PB) strongly induces in the liver the expression of many genes encoding detoxication enzymes, such as the aldehyde dehydrogenase type 2 in the mouse (Aldh2).	Phenobarbital	0-13	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	165-170
11027630-0	2000	Phenobarbital-elicited activation of nuclear receptor CAR in induction of cytochrome P450 genes.	Phenobarbital	0-13	CXADR pseudogene 1	Homo sapiens	54-57
11027630-3	2000	In response to PB exposure, CAR in the cytoplasm translocates into the nucleus, forms a heterodimer with the retinoid X receptor, and activates the PB response enhancer element leading to the concerted induction of numerous genes.	Phenobarbital	15-17	CXADR pseudogene 1	Homo sapiens	28-31
11027630-3	2000	In response to PB exposure, CAR in the cytoplasm translocates into the nucleus, forms a heterodimer with the retinoid X receptor, and activates the PB response enhancer element leading to the concerted induction of numerous genes.	Phenobarbital	15-17	retinoid X receptor alpha	Homo sapiens	109-128
11027630-3	2000	In response to PB exposure, CAR in the cytoplasm translocates into the nucleus, forms a heterodimer with the retinoid X receptor, and activates the PB response enhancer element leading to the concerted induction of numerous genes.	Phenobarbital	148-150	CXADR pseudogene 1	Homo sapiens	28-31
11027641-1	2000	The effects of 5alpha-androsten-3alpha-ol (ASE), and retinoic acids (RAs) and their precursors on the phenobarbital (PB)-mediated induction of CYP2B1 and 2B2 were examined in cultured rat hepatocytes.	Phenobarbital	102-115	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	143-157
11027641-1	2000	The effects of 5alpha-androsten-3alpha-ol (ASE), and retinoic acids (RAs) and their precursors on the phenobarbital (PB)-mediated induction of CYP2B1 and 2B2 were examined in cultured rat hepatocytes.	Phenobarbital	117-119	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	143-157
11129524-1	2000	Phenobarbital (PB) strongly induces in the liver the expression of many genes encoding detoxication enzymes, such as the aldehyde dehydrogenase type 2 in the mouse (Aldh2).	Phenobarbital	15-17	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	165-170
11129524-3	2000	In a previous report, the genetic analysis of both the C57BL/6J (B6) x DBA/2J (D2) F1 and the (F1 x F1) F2 led us to the hypothesis that Aldh2 responsiveness to PB was under the control of one major locus independent of the structural gene.	Phenobarbital	161-163	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	137-142
11033069-2	2000	This minireview deals with the mechanisms by which phenobarbital and phenobarbital-type chemicals induce cytochrome P450 and other genes, and summarises the knowledge on the role of the constitutively active receptor CAR in the induction process.	Phenobarbital	51-64	CXADR pseudogene 1	Homo sapiens	217-220
11033069-2	2000	This minireview deals with the mechanisms by which phenobarbital and phenobarbital-type chemicals induce cytochrome P450 and other genes, and summarises the knowledge on the role of the constitutively active receptor CAR in the induction process.	Phenobarbital	69-82	CXADR pseudogene 1	Homo sapiens	217-220
11005856-5	2000	Furthermore, CXR binds to a previously identified phenobarbital-responsive enhancer unit (PBRU) in the 5"-flanking region of the chicken CYP2H1 gene.	Phenobarbital	50-63	nuclear receptor subfamily 1 group I member 3	Gallus gallus	13-16
11005856-5	2000	Furthermore, CXR binds to a previously identified phenobarbital-responsive enhancer unit (PBRU) in the 5"-flanking region of the chicken CYP2H1 gene.	Phenobarbital	50-63	cytochrome P450 2H1	Gallus gallus	137-143
10945841-5	2000	with four daily doses of PB demonstrated markedly induced levels of CYP2B1, CYP2B2, and CYP3A1 mRNA in the striatum and cerebellum.	Phenobarbital	25-27	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	76-82
10998257-1	2000	Rat liver contains two class 1 aldehyde dehydrogenases (ALDHs): a constitutive isozyme (ALDH1) and a phenobarbital-inducible isozyme (ALDH-PB).	Phenobarbital	101-114	aldehyde dehydrogenase family 1, subfamily A7	Rattus norvegicus	134-141
11016633-4	2000	We have now tested this hypothesis by analyzing the potency of phenobarbital as a liver tumor promoter in male Cx32-wild-type (Cx32(Y/+)) and Cx32-null (Cx32(Y/-)) mice.	Phenobarbital	63-76	gap junction protein, beta 1	Mus musculus	111-115
11016633-8	2000	Phenobarbital led to a approximately 5-fold increase in the volume fraction occupied by glucose-6-phosphatase-deficient liver lesions in Cx32(Y/+) mice, whereas there was no such increase in Cx32(Y/-) mice.	Phenobarbital	0-13	gap junction protein, beta 1	Mus musculus	137-141
11016633-10	2000	Whereas phenobarbital clearly promoted the occurrence of numerous large hepatomas in Cx32(Y/+) mice, no such effect was seen in Cx32(Y/-) mice.	Phenobarbital	8-21	gap junction protein, beta 1	Mus musculus	85-89
11016633-11	2000	These results demonstrate, for the first time, that functional Cx32 protein is required for tumor promotion by phenobarbital.	Phenobarbital	111-124	gap junction protein, beta 1	Mus musculus	63-67
10945841-5	2000	with four daily doses of PB demonstrated markedly induced levels of CYP2B1, CYP2B2, and CYP3A1 mRNA in the striatum and cerebellum.	Phenobarbital	25-27	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	68-74
10945841-5	2000	with four daily doses of PB demonstrated markedly induced levels of CYP2B1, CYP2B2, and CYP3A1 mRNA in the striatum and cerebellum.	Phenobarbital	25-27	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	88-94
10945841-6	2000	In contrast, 1 or 2 days of PB treatment resulted in unchanged or even slightly decreased levels of CYP2B1 and CYP2B2 in the brain, although the latter treatments produced marked induction of the corresponding genes in the liver.	Phenobarbital	28-30	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	100-106
10945841-6	2000	In contrast, 1 or 2 days of PB treatment resulted in unchanged or even slightly decreased levels of CYP2B1 and CYP2B2 in the brain, although the latter treatments produced marked induction of the corresponding genes in the liver.	Phenobarbital	28-30	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	111-117
10945841-8	2000	Substantial activation of cerebral CYP2B1, CYP2B2, and CYP3A1 mRNA levels also resulted when animals were treated with the neuroactive drugs diphenylhydantoin and amitryptiline, and with the potential PB-like xenobiotic inducers trans-stilbene oxide and diallyl sulfide, whereas dichlorodiphenyltrichloroethane was less efficacious.	Phenobarbital	201-203	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	35-41
10945841-8	2000	Substantial activation of cerebral CYP2B1, CYP2B2, and CYP3A1 mRNA levels also resulted when animals were treated with the neuroactive drugs diphenylhydantoin and amitryptiline, and with the potential PB-like xenobiotic inducers trans-stilbene oxide and diallyl sulfide, whereas dichlorodiphenyltrichloroethane was less efficacious.	Phenobarbital	201-203	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	43-49
10945841-8	2000	Substantial activation of cerebral CYP2B1, CYP2B2, and CYP3A1 mRNA levels also resulted when animals were treated with the neuroactive drugs diphenylhydantoin and amitryptiline, and with the potential PB-like xenobiotic inducers trans-stilbene oxide and diallyl sulfide, whereas dichlorodiphenyltrichloroethane was less efficacious.	Phenobarbital	201-203	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	55-61
10918498-7	2000	Exogenously added TNF-alpha was also effective in repressing PB induction, consistent with other reports indicating that inflammatory cytokines are capable of suppressing expression of biotransformation enzyme systems.	Phenobarbital	61-63	tumor necrosis factor	Rattus norvegicus	18-27
10924340-4	2000	In parallel, IL-6 decreases both rifampicin- and phenobarbital-mediated induction of CYP2B6, CYP2C8, CYP2C9, and CYP3A4.	Phenobarbital	49-62	interleukin 6	Homo sapiens	13-17
10924340-4	2000	In parallel, IL-6 decreases both rifampicin- and phenobarbital-mediated induction of CYP2B6, CYP2C8, CYP2C9, and CYP3A4.	Phenobarbital	49-62	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	85-91
10924340-4	2000	In parallel, IL-6 decreases both rifampicin- and phenobarbital-mediated induction of CYP2B6, CYP2C8, CYP2C9, and CYP3A4.	Phenobarbital	49-62	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	93-99
10924340-4	2000	In parallel, IL-6 decreases both rifampicin- and phenobarbital-mediated induction of CYP2B6, CYP2C8, CYP2C9, and CYP3A4.	Phenobarbital	49-62	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	101-107
10924340-4	2000	In parallel, IL-6 decreases both rifampicin- and phenobarbital-mediated induction of CYP2B6, CYP2C8, CYP2C9, and CYP3A4.	Phenobarbital	49-62	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	113-119
11025406-5	2000	Miconazole (3 days) and phenobarbital (3 and 14 days) achieved cytochrome P450 inhibition and induction, respectively.	Phenobarbital	24-37	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	63-78
10825474-1	2000	Phenobarbital (PB) was shown to induce the major PB-inducible cytochrome P450 (CYP) isoforms, CYP2B1/2, in perivenular hepatocytes by a single injection, and in midzonal and periportal hepatocytes in addition to perivenular hepatocytes by injections of the same dosage once a day for 3 days in rat livers.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	94-102
11037111-4	2000	BFC was metabolized by both untreated and sodium phenobarbitone (NaPB)-treated rat hepatocytes in a time- and concentration-dependent manner to the highly fluorescent product 7-hydroxy-4-trifluoromethylcoumarin (HFC).	Phenobarbital	42-63	NSF attachment protein beta	Rattus norvegicus	65-69
10965017-2	2000	Initiation was induced by a single dose of diethylnitrosamine (DEN), followed by dietary administration of the promoter sodium phenobarbital (NaPB) 2 weeks later, for 6 weeks.	Phenobarbital	127-140	NSF attachment protein beta	Rattus norvegicus	142-146
10825474-1	2000	Phenobarbital (PB) was shown to induce the major PB-inducible cytochrome P450 (CYP) isoforms, CYP2B1/2, in perivenular hepatocytes by a single injection, and in midzonal and periportal hepatocytes in addition to perivenular hepatocytes by injections of the same dosage once a day for 3 days in rat livers.	Phenobarbital	49-51	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	62-77
10825474-0	2000	Effect of phenobarbital on intralobular expression of CYP2B1/2 in livers of rats: difference in the expression between single and repetitive administrations.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	54-60
10825474-1	2000	Phenobarbital (PB) was shown to induce the major PB-inducible cytochrome P450 (CYP) isoforms, CYP2B1/2, in perivenular hepatocytes by a single injection, and in midzonal and periportal hepatocytes in addition to perivenular hepatocytes by injections of the same dosage once a day for 3 days in rat livers.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	62-77
10825474-1	2000	Phenobarbital (PB) was shown to induce the major PB-inducible cytochrome P450 (CYP) isoforms, CYP2B1/2, in perivenular hepatocytes by a single injection, and in midzonal and periportal hepatocytes in addition to perivenular hepatocytes by injections of the same dosage once a day for 3 days in rat livers.	Phenobarbital	49-51	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	79-82
10825474-1	2000	Phenobarbital (PB) was shown to induce the major PB-inducible cytochrome P450 (CYP) isoforms, CYP2B1/2, in perivenular hepatocytes by a single injection, and in midzonal and periportal hepatocytes in addition to perivenular hepatocytes by injections of the same dosage once a day for 3 days in rat livers.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	79-82
10825474-1	2000	Phenobarbital (PB) was shown to induce the major PB-inducible cytochrome P450 (CYP) isoforms, CYP2B1/2, in perivenular hepatocytes by a single injection, and in midzonal and periportal hepatocytes in addition to perivenular hepatocytes by injections of the same dosage once a day for 3 days in rat livers.	Phenobarbital	49-51	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	94-102
10825474-1	2000	Phenobarbital (PB) was shown to induce the major PB-inducible cytochrome P450 (CYP) isoforms, CYP2B1/2, in perivenular hepatocytes by a single injection, and in midzonal and periportal hepatocytes in addition to perivenular hepatocytes by injections of the same dosage once a day for 3 days in rat livers.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	94-102
10825474-1	2000	Phenobarbital (PB) was shown to induce the major PB-inducible cytochrome P450 (CYP) isoforms, CYP2B1/2, in perivenular hepatocytes by a single injection, and in midzonal and periportal hepatocytes in addition to perivenular hepatocytes by injections of the same dosage once a day for 3 days in rat livers.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	62-77
10936227-3	2000	The nature of CYP isoforms involved in this covalent binding was investigated by using cultured rabbit hepatocytes treated or not with various CYP inducers (CYP1A1/2 by beta-naphthoflavone, CYP2B4 by phenobarbital, CYP3A6 by rifampicine, CYP4A by clofibrate) and human liver and bronchial CYP-expressing cells.	Phenobarbital	200-213	cytochrome P450 2B4	Oryctolagus cuniculus	190-196
10825474-1	2000	Phenobarbital (PB) was shown to induce the major PB-inducible cytochrome P450 (CYP) isoforms, CYP2B1/2, in perivenular hepatocytes by a single injection, and in midzonal and periportal hepatocytes in addition to perivenular hepatocytes by injections of the same dosage once a day for 3 days in rat livers.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	79-82
10871056-1	2000	Xanthates have previously been shown to inactivate the phenobarbital-inducible rat cytochrome P450 2B1 as well as its human homologue P450 2B6.	Phenobarbital	55-68	cytochrome P450 2B1	Rattus norvegicus	83-102
11180198-1	2000	In order to find what form of hepatic cytochrome P450 (CYP) is involved in the metabolism of parathion to form paraoxon, rats were pretreated with the enzyme inhibitors, such as SKF 525-A and ketoconazole or enzyme inducers, such as dexamethasone, isoniazid, phenobarbital, and 3-methylcholanthrene.	Phenobarbital	259-272	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	38-53
11180198-1	2000	In order to find what form of hepatic cytochrome P450 (CYP) is involved in the metabolism of parathion to form paraoxon, rats were pretreated with the enzyme inhibitors, such as SKF 525-A and ketoconazole or enzyme inducers, such as dexamethasone, isoniazid, phenobarbital, and 3-methylcholanthrene.	Phenobarbital	259-272	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	55-58
10859158-5	2000	The formation of III was inhibited to a significant extent by carbon monoxide, metyrapone, SKF 525-A, and cytochrome c, suggesting the participation of PB-induced microsomal cytochrome P-450 system in the conversion of I to III.	Phenobarbital	152-154	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	174-190
10859158-10	2000	This suggests that PB-induced cytochrome P-450-catalyzed reactive metabolites may be responsible for the toxic effects caused by I.	Phenobarbital	19-21	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	30-46
10942533-0	2000	Promotion of hepatocarcinogenesis by phenobarbital in c-myc/TGF-alpha transgenic mice.	Phenobarbital	37-50	transforming growth factor alpha	Mus musculus	60-69
10942533-9	2000	We believe that the PB-dependent modification of tumorigenesis in the livers of c-myc/TGF-alpha mice was predominantly a result of the ability of this drug to block cell death during the early stages of tumor development.	Phenobarbital	20-22	transforming growth factor alpha	Mus musculus	86-95
10873607-4	2000	Model inducers like rifampicin, phenobarbital, or 3-methylcholanthrene and beta-naphtoflavone were able to induce CYP1A or CYP3A4 as well as EROD or T6H activities for up to 30 days.	Phenobarbital	32-45	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	123-129
10828207-0	2000	EGF receptors of hepatocytes from rats treated with phenobarbital are sensitized to down-regulation by phenobarbital in culture.	Phenobarbital	52-65	epidermal growth factor like 1	Rattus norvegicus	0-3
10869407-0	2000	Latent overexpression of hepatic CYP2C7 in adult male and female rats neonatally exposed to phenobarbital: a developmental profile of gender-dependent P450s.	Phenobarbital	92-105	cytochrome P450, family 2, subfamily c, polypeptide 7	Rattus norvegicus	33-39
10869407-3	2000	Some of the cytochrome P450s (CYP), i. e., CYP2A1, 2A2, 2C6, 3A1, and 3A2, exhibit the typical transient response in which isoform levels (mRNA, protein, and/or specific catalytic activity) rise precipitously at the time of phenobarbital administration and rapidly decline to preinduction levels after withdrawal of the barbiturate.	Phenobarbital	224-237	cytochrome P450, family 2, subfamily a, polypeptide 1	Rattus norvegicus	43-49
10837011-4	2000	Various hepatic promoters, including phenobarbital and several peroxisomal proliferators, have been shown to inhibit TGF-beta-induced apoptosis in rat hepatocytes.	Phenobarbital	37-50	transforming growth factor, beta 1	Rattus norvegicus	117-125
10820145-5	2000	As expected, the mRNA levels of Cyp3a11, Cyp2b10, and Cyp1a2 were induced by a single dose of dexamethasone (100 mg/kg), phenobarbital (80 mg/kg), and 3-methylcholanthrene (80 mg/kg), respectively.	Phenobarbital	121-134	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	32-39
10820145-5	2000	As expected, the mRNA levels of Cyp3a11, Cyp2b10, and Cyp1a2 were induced by a single dose of dexamethasone (100 mg/kg), phenobarbital (80 mg/kg), and 3-methylcholanthrene (80 mg/kg), respectively.	Phenobarbital	121-134	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	41-48
10820145-5	2000	As expected, the mRNA levels of Cyp3a11, Cyp2b10, and Cyp1a2 were induced by a single dose of dexamethasone (100 mg/kg), phenobarbital (80 mg/kg), and 3-methylcholanthrene (80 mg/kg), respectively.	Phenobarbital	121-134	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	54-60
11105834-7	2000	RESULTS: Thirty-five PB-treated patients (27.6%) experienced SHS.	Phenobarbital	21-23	polyglutamine binding protein 1	Homo sapiens	61-64
11105834-8	2000	In these patients SHS developed during the first 7 months of therapy and regressed after PB discontinuation or, in 2 cases, after dosage reduction.	Phenobarbital	89-91	polyglutamine binding protein 1	Homo sapiens	18-21
10828267-8	2000	When blood cell-derived cultures were exposed to the prototypical CYP1A and CYP3A inducers, i.e., beta-naphthoflavone (beta-NF), dexamethasone (DEX) or phenobarbital, generally little or no inductive response was manifested.	Phenobarbital	152-165	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	76-81
10828207-0	2000	EGF receptors of hepatocytes from rats treated with phenobarbital are sensitized to down-regulation by phenobarbital in culture.	Phenobarbital	103-116	epidermal growth factor like 1	Rattus norvegicus	0-3
10828207-1	2000	Hepatocytes from Fisher 344 rats treated with the liver tumor promoter phenobarbital (PhB; 0.1% in the drinking water, 2-3 months) exhibit reduced epidermal growth factor (EGF) binding and EGF-induced mitogenesis in culture.	Phenobarbital	71-84	epidermal growth factor like 1	Rattus norvegicus	147-170
10828207-1	2000	Hepatocytes from Fisher 344 rats treated with the liver tumor promoter phenobarbital (PhB; 0.1% in the drinking water, 2-3 months) exhibit reduced epidermal growth factor (EGF) binding and EGF-induced mitogenesis in culture.	Phenobarbital	71-84	epidermal growth factor like 1	Rattus norvegicus	172-175
10828207-1	2000	Hepatocytes from Fisher 344 rats treated with the liver tumor promoter phenobarbital (PhB; 0.1% in the drinking water, 2-3 months) exhibit reduced epidermal growth factor (EGF) binding and EGF-induced mitogenesis in culture.	Phenobarbital	71-84	epidermal growth factor like 1	Rattus norvegicus	189-192
10828207-1	2000	Hepatocytes from Fisher 344 rats treated with the liver tumor promoter phenobarbital (PhB; 0.1% in the drinking water, 2-3 months) exhibit reduced epidermal growth factor (EGF) binding and EGF-induced mitogenesis in culture.	Phenobarbital	86-89	epidermal growth factor like 1	Rattus norvegicus	147-170
10828207-1	2000	Hepatocytes from Fisher 344 rats treated with the liver tumor promoter phenobarbital (PhB; 0.1% in the drinking water, 2-3 months) exhibit reduced epidermal growth factor (EGF) binding and EGF-induced mitogenesis in culture.	Phenobarbital	86-89	epidermal growth factor like 1	Rattus norvegicus	172-175
10828207-1	2000	Hepatocytes from Fisher 344 rats treated with the liver tumor promoter phenobarbital (PhB; 0.1% in the drinking water, 2-3 months) exhibit reduced epidermal growth factor (EGF) binding and EGF-induced mitogenesis in culture.	Phenobarbital	86-89	epidermal growth factor like 1	Rattus norvegicus	189-192
10828207-7	2000	Differentiated hepatocyte function was required for PhB-induced EGFr down-regulation since HepG2 and rat liver epithelial cells were unresponsive, but involvement of CYP2B1/2 activity was discounted by the failure of metyrapone to inhibit the response in PhB-induced hepatocytes.	Phenobarbital	52-55	epidermal growth factor receptor	Homo sapiens	64-68
11180194-1	2000	In order to find what types of hepatic cytochrome P450 (CYP) isozymes are involved in the metabolism of 2-(allylthio)pyrazine (2-AP) in rats, enzyme inducers, such as phenobarbital, 3-methylcholanthrene, dexamethasone, or isoniazid, and an enzyme inhibitor, such as SKF 525-A were pretreated.	Phenobarbital	167-180	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-54
10773077-1	2000	The phenobarbital-inducible rat cytochrome P450 (CYP) 2B1 and 2B2 proteins are encoded by homologous genes whose promoters contain a mammalian-apparent long terminal repeat retrotransposon (MaLR).	Phenobarbital	4-17	cytochrome P450 2B1	Rattus norvegicus	32-65
10788445-0	2000	A conserved nuclear receptor consensus sequence (DR-4) mediates transcriptional activation of the chicken CYP2H1 gene by phenobarbital in a hepatoma cell line.	Phenobarbital	121-134	cytochrome P450 2H1	Gallus gallus	106-112
10788445-4	2000	This motif resembles phenobarbital response elements in the flanking regions of three phenobarbital-inducible genes, rat CYP2B2, mouse Cyp2b10, and human CYP2B6.	Phenobarbital	21-34	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	121-127
10788445-4	2000	This motif resembles phenobarbital response elements in the flanking regions of three phenobarbital-inducible genes, rat CYP2B2, mouse Cyp2b10, and human CYP2B6.	Phenobarbital	21-34	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	135-142
10788445-4	2000	This motif resembles phenobarbital response elements in the flanking regions of three phenobarbital-inducible genes, rat CYP2B2, mouse Cyp2b10, and human CYP2B6.	Phenobarbital	21-34	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	154-160
10788445-4	2000	This motif resembles phenobarbital response elements in the flanking regions of three phenobarbital-inducible genes, rat CYP2B2, mouse Cyp2b10, and human CYP2B6.	Phenobarbital	86-99	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	121-127
10788445-4	2000	This motif resembles phenobarbital response elements in the flanking regions of three phenobarbital-inducible genes, rat CYP2B2, mouse Cyp2b10, and human CYP2B6.	Phenobarbital	86-99	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	135-142
10788445-4	2000	This motif resembles phenobarbital response elements in the flanking regions of three phenobarbital-inducible genes, rat CYP2B2, mouse Cyp2b10, and human CYP2B6.	Phenobarbital	86-99	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	154-160
10788445-6	2000	Evidence for evolutionary conservation of this recognition site was indicated by activation in LMH cells of a mouse Cyp2b10 phenobarbital-responsive enhancer by the same spectrum of inducers that activate the CYP2H1 264-bp PBRU.	Phenobarbital	124-137	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	116-123
10788445-6	2000	Evidence for evolutionary conservation of this recognition site was indicated by activation in LMH cells of a mouse Cyp2b10 phenobarbital-responsive enhancer by the same spectrum of inducers that activate the CYP2H1 264-bp PBRU.	Phenobarbital	124-137	cytochrome P450 2H1	Gallus gallus	209-215
10775455-9	2000	On the other hand, pregnenolone 16alpha-carbonitrile and phenobarbital suppressed CYP3A41 level to half that of untreated female mice.	Phenobarbital	57-70	cytochrome P450, family 3, subfamily a, polypeptide 41A	Mus musculus	82-89
11180194-1	2000	In order to find what types of hepatic cytochrome P450 (CYP) isozymes are involved in the metabolism of 2-(allylthio)pyrazine (2-AP) in rats, enzyme inducers, such as phenobarbital, 3-methylcholanthrene, dexamethasone, or isoniazid, and an enzyme inhibitor, such as SKF 525-A were pretreated.	Phenobarbital	167-180	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	56-59
10772642-9	2000	Analysis of chemical-induced differences in gene expression by bDNA signal amplification indicated that 3-methylcholanthrene induced CYP1A1 and CYP1A2 mRNA levels 670- and 11-fold, respectively; PB induced CYP2B1/2 expression 71-fold; pregnenolone-16alpha-carbonitrile induced CYP3A1/23 expression 34-fold; and clofibric acid induced CYP4A2/3 expression 4.7-fold.	Phenobarbital	195-197	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	144-150
10772642-9	2000	Analysis of chemical-induced differences in gene expression by bDNA signal amplification indicated that 3-methylcholanthrene induced CYP1A1 and CYP1A2 mRNA levels 670- and 11-fold, respectively; PB induced CYP2B1/2 expression 71-fold; pregnenolone-16alpha-carbonitrile induced CYP3A1/23 expression 34-fold; and clofibric acid induced CYP4A2/3 expression 4.7-fold.	Phenobarbital	195-197	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	206-212
10772642-8	2000	Male Sprague-Dawley rats were administered 3-methylcholanthrene, PB, isoniazid, pregnenolone-16alpha-carbonitrile, or clofibric acid to induce transcription of CYP1A1, CYP1A2, CYP2B1/2, CYP2E1, CYP3A1/23, and CYP4A2/3 mRNA, respectively.	Phenobarbital	65-67	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	160-166
10772642-9	2000	Analysis of chemical-induced differences in gene expression by bDNA signal amplification indicated that 3-methylcholanthrene induced CYP1A1 and CYP1A2 mRNA levels 670- and 11-fold, respectively; PB induced CYP2B1/2 expression 71-fold; pregnenolone-16alpha-carbonitrile induced CYP3A1/23 expression 34-fold; and clofibric acid induced CYP4A2/3 expression 4.7-fold.	Phenobarbital	195-197	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	277-283
10772642-9	2000	Analysis of chemical-induced differences in gene expression by bDNA signal amplification indicated that 3-methylcholanthrene induced CYP1A1 and CYP1A2 mRNA levels 670- and 11-fold, respectively; PB induced CYP2B1/2 expression 71-fold; pregnenolone-16alpha-carbonitrile induced CYP3A1/23 expression 34-fold; and clofibric acid induced CYP4A2/3 expression 4.7-fold.	Phenobarbital	195-197	cytochrome P450, family 4, subfamily a, polypeptide 2	Rattus norvegicus	334-340
10729196-12	2000	Upon incubation with phenobarbital and rifampin (rifampicin), human hepatocytes increased CYP 2B6, 3A4, and 3A5 among others.	Phenobarbital	21-34	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	90-97
10757780-5	2000	However, CAR transactivation is increased in the presence of 1,4-bis[2-(3, 5-dichloropyridyloxy)]benzene (TCPOBOP), the most potent known member of the phenobarbital-like class of CYP-inducing agents.	Phenobarbital	152-165	CXADR pseudogene 1	Homo sapiens	9-12
10757780-5	2000	However, CAR transactivation is increased in the presence of 1,4-bis[2-(3, 5-dichloropyridyloxy)]benzene (TCPOBOP), the most potent known member of the phenobarbital-like class of CYP-inducing agents.	Phenobarbital	152-165	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	180-183
10788562-4	2000	We have shown that serum TSH is increased the most in rats treated with the microsomal enzyme inducers phenobarbital (PB) or pregnenolone-16alpha-carbonitrile (PCN), whereas TSH is affected less in rats treated with 3-methylcholanthrene (3MC) and Aroclor 1254 (PCB).	Phenobarbital	103-116	pyruvate carboxylase	Rattus norvegicus	261-264
10770516-5	2000	RESULTS: The patients on AEDs inducing the cytochrome P450 (carbamazepine, phenytoin, phenobarbital, primidone), had higher fasting and 6h-PML plasma tHcy concentrations than the controls (P = 0.01 and P&lt;0.001).	Phenobarbital	86-99	PML nuclear body scaffold	Homo sapiens	139-142
10781875-0	2000	Induction of cytochrome P450 2B1-mRNA and pentoxyresorufin O-depentylation after exposure of precision-cut rat liver slices to phenobarbital.	Phenobarbital	127-140	cytochrome P450 2B1	Rattus norvegicus	13-32
10781875-2	2000	After exposure of the slices to 100 microM phenobarbital, CYP2B1-mRNA increased by about 10- or 60-fold after 6 or 24 h, respectively.	Phenobarbital	43-56	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	58-64
10762607-1	2000	Phenobarbital and other xenobiotics induce drug-metabolizing enzymes, including glutathione S-transferase A1/A2 (rGSTA1/A2).	Phenobarbital	0-13	glutathione S-transferase alpha 1	Rattus norvegicus	113-122
10762607-2	2000	We examined the mechanism of induction of rGSTA1/A2 in rat livers after phenobarbital treatment.	Phenobarbital	72-85	glutathione S-transferase alpha 1	Rattus norvegicus	42-48
10762607-3	2000	The induction of rGSTA1/A2 was not uniform across the hepatic lobule; steady-state transcript levels were threefold higher in perivenous hepatocytes relative to periportal hepatocytes when examined by in situ hybridization 12 h after a single dose of phenobarbital.	Phenobarbital	251-264	glutathione S-transferase alpha 1	Rattus norvegicus	17-26
10762607-5	2000	The transcriptional activity of the rGSTA1/A2 gene was increased 3.5- to 5.5-fold in whole liver by phenobarbital, but activities were the same in enriched periportal and perivenous subpopulations of hepatocytes from phenobarbital-treated animals.	Phenobarbital	100-113	glutathione S-transferase alpha 1	Rattus norvegicus	36-45
10762607-5	2000	The transcriptional activity of the rGSTA1/A2 gene was increased 3.5- to 5.5-fold in whole liver by phenobarbital, but activities were the same in enriched periportal and perivenous subpopulations of hepatocytes from phenobarbital-treated animals.	Phenobarbital	217-230	glutathione S-transferase alpha 1	Rattus norvegicus	36-45
10762607-6	2000	The half-life of rGSTA1/A2 mRNA in control animals was 3.6 h, whereas it was 10.2 h in phenobarbital-treated animals.	Phenobarbital	87-100	glutathione S-transferase alpha 1	Rattus norvegicus	17-26
10762607-7	2000	We conclude that phenobarbital induces rGSTA1/A2 expression by increasing transcriptional activity across the lobule but induction of rGSTA1/A2 is greater in perivenous hepatocytes due to localized stabilization of mRNA transcripts.	Phenobarbital	17-30	glutathione S-transferase alpha 1	Rattus norvegicus	39-45
10788562-8	2000	T(4) UDP-GT activity was increased in rats treated with PB (120%), PCN (250 to 400%), 3MC (400 to 600%), or PCB (300 to 430%).	Phenobarbital	56-58	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	5-11
10788562-9	2000	In contrast, T(3) UDP-GT activity was increased in rats treated with PB (90%) or PCN (120 to 200%), whereas 3MC and PCB treatments did not have an appreciable effect.	Phenobarbital	69-71	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	18-24
10702363-5	2000	Furthermore, 3MC and PCB do not increase serum TSH, whereas PB and PCN do, because type-II ORD activity in the pituitary of 3MC- and PCB-treated rats is increased greater than in rats treated with PB or PCN.	Phenobarbital	60-62	pyruvate carboxylase	Rattus norvegicus	133-136
10817630-4	2000	Phenobarbital (PB) administration (0.1% in drinking water; 15 days) elicited an enhancement in liver microsomal functions, lipid peroxidation, and GSH content, without changes in oxidative stress-related enzymatic activities, except for the elevation in those of glutathione reductase and glutathione-S-transferase, compared to control rats.	Phenobarbital	0-13	glutathione-disulfide reductase	Rattus norvegicus	263-284
10817630-4	2000	Phenobarbital (PB) administration (0.1% in drinking water; 15 days) elicited an enhancement in liver microsomal functions, lipid peroxidation, and GSH content, without changes in oxidative stress-related enzymatic activities, except for the elevation in those of glutathione reductase and glutathione-S-transferase, compared to control rats.	Phenobarbital	0-13	hematopoietic prostaglandin D synthase	Rattus norvegicus	289-314
10817630-4	2000	Phenobarbital (PB) administration (0.1% in drinking water; 15 days) elicited an enhancement in liver microsomal functions, lipid peroxidation, and GSH content, without changes in oxidative stress-related enzymatic activities, except for the elevation in those of glutathione reductase and glutathione-S-transferase, compared to control rats.	Phenobarbital	15-17	glutathione-disulfide reductase	Rattus norvegicus	263-284
10817630-4	2000	Phenobarbital (PB) administration (0.1% in drinking water; 15 days) elicited an enhancement in liver microsomal functions, lipid peroxidation, and GSH content, without changes in oxidative stress-related enzymatic activities, except for the elevation in those of glutathione reductase and glutathione-S-transferase, compared to control rats.	Phenobarbital	15-17	hematopoietic prostaglandin D synthase	Rattus norvegicus	289-314
10746936-11	2000	Many EAF in PB-treated animals contained very large numbers of p53-positive cells.	Phenobarbital	12-14	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	63-66
10751624-0	2000	Subchronic administration of phenobarbital alters the mutation spectrum of lacI in the livers of Big Blue transgenic mice.	Phenobarbital	29-42	tissue factor pathway inhibitor	Mus musculus	75-79
10751624-7	2000	It is postulated that the increase in transversions at G:C base pairs found in the PHE-derived spectrum is likely due to oxidative damage as a result of induction of CYP2B isozymes by the chronic administration of PHE.	Phenobarbital	83-86	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	166-171
10751624-7	2000	It is postulated that the increase in transversions at G:C base pairs found in the PHE-derived spectrum is likely due to oxidative damage as a result of induction of CYP2B isozymes by the chronic administration of PHE.	Phenobarbital	214-217	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	166-171
10751624-9	2000	The PHE-derived spectrum of lacI mutants from the liver of Big Blue(R) B6C3F1 male mice was remarkably similar (p=0.8) to that generated by oxazepam (OX), a compound which also induces CYP2B isozymes following chronic administration of the drug.	Phenobarbital	4-7	tissue factor pathway inhibitor	Mus musculus	28-32
10751624-9	2000	The PHE-derived spectrum of lacI mutants from the liver of Big Blue(R) B6C3F1 male mice was remarkably similar (p=0.8) to that generated by oxazepam (OX), a compound which also induces CYP2B isozymes following chronic administration of the drug.	Phenobarbital	4-7	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	185-190
10696073-7	2000	CYP3A5 was induced 8-fold by dexamethasone and 11-fold by phenobarbital.	Phenobarbital	58-71	cytochrome P450 family 3 subfamily A member 5	Homo sapiens	0-6
10712264-4	2000	Although expression of MRP3 was also induced by administration of phenobarbital, that of cMOAT/MRP2, MRP1, and MRP6 was not affected by any of these treatments.	Phenobarbital	66-79	ATP binding cassette subfamily C member 3	Rattus norvegicus	23-27
10681370-1	2000	Cytochrome P-4503A, CYP2B, and P-450 reductase are induced by glucocorticoids, antiglucocorticoids such as pregnenolone 16alpha-carbonitrile, and drugs such as rifampin and phenobarbital.	Phenobarbital	173-186	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	20-25
10681370-10	2000	Phenobarbital induced CYP3A, CYP2B, and P-450 reductase in all mice, but the amplitude of induction was diminished 37% in glucocorticoid receptor-null mice.	Phenobarbital	0-13	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	22-27
10681370-10	2000	Phenobarbital induced CYP3A, CYP2B, and P-450 reductase in all mice, but the amplitude of induction was diminished 37% in glucocorticoid receptor-null mice.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	29-34
10681370-10	2000	Phenobarbital induced CYP3A, CYP2B, and P-450 reductase in all mice, but the amplitude of induction was diminished 37% in glucocorticoid receptor-null mice.	Phenobarbital	0-13	nuclear receptor subfamily 3, group C, member 1	Mus musculus	122-145
10805060-0	2000	CYP2C19 polymorphism effect on phenobarbitone.	Phenobarbital	31-45	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	0-7
10885034-1	2000	Neuro-, hepato- and geno-toxic effects of the industrial xenobiotic, acrylamide, were studied in intact rats and in rats with induced phenobarbital- and 3-methylholanthren-dependent isoforms of cytochrome P-450.	Phenobarbital	134-147	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	194-210
10700573-3	2000	We examined whether the commonly used AEDs, diazepam (DZP), carbamazepine (CBZ), phenobarbital (PB), phenytoin (PHT), and VPA, can inhibit activation of the nuclear transcription factor kappa B (NF-kappaB), in human monocytic leukemia cells (THP-1) and in human glioma cells (A-172).	Phenobarbital	81-94	GLI family zinc finger 2	Homo sapiens	242-247
10679274-1	2000	The phenobarbitone (PB) responsiveness of the 5"-proximal region of the CYP2B1/B2 gene was examined in detail with plasmid DNA constructs containing G-free cassette as reporter, using in vivo targeting of the same DNA constructs into rat liver as galactosylated-polylysine complexes.	Phenobarbital	4-18	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	72-78
10679274-1	2000	The phenobarbitone (PB) responsiveness of the 5"-proximal region of the CYP2B1/B2 gene was examined in detail with plasmid DNA constructs containing G-free cassette as reporter, using in vivo targeting of the same DNA constructs into rat liver as galactosylated-polylysine complexes.	Phenobarbital	20-22	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	72-78
10672003-8	2000	Ca2+ thus appeared to mediate PB action likely via Ca2+/calmodulin-dependent protein kinase II, as KN62, a specific inhibitor of this enzyme, also dramatically inhibited PB induction of the Cyp2b9/10 genes.	Phenobarbital	30-32	calcium/calmodulin-dependent protein kinase II gamma	Mus musculus	51-94
10672003-8	2000	Ca2+ thus appeared to mediate PB action likely via Ca2+/calmodulin-dependent protein kinase II, as KN62, a specific inhibitor of this enzyme, also dramatically inhibited PB induction of the Cyp2b9/10 genes.	Phenobarbital	30-32	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	190-196
10672003-8	2000	Ca2+ thus appeared to mediate PB action likely via Ca2+/calmodulin-dependent protein kinase II, as KN62, a specific inhibitor of this enzyme, also dramatically inhibited PB induction of the Cyp2b9/10 genes.	Phenobarbital	170-172	calcium/calmodulin-dependent protein kinase II gamma	Mus musculus	51-94
10672003-8	2000	Ca2+ thus appeared to mediate PB action likely via Ca2+/calmodulin-dependent protein kinase II, as KN62, a specific inhibitor of this enzyme, also dramatically inhibited PB induction of the Cyp2b9/10 genes.	Phenobarbital	170-172	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	190-196
10672003-0	2000	Regulation of phenobarbital induction of the cytochrome P450 2b9/10 genes in primary mouse hepatocyte culture.	Phenobarbital	14-27	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	45-64
10672003-5	2000	The cGMP-dependent protein kinase (PKG) seems to play a positive role as PKG inhibitor reduced the PB-induced level of Cyp2b9/10 mRNA.	Phenobarbital	99-101	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	119-125
10672003-7	2000	Firstly, measurements of intracellular Fura-2 fluorescence ratio in murine hepatocytes showed that long-term PB incubation (24 and 48 h) led to a significant increase of [Ca2+]i. Secondly, treatment with an intracellular Ca2+ chelator (BAPTA-AM) nearly completely abolished PB-induced Cyp2b9/10 expression.	Phenobarbital	109-111	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	285-291
10805060-2	2000	OBJECTIVE: The aim of this study was to clarify the effect of genetic polymorphisms of CYP2C19 on the pharmacokinetics of phenobarbitone (PB) using a nonlinear mixed-effects model (NONMEM) analysis in Japanese adults with epilepsy.	Phenobarbital	122-136	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	87-94
10805060-2	2000	OBJECTIVE: The aim of this study was to clarify the effect of genetic polymorphisms of CYP2C19 on the pharmacokinetics of phenobarbitone (PB) using a nonlinear mixed-effects model (NONMEM) analysis in Japanese adults with epilepsy.	Phenobarbital	138-140	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	87-94
10805060-9	2000	CONCLUSION: In this study, we first demonstrated the effect of the CYP2C19 polymorphism on pharmacokinetics of PB by genotyping.	Phenobarbital	111-113	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	67-74
10718121-4	2000	Dexamethasone and phenobarbitone pretreatment enhanced MI-complexation by DTZ (36% and 11% of total CYP complexed, respectively), whereas beta-naphthoflavone induction was without effect.	Phenobarbital	18-32	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	100-103
10484068-1	1999	Results of previous studies have substantiated a negative modulatory role for cyclic AMP (cAMP) and protein kinase A (PKA) dependent processes on the phenobarbital (PB) induction response in hepatocytes.	Phenobarbital	150-163	cathelicidin antimicrobial peptide	Rattus norvegicus	78-95
10620362-12	2000	Finally, in both chicken embryo liver and chicken hepatoma cells (LMH), CYP3A37 mRNA was increased after treatment with typical CYP3A inducers, such as metyrapone, phenobarbital, dexamethasone, and pregnenolone 16alpha-carbonitrile, but not rifampicin.	Phenobarbital	164-177	cytochrome P450 family 3 subfamily A member 5	Gallus gallus	72-79
10620362-12	2000	Finally, in both chicken embryo liver and chicken hepatoma cells (LMH), CYP3A37 mRNA was increased after treatment with typical CYP3A inducers, such as metyrapone, phenobarbital, dexamethasone, and pregnenolone 16alpha-carbonitrile, but not rifampicin.	Phenobarbital	164-177	cytochrome P450 family 3 subfamily A member 5	Gallus gallus	72-77
10670821-6	2000	Potentiation of thioacetamide hepatotoxicity by phenobarbital pretreatment was demonstrated at morphological level, and by significant increases in the activities of serum aspartate aminotransferase and gamma-glutamyl transferase, and in the levels of total bilirubin.	Phenobarbital	48-61	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	172-198
10670821-6	2000	Potentiation of thioacetamide hepatotoxicity by phenobarbital pretreatment was demonstrated at morphological level, and by significant increases in the activities of serum aspartate aminotransferase and gamma-glutamyl transferase, and in the levels of total bilirubin.	Phenobarbital	48-61	gamma-glutamyltransferase 1	Rattus norvegicus	203-229
10670824-14	2000	Induction of CYP2B/1/2, CYP3A1/2 and NADPH cytochrome P450 reductase was observed in rats treated with 50 mg/kg phenobarbital by intraperitoneal injection.	Phenobarbital	112-125	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	24-32
10670824-14	2000	Induction of CYP2B/1/2, CYP3A1/2 and NADPH cytochrome P450 reductase was observed in rats treated with 50 mg/kg phenobarbital by intraperitoneal injection.	Phenobarbital	112-125	cytochrome p450 oxidoreductase	Rattus norvegicus	37-68
10613740-5	2000	Repetitive doses of CCl(4) in the presence or absence of phenobarbital resulted in increased injury and fibrosis in IL-6 -/- compared with +/+ livers.	Phenobarbital	57-70	interleukin 6	Mus musculus	116-120
10529397-0	1999	Phosphorylation/Dephosphorylation steps are crucial for the induction of CYP2B1 and CYP2B2 gene expression by phenobarbital.	Phenobarbital	110-123	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	73-79
10529397-0	1999	Phosphorylation/Dephosphorylation steps are crucial for the induction of CYP2B1 and CYP2B2 gene expression by phenobarbital.	Phenobarbital	110-123	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	84-90
10529397-1	1999	The effects of several protein kinase activators and protein phosphatase inhibitors on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes were investigated.	Phenobarbital	91-104	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	137-143
10529397-1	1999	The effects of several protein kinase activators and protein phosphatase inhibitors on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes were investigated.	Phenobarbital	91-104	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	148-154
10529397-1	1999	The effects of several protein kinase activators and protein phosphatase inhibitors on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes were investigated.	Phenobarbital	91-104	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	156-166
10529397-1	1999	The effects of several protein kinase activators and protein phosphatase inhibitors on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes were investigated.	Phenobarbital	106-108	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	137-143
10529397-1	1999	The effects of several protein kinase activators and protein phosphatase inhibitors on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes were investigated.	Phenobarbital	106-108	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	148-154
10529397-1	1999	The effects of several protein kinase activators and protein phosphatase inhibitors on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes were investigated.	Phenobarbital	106-108	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	156-166
11996099-1	2000	In contrast to the well-known Ah receptor-mediated regulation of the CYP1A1 gene by polycyclic aromatic hydrocarbons, the molecular mechanism by which phenobarbital (PB) and PB-like inducers affect transcription of CYP genes remains unknown; no receptor for these chemicals has been found to date.	Phenobarbital	174-176	aryl hydrocarbon receptor	Homo sapiens	30-41
11996099-1	2000	In contrast to the well-known Ah receptor-mediated regulation of the CYP1A1 gene by polycyclic aromatic hydrocarbons, the molecular mechanism by which phenobarbital (PB) and PB-like inducers affect transcription of CYP genes remains unknown; no receptor for these chemicals has been found to date.	Phenobarbital	174-176	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	69-75
11996099-3	2000	The phenobarbital-responsive enhancer unit (PBRU) of CYP2B gene family members contain two potential nuclear receptor binding sites (NR1 and NR2) that flank a nuclear factor 1 (NF-1) binding motif.	Phenobarbital	4-17	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	53-58
11996099-3	2000	The phenobarbital-responsive enhancer unit (PBRU) of CYP2B gene family members contain two potential nuclear receptor binding sites (NR1 and NR2) that flank a nuclear factor 1 (NF-1) binding motif.	Phenobarbital	4-17	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	133-136
11996099-3	2000	The phenobarbital-responsive enhancer unit (PBRU) of CYP2B gene family members contain two potential nuclear receptor binding sites (NR1 and NR2) that flank a nuclear factor 1 (NF-1) binding motif.	Phenobarbital	4-17	neurofibromin 1	Homo sapiens	177-181
11996099-7	2000	It is also possible that the pleiotropic effects of PB can, in part, be explained by the ability of the CAR-RXR heterodimer to bind to a variety of nuclear receptor binding motifs.	Phenobarbital	52-54	CXADR pseudogene 1	Homo sapiens	104-107
11201056-0	2000	Regulation of phenobarbital-induction of CYP2B and CYP3A genes in rat cultured hepatocytes: involvement of several serine/threonine protein kinases and phosphatases.	Phenobarbital	14-27	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	51-56
11201056-2	2000	Different inhibitors or activators of protein kinases or phosphatases were assessed for their ability to modulate PB-induction of CYP2B and CYP3A mRNA expression.	Phenobarbital	114-116	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	140-145
11201056-4	2000	The present data further suggested that Ca2+/calmodulin-dependent protein kinases II (independently of Ca2+) and extracellular signal-regulated kinases 1/2 (ERK1/2) might function respectively as positive and negative regulator in the PB-induction of CYP2B and CYP3A.	Phenobarbital	235-237	mitogen activated protein kinase 3	Rattus norvegicus	113-155
11201056-4	2000	The present data further suggested that Ca2+/calmodulin-dependent protein kinases II (independently of Ca2+) and extracellular signal-regulated kinases 1/2 (ERK1/2) might function respectively as positive and negative regulator in the PB-induction of CYP2B and CYP3A.	Phenobarbital	235-237	mitogen activated protein kinase 3	Rattus norvegicus	157-163
11201056-4	2000	The present data further suggested that Ca2+/calmodulin-dependent protein kinases II (independently of Ca2+) and extracellular signal-regulated kinases 1/2 (ERK1/2) might function respectively as positive and negative regulator in the PB-induction of CYP2B and CYP3A.	Phenobarbital	235-237	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	261-266
11201056-6	2000	We conclude that a complex network of phosphorylation/dephosphorylation events might be crucial for PB-induction of rat CYP2B and CYP3A.	Phenobarbital	100-102	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	130-135
10611137-11	2000	Previous studies demonstrated that UGT1A1 inducers like phenobarbital have no effect on T4 conjugation ().	Phenobarbital	56-69	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	35-41
10712746-0	2000	Phenobarbital increases DNA adduct and metabolites formed by ochratoxin A: role of CYP 2C9 and microsomal glutathione-S-transferase.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-90
10600163-0	1999	Transcriptional regulation of 5-aminolevulinate synthase by phenobarbital and cAMP-dependent protein kinase.	Phenobarbital	60-73	5'-aminolevulinate synthase 1	Rattus norvegicus	30-56
10600163-4	1999	In this report we examine the mechanisms by which phenobarbital and cAMP regulate housekeeping ALA-S expression.	Phenobarbital	50-63	5'-aminolevulinate synthase 1	Rattus norvegicus	95-100
10600163-5	1999	We have determined that cAMP and phenobarbital effects are additive and the combined action is necessary to observe the cAMP effect on ALA-S mRNA in rat hepatocytes.	Phenobarbital	33-46	5'-aminolevulinate synthase 1	Rattus norvegicus	135-140
10600163-8	1999	A 870-bp fragment of ALA-S 5"-flanking region is able to provide cAMP and phenobarbital stimulation to chloramphenicol O-acetyltranferase fusion vectors in transiently transfected HepG2 cells.	Phenobarbital	74-87	5'-aminolevulinate synthase 1	Homo sapiens	21-26
10600163-12	1999	Finally, heme addition greatly decreases the basal and phenobarbital or cAMP analog-mediated induction of ALA-S promoter activity.	Phenobarbital	55-68	5'-aminolevulinate synthase 1	Rattus norvegicus	106-111
10600163-13	1999	The present work provides evidence that cAMP, through PKA-mediated CREB phosphorylation, and phenobarbital induce ALA-S expression at the transcriptional level, while heme represses it.	Phenobarbital	93-106	5'-aminolevulinate synthase 1	Rattus norvegicus	114-119
10598746-11	1999	Microsomes from phenobarbitone and isoniazid-pretreated animals significantly (p &lt; 0.05) enhanced the formation of AQ4 from AQ4N indicating a role for CYP2B and 2E respectively.	Phenobarbital	16-30	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	154-166
10598750-3	1999	In the present study the salicylate-hydroxylation assay was used to examine whether CYP induction by the administration of dexamethasone, phenobarbital or beta-naphthoflavone to the male rat led to oxidative stress in vivo.	Phenobarbital	138-151	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	84-87
10598750-9	1999	Phenobarbital led to a 4.7-fold increase in 2,3-DHB plasma concentration under conditions that induced CYP P4502B and 3A.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	103-106
10529397-4	1999	The addition of genistein to vanadate-treated hepatocytes partially recovered the induction of CYP2B1/2B1 gene expression by PB.	Phenobarbital	125-127	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	95-105
10484068-1	1999	Results of previous studies have substantiated a negative modulatory role for cyclic AMP (cAMP) and protein kinase A (PKA) dependent processes on the phenobarbital (PB) induction response in hepatocytes.	Phenobarbital	150-163	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	100-116
10484068-1	1999	Results of previous studies have substantiated a negative modulatory role for cyclic AMP (cAMP) and protein kinase A (PKA) dependent processes on the phenobarbital (PB) induction response in hepatocytes.	Phenobarbital	150-163	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	118-121
10484068-1	1999	Results of previous studies have substantiated a negative modulatory role for cyclic AMP (cAMP) and protein kinase A (PKA) dependent processes on the phenobarbital (PB) induction response in hepatocytes.	Phenobarbital	165-167	cathelicidin antimicrobial peptide	Rattus norvegicus	78-95
10484068-1	1999	Results of previous studies have substantiated a negative modulatory role for cyclic AMP (cAMP) and protein kinase A (PKA) dependent processes on the phenobarbital (PB) induction response in hepatocytes.	Phenobarbital	165-167	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	100-116
10484068-1	1999	Results of previous studies have substantiated a negative modulatory role for cyclic AMP (cAMP) and protein kinase A (PKA) dependent processes on the phenobarbital (PB) induction response in hepatocytes.	Phenobarbital	165-167	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	118-121
10528997-2	1999	The dihydrodiol is metabolized at a rate of 2.4 nmol/nmol of cytochrome P450 1A1/min with microsomes from 3-methylcholanthrene-treated rats, a rate more than 10-fold higher than that observed with microsomes from control or phenobarbital-treated rats.	Phenobarbital	224-237	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	61-80
10497137-3	1999	Immunoblot analysis of enterocyte microsomes from rats treated with beta-naphthoflavone, dexamethasone, or phenobarbital revealed unchanged, diminished, or slightly increased levels of CYP2J4 protein, respectively, relative to vehicle-treated rats, whereas rats treated with pyrazole (200 mg/kg) had 3- to 4-fold increased levels of CYP2J4.	Phenobarbital	107-120	cytochrome P450, family 2, subfamily j, polypeptide 4	Rattus norvegicus	185-191
10497137-3	1999	Immunoblot analysis of enterocyte microsomes from rats treated with beta-naphthoflavone, dexamethasone, or phenobarbital revealed unchanged, diminished, or slightly increased levels of CYP2J4 protein, respectively, relative to vehicle-treated rats, whereas rats treated with pyrazole (200 mg/kg) had 3- to 4-fold increased levels of CYP2J4.	Phenobarbital	107-120	cytochrome P450, family 2, subfamily j, polypeptide 4	Rattus norvegicus	333-339
10522495-1	1999	The effects of cytochrome P-450 (CYP) induction by phenobarbital (PB), CYP 2B, 2C, and 3A inducer in mammalians, on triphenyltin metabolism and toxicity in hamsters were studied.	Phenobarbital	51-64	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	15-31
10522495-1	1999	The effects of cytochrome P-450 (CYP) induction by phenobarbital (PB), CYP 2B, 2C, and 3A inducer in mammalians, on triphenyltin metabolism and toxicity in hamsters were studied.	Phenobarbital	51-64	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	33-36
10522495-1	1999	The effects of cytochrome P-450 (CYP) induction by phenobarbital (PB), CYP 2B, 2C, and 3A inducer in mammalians, on triphenyltin metabolism and toxicity in hamsters were studied.	Phenobarbital	66-68	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	15-31
10522495-1	1999	The effects of cytochrome P-450 (CYP) induction by phenobarbital (PB), CYP 2B, 2C, and 3A inducer in mammalians, on triphenyltin metabolism and toxicity in hamsters were studied.	Phenobarbital	66-68	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	33-36
10522495-3	1999	Although the triphenyltin produced marked but reversible hyperglycemia and hypertriglyceridemia in PB-untreated hamsters, the pretreatment of hamsters with PB, which increased levels of CYP, suppressed the diabetogenic effects compared with PB-untreated hamsters.	Phenobarbital	156-158	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	186-189
10522495-3	1999	Although the triphenyltin produced marked but reversible hyperglycemia and hypertriglyceridemia in PB-untreated hamsters, the pretreatment of hamsters with PB, which increased levels of CYP, suppressed the diabetogenic effects compared with PB-untreated hamsters.	Phenobarbital	156-158	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	186-189
10522495-11	1999	Especially, based on effects of PB and other CYP inducers, PB induction has a key role in suppressing the diabetogenic action of triphenyltin, i.e. by decreasing triphenyltin accumulation in the hamsters.	Phenobarbital	59-61	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	45-48
10462436-3	1999	Roles for three "orphan" nuclear receptor superfamily members, designated CAR, PXR, and PPAR, in respectively mediating the induction of hepatic P450s belonging to families CYP2, CYP3, and CYP4 in response to the prototypical inducers phenobarbital (CAR), pregnenolone 16alpha-carbonitrile and rifampicin (PXR), and clofibric acid (PPAR) have now been established.	Phenobarbital	235-248	CXADR pseudogene 1	Homo sapiens	74-77
10462436-3	1999	Roles for three "orphan" nuclear receptor superfamily members, designated CAR, PXR, and PPAR, in respectively mediating the induction of hepatic P450s belonging to families CYP2, CYP3, and CYP4 in response to the prototypical inducers phenobarbital (CAR), pregnenolone 16alpha-carbonitrile and rifampicin (PXR), and clofibric acid (PPAR) have now been established.	Phenobarbital	235-248	nuclear receptor subfamily 1 group I member 2	Homo sapiens	79-82
10462436-3	1999	Roles for three "orphan" nuclear receptor superfamily members, designated CAR, PXR, and PPAR, in respectively mediating the induction of hepatic P450s belonging to families CYP2, CYP3, and CYP4 in response to the prototypical inducers phenobarbital (CAR), pregnenolone 16alpha-carbonitrile and rifampicin (PXR), and clofibric acid (PPAR) have now been established.	Phenobarbital	235-248	peroxisome proliferator activated receptor alpha	Homo sapiens	88-92
10550479-9	1999	These results suggest that the CYP 2B1/2 induction and Cx32 decrease in centrilobular hepatocytes, similarly to those thought to be involved in the hepatic promotion mechanism of phenobarbital, may also play important roles in clofibrate actions in the liver, in addition to its causation of oxidative DNA injury.	Phenobarbital	179-192	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	31-38
10550479-9	1999	These results suggest that the CYP 2B1/2 induction and Cx32 decrease in centrilobular hepatocytes, similarly to those thought to be involved in the hepatic promotion mechanism of phenobarbital, may also play important roles in clofibrate actions in the liver, in addition to its causation of oxidative DNA injury.	Phenobarbital	179-192	gap junction protein, beta 1	Rattus norvegicus	55-59
10462436-3	1999	Roles for three "orphan" nuclear receptor superfamily members, designated CAR, PXR, and PPAR, in respectively mediating the induction of hepatic P450s belonging to families CYP2, CYP3, and CYP4 in response to the prototypical inducers phenobarbital (CAR), pregnenolone 16alpha-carbonitrile and rifampicin (PXR), and clofibric acid (PPAR) have now been established.	Phenobarbital	235-248	peptidylprolyl isomerase F	Homo sapiens	179-183
10462436-3	1999	Roles for three "orphan" nuclear receptor superfamily members, designated CAR, PXR, and PPAR, in respectively mediating the induction of hepatic P450s belonging to families CYP2, CYP3, and CYP4 in response to the prototypical inducers phenobarbital (CAR), pregnenolone 16alpha-carbonitrile and rifampicin (PXR), and clofibric acid (PPAR) have now been established.	Phenobarbital	235-248	CXADR pseudogene 1	Homo sapiens	250-253
10462436-3	1999	Roles for three "orphan" nuclear receptor superfamily members, designated CAR, PXR, and PPAR, in respectively mediating the induction of hepatic P450s belonging to families CYP2, CYP3, and CYP4 in response to the prototypical inducers phenobarbital (CAR), pregnenolone 16alpha-carbonitrile and rifampicin (PXR), and clofibric acid (PPAR) have now been established.	Phenobarbital	235-248	nuclear receptor subfamily 1 group I member 2	Homo sapiens	306-309
10462436-3	1999	Roles for three "orphan" nuclear receptor superfamily members, designated CAR, PXR, and PPAR, in respectively mediating the induction of hepatic P450s belonging to families CYP2, CYP3, and CYP4 in response to the prototypical inducers phenobarbital (CAR), pregnenolone 16alpha-carbonitrile and rifampicin (PXR), and clofibric acid (PPAR) have now been established.	Phenobarbital	235-248	peroxisome proliferator activated receptor alpha	Homo sapiens	332-336
10462443-1	1999	The effect of the synthetic glucocorticoid, dexamethasone, and phenobarbital upon the expression of Cyp2b9 and Cyp2b10, major CYP2B subfamilies in the mouse, was differentiated in C57BL/6 mouse liver and hepatocytes in primary culture.	Phenobarbital	63-76	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	100-106
10462443-1	1999	The effect of the synthetic glucocorticoid, dexamethasone, and phenobarbital upon the expression of Cyp2b9 and Cyp2b10, major CYP2B subfamilies in the mouse, was differentiated in C57BL/6 mouse liver and hepatocytes in primary culture.	Phenobarbital	63-76	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	111-118
10462443-1	1999	The effect of the synthetic glucocorticoid, dexamethasone, and phenobarbital upon the expression of Cyp2b9 and Cyp2b10, major CYP2B subfamilies in the mouse, was differentiated in C57BL/6 mouse liver and hepatocytes in primary culture.	Phenobarbital	63-76	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	126-131
10462443-4	1999	Phenobarbital increased Cyp2b10 expression more than did Cyp2b9 in both sexes.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	24-31
10460800-4	1999	NNAL glucuronidation was induced in liver microsomes from rats treated with family 2 UGT inducers including phenobarbitol and 3, 5-di-tert-butyl-4-hydroxytoluene, which exhibited 1.7- and 2.6-fold higher rates of glucuronidation than microsomes from control rats.	Phenobarbital	108-121	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	85-88
10460791-10	1999	PB treatment in female rats resulted in a 5-fold increase in N-AIAPP formation, showing that CYP2B1/2 were also susceptible to N-alkylation mediated by AIA.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	93-99
10460791-4	1999	Phenobarbital (PB) pretreatment, which induces CYP2B1/2 and 3A1/2 in male rats, increased N-vinylPP formation after TTMS administration.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	47-53
10460791-4	1999	Phenobarbital (PB) pretreatment, which induces CYP2B1/2 and 3A1/2 in male rats, increased N-vinylPP formation after TTMS administration.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	47-53
10460791-6	1999	This conclusion was supported by demonstrating a 15-fold increase in TTMSinduced N-vinylPP formation in female rats after CYP2B1/2 induction with PB pretreatment.	Phenobarbital	146-148	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	122-128
10454578-0	1999	Phenobarbital-responsive nuclear translocation of the receptor CAR in induction of the CYP2B gene.	Phenobarbital	0-13	nuclear receptor subfamily 1, group I, member 3	Mus musculus	63-66
10454503-1	1999	Several of the hepatic microsomal cytochromes P-450 (CYP) including CYP3A are inducible by phenobarbital (PB).	Phenobarbital	91-104	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	68-73
10454503-1	1999	Several of the hepatic microsomal cytochromes P-450 (CYP) including CYP3A are inducible by phenobarbital (PB).	Phenobarbital	106-108	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	68-73
10454503-2	1999	However, the intracellular pathways involved in the action of PB on CYP3A remain poorly known.	Phenobarbital	62-64	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	68-73
10454503-3	1999	With the aim to unravel some of the main aspects of PB signaling, we first devised a simple model of mouse cultured primary hepatocytes in which CYP3A mRNA and protein were strongly induced by PB in the absence of dexamethasone and were at maximum levels after a 48-h treatment with a 2-mM dose of PB.	Phenobarbital	52-54	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	145-150
10454503-3	1999	With the aim to unravel some of the main aspects of PB signaling, we first devised a simple model of mouse cultured primary hepatocytes in which CYP3A mRNA and protein were strongly induced by PB in the absence of dexamethasone and were at maximum levels after a 48-h treatment with a 2-mM dose of PB.	Phenobarbital	193-195	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	145-150
10454503-3	1999	With the aim to unravel some of the main aspects of PB signaling, we first devised a simple model of mouse cultured primary hepatocytes in which CYP3A mRNA and protein were strongly induced by PB in the absence of dexamethasone and were at maximum levels after a 48-h treatment with a 2-mM dose of PB.	Phenobarbital	193-195	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	145-150
10454503-4	1999	Under these culture conditions, we studied the effects of inhibitors and activators of different protein kinases or phosphatases on CYP3A mRNA and protein induction by PB.	Phenobarbital	168-170	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	132-137
10454503-7	1999	Inhibition of Ca(2+)/calmodulin-dependent protein kinase by KN-62 or the intracellular Ca(2+) chelator BAPTA-AM produced an inhibition of CYP3A induction by PB.	Phenobarbital	157-159	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	138-143
10454503-9	1999	Taken together, our results suggest that CYP3A induction by PB is regulated positively by calmodulin-dependent protein kinase and cGMP-dependent protein kinase, and negatively by PKA in mouse hepatocytes in primary culture.	Phenobarbital	60-62	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	41-46
10454578-0	1999	Phenobarbital-responsive nuclear translocation of the receptor CAR in induction of the CYP2B gene.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	87-92
10454578-1	1999	The constitutively active receptor (CAR) transactivates a distal enhancer called the phenobarbital (PB)-responsive enhancer module (PBREM) found in PB-inducible CYP2B genes.	Phenobarbital	85-98	nuclear receptor subfamily 1, group I, member 3	Mus musculus	36-39
10454578-1	1999	The constitutively active receptor (CAR) transactivates a distal enhancer called the phenobarbital (PB)-responsive enhancer module (PBREM) found in PB-inducible CYP2B genes.	Phenobarbital	85-98	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	161-166
10454578-1	1999	The constitutively active receptor (CAR) transactivates a distal enhancer called the phenobarbital (PB)-responsive enhancer module (PBREM) found in PB-inducible CYP2B genes.	Phenobarbital	100-102	nuclear receptor subfamily 1, group I, member 3	Mus musculus	36-39
10454578-1	1999	The constitutively active receptor (CAR) transactivates a distal enhancer called the phenobarbital (PB)-responsive enhancer module (PBREM) found in PB-inducible CYP2B genes.	Phenobarbital	100-102	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	161-166
10454578-1	1999	The constitutively active receptor (CAR) transactivates a distal enhancer called the phenobarbital (PB)-responsive enhancer module (PBREM) found in PB-inducible CYP2B genes.	Phenobarbital	132-134	nuclear receptor subfamily 1, group I, member 3	Mus musculus	36-39
10454578-1	1999	The constitutively active receptor (CAR) transactivates a distal enhancer called the phenobarbital (PB)-responsive enhancer module (PBREM) found in PB-inducible CYP2B genes.	Phenobarbital	132-134	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	161-166
10454578-2	1999	CAR dramatically increases its binding to PBREM in livers of PB-treated mice.	Phenobarbital	42-44	nuclear receptor subfamily 1, group I, member 3	Mus musculus	0-3
10454578-3	1999	We have investigated the cellular mechanism of PB-induced increase of CAR binding.	Phenobarbital	47-49	nuclear receptor subfamily 1, group I, member 3	Mus musculus	70-73
10454578-4	1999	Western blot analyses of mouse livers revealed an extensive nuclear accumulation of CAR following PB treatment.	Phenobarbital	98-100	nuclear receptor subfamily 1, group I, member 3	Mus musculus	84-87
10454578-6	1999	PB-elicited nuclear accumulation of CAR appears to be a general step regulating the induction of CYP2B genes, since treatments with other PB-type inducers result in the same nuclear accumulation of CAR.	Phenobarbital	0-2	nuclear receptor subfamily 1, group I, member 3	Mus musculus	36-39
10454578-6	1999	PB-elicited nuclear accumulation of CAR appears to be a general step regulating the induction of CYP2B genes, since treatments with other PB-type inducers result in the same nuclear accumulation of CAR.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	97-102
10454578-6	1999	PB-elicited nuclear accumulation of CAR appears to be a general step regulating the induction of CYP2B genes, since treatments with other PB-type inducers result in the same nuclear accumulation of CAR.	Phenobarbital	0-2	nuclear receptor subfamily 1, group I, member 3	Mus musculus	198-201
10454578-7	1999	Both immunoprecipitation and immunohistochemistry studies show cytoplasmic localization of CAR in the livers of nontreated mice, indicating that CAR translocates into nuclei following PB treatment.	Phenobarbital	184-186	nuclear receptor subfamily 1, group I, member 3	Mus musculus	91-94
10454578-7	1999	Both immunoprecipitation and immunohistochemistry studies show cytoplasmic localization of CAR in the livers of nontreated mice, indicating that CAR translocates into nuclei following PB treatment.	Phenobarbital	184-186	nuclear receptor subfamily 1, group I, member 3	Mus musculus	145-148
10454578-9	1999	Thus, the CAR-mediated transactivation of PBREM in vivo becomes PB responsive through an okadaic acid-sensitive nuclear translocation process.	Phenobarbital	42-44	nuclear receptor subfamily 1, group I, member 3	Mus musculus	10-13
10423399-0	1999	Cis-acting sequences from the rat cytochrome P450 2B1 gene confer pulmonary and phenobarbital-inducible expression in transgenic mice.	Phenobarbital	80-93	cytochrome P450 2B1	Rattus norvegicus	34-53
10423399-4	1999	The constitutive expression of CYP2B1 and CYP2B2 in liver is low, but inducible by PB, whereas the pulmonary expression of CYP2B1 is not induced by PB.	Phenobarbital	83-85	cytochrome P450 2B1	Rattus norvegicus	31-37
10423399-4	1999	The constitutive expression of CYP2B1 and CYP2B2 in liver is low, but inducible by PB, whereas the pulmonary expression of CYP2B1 is not induced by PB.	Phenobarbital	83-85	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	42-48
10486655-9	1999	Following explanation can be hypothesis: several antihypertensive drugs are liver-metabolised by microsomal cytochrome P450 3A4 isoform that could explain a significantly decreased half-life in association with enzymatic inducers, such as rifampicine or antiepileptic drugs (phenobarbital, phenytoin or carbamazepine).	Phenobarbital	275-288	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	108-127
10426811-4	1999	Acute treatment of B6C3F1 mice with phenobarbital resulted in increased levels of bcl-2 and decreased levels of bax protein, while acute treatment with WY-14,643 resulted in increased bcl-2 and BAG-1 protein in the liver.	Phenobarbital	36-49	B cell leukemia/lymphoma 2	Mus musculus	82-87
10426785-0	1999	Effect of lindane and phenobarbital on cyclooxygenase-2 expression and prostanoid synthesis by Kupffer cells.	Phenobarbital	22-35	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	39-55
10426811-4	1999	Acute treatment of B6C3F1 mice with phenobarbital resulted in increased levels of bcl-2 and decreased levels of bax protein, while acute treatment with WY-14,643 resulted in increased bcl-2 and BAG-1 protein in the liver.	Phenobarbital	36-49	BCL2-associated X protein	Mus musculus	112-115
10426785-5	1999	Similarly, PB, which shares several effects with lindane in rat liver, also clearly induced COX-2.	Phenobarbital	11-13	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	92-97
10553719-12	1999	Both the demethylation and the denitrosation of tauromustine were increased 3-fold in liver microsomes from rat pretreated with phenobarbital, whereas treatment with cyanopregnenolone enhanced the denitrosation 11-fold, indicating the involvement of CYP3A.	Phenobarbital	128-141	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	250-255
10449034-7	1999	Phenobarbital, a potent liver tumor promoter, inhibited apoptosis in c-myc hepatocytes but not in wild-type hepatocytes, decreased p53 and bax, and increased bcl-2 protein levels.	Phenobarbital	0-13	transformation related protein 53, pseudogene	Mus musculus	131-134
10449034-7	1999	Phenobarbital, a potent liver tumor promoter, inhibited apoptosis in c-myc hepatocytes but not in wild-type hepatocytes, decreased p53 and bax, and increased bcl-2 protein levels.	Phenobarbital	0-13	BCL2-associated X protein	Mus musculus	139-142
10449034-7	1999	Phenobarbital, a potent liver tumor promoter, inhibited apoptosis in c-myc hepatocytes but not in wild-type hepatocytes, decreased p53 and bax, and increased bcl-2 protein levels.	Phenobarbital	0-13	B cell leukemia/lymphoma 2	Mus musculus	158-163
10462055-1	1999	Exposure to benzene was recently reported to lower the cytochrome P450 (CYP) content in phenobarbital-pretreated rats in vivo (Gut et al., Environ.	Phenobarbital	88-101	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	55-70
10462055-1	1999	Exposure to benzene was recently reported to lower the cytochrome P450 (CYP) content in phenobarbital-pretreated rats in vivo (Gut et al., Environ.	Phenobarbital	88-101	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	72-75
10447669-0	1999	Modulation of murine phenobarbital-inducible CYP2A5, CYP2B10 and CYP1A enzymes by inhibitors of protein kinases and phosphatases.	Phenobarbital	21-34	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	45-51
10447669-0	1999	Modulation of murine phenobarbital-inducible CYP2A5, CYP2B10 and CYP1A enzymes by inhibitors of protein kinases and phosphatases.	Phenobarbital	21-34	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	53-60
10447669-2	1999	In this study, the involvement of several protein kinase and phosphatase pathways on constitutive and phenobarbital-induced activities of CYP2A5, CYP2B10 and CYP1A1/2 in primary mouse hepatocytes was determined using well-defined chemical modulators of intracellular protein phosphorylation and desphosphorylation events.	Phenobarbital	102-115	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	138-144
10447669-2	1999	In this study, the involvement of several protein kinase and phosphatase pathways on constitutive and phenobarbital-induced activities of CYP2A5, CYP2B10 and CYP1A1/2 in primary mouse hepatocytes was determined using well-defined chemical modulators of intracellular protein phosphorylation and desphosphorylation events.	Phenobarbital	102-115	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	146-153
10447669-2	1999	In this study, the involvement of several protein kinase and phosphatase pathways on constitutive and phenobarbital-induced activities of CYP2A5, CYP2B10 and CYP1A1/2 in primary mouse hepatocytes was determined using well-defined chemical modulators of intracellular protein phosphorylation and desphosphorylation events.	Phenobarbital	102-115	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	158-164
10447669-3	1999	A 48-h treatment of the hepatocytes with 2-aminopurine, a nonspecific serine/threonine kinase inhibitor, elicited dose-dependent increases in both basal and phenobarbital-induced CYP2A5 catalytic activity (assayed as coumarin 7-hydroxylation), the maximal induction being 60-fold greater than the control value upon cotreatment with 1.5 mM phenobarbital and 10 mM 2-aminopurine.	Phenobarbital	157-170	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	179-185
10447669-3	1999	A 48-h treatment of the hepatocytes with 2-aminopurine, a nonspecific serine/threonine kinase inhibitor, elicited dose-dependent increases in both basal and phenobarbital-induced CYP2A5 catalytic activity (assayed as coumarin 7-hydroxylation), the maximal induction being 60-fold greater than the control value upon cotreatment with 1.5 mM phenobarbital and 10 mM 2-aminopurine.	Phenobarbital	340-353	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	179-185
10447669-4	1999	In contrast, phenobarbital induction of CYP2B10 (pentoxyresorufin O-deethylase) and CYP1A1/2 (ethoxyresorufin O-deethylase) activities were blocked by 2-aminopurine.	Phenobarbital	13-26	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	40-47
10447669-4	1999	In contrast, phenobarbital induction of CYP2B10 (pentoxyresorufin O-deethylase) and CYP1A1/2 (ethoxyresorufin O-deethylase) activities were blocked by 2-aminopurine.	Phenobarbital	13-26	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	84-92
10447669-7	1999	The serine/threonine phosphatase inhibitors tautomycin, calyculin A and okadaic acid all reduced both basal and phenobarbital-induced CYP2A5, CYP2B10 and CYP1A1/2 activities.	Phenobarbital	112-125	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	134-140
10447669-7	1999	The serine/threonine phosphatase inhibitors tautomycin, calyculin A and okadaic acid all reduced both basal and phenobarbital-induced CYP2A5, CYP2B10 and CYP1A1/2 activities.	Phenobarbital	112-125	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	142-149
10447669-7	1999	The serine/threonine phosphatase inhibitors tautomycin, calyculin A and okadaic acid all reduced both basal and phenobarbital-induced CYP2A5, CYP2B10 and CYP1A1/2 activities.	Phenobarbital	112-125	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	154-160
10454249-6	1999	In animals given PB, eosinophilic swelling of hepatocytes was prominent, and the hepatocytes showed strongly positive reactions for CYP 1A1 and 3A2.	Phenobarbital	17-19	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	132-139
10423176-7	1999	In microsomes from mice pretreated with phenobarbital (a CYP2B-selective inducer), 3-methylcholanthrene (a CYP1A-selective inducer), pregnenolone-16alpha-carbonitrile (a CYP3A-selective inducer), and EtOH (a CYP2E-selective inducer), an increase in the rates of oxidation was seen only in microsomes from EtOH-treated animals.	Phenobarbital	40-53	ATPase, H+ transporting, lysosomal accessory protein 1	Mus musculus	146-153
10403793-0	1999	EGF-Induced receptor autophosphorylation in primary hepatocytes isolated from phenobarbitone-treated mice.	Phenobarbital	78-92	epidermal growth factor	Mus musculus	0-3
10403793-2	1999	Here, epidermal growth factor receptor (EGFR) expression and receptor autophosphorylation was determined in hepatocytes isolated from control and PB-treated mice.	Phenobarbital	146-148	epidermal growth factor receptor	Mus musculus	6-38
10403793-3	1999	There was a decrease in the level of EGFR expression in hepatocytes isolated from mice following PB administration when compared to controls.	Phenobarbital	97-99	epidermal growth factor receptor	Mus musculus	37-41
10403793-5	1999	Following PB treatment, the degree of basal receptor phosphorylation (in the absence of EGF) was significantly greater and therefore the fold rise in EGFR phosphorylation in isolated hepatocytes was lower than in controls.	Phenobarbital	10-12	epidermal growth factor receptor	Mus musculus	150-154
10385683-0	1999	Mimicry in primary rat hepatocyte cultures of the in vivo perivenous induction by phenobarbital of cytochrome P-450 2B1 mRNA: role of epidermal growth factor and perivenous oxygen tension.	Phenobarbital	82-95	cytochrome P450 2B1	Rattus norvegicus	99-119
10385683-1	1999	Treatment of male rats with phenobarbital (PB) results in a perivenous and mid-zonal pattern of cytochrome P-450 (CYP)2B1 mRNA expression within the liver acinus.	Phenobarbital	28-41	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	96-121
10385683-1	1999	Treatment of male rats with phenobarbital (PB) results in a perivenous and mid-zonal pattern of cytochrome P-450 (CYP)2B1 mRNA expression within the liver acinus.	Phenobarbital	43-45	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	96-121
10385683-6	1999	Within 3 days, phenobarbital induced CYP2B1 mRNA to maximal levels under arterial pO2 and to about 40% of maximal levels under venous pO2.	Phenobarbital	15-28	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	37-43
10385683-8	1999	EGF suppressed CYP2B1 mRNA induction by PB only under arterial but not under venous pO2, whereas GH, T4, and T3 inhibited induction under both arterial and venous pO2.	Phenobarbital	40-42	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	15-21
10385683-9	1999	Thus, in hepatocyte cultures, an O2 gradient in conjunction with EGF mimicked the perivenous induction by PB of the CYP2B1 gene observed in the liver in vivo.	Phenobarbital	106-108	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	116-122
10547882-0	1999	[Change in the rat liver microsomal monooxygenase system upon induction with phenobarbital in acute pancreatitis].	Phenobarbital	77-90	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	25-49
10547882-1	1999	While injecting phenobarbital (PB) into the rats, on the second day of an experimental pancreatitis, cytochrome P450 2B1 and 2C6 activities were found, on the forth day of disease, as being considerably higher in comparison with data obtained in sham-operated control animals.	Phenobarbital	16-29	cytochrome P450 2B1	Rattus norvegicus	101-128
10547882-1	1999	While injecting phenobarbital (PB) into the rats, on the second day of an experimental pancreatitis, cytochrome P450 2B1 and 2C6 activities were found, on the forth day of disease, as being considerably higher in comparison with data obtained in sham-operated control animals.	Phenobarbital	31-33	cytochrome P450 2B1	Rattus norvegicus	101-128
10348806-3	1999	The major phenobarbital-inducible form of cytochrome P-450 in male rat liver microsomes, CYP2B1, is capable of catalyzing O-dealkylations.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	42-58
10373399-2	1999	Pretreatment with phenobarbital (PB), 3-methylcholanthrene (3MC), and PB plus 3MC elicited significant induction of multiple CYP enzymes in alligator, as detected by antibodies to CYP1A, CYP2B, CYP2C, CYP2E, CYP2K, and CYP3A.	Phenobarbital	18-31	cytochrome P450 3A21	Alligator mississippiensis	219-224
10373399-2	1999	Pretreatment with phenobarbital (PB), 3-methylcholanthrene (3MC), and PB plus 3MC elicited significant induction of multiple CYP enzymes in alligator, as detected by antibodies to CYP1A, CYP2B, CYP2C, CYP2E, CYP2K, and CYP3A.	Phenobarbital	70-72	cytochrome P450 3A21	Alligator mississippiensis	219-224
10418970-13	1999	In contrast, cells that had been preincubated prior to freezing had an excellent plating efficiency (approximately 60%) and responded to classical CYP inducers dexamethasone, beta-naphthoflavone and phenobarbital in a manner indistinguishable from that of fresh hepatocytes.	Phenobarbital	199-212	peptidylprolyl isomerase G	Homo sapiens	147-150
10348806-3	1999	The major phenobarbital-inducible form of cytochrome P-450 in male rat liver microsomes, CYP2B1, is capable of catalyzing O-dealkylations.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	89-95
10433360-6	1999	IL-1beta inhibited both allylisopropylamide- and phenobarbital-inducible delta-ALAS activities in the liver.	Phenobarbital	49-62	interleukin 1 beta	Rattus norvegicus	0-8
10433360-6	1999	IL-1beta inhibited both allylisopropylamide- and phenobarbital-inducible delta-ALAS activities in the liver.	Phenobarbital	49-62	5'-aminolevulinate synthase 1	Rattus norvegicus	79-83
10405987-6	1999	The cytochrome P-450 content increased by 34.5% in phenobarbital treated female rats in the age of 12 months in comparison with control animals.	Phenobarbital	51-64	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	4-20
10336559-6	1999	Moreover, phenobarbital, an inducer of hepatic CYP4B1 in the rabbit, also induced 12-HETE and 12-HETrE synthesis.	Phenobarbital	10-23	cytochrome P450 4B1	Oryctolagus cuniculus	47-53
10336559-7	1999	Antibodies against CYP4B1, but not against CYP4A1, inhibited hypoxia-, clofibrate-, and phenobarbital-induced 12-HETE and 12-HETrE synthesis.	Phenobarbital	88-101	cytochrome P450 4B1	Oryctolagus cuniculus	19-25
10471061-11	1999	We also found that CYP2B6 is induced at protein and mRNA levels by phenobarbital (2 mM) and cyclophosphamide (1 mM), an anticancer drug known to be metabolized by CYP2B6.	Phenobarbital	67-80	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	19-25
10471061-11	1999	We also found that CYP2B6 is induced at protein and mRNA levels by phenobarbital (2 mM) and cyclophosphamide (1 mM), an anticancer drug known to be metabolized by CYP2B6.	Phenobarbital	67-80	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	163-169
10215695-3	1999	In the present study, we examined the effects of insulin on pyridine-, phenobarbital-, and ciprofibrate-mediated expression of CYP2E1, CYP2B, CYP3A, and CYP4A in primary cultured rat hepatocytes.	Phenobarbital	71-84	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	127-133
10403658-0	1999	The UDP-glucuronyltransferase inducers, phenobarbital and pregnenolone-16alpha-carbonitrile, enhance thyroid-follicular cell apoptosis: association with TGF-beta1 expression.	Phenobarbital	40-53	transforming growth factor, beta 1	Rattus norvegicus	153-162
10403658-12	1999	In PB- and PCN-treated rats, a moderate increase in apoptosis coincided with similar increases in TGF-beta1 immunoreactive thyroid-follicular cells.	Phenobarbital	3-5	transforming growth factor, beta 1	Rattus norvegicus	98-107
10403658-13	1999	In summary, PB and PCN increase apoptosis and the percentage of TGF-beta1 positive thyroid-follicular cells.	Phenobarbital	12-14	transforming growth factor, beta 1	Rattus norvegicus	64-73
10796078-0	1999	Positive regulation of the rat CYP2B2 phenobarbital response unit by the nuclear receptor hexamer half-site.nuclear factor 1 complex.	Phenobarbital	38-51	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	31-37
10796078-1	1999	A distal 163-bp fragment mediates phenobarbital responsiveness of the rat CYP2B2 gene.	Phenobarbital	34-47	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	74-80
10796078-6	1999	We introduced into the rat CYP2B2 hexamer half-site the specific mutational change previously introduced into the Cyp2b10 sequence, where its effect was to increase the basal level of expression and to abolish phenobarbital responsiveness.	Phenobarbital	210-223	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	27-33
10796078-6	1999	We introduced into the rat CYP2B2 hexamer half-site the specific mutational change previously introduced into the Cyp2b10 sequence, where its effect was to increase the basal level of expression and to abolish phenobarbital responsiveness.	Phenobarbital	210-223	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	114-121
10220487-5	1999	Phenobarbital, 3-methylcholanthrene, and clofibrate enhanced the glucuronidation of LF 4.0212 on positions 2, 3, and 4 of the thioxyloside ring, thus indicating that several UGT isoforms were involved in this process.	Phenobarbital	0-13	beta-1,3-glucuronyltransferase 2	Homo sapiens	174-177
10215695-3	1999	In the present study, we examined the effects of insulin on pyridine-, phenobarbital-, and ciprofibrate-mediated expression of CYP2E1, CYP2B, CYP3A, and CYP4A in primary cultured rat hepatocytes.	Phenobarbital	71-84	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	142-147
10215695-9	1999	Omitting insulin from the medium resulted in a 50% decrease in CYP3A mRNA levels in response to phenobarbital treatment and a 30% decrease in CYP4A mRNA levels in response to ciprofibrate treatment, relative to the level obtained in response to these treatments in the presence of 1 microM insulin.	Phenobarbital	96-109	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	63-68
9890442-3	1999	Culturing in the absence of insulin produced 1.5-2-fold increases in the induction magnitude of CYP2B1 and CYP2B2 mRNA expression resulting from PB exposures, without altering the bell-shaped dose-response curve characteristic of this agent.	Phenobarbital	145-147	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	96-102
10378774-4	1999	32P-postlabeling analysis of dAp and dGp, which were modified by NMA activated with microsomes of rats pretreated with phenobarbital (PB), and directly labeled resulted in each case in the appearance of one single adduct spot.	Phenobarbital	119-132	dacapo	Drosophila melanogaster	29-32
10378774-4	1999	32P-postlabeling analysis of dAp and dGp, which were modified by NMA activated with microsomes of rats pretreated with phenobarbital (PB), and directly labeled resulted in each case in the appearance of one single adduct spot.	Phenobarbital	134-136	dacapo	Drosophila melanogaster	29-32
10207164-5	1999	PBGD-deficient mice (PBGD-/-) imitate acute porphyria through massive induction of hepatic delta-aminolevulinic acid synthase by drugs such as phenobarbital.	Phenobarbital	143-156	hydroxymethylbilane synthase	Mus musculus	0-4
10072770-0	1999	Phenobarbital responsiveness conferred by the 5"-flanking region of the rat CYP2B2 gene in transgenic mice.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	76-82
10072770-5	1999	DNA affinity enrichment techniques and immunoblotting and electromobility shift assays were used to determine that nuclear factor 1 (NF-1) interacts strongly with a site centered at -2200bp in the PB responsive unit (PBRU) of CYP2B2.	Phenobarbital	197-199	neurofibromin 1	Mus musculus	133-137
10072770-6	1999	To test the functional contribution of NF-1 in PB activation, we introduced specific mutations within the PBRU NF-1 element and demonstrated that these mutations completely ablate the binding interaction.	Phenobarbital	47-49	neurofibromin 1	Mus musculus	39-43
10072770-7	1999	However, transgenic mice incorporating the mutant NF-1 sequence within an otherwise wild-type -2500/CYP2B2 transgene maintained full PB responsiveness.	Phenobarbital	133-135	neurofibromin 1	Mus musculus	50-54
10064569-0	1999	Induction of CYP1A2 by phenobarbital in the livers of aryl hydrocarbon-responsive and -nonresponsive mice.	Phenobarbital	23-36	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	13-19
10064569-1	1999	The effects of phenobarbital treatment on the expression of the cytochrome P-450 (CYP or P-450) enzyme CYP1A2 in the livers of mice of various strains were examined.	Phenobarbital	15-28	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	103-109
10064569-3	1999	The induction of CYP2B10, which is known as a phenobarbital-inducible P-450 in mice, was prominent in the livers of all five strains examined, whereas clear inductive effects on the P-450 CYP2B9 were not observed in female C57BL/6 and female DBA/2NCrj mice.	Phenobarbital	46-59	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	17-24
10064569-4	1999	These results indicate that CYP1A2 is a member of the family of phenobarbital-inducible genes in mice and suggest that the aryl hydrocarbon receptor-dependent induction pathway is not involved in the induction of CYP1A2.	Phenobarbital	64-77	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	28-34
10064569-8	1999	1-fold), suggesting that the induction of CYP1A2 by phenobarbital is mainly determined at a pretranslational level.	Phenobarbital	52-65	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	42-48
10219967-9	1999	Induction of CYP3A4-dependent reporter gene expression and enhancement of the induction by the glucocorticoid receptor was also observed with pregnenolone-16alpha-carbonitrile (PCN), rifampicin, phenytoin, carbamazepine, phenylbutazone and phenobarbitone, all known in vivo inducers of CYP3A4 in man.	Phenobarbital	240-254	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	13-19
10219967-9	1999	Induction of CYP3A4-dependent reporter gene expression and enhancement of the induction by the glucocorticoid receptor was also observed with pregnenolone-16alpha-carbonitrile (PCN), rifampicin, phenytoin, carbamazepine, phenylbutazone and phenobarbitone, all known in vivo inducers of CYP3A4 in man.	Phenobarbital	240-254	nuclear receptor subfamily 3 group C member 1	Homo sapiens	95-118
10096772-8	1999	The simultaneous treatment of the cocultures with phenobarbital and LPS (10 ng/ml) or 3-methylcholanthrene and LPS (10 ng/ml) resulted in a strong down-regulation (85%) of the phenobarbital-induced cytochrome P450 (CYP) isoform CYP2B1 in the hepatocytes whereas the 3-methylcholanthrene-induced isoform CYP1A1 was only weakly affected (15%).	Phenobarbital	50-63	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	198-213
10096772-8	1999	The simultaneous treatment of the cocultures with phenobarbital and LPS (10 ng/ml) or 3-methylcholanthrene and LPS (10 ng/ml) resulted in a strong down-regulation (85%) of the phenobarbital-induced cytochrome P450 (CYP) isoform CYP2B1 in the hepatocytes whereas the 3-methylcholanthrene-induced isoform CYP1A1 was only weakly affected (15%).	Phenobarbital	50-63	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	215-218
10096772-8	1999	The simultaneous treatment of the cocultures with phenobarbital and LPS (10 ng/ml) or 3-methylcholanthrene and LPS (10 ng/ml) resulted in a strong down-regulation (85%) of the phenobarbital-induced cytochrome P450 (CYP) isoform CYP2B1 in the hepatocytes whereas the 3-methylcholanthrene-induced isoform CYP1A1 was only weakly affected (15%).	Phenobarbital	50-63	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	228-234
10096772-8	1999	The simultaneous treatment of the cocultures with phenobarbital and LPS (10 ng/ml) or 3-methylcholanthrene and LPS (10 ng/ml) resulted in a strong down-regulation (85%) of the phenobarbital-induced cytochrome P450 (CYP) isoform CYP2B1 in the hepatocytes whereas the 3-methylcholanthrene-induced isoform CYP1A1 was only weakly affected (15%).	Phenobarbital	50-63	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	303-309
10096772-8	1999	The simultaneous treatment of the cocultures with phenobarbital and LPS (10 ng/ml) or 3-methylcholanthrene and LPS (10 ng/ml) resulted in a strong down-regulation (85%) of the phenobarbital-induced cytochrome P450 (CYP) isoform CYP2B1 in the hepatocytes whereas the 3-methylcholanthrene-induced isoform CYP1A1 was only weakly affected (15%).	Phenobarbital	176-189	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	198-213
10096772-8	1999	The simultaneous treatment of the cocultures with phenobarbital and LPS (10 ng/ml) or 3-methylcholanthrene and LPS (10 ng/ml) resulted in a strong down-regulation (85%) of the phenobarbital-induced cytochrome P450 (CYP) isoform CYP2B1 in the hepatocytes whereas the 3-methylcholanthrene-induced isoform CYP1A1 was only weakly affected (15%).	Phenobarbital	176-189	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	215-218
10096772-8	1999	The simultaneous treatment of the cocultures with phenobarbital and LPS (10 ng/ml) or 3-methylcholanthrene and LPS (10 ng/ml) resulted in a strong down-regulation (85%) of the phenobarbital-induced cytochrome P450 (CYP) isoform CYP2B1 in the hepatocytes whereas the 3-methylcholanthrene-induced isoform CYP1A1 was only weakly affected (15%).	Phenobarbital	176-189	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	228-234
10096772-8	1999	The simultaneous treatment of the cocultures with phenobarbital and LPS (10 ng/ml) or 3-methylcholanthrene and LPS (10 ng/ml) resulted in a strong down-regulation (85%) of the phenobarbital-induced cytochrome P450 (CYP) isoform CYP2B1 in the hepatocytes whereas the 3-methylcholanthrene-induced isoform CYP1A1 was only weakly affected (15%).	Phenobarbital	176-189	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	303-309
10036213-2	1999	CLO, PB, and PCN induced histological liver hypertrophy, increases in liver weights, in microsomal protein and cytochrome P450 contents as well as increases in specific UGT activities.	Phenobarbital	5-7	solute carrier family 35 (UDP-galactose transporter), member A2	Mus musculus	169-172
9927535-3	1999	PURPOSE: To examine the effect of long-term administration of phenobarbital in liver regeneration after HTX with regard to CCl4-induced cirrhotic rat model.	Phenobarbital	62-75	C-C motif chemokine ligand 4	Rattus norvegicus	123-127
10096431-0	1999	c-fos gene expression in rat liver is induced by phenobarbital.	Phenobarbital	49-62	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
10096431-3	1999	Gene expression, determined by the mRNA level, and FOS protein were increased after 52 weeks of treatment in arylamine initiated as well as in phenobarbital only treated animals.	Phenobarbital	143-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	51-54
10096431-4	1999	Expression of c-fos seems to be a phenobarbital induced effect that is independent of additional initiator treatments.	Phenobarbital	34-47	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-19
10096431-6	1999	The results indicate that phenobarbital, a widely used tumor promoter, induces c-fos expression.	Phenobarbital	26-39	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-84
9854036-11	1999	Mouse GSTT1 mRNA is induced in liver by phenobarbital, but not by butylated hydroxyanisole, beta-napthoflavone or isosafrole.	Phenobarbital	40-53	glutathione S-transferase, theta 1	Mus musculus	6-11
9862866-3	1999	AGP gene expression remained inducible by IL-1, IL-6, and phenobarbital (PB) in GH-treated hepatocytes.	Phenobarbital	73-75	gonadotropin releasing hormone receptor	Rattus norvegicus	80-82
10098905-8	1999	UGT 2B1 mRNA, typically induced by phenobarbital-like compounds, was not significantly affected.	Phenobarbital	35-48	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	0-7
10487415-10	1999	Although CYP2C8 has been shown to be phenobarbital inducible, neither a barbiturate-responsive regulatory sequence (a Barbie box) nor a phenobarbital-responsive enhancer module (PBREM) was found within the upstream region analyzed.	Phenobarbital	37-50	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	9-15
10379985-6	1999	Phenobarbitone induced (2-6-fold) coumarin 7-hydroxylase, cortisol 6beta-hydroxylase, S-mephenytoin N-demethylase, phenoxazone hydroxylase and benzyloxyresorufin O-dealkylase activities, but not the O-dealkylations of pentoxyresorufin or other alkoxyresorufins, in monkey.	Phenobarbital	0-14	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	34-56
10191271-3	1999	During the cloning process, an additional closely related gene was also isolated and named Aldh-pb, owing to its high amino acid sequence identity (92%) with the rat phenobarbitol-inducible ALDH protein (ALDH-PB).	Phenobarbital	166-179	aldehyde dehydrogenase family 1, subfamily A7	Rattus norvegicus	91-98
10191271-3	1999	During the cloning process, an additional closely related gene was also isolated and named Aldh-pb, owing to its high amino acid sequence identity (92%) with the rat phenobarbitol-inducible ALDH protein (ALDH-PB).	Phenobarbital	166-179	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	190-194
10191271-3	1999	During the cloning process, an additional closely related gene was also isolated and named Aldh-pb, owing to its high amino acid sequence identity (92%) with the rat phenobarbitol-inducible ALDH protein (ALDH-PB).	Phenobarbital	166-179	aldehyde dehydrogenase family 1, subfamily A7	Rattus norvegicus	204-211
10037683-0	1999	The repressed nuclear receptor CAR responds to phenobarbital in activating the human CYP2B6 gene.	Phenobarbital	47-60	CXADR pseudogene 1	Homo sapiens	31-34
10037683-0	1999	The repressed nuclear receptor CAR responds to phenobarbital in activating the human CYP2B6 gene.	Phenobarbital	47-60	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	85-91
10037683-1	1999	The endogenous CYP2B6 gene becomes phenobarbital (PB) inducible in androstenol-treated HepG2 cells either transiently or stably transfected with a nuclear receptor CAR expression vector.	Phenobarbital	35-48	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	15-21
10037683-1	1999	The endogenous CYP2B6 gene becomes phenobarbital (PB) inducible in androstenol-treated HepG2 cells either transiently or stably transfected with a nuclear receptor CAR expression vector.	Phenobarbital	35-48	CXADR pseudogene 1	Homo sapiens	164-167
10037683-1	1999	The endogenous CYP2B6 gene becomes phenobarbital (PB) inducible in androstenol-treated HepG2 cells either transiently or stably transfected with a nuclear receptor CAR expression vector.	Phenobarbital	50-52	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	15-21
10037683-1	1999	The endogenous CYP2B6 gene becomes phenobarbital (PB) inducible in androstenol-treated HepG2 cells either transiently or stably transfected with a nuclear receptor CAR expression vector.	Phenobarbital	50-52	CXADR pseudogene 1	Homo sapiens	164-167
10037683-4	1999	In a stably transfected HepG2 cell line, both PBREM and NR1 are activated by PB and PB-type compounds such as chlorinated pesticides, polychlorinated biphenyls and chlorpromazine.	Phenobarbital	77-79	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	56-59
10037683-6	1999	Thus, activation of the repressed nuclear receptor CAR appears to be a versatile mediator that regulates PB induction of the CYP2B and other genes.	Phenobarbital	105-107	CXADR pseudogene 1	Homo sapiens	51-54
10037683-6	1999	Thus, activation of the repressed nuclear receptor CAR appears to be a versatile mediator that regulates PB induction of the CYP2B and other genes.	Phenobarbital	105-107	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	125-130
10064562-1	1999	In the present study, we evaluated the inducibility of cytochrome P-450 (CYP) CYP1A, CYP2B, CYP3A, and CYP4A by beta-naphthoflavone, phenobarbital, dexamethasone, and clofibric acid, respectively, in primary hepatocyte cultures prepared from both fresh and cryopreserved rat hepatocytes.	Phenobarbital	133-146	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	55-71
10064562-1	1999	In the present study, we evaluated the inducibility of cytochrome P-450 (CYP) CYP1A, CYP2B, CYP3A, and CYP4A by beta-naphthoflavone, phenobarbital, dexamethasone, and clofibric acid, respectively, in primary hepatocyte cultures prepared from both fresh and cryopreserved rat hepatocytes.	Phenobarbital	133-146	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	73-76
10064562-1	1999	In the present study, we evaluated the inducibility of cytochrome P-450 (CYP) CYP1A, CYP2B, CYP3A, and CYP4A by beta-naphthoflavone, phenobarbital, dexamethasone, and clofibric acid, respectively, in primary hepatocyte cultures prepared from both fresh and cryopreserved rat hepatocytes.	Phenobarbital	133-146	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	92-97
10036216-0	1999	Phenobarbital induction of CYP2B1/2 in primary hepatocytes: endocrine regulation and evidence for a single pathway for multiple inducers.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	27-33
10036216-1	1999	Phenobarbital (PB) and many structurally unrelated chemicals induce the protein and mRNA of P450 cytochromes CYP2B1, CYP2B2, CYP3A1, and specific phase II enzymes to a greater extent in Fischer 344 (F344) than in Wistar Furth (WF) female rats.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	109-115
10036216-1	1999	Phenobarbital (PB) and many structurally unrelated chemicals induce the protein and mRNA of P450 cytochromes CYP2B1, CYP2B2, CYP3A1, and specific phase II enzymes to a greater extent in Fischer 344 (F344) than in Wistar Furth (WF) female rats.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	117-123
10036216-1	1999	Phenobarbital (PB) and many structurally unrelated chemicals induce the protein and mRNA of P450 cytochromes CYP2B1, CYP2B2, CYP3A1, and specific phase II enzymes to a greater extent in Fischer 344 (F344) than in Wistar Furth (WF) female rats.	Phenobarbital	0-13	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	125-131
10036216-1	1999	Phenobarbital (PB) and many structurally unrelated chemicals induce the protein and mRNA of P450 cytochromes CYP2B1, CYP2B2, CYP3A1, and specific phase II enzymes to a greater extent in Fischer 344 (F344) than in Wistar Furth (WF) female rats.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	109-115
10036216-1	1999	Phenobarbital (PB) and many structurally unrelated chemicals induce the protein and mRNA of P450 cytochromes CYP2B1, CYP2B2, CYP3A1, and specific phase II enzymes to a greater extent in Fischer 344 (F344) than in Wistar Furth (WF) female rats.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	117-123
10036216-1	1999	Phenobarbital (PB) and many structurally unrelated chemicals induce the protein and mRNA of P450 cytochromes CYP2B1, CYP2B2, CYP3A1, and specific phase II enzymes to a greater extent in Fischer 344 (F344) than in Wistar Furth (WF) female rats.	Phenobarbital	15-17	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	125-131
10036216-9	1999	CYP2B1/2B2 expression following induction by PB and HCB was subject to identical patterns of inhibition by okadaic acid, cAMP, and GH.	Phenobarbital	45-47	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	0-6
10205668-1	1999	The induction of cytochrome P450 2B1 and 2B2 in rat liver in response to phenobarbital is mediated at the transcriptional level.	Phenobarbital	73-86	cytochrome P450 2B1	Rattus norvegicus	17-44
9934848-0	1999	Phenobarbital promotes liver growth in c-myc/TGF-alpha transgenic mice by inducing hypertrophy and inhibiting apoptosis.	Phenobarbital	0-13	transforming growth factor alpha	Mus musculus	45-54
9934848-10	1999	Throughout the study, PB-treated animals showed markedly lower levels of TGF-beta1 ligand, coincident with an elevated level of the anti-apoptotic protein Bcl-2.	Phenobarbital	22-24	transforming growth factor, beta 1	Mus musculus	73-82
9934848-10	1999	Throughout the study, PB-treated animals showed markedly lower levels of TGF-beta1 ligand, coincident with an elevated level of the anti-apoptotic protein Bcl-2.	Phenobarbital	22-24	B cell leukemia/lymphoma 2	Mus musculus	155-160
9934848-13	1999	We conclude from our data that PB stimulates liver growth in double transgenic c-myc/TGF-alpha mice by induction of liver hypertrophy and inhibition of apoptosis, brought about by both a decrease in signaling through the TGF-beta pathway and an increase in Bcl-2.	Phenobarbital	31-33	transforming growth factor alpha	Mus musculus	85-94
9934848-13	1999	We conclude from our data that PB stimulates liver growth in double transgenic c-myc/TGF-alpha mice by induction of liver hypertrophy and inhibition of apoptosis, brought about by both a decrease in signaling through the TGF-beta pathway and an increase in Bcl-2.	Phenobarbital	31-33	transforming growth factor, beta 1	Mus musculus	221-229
9934848-13	1999	We conclude from our data that PB stimulates liver growth in double transgenic c-myc/TGF-alpha mice by induction of liver hypertrophy and inhibition of apoptosis, brought about by both a decrease in signaling through the TGF-beta pathway and an increase in Bcl-2.	Phenobarbital	31-33	B cell leukemia/lymphoma 2	Mus musculus	257-262
9862866-3	1999	AGP gene expression remained inducible by IL-1, IL-6, and phenobarbital (PB) in GH-treated hepatocytes.	Phenobarbital	58-71	orosomucoid 1	Rattus norvegicus	0-3
9862866-3	1999	AGP gene expression remained inducible by IL-1, IL-6, and phenobarbital (PB) in GH-treated hepatocytes.	Phenobarbital	58-71	gonadotropin releasing hormone receptor	Rattus norvegicus	80-82
9862866-3	1999	AGP gene expression remained inducible by IL-1, IL-6, and phenobarbital (PB) in GH-treated hepatocytes.	Phenobarbital	73-75	orosomucoid 1	Rattus norvegicus	0-3
9890448-6	1999	Results obtained by using chemical inhibitors or antibodies selectively active against specific CYPs provide a direct evidence for the involvement of CYP2C11, CYP3A2, and CYP2B1/2, indicating that each of them contributed about 40-50% of the diazinon metabolism, in hepatic microsomes from untreated, phenobarbital-, and dexamethasone-treated rats, respectively.	Phenobarbital	301-314	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	150-157
9890448-6	1999	Results obtained by using chemical inhibitors or antibodies selectively active against specific CYPs provide a direct evidence for the involvement of CYP2C11, CYP3A2, and CYP2B1/2, indicating that each of them contributed about 40-50% of the diazinon metabolism, in hepatic microsomes from untreated, phenobarbital-, and dexamethasone-treated rats, respectively.	Phenobarbital	301-314	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	159-165
9890448-6	1999	Results obtained by using chemical inhibitors or antibodies selectively active against specific CYPs provide a direct evidence for the involvement of CYP2C11, CYP3A2, and CYP2B1/2, indicating that each of them contributed about 40-50% of the diazinon metabolism, in hepatic microsomes from untreated, phenobarbital-, and dexamethasone-treated rats, respectively.	Phenobarbital	301-314	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	171-177
9890448-7	1999	The higher diazoxon/pyrimidinol ratio observed after phenobarbital-treatment together with the significantly more effective inhibition toward diazoxon production exerted by metyrapone in microsomes from phenobarbital-treated rats supports the conclusion that CYP2B1/2 catalyze preferentially the production of diazoxon.	Phenobarbital	203-216	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	259-265
9890442-3	1999	Culturing in the absence of insulin produced 1.5-2-fold increases in the induction magnitude of CYP2B1 and CYP2B2 mRNA expression resulting from PB exposures, without altering the bell-shaped dose-response curve characteristic of this agent.	Phenobarbital	145-147	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	107-113
9890442-4	1999	However, for the CYP3A1 gene, insulin removal led to a pronounced shift in both the PB-induction magnitude and dose-response relationships of the induction response, with higher levels of CYP3A1 expression resulting from exposures to lower concentrations of inducer.	Phenobarbital	84-86	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	17-23
9808766-0	1998	A major phenobarbital-inducible P450 isozyme, CYP2A14, in the Chinese hamster liver: purification, characterization, and cDNA cloning.	Phenobarbital	8-21	Cytochrome P-450 2A14	Cricetulus griseus	46-53
10591051-5	1999	SKF-525A pretreatment diminished the protective effect of selegiline against DSP-4, while phenobarbital pretreatment decreased its MAO-B inhibitory potency.	Phenobarbital	90-103	monoamine oxidase B	Homo sapiens	131-136
10205826-0	1999	[Interstrain differences in enzymatic activity of CYP2B1 and expression of its gene in the rat liver during induction with phenobarbital and triphenyldioxane].	Phenobarbital	123-136	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	50-56
10205826-1	1999	The interstrain differences in hepatic 7-pentoxyresorufin-O-dealkylase and 16 beta-androstendione hydroxylase activities specific for cytochrome P450 2B1 have been found in Sprague-Dawley, Brattleboro and Wistar rats treated with with phenobarbital, triphenyldioxane.	Phenobarbital	235-248	cytochrome P450 2B1	Rattus norvegicus	134-153
10205826-4	1999	Thus, differences in transcriptional activity of CYP2B1 gene during induction by phenobarbital and triphenyldioxane may be one of reasons for interstrain differences between enzymatic activities of rat liver cytochrome P4502B1.	Phenobarbital	81-94	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	49-55
9882693-0	1999	Analysis of a phenobarbital-responsive enhancer sequence located in the 5" flanking region of the chicken CYP2H1 gene: identification and characterization of functional protein-binding sites.	Phenobarbital	14-27	cytochrome P450 2H1	Gallus gallus	106-112
9882693-1	1999	We previously identified in the chicken CYP2H1 gene an upstream enhancer domain (-5900/-1100) that responds to phenobarbital.	Phenobarbital	111-124	cytochrome P450 2H1	Gallus gallus	40-46
9974185-1	1999	We examined hepatic cytochrome P450 (CYP) induction in rat foetuses and neonates by phenobarbital administered through placenta or breast feeding.	Phenobarbital	84-97	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	20-35
9974185-1	1999	We examined hepatic cytochrome P450 (CYP) induction in rat foetuses and neonates by phenobarbital administered through placenta or breast feeding.	Phenobarbital	84-97	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	37-40
10022238-9	1998	When introduced into primary rat liver cell cultures by transient transfection, hPPAR alpha-6/29 prevented the suppression of hepatocyte apoptosis by the PP nafenopin, but not that seen in response to phenobarbitone (PB), a non-genotoxic carcinogen whose action does not involve PPAR alpha.	Phenobarbital	217-219	peroxisome proliferator activated receptor alpha	Homo sapiens	80-85
10022238-9	1998	When introduced into primary rat liver cell cultures by transient transfection, hPPAR alpha-6/29 prevented the suppression of hepatocyte apoptosis by the PP nafenopin, but not that seen in response to phenobarbitone (PB), a non-genotoxic carcinogen whose action does not involve PPAR alpha.	Phenobarbital	217-219	peroxisome proliferator activated receptor alpha	Rattus norvegicus	81-91
9872399-0	1998	The influence of phenobarbital on cytochromes and reactive oxygen species in erythropoietin producing HepG2 cells.	Phenobarbital	17-30	erythropoietin	Homo sapiens	77-91
9872399-1	1998	Light absorption photometry of HepG2 cells treated with phenobarbital for enhancing the content of cytochrome P-450 and the synthesis of erythropoietin revealed an influence on all cytochromes detectable in the wavelength range between 400 and 620 nm.	Phenobarbital	56-69	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	99-115
9872399-1	1998	Light absorption photometry of HepG2 cells treated with phenobarbital for enhancing the content of cytochrome P-450 and the synthesis of erythropoietin revealed an influence on all cytochromes detectable in the wavelength range between 400 and 620 nm.	Phenobarbital	56-69	erythropoietin	Homo sapiens	137-151
9794803-8	1998	Phenobarbital showed significant induction of GSTT1 only in male rat liver and had little effect in female rat liver.	Phenobarbital	0-13	glutathione S-transferase theta 1	Rattus norvegicus	46-51
9802338-0	1998	Interactions of gender, growth hormone, and phenobarbital induction on murine Cyp2b expression.	Phenobarbital	44-57	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	78-83
9802338-1	1998	The interactions of gender, growth hormone, and phenobarbital induction on Cyp2b expression were examined in phenotypically normal (lit/+) and growth-hormone deficient "little" (lit/lit) mice.	Phenobarbital	48-61	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	75-80
9802338-3	1998	Phenobarbital administration to lit/+ mice increased the expression of the two Cyp2b isoforms in the males by 3- to 4-fold, but produced an approximately 75% reduction in the female-expressed proteins.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	79-84
9802338-8	1998	In spite of an apparent high degree of sequence homology between the rat CYP2B and murine Cyp2b gene families, the present findings highlight fundamental differences in their constitutive and gender-dependent expression, growth hormone regulation, and phenobarbital inducibility.	Phenobarbital	252-265	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	73-78
9802338-8	1998	In spite of an apparent high degree of sequence homology between the rat CYP2B and murine Cyp2b gene families, the present findings highlight fundamental differences in their constitutive and gender-dependent expression, growth hormone regulation, and phenobarbital inducibility.	Phenobarbital	252-265	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	90-95
9806796-3	1998	The addition of 5 nM insulin to hepatocytes culture led to a significant decrease of both basal and phenobarbital-induced ALA-S mRNA in a dose-dependent manner, as measured by Northern and slot-blot analysis.	Phenobarbital	100-113	insulin	Homo sapiens	21-28
9853405-2	1998	To seek information on the target site of PB, reflecting the induction of hepatic enzymes, we examined here the effect of picrotoxin on PB-mediated induction of hepatic cytochrome P450 and UDP-glucuronosyltransferase in vivo in rats.	Phenobarbital	136-138	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	189-216
9972461-7	1998	Western blotting studies indicated that hepatic microsomal proteins immunoreactive with polyclonal antisera to R. norvegicus CYP2B1 or CYP3A1 were induced, in a dose-responsive manner, by PB in the cotton rats.	Phenobarbital	188-190	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	125-131
9972461-7	1998	Western blotting studies indicated that hepatic microsomal proteins immunoreactive with polyclonal antisera to R. norvegicus CYP2B1 or CYP3A1 were induced, in a dose-responsive manner, by PB in the cotton rats.	Phenobarbital	188-190	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	135-141
9806796-3	1998	The addition of 5 nM insulin to hepatocytes culture led to a significant decrease of both basal and phenobarbital-induced ALA-S mRNA in a dose-dependent manner, as measured by Northern and slot-blot analysis.	Phenobarbital	100-113	5'-aminolevulinate synthase 1	Homo sapiens	122-127
9806796-8	1998	Our results demonstrate that the insulin effect is dominant; it overrides 8-CPT-cAMP plus phenobarbital-mediated induction.	Phenobarbital	90-103	insulin	Homo sapiens	33-40
9928666-4	1998	For example, phenobarbital (PB) and pregnenolone-16alpha-carbonitrile (PCN) increase serum levels of TSH, while 3-methylcholanthrene (3MC) and Aroclor 1254 (PCB) do not.	Phenobarbital	13-26	pyruvate carboxylase	Rattus norvegicus	157-160
9928666-4	1998	For example, phenobarbital (PB) and pregnenolone-16alpha-carbonitrile (PCN) increase serum levels of TSH, while 3-methylcholanthrene (3MC) and Aroclor 1254 (PCB) do not.	Phenobarbital	28-30	pyruvate carboxylase	Rattus norvegicus	157-160
9928666-8	1998	PB and PCN, UDP-GT inducing compounds which increase serum TSH, increased the percentage of TGF-beta1-positive follicular cells and increased apoptosis.	Phenobarbital	0-2	transforming growth factor, beta 1	Rattus norvegicus	92-101
9928666-6	1998	In a previous study in our laboratory, rats were treated for various times (up to 90 days) with PB and PCN, which increased TGF-beta1 protein and apoptosis.	Phenobarbital	96-98	transforming growth factor, beta 1	Rattus norvegicus	124-133
9806150-7	1998	We conclude that inhibition of spontaneous apoptosis induced by either phenobarbital or clofibrate is accompanied by increases in the endogenous levels of peroxides and by significant induction of catalase gene expression.	Phenobarbital	71-84	catalase	Rattus norvegicus	197-205
9763409-1	1998	Cytochrome P450 2B1 clones were isolated from a phenobarbital-induced Wistar-Kyoto (WKY) hepatic cDNA library and were found to contain a Glu-322 --&gt; Val substitution, compared with wild-type 2B1 from Sprague-Dawley rats.	Phenobarbital	48-61	cytochrome P450 2B1	Rattus norvegicus	0-19
9781726-10	1998	The administration of phenobarbital, a cytochrome P-450 inducer and of nitro-L-arginine methyl ester, a NOS inhibitor, prevented cGMP production and abolished the overexpression of HO-1 mRNA.	Phenobarbital	22-35	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-55
9781726-10	1998	The administration of phenobarbital, a cytochrome P-450 inducer and of nitro-L-arginine methyl ester, a NOS inhibitor, prevented cGMP production and abolished the overexpression of HO-1 mRNA.	Phenobarbital	22-35	heme oxygenase 1	Rattus norvegicus	181-185
9742082-0	1998	The nuclear orphan receptor CAR-retinoid X receptor heterodimer activates the phenobarbital-responsive enhancer module of the CYP2B gene.	Phenobarbital	78-91	CXADR pseudogene 1	Homo sapiens	28-31
10323327-2	1998	ALDHI is mainly increased by phenobarbital-type inducers; polycyclic aromatic hydrocarbons (PAHs), such as 3- methylcholanthrene (3MC), increase ALDH3c enzyme activity in all rat species currently tested.	Phenobarbital	29-42	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	145-150
10323328-3	1998	Phenobarbital- type inducers increase ALDH1 activity while polycyclic aromatic hydrocarbons (such as benzo[alpha]pyrene) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increase ALDH3c isoenzyme activity.	Phenobarbital	0-13	aldehyde dehydrogenase 2 family member	Rattus norvegicus	38-43
10323328-3	1998	Phenobarbital- type inducers increase ALDH1 activity while polycyclic aromatic hydrocarbons (such as benzo[alpha]pyrene) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increase ALDH3c isoenzyme activity.	Phenobarbital	0-13	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	177-182
10323328-4	1998	Two rat substrains were isolated according to a different induction of hepatic ALDH after treatment with phenobarbital (PB).	Phenobarbital	105-118	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	79-83
9742071-0	1998	Effect of 3-methylcholanthrene administration on expression of cytochrome P-450 isoforms induced by phenobarbital in rat hepatocytes.	Phenobarbital	100-113	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	63-79
9742071-2	1998	Thus, we examined the amount of phenobarbital (PB)-inducible P-450 isoforms (P-450 2B1/2B2) in hepatocytes from rats injected first with PB and then with 3-methylcholanthrene (MC) (PB+MC-treated animals) by quantitative immunohistochemistry.	Phenobarbital	32-45	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	83-90
9742071-2	1998	Thus, we examined the amount of phenobarbital (PB)-inducible P-450 isoforms (P-450 2B1/2B2) in hepatocytes from rats injected first with PB and then with 3-methylcholanthrene (MC) (PB+MC-treated animals) by quantitative immunohistochemistry.	Phenobarbital	47-49	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	83-90
9742071-4	1998	In PB-treated animals, P-450 2B1/2B2 content increased in perivenular and midzonal hepatocytes.	Phenobarbital	3-5	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	29-36
9742071-5	1998	In PB+MC-treated animals, however, the PB-induced increase in 2B1/2B2 content was suppressed in perivenular hepatocytes but promoted in midzonal hepatocytes.	Phenobarbital	3-5	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	62-69
9742071-5	1998	In PB+MC-treated animals, however, the PB-induced increase in 2B1/2B2 content was suppressed in perivenular hepatocytes but promoted in midzonal hepatocytes.	Phenobarbital	39-41	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	62-69
9742071-8	1998	The promotion of the increase in P-450 2B1/2B2 content in midzonal hepatocytes in PB+MC-treated animals probably corresponds to the strong hybridization signal, whereas there appeared to be a divergence between the intensity of the signal and the content in perivenular hepatocytes.	Phenobarbital	82-84	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	39-46
9742082-0	1998	The nuclear orphan receptor CAR-retinoid X receptor heterodimer activates the phenobarbital-responsive enhancer module of the CYP2B gene.	Phenobarbital	78-91	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	126-131
9742082-1	1998	PBREM, the phenobarbital-responsive enhancer module of the cytochrome P-450 Cyp2b10 gene, contains two potential nuclear receptor binding sites, NR1 and NR2.	Phenobarbital	11-24	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	76-83
9742082-1	1998	PBREM, the phenobarbital-responsive enhancer module of the cytochrome P-450 Cyp2b10 gene, contains two potential nuclear receptor binding sites, NR1 and NR2.	Phenobarbital	11-24	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	145-148
9742082-2	1998	Consistent with the finding that anti-retinoid X receptor (RXR) could supershift the NR1-nuclear protein complex, DNA affinity chromatography with NR1 oligonucleotides enriched the nuclear orphan receptor RXR from the hepatic nuclear extracts of phenobarbital-treated mice.	Phenobarbital	246-259	retinoid X receptor alpha	Homo sapiens	59-62
9742082-2	1998	Consistent with the finding that anti-retinoid X receptor (RXR) could supershift the NR1-nuclear protein complex, DNA affinity chromatography with NR1 oligonucleotides enriched the nuclear orphan receptor RXR from the hepatic nuclear extracts of phenobarbital-treated mice.	Phenobarbital	246-259	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	147-150
9742082-2	1998	Consistent with the finding that anti-retinoid X receptor (RXR) could supershift the NR1-nuclear protein complex, DNA affinity chromatography with NR1 oligonucleotides enriched the nuclear orphan receptor RXR from the hepatic nuclear extracts of phenobarbital-treated mice.	Phenobarbital	246-259	retinoid X receptor alpha	Homo sapiens	205-208
9742082-4	1998	In the phenobarbital-treated mice, the binding of both CAR and RXR was rapidly increased before the induction of CYP2B10 mRNA.	Phenobarbital	7-20	nuclear receptor subfamily 1, group I, member 3	Mus musculus	55-58
9742082-4	1998	In the phenobarbital-treated mice, the binding of both CAR and RXR was rapidly increased before the induction of CYP2B10 mRNA.	Phenobarbital	7-20	retinoid X receptor alpha	Homo sapiens	63-66
9742082-4	1998	In the phenobarbital-treated mice, the binding of both CAR and RXR was rapidly increased before the induction of CYP2B10 mRNA.	Phenobarbital	7-20	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	113-120
9742082-7	1998	A CAR-RXR heterodimer has thus been characterized as a trans-acting factor for the phenobarbital-inducible Cyp2b10 gene.	Phenobarbital	83-96	CXADR pseudogene 1	Homo sapiens	2-5
9742082-7	1998	A CAR-RXR heterodimer has thus been characterized as a trans-acting factor for the phenobarbital-inducible Cyp2b10 gene.	Phenobarbital	83-96	retinoid X receptor alpha	Homo sapiens	6-9
9742082-7	1998	A CAR-RXR heterodimer has thus been characterized as a trans-acting factor for the phenobarbital-inducible Cyp2b10 gene.	Phenobarbital	83-96	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	107-114
9792038-2	1998	At low concentrations of 0.5-2 mmol/L, phenobarbital enhances DNA synthesis of normal adult rat hepatocytes in the presence of epidermal growth factor (EGF) and/or dexamethasone.	Phenobarbital	39-52	epidermal growth factor like 1	Rattus norvegicus	127-150
9736044-5	1998	However, hepatic HGF levels were decreased despite an increased number of mitotic hepatocytes and increased or unchanged plasma HGF levels in rats given phenobarbital and in rats after dimethylnitrosamine intoxication, which can induce hepatic necrosis after apoptosis of hepatic stellate cells.	Phenobarbital	153-166	hepatocyte growth factor	Rattus norvegicus	17-20
9751125-6	1998	Phenobarbital inhibited both TGF-beta and bleomycin-induced apoptosis and the normal regulation of p53, bcl-2, and bax.	Phenobarbital	0-13	transforming growth factor, beta 1	Mus musculus	29-37
9751125-6	1998	Phenobarbital inhibited both TGF-beta and bleomycin-induced apoptosis and the normal regulation of p53, bcl-2, and bax.	Phenobarbital	0-13	transformation related protein 53, pseudogene	Mus musculus	99-102
9751125-6	1998	Phenobarbital inhibited both TGF-beta and bleomycin-induced apoptosis and the normal regulation of p53, bcl-2, and bax.	Phenobarbital	0-13	B cell leukemia/lymphoma 2	Mus musculus	104-109
9751125-6	1998	Phenobarbital inhibited both TGF-beta and bleomycin-induced apoptosis and the normal regulation of p53, bcl-2, and bax.	Phenobarbital	0-13	BCL2-associated X protein	Mus musculus	115-118
9792038-5	1998	Furthermore, phenobarbital inhibits DNA synthesis of transforming growth factor-alpha-stimulated primary hepatocytes from normal adult rats in a dose-dependent manner within a concentration range of 3-6 mmol/L.	Phenobarbital	13-26	myotrophin	Rattus norvegicus	66-79
9792038-6	1998	When normal adult rat hepatocytes are led to undergo multiple proliferative cycles upon stimulation with hepatocyte growth factor (HGF) and EGF in the chemically defined hepatocyte growth medium (HGM), 3 mmol/L phenobarbital also remarkably suppresses DNA synthesis.	Phenobarbital	211-224	hepatocyte growth factor	Rattus norvegicus	105-129
9737965-5	1998	PHS-1 was incubated with teratogen (phenytoin, mephenytoin, trimethadione, phenobarbital, and major metabolites) or its vehicle and the free radical spin trap alpha-phenyl-N-t-butylnitrone, and incubations were analyzed by EPR spectrometry.	Phenobarbital	75-88	prostaglandin-endoperoxide synthase 1	Homo sapiens	0-5
9753209-3	1998	Known inducers of CYP3A, such as rifampin, phenytoin, carbamazepine, and phenobarbital, increase the urinary excretion of 6beta-hydroxycortisol and the ratio of 6beta-hydroxycortisol to cortisol.	Phenobarbital	73-86	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	18-23
28976694-2	1998	At low concentrations of 0.5-2 mmol/L, phenobarbital enhances DNA synthesis of normal adult rat hepatocytes in the presence of epidermal growth factor (EGF) and/or dexamethasone.	Phenobarbital	39-52	epidermal growth factor like 1	Rattus norvegicus	127-150
28976694-2	1998	At low concentrations of 0.5-2 mmol/L, phenobarbital enhances DNA synthesis of normal adult rat hepatocytes in the presence of epidermal growth factor (EGF) and/or dexamethasone.	Phenobarbital	39-52	epidermal growth factor like 1	Rattus norvegicus	152-155
9792038-2	1998	At low concentrations of 0.5-2 mmol/L, phenobarbital enhances DNA synthesis of normal adult rat hepatocytes in the presence of epidermal growth factor (EGF) and/or dexamethasone.	Phenobarbital	39-52	epidermal growth factor like 1	Rattus norvegicus	152-155
28976694-5	1998	Furthermore, phenobarbital inhibits DNA synthesis of transforming growth factor-a-stimulated primary hepatocytes from normal adult rats in a dose-dependent manner within a concentration range of 3-6 mmol/L.	Phenobarbital	13-26	myotrophin	Rattus norvegicus	66-79
9874281-4	1998	In addition, modulation of the AGP induction by CAM, PB, EE2 and DEX in the diabetic state was examined.	Phenobarbital	53-55	orosomucoid 1	Rattus norvegicus	31-34
28976694-6	1998	When normal adult rat hepatocytes are led to undergo multiple proliferative cycles upon stimulation with hepatocyte growth factor (HGF) and EGF in the chemically defined hepatocyte growth medium (HGM), 3 mmol/L phenobarbital also remarkably suppresses DNA synthesis.	Phenobarbital	211-224	hepatocyte growth factor	Rattus norvegicus	105-129
9874281-7	1998	In addition, AGP induction by CAM, EE2 and DEX were attenuated in streptozotocin-induced diabetic rats, whereas the PB-induced increase in AGP levels was potentiated in diabetic rats.	Phenobarbital	116-118	orosomucoid 1	Rattus norvegicus	139-142
9705199-0	1998	Evidence for involvement of cAMP-dependent pathway in the phenobarbital-induced expression of a novel hamster cytochrome P450, CYP3A31.	Phenobarbital	58-71	cathelicidin antimicrobial peptide	Mesocricetus auratus	28-32
18967308-2	1998	The resolution of binary mixtures of phenobarbital and phenytoin has been accomplished by using partial least squares (PLS-1) regression analysis.	Phenobarbital	37-50	plastin 1	Homo sapiens	119-124
9789950-3	1998	Immunohistochemical assessment of altered p53 expression on liver sections with polyclonal serum (CM5) resulted in positive staining in 17/21 benzo(a)pyrene-, 1/18 thioacetamide-, 2/21 clofibric acid-, 2/21 phenobarbitone-, 7/19 ethinylestradiol-, 1/21 tryptophan-, 3/19 thyroxine-, and 1/21 fructose-treated rats and in 2/19 controls.	Phenobarbital	207-221	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	42-45
9705199-0	1998	Evidence for involvement of cAMP-dependent pathway in the phenobarbital-induced expression of a novel hamster cytochrome P450, CYP3A31.	Phenobarbital	58-71	cytochrome P450 3A31	Mesocricetus auratus	127-134
9705199-2	1998	In primary hepatocyte cultures, CYP3A31 is dramatically induced by phenobarbital.	Phenobarbital	67-80	cytochrome P450 3A31	Mesocricetus auratus	32-39
9705199-3	1998	To elucidate the mechanism of this induction, we first studied the effects of cAMP on phenobarbital-induced CYP3A31 expression using forskolin and N6,O2"-dibutyryl cAMP in hepatocyte cultures.	Phenobarbital	86-99	cathelicidin antimicrobial peptide	Mesocricetus auratus	78-82
9705199-3	1998	To elucidate the mechanism of this induction, we first studied the effects of cAMP on phenobarbital-induced CYP3A31 expression using forskolin and N6,O2"-dibutyryl cAMP in hepatocyte cultures.	Phenobarbital	86-99	cytochrome P450 3A31	Mesocricetus auratus	108-115
9705199-3	1998	To elucidate the mechanism of this induction, we first studied the effects of cAMP on phenobarbital-induced CYP3A31 expression using forskolin and N6,O2"-dibutyryl cAMP in hepatocyte cultures.	Phenobarbital	86-99	cathelicidin antimicrobial peptide	Mesocricetus auratus	164-168
9705199-4	1998	At 100 microM, forskolin significantly inhibited both the phenobarbital-induced CYP3A31 mRNAs expression and the testosterone 6beta-hydroxylation activity related to the CYP3A subfamily in rats, whereas 0.1 microM forskolin potentiated the phenobarbital induction of CYP3A31 mRNA and the testosterone 6beta-hydroxylation activity.	Phenobarbital	58-71	cytochrome P450 3A31	Mesocricetus auratus	80-87
9705199-4	1998	At 100 microM, forskolin significantly inhibited both the phenobarbital-induced CYP3A31 mRNAs expression and the testosterone 6beta-hydroxylation activity related to the CYP3A subfamily in rats, whereas 0.1 microM forskolin potentiated the phenobarbital induction of CYP3A31 mRNA and the testosterone 6beta-hydroxylation activity.	Phenobarbital	58-71	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	80-85
9705199-4	1998	At 100 microM, forskolin significantly inhibited both the phenobarbital-induced CYP3A31 mRNAs expression and the testosterone 6beta-hydroxylation activity related to the CYP3A subfamily in rats, whereas 0.1 microM forskolin potentiated the phenobarbital induction of CYP3A31 mRNA and the testosterone 6beta-hydroxylation activity.	Phenobarbital	58-71	cytochrome P450 3A31	Mesocricetus auratus	267-274
9705199-5	1998	Treatment with N6,O2"-dibutyryl cAMP resulted in an inhibition of phenobarbital-induced CYP3A31 gene expression and testosterone 6beta-hydroxylation activity.	Phenobarbital	66-79	cathelicidin antimicrobial peptide	Mesocricetus auratus	32-36
9738950-7	1998	In HepG2 cells, the expression of MRP3 was induced by phenobarbital.	Phenobarbital	54-67	ATP binding cassette subfamily C member 3	Homo sapiens	34-38
9705199-5	1998	Treatment with N6,O2"-dibutyryl cAMP resulted in an inhibition of phenobarbital-induced CYP3A31 gene expression and testosterone 6beta-hydroxylation activity.	Phenobarbital	66-79	cytochrome P450 3A31	Mesocricetus auratus	88-95
9705199-6	1998	Increasing amounts of transfected cAMP-response element binding proteins (CREB) or CREB-binding proteins in hamster hepatocytes reduced the phenobarbital-induction of CYP3A31 mRNAs expression.	Phenobarbital	140-153	cathelicidin antimicrobial peptide	Mesocricetus auratus	34-38
9705199-6	1998	Increasing amounts of transfected cAMP-response element binding proteins (CREB) or CREB-binding proteins in hamster hepatocytes reduced the phenobarbital-induction of CYP3A31 mRNAs expression.	Phenobarbital	140-153	cytochrome P450 3A31	Mesocricetus auratus	167-174
9705199-7	1998	These results suggest that in vitro induction of CYP3A31 by phenobarbital in Syrian hamster hepatocytes is regulated by a cAMP-dependent pathway.	Phenobarbital	60-73	cytochrome P450 3A31	Mesocricetus auratus	49-56
9705199-7	1998	These results suggest that in vitro induction of CYP3A31 by phenobarbital in Syrian hamster hepatocytes is regulated by a cAMP-dependent pathway.	Phenobarbital	60-73	cathelicidin antimicrobial peptide	Mesocricetus auratus	122-126
9664123-5	1998	PB and BNF treatments markedly induced the amount of GST proteins in all the tissues studied with the maximum induction in the cytosol after 4 days of PB and 10 days of BNF treatments, respectively.	Phenobarbital	0-2	natriuretic peptide B	Rattus norvegicus	169-172
9698295-0	1998	Differential regulation of individual sulfotransferase isoforms by phenobarbital in male rat liver.	Phenobarbital	67-80	carbohydrate sulfotransferase 10	Rattus norvegicus	38-54
9698295-2	1998	In the present study, male Sprague-Dawley rats were treated for 3 consecutive days with doses of phenobarbital (PB) that induce cytochrome P450 2B1/2 expression.	Phenobarbital	97-110	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	128-149
9698295-2	1998	In the present study, male Sprague-Dawley rats were treated for 3 consecutive days with doses of phenobarbital (PB) that induce cytochrome P450 2B1/2 expression.	Phenobarbital	112-114	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	128-149
9698295-4	1998	PB suppressed SULT1A1 mRNA levels, increased the expression of the SULT-Dopa/tyrosine isoform, and did not produce significant changes in SULT1C1 and SULT1E2 mRNA expression.	Phenobarbital	0-2	sulfotransferase family 1A member 1	Rattus norvegicus	14-21
9698295-4	1998	PB suppressed SULT1A1 mRNA levels, increased the expression of the SULT-Dopa/tyrosine isoform, and did not produce significant changes in SULT1C1 and SULT1E2 mRNA expression.	Phenobarbital	0-2	carbohydrate sulfotransferase 10	Rattus norvegicus	14-18
9698295-5	1998	In rats injected with the highest test dose of PB (100 mg/kg), hepatic SULT1A1 mRNA levels were decreased to approximately 42% of control levels and SULT-Dopa/tyrosine mRNA levels were increased to approximately 417% of vehicle-treated control levels.	Phenobarbital	47-49	sulfotransferase family 1A member 1	Rattus norvegicus	71-78
9698295-5	1998	In rats injected with the highest test dose of PB (100 mg/kg), hepatic SULT1A1 mRNA levels were decreased to approximately 42% of control levels and SULT-Dopa/tyrosine mRNA levels were increased to approximately 417% of vehicle-treated control levels.	Phenobarbital	47-49	carbohydrate sulfotransferase 10	Rattus norvegicus	71-75
9698295-9	1998	These studies support a complex role for PB-mediated effects on the SULT multigene family in rat liver.	Phenobarbital	41-43	carbohydrate sulfotransferase 10	Rattus norvegicus	68-72
9698295-10	1998	Because individual SULT1 and SULT2 enzyme isoforms are known to metabolize a variety of potentially toxic substrates, varied responses to PB among members of the SULT multigene family might have important implications for xenobiotic hepatotoxicity.	Phenobarbital	138-140	carbohydrate sulfotransferase 10	Rattus norvegicus	19-23
9875460-1	1998	Glutathione S-transferase placental form (GST-P) positive foci development and its expression in liver exposed by nongenotoxic carcinogens phenobarbital (PB) and clofibrate (CF), and genotoxic carcinogen 2-amino-3-methylimidazo[4,5-f] quinoline (IQ) were investigated as a measure of carcinogenic potential of these chemicals.	Phenobarbital	139-152	glutathione S-transferase pi 1	Rattus norvegicus	0-47
9875460-1	1998	Glutathione S-transferase placental form (GST-P) positive foci development and its expression in liver exposed by nongenotoxic carcinogens phenobarbital (PB) and clofibrate (CF), and genotoxic carcinogen 2-amino-3-methylimidazo[4,5-f] quinoline (IQ) were investigated as a measure of carcinogenic potential of these chemicals.	Phenobarbital	154-156	glutathione S-transferase pi 1	Rattus norvegicus	0-47
9744545-18	1998	Immunohistochemical staining of TGF-alpha and GST-P using serial liver sections demonstrated that the TGF-alpha-positive foci comprised a sub-population of the GST-P-positive lesions, being approximately 1/8-1/10th as common in livers of animals treated with PB.	Phenobarbital	259-261	transforming growth factor alpha	Rattus norvegicus	102-111
9683175-9	1998	A reduction in p53 protein, but not transcript levels, was observed in hepatocytes exposed to PB.	Phenobarbital	94-96	transformation related protein 53, pseudogene	Mus musculus	15-18
9726815-4	1998	Phenobarbital treatment increased the number of CYP2A5-positive centrilobular hepatocytes and the CYP2A5-positive areas were extended into the middle zone in all strains, but periportal hepatocytes remained negative.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	48-54
9726815-4	1998	Phenobarbital treatment increased the number of CYP2A5-positive centrilobular hepatocytes and the CYP2A5-positive areas were extended into the middle zone in all strains, but periportal hepatocytes remained negative.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	98-104
9726815-5	1998	Fifty percent of the spontaneous foci in untreated mice, over 90% of the foci in mice treated with NDEA or phenobarbital and all of the hepatocellular adenomas and carcinomas displayed positive immunostaining and a strong CYP2A5 mRNA signal by in situ hybridization.	Phenobarbital	107-120	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	222-228
9661906-4	1998	After a single injection with diethylnitrosamine and subsequent treatment with phenobarbitol for 6 months, Mgat3+/+ and Mgat3+/- mice had grossly enlarged livers that contained numerous tumors.	Phenobarbital	79-92	mannoside acetylglucosaminyltransferase 3	Mus musculus	107-112
9683175-10	1998	Additionally, PB delayed and attenuated p53 protein induction during DNA damage, which suggests that changes in the p53 protein may be contributing to the attenuated G1 checkpoint response caused by PB.	Phenobarbital	14-16	transformation related protein 53, pseudogene	Mus musculus	40-43
9683175-10	1998	Additionally, PB delayed and attenuated p53 protein induction during DNA damage, which suggests that changes in the p53 protein may be contributing to the attenuated G1 checkpoint response caused by PB.	Phenobarbital	14-16	transformation related protein 53, pseudogene	Mus musculus	116-119
9683175-10	1998	Additionally, PB delayed and attenuated p53 protein induction during DNA damage, which suggests that changes in the p53 protein may be contributing to the attenuated G1 checkpoint response caused by PB.	Phenobarbital	199-201	transformation related protein 53, pseudogene	Mus musculus	116-119
9715508-1	1998	The tumorigenic potential of phenobarbital was examined in a 26-wk carcinogenesis bioassay using p53 heterozygous mice and wild-type controls.	Phenobarbital	29-42	transformation related protein 53, pseudogene	Mus musculus	97-100
9720140-6	1998	PCNA labeling index measurements of liver hepatocytes confirmed that there was a significant increase in the growth fraction of hepatocytes during PB treatment.	Phenobarbital	147-149	proliferating cell nuclear antigen	Rattus norvegicus	0-4
9637786-0	1998	Phenobarbital suppresses growth and accelerates restoration of differentiation markers of primary culture rat hepatocytes in the chemically defined hepatocyte growth medium containing hepatocyte growth factor and epidermal growth factor.	Phenobarbital	0-13	hepatocyte growth factor	Rattus norvegicus	184-208
9637786-1	1998	Phenobarbital (PB), a liver-tumor promoter, at a concentration of 3 mM dramatically inhibited the growth of adult rat hepatocytes in the chemically defined medium, HGM, with added hepatocyte growth factor (HGF) and epidermal growth factor (EGF).	Phenobarbital	0-13	hepatocyte growth factor	Rattus norvegicus	180-204
9637786-1	1998	Phenobarbital (PB), a liver-tumor promoter, at a concentration of 3 mM dramatically inhibited the growth of adult rat hepatocytes in the chemically defined medium, HGM, with added hepatocyte growth factor (HGF) and epidermal growth factor (EGF).	Phenobarbital	0-13	hepatocyte growth factor	Rattus norvegicus	206-209
9637786-1	1998	Phenobarbital (PB), a liver-tumor promoter, at a concentration of 3 mM dramatically inhibited the growth of adult rat hepatocytes in the chemically defined medium, HGM, with added hepatocyte growth factor (HGF) and epidermal growth factor (EGF).	Phenobarbital	15-17	hepatocyte growth factor	Rattus norvegicus	180-204
9637786-1	1998	Phenobarbital (PB), a liver-tumor promoter, at a concentration of 3 mM dramatically inhibited the growth of adult rat hepatocytes in the chemically defined medium, HGM, with added hepatocyte growth factor (HGF) and epidermal growth factor (EGF).	Phenobarbital	15-17	hepatocyte growth factor	Rattus norvegicus	206-209
9637786-5	1998	Additionally, PB strongly suppressed expression of the mRNA for alpha-fetoprotein, a protein primarily expressed by fetal liver, and the accelerative effect of PB on restoration of mature hepatocyte markers showed a correlation with the up-regulation of the hepatocyte-enriched transcription factors HNF3 and HNF4.	Phenobarbital	14-16	alpha-fetoprotein	Rattus norvegicus	64-81
9637786-5	1998	Additionally, PB strongly suppressed expression of the mRNA for alpha-fetoprotein, a protein primarily expressed by fetal liver, and the accelerative effect of PB on restoration of mature hepatocyte markers showed a correlation with the up-regulation of the hepatocyte-enriched transcription factors HNF3 and HNF4.	Phenobarbital	14-16	forkhead box E3	Rattus norvegicus	300-304
9637786-5	1998	Additionally, PB strongly suppressed expression of the mRNA for alpha-fetoprotein, a protein primarily expressed by fetal liver, and the accelerative effect of PB on restoration of mature hepatocyte markers showed a correlation with the up-regulation of the hepatocyte-enriched transcription factors HNF3 and HNF4.	Phenobarbital	14-16	hepatocyte nuclear factor 4, alpha	Rattus norvegicus	309-313
9637786-5	1998	Additionally, PB strongly suppressed expression of the mRNA for alpha-fetoprotein, a protein primarily expressed by fetal liver, and the accelerative effect of PB on restoration of mature hepatocyte markers showed a correlation with the up-regulation of the hepatocyte-enriched transcription factors HNF3 and HNF4.	Phenobarbital	160-162	forkhead box E3	Rattus norvegicus	300-304
9637786-5	1998	Additionally, PB strongly suppressed expression of the mRNA for alpha-fetoprotein, a protein primarily expressed by fetal liver, and the accelerative effect of PB on restoration of mature hepatocyte markers showed a correlation with the up-regulation of the hepatocyte-enriched transcription factors HNF3 and HNF4.	Phenobarbital	160-162	hepatocyte nuclear factor 4, alpha	Rattus norvegicus	309-313
9673412-7	1998	When PB was administered in vitro simultaneously to rat hepatocytes with TNF, the decrease observed for GST mu subunit was suppressed while total GST activity and GST alpha content were not affected.	Phenobarbital	5-7	tumor necrosis factor	Rattus norvegicus	73-76
9663807-4	1998	Evidence suggests that CYP2C9 substrates may also be induced variably by carbamazepine, ethanol and phenobarbitone.	Phenobarbital	100-114	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	23-29
9625027-3	1998	Other medications, e.g., rifampin and phenobarbital, which also induce p450 3A activity, have been reported to significantly decrease cyclosporine (CsA) concentrations.	Phenobarbital	38-51	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	148-151
9578594-1	1998	The molecular mechanisms by which dimethyl sulfoxide (DMSO) enhances CYP3A protein in phenobarbital-treated primary cultured rat hepatocytes were examined.	Phenobarbital	86-99	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	69-74
9678251-0	1998	Identification of sequences involved in both basal expression and phenobarbital induction of a CYP2B2 gene using in vitro transcription system.	Phenobarbital	66-79	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	95-101
9678251-7	1998	The use of synthetic oligonucleotides as competitor in vitro transcription assays indicated the importance for transcriptional control of the CYP2B2 gene of sequences located between -183 and -199 and -31 and -72 that were identified previously [1] as binding rat liver nuclear proteins that are enriched or activated in vivo by phenobarbital.	Phenobarbital	329-342	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	142-148
9606477-7	1998	Phenytoin, phenobarbital, and carbamazepine induce CYP and UGT enzymes.	Phenobarbital	11-24	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	51-54
9606477-7	1998	Phenytoin, phenobarbital, and carbamazepine induce CYP and UGT enzymes.	Phenobarbital	11-24	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	59-62
9673412-8	1998	When hepatocytes were treated with TNF after PB given in vivo directly to the rat by i.p.	Phenobarbital	45-47	tumor necrosis factor	Rattus norvegicus	35-38
9673412-11	1998	Then, PB could prevent some TNF toxic effects.	Phenobarbital	6-8	tumor necrosis factor	Rattus norvegicus	28-31
9628589-0	1998	Nuclear factor-1 motif and redundant regulatory elements comprise phenobarbital-responsive enhancer in CYP2B1/2.	Phenobarbital	66-79	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	103-111
10076536-5	1998	Only dexamethasone (Dex) produced effects on Fluva-inducible CYP2B1/2 mRNA expression that differed from those produced on PB-inducible CYP2B1/2 mRNA expression.	Phenobarbital	123-125	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	136-142
10076536-6	1998	Dex concentrations up to 10(-7) M of potentiated PB (10(-4) M)-mediated CYP2B1/2 mRNA induction, while higher Dex concentrations produced a progressive reduction in PB-induced CYP2B1/2 mRNA levels.	Phenobarbital	49-51	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	72-78
10076536-6	1998	Dex concentrations up to 10(-7) M of potentiated PB (10(-4) M)-mediated CYP2B1/2 mRNA induction, while higher Dex concentrations produced a progressive reduction in PB-induced CYP2B1/2 mRNA levels.	Phenobarbital	165-167	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	176-182
9630843-4	1998	Liver microsomes isolated from rats pretreated with phenobarbital (PB-microsomes) did not have increased FMO activity but had increased activities for hydroxylating the testosterone at 6 beta-(CYP3A1), 16 beta-(CYP2B1), and 2 beta-(CYP3A1) positions.	Phenobarbital	52-65	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	193-199
9630843-4	1998	Liver microsomes isolated from rats pretreated with phenobarbital (PB-microsomes) did not have increased FMO activity but had increased activities for hydroxylating the testosterone at 6 beta-(CYP3A1), 16 beta-(CYP2B1), and 2 beta-(CYP3A1) positions.	Phenobarbital	52-65	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	211-217
9630843-4	1998	Liver microsomes isolated from rats pretreated with phenobarbital (PB-microsomes) did not have increased FMO activity but had increased activities for hydroxylating the testosterone at 6 beta-(CYP3A1), 16 beta-(CYP2B1), and 2 beta-(CYP3A1) positions.	Phenobarbital	52-65	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	232-238
9571231-6	1998	In contrast, induction of CYP 2B1/2 by phenobarbital was markedly stronger in hepatocytes cultured on Matrigel.	Phenobarbital	39-52	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	26-33
9628589-14	1998	These studies indicate that the CYP2B2 phenobarbital-responsive enhancer contains multiple constitutive and phenobarbital-responsive elements.	Phenobarbital	39-52	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	32-38
9628589-14	1998	These studies indicate that the CYP2B2 phenobarbital-responsive enhancer contains multiple constitutive and phenobarbital-responsive elements.	Phenobarbital	108-121	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	32-38
9628589-16	1998	The only difference detected was a complex that was substantially reduced by phenobarbital treatment and mapped to the 3" side of the NF-1 site.	Phenobarbital	77-90	neurofibromin 1	Rattus norvegicus	134-138
9628589-2	1998	A 163-bp fragment at about -2.2 Kb in CYP2B2 has been shown to mediate phenobarbital induction in primary rat hepatocytes (Trottier, et al.	Phenobarbital	71-84	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	38-44
9630465-2	1998	Phenobarbital (PB)-pretreatment of mice induced P450s 3A and 2B and markedly increased serum alanine aminotransferase (ALT) activity after cocaine or norcocaine administration.	Phenobarbital	0-13	glutamic pyruvic transaminase, soluble	Mus musculus	93-117
9685045-9	1998	Significant increases in immunodetectable levels of CYP 2B were, however, detected in toxaphene-treated mice, and are consistent with earlier reports demonstrating that toxaphene, like many other pesticides, induces the phenobarbital-inducible subfamily of CYP.	Phenobarbital	220-233	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	52-55
9685045-9	1998	Significant increases in immunodetectable levels of CYP 2B were, however, detected in toxaphene-treated mice, and are consistent with earlier reports demonstrating that toxaphene, like many other pesticides, induces the phenobarbital-inducible subfamily of CYP.	Phenobarbital	220-233	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	257-260
9630465-5	1998	In contrast to the marked induction of P450s 3A and 2B, P450 2C was increased only 2.5-fold by PB and to an even lesser extent by Dex or PCP.	Phenobarbital	95-97	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	56-63
9571220-12	1998	Oral administration of phenobarbital or acetone increased CYP2B and CYP2E1 activities in rat liver but had no significant effect on P450 activities in subcompartments of rat lung.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	68-74
9630454-1	1998	Phenobarbital (PB)-mediated induction of five forms of cytochrome P450 (CYP2B1, CYP2B2, CYP3A1, CYP2A1, and CYP2C6) and epoxide hydrolase is highly suppressed, at the transcriptional level, in Wistar Furth (WF) relative to Fischer 344 (F344) female rats.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	72-78
9630465-2	1998	Phenobarbital (PB)-pretreatment of mice induced P450s 3A and 2B and markedly increased serum alanine aminotransferase (ALT) activity after cocaine or norcocaine administration.	Phenobarbital	0-13	glutamic pyruvic transaminase, soluble	Mus musculus	119-122
9630454-1	1998	Phenobarbital (PB)-mediated induction of five forms of cytochrome P450 (CYP2B1, CYP2B2, CYP3A1, CYP2A1, and CYP2C6) and epoxide hydrolase is highly suppressed, at the transcriptional level, in Wistar Furth (WF) relative to Fischer 344 (F344) female rats.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	80-86
9630465-2	1998	Phenobarbital (PB)-pretreatment of mice induced P450s 3A and 2B and markedly increased serum alanine aminotransferase (ALT) activity after cocaine or norcocaine administration.	Phenobarbital	15-17	glutamic pyruvic transaminase, soluble	Mus musculus	93-117
9630454-1	1998	Phenobarbital (PB)-mediated induction of five forms of cytochrome P450 (CYP2B1, CYP2B2, CYP3A1, CYP2A1, and CYP2C6) and epoxide hydrolase is highly suppressed, at the transcriptional level, in Wistar Furth (WF) relative to Fischer 344 (F344) female rats.	Phenobarbital	0-13	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	88-94
9630465-2	1998	Phenobarbital (PB)-pretreatment of mice induced P450s 3A and 2B and markedly increased serum alanine aminotransferase (ALT) activity after cocaine or norcocaine administration.	Phenobarbital	15-17	glutamic pyruvic transaminase, soluble	Mus musculus	119-122
9630454-1	1998	Phenobarbital (PB)-mediated induction of five forms of cytochrome P450 (CYP2B1, CYP2B2, CYP3A1, CYP2A1, and CYP2C6) and epoxide hydrolase is highly suppressed, at the transcriptional level, in Wistar Furth (WF) relative to Fischer 344 (F344) female rats.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily a, polypeptide 1	Rattus norvegicus	96-102
9630454-1	1998	Phenobarbital (PB)-mediated induction of five forms of cytochrome P450 (CYP2B1, CYP2B2, CYP3A1, CYP2A1, and CYP2C6) and epoxide hydrolase is highly suppressed, at the transcriptional level, in Wistar Furth (WF) relative to Fischer 344 (F344) female rats.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	108-114
9571149-2	1998	Furthermore, phenobarbital (1 and 2 mM) induces mrp2 gene expression, probably explaining the increase in bile-salt-independent bile flow caused by phenobarbital, while the cholestatic drug ethinyl estradiol (10(-6) M) leads to an increase in mrp2 mRNA but decreases Mrp2 protein level probably via a posttranscriptional mechanism.	Phenobarbital	13-26	ATP binding cassette subfamily B member 4	Rattus norvegicus	48-52
9630454-1	1998	Phenobarbital (PB)-mediated induction of five forms of cytochrome P450 (CYP2B1, CYP2B2, CYP3A1, CYP2A1, and CYP2C6) and epoxide hydrolase is highly suppressed, at the transcriptional level, in Wistar Furth (WF) relative to Fischer 344 (F344) female rats.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	72-78
9630454-1	1998	Phenobarbital (PB)-mediated induction of five forms of cytochrome P450 (CYP2B1, CYP2B2, CYP3A1, CYP2A1, and CYP2C6) and epoxide hydrolase is highly suppressed, at the transcriptional level, in Wistar Furth (WF) relative to Fischer 344 (F344) female rats.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	80-86
9630454-1	1998	Phenobarbital (PB)-mediated induction of five forms of cytochrome P450 (CYP2B1, CYP2B2, CYP3A1, CYP2A1, and CYP2C6) and epoxide hydrolase is highly suppressed, at the transcriptional level, in Wistar Furth (WF) relative to Fischer 344 (F344) female rats.	Phenobarbital	15-17	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	88-94
9630454-1	1998	Phenobarbital (PB)-mediated induction of five forms of cytochrome P450 (CYP2B1, CYP2B2, CYP3A1, CYP2A1, and CYP2C6) and epoxide hydrolase is highly suppressed, at the transcriptional level, in Wistar Furth (WF) relative to Fischer 344 (F344) female rats.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily a, polypeptide 1	Rattus norvegicus	96-102
9630454-1	1998	Phenobarbital (PB)-mediated induction of five forms of cytochrome P450 (CYP2B1, CYP2B2, CYP3A1, CYP2A1, and CYP2C6) and epoxide hydrolase is highly suppressed, at the transcriptional level, in Wistar Furth (WF) relative to Fischer 344 (F344) female rats.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	108-114
9630454-8	1998	The LFD suppressed PB-induction of CYP mRNA and protein in WF but not F344 rats.	Phenobarbital	19-21	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	35-38
9571149-2	1998	Furthermore, phenobarbital (1 and 2 mM) induces mrp2 gene expression, probably explaining the increase in bile-salt-independent bile flow caused by phenobarbital, while the cholestatic drug ethinyl estradiol (10(-6) M) leads to an increase in mrp2 mRNA but decreases Mrp2 protein level probably via a posttranscriptional mechanism.	Phenobarbital	13-26	ATP binding cassette subfamily B member 4	Rattus norvegicus	243-247
9571149-2	1998	Furthermore, phenobarbital (1 and 2 mM) induces mrp2 gene expression, probably explaining the increase in bile-salt-independent bile flow caused by phenobarbital, while the cholestatic drug ethinyl estradiol (10(-6) M) leads to an increase in mrp2 mRNA but decreases Mrp2 protein level probably via a posttranscriptional mechanism.	Phenobarbital	13-26	ATP binding cassette subfamily C member 2	Rattus norvegicus	267-271
9571149-2	1998	Furthermore, phenobarbital (1 and 2 mM) induces mrp2 gene expression, probably explaining the increase in bile-salt-independent bile flow caused by phenobarbital, while the cholestatic drug ethinyl estradiol (10(-6) M) leads to an increase in mrp2 mRNA but decreases Mrp2 protein level probably via a posttranscriptional mechanism.	Phenobarbital	148-161	ATP binding cassette subfamily B member 4	Rattus norvegicus	48-52
9559668-0	1998	Phenobarbital induces cytochrome P4501A2 hnRNA, mRNA and protein in the liver of C57BL/6J wild type and aryl hydrocarbon receptor knock-out mice.	Phenobarbital	0-13	aryl-hydrocarbon receptor	Mus musculus	104-129
9525968-0	1998	The CYP2B2 phenobarbital response unit contains an accessory factor element and a putative glucocorticoid response element essential for conferring maximal phenobarbital responsiveness.	Phenobarbital	11-24	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	4-10
9525968-0	1998	The CYP2B2 phenobarbital response unit contains an accessory factor element and a putative glucocorticoid response element essential for conferring maximal phenobarbital responsiveness.	Phenobarbital	156-169	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	4-10
9525968-2	1998	One of the major unsolved problems in xenobiotic metabolism is the molecular mechanism whereby phenobarbital induces hepatic enzymes, particularly CYP2B1 and CYP2B2 in rat liver.	Phenobarbital	95-108	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	147-153
9525968-2	1998	One of the major unsolved problems in xenobiotic metabolism is the molecular mechanism whereby phenobarbital induces hepatic enzymes, particularly CYP2B1 and CYP2B2 in rat liver.	Phenobarbital	95-108	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	158-164
9525968-3	1998	By using primary rat hepatocytes for transfection analyses, we previously identified in the CYP2B2 5"-flank a 163-base pair Sau3AI fragment that confers phenobarbital inducibility on a cat reporter gene and that has the properties of a transcriptional enhancer.	Phenobarbital	153-166	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	92-98
9525968-9	1998	Taken together, the results indicate that phenobarbital induction of CYP2B2 requires interactions among multiple regulatory proteins and cis-acting elements constituting a phenobarbital response unit.	Phenobarbital	42-55	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	69-75
9525968-9	1998	Taken together, the results indicate that phenobarbital induction of CYP2B2 requires interactions among multiple regulatory proteins and cis-acting elements constituting a phenobarbital response unit.	Phenobarbital	172-185	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	69-75
9547348-0	1998	Activation by diverse xenochemicals of the 51-base pair phenobarbital-responsive enhancer module in the CYP2B10 gene.	Phenobarbital	56-69	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	104-111
9547348-1	1998	By extending previous studies of the phenobarbital (PB)-responsive 132-base pair (bp) enhancer sequence in the CYP2B10 gene, we have delimited a 51-bp enhancer element that is fully inducible by PB in mouse primary hepatocytes.	Phenobarbital	37-50	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	111-118
9547348-1	1998	By extending previous studies of the phenobarbital (PB)-responsive 132-base pair (bp) enhancer sequence in the CYP2B10 gene, we have delimited a 51-bp enhancer element that is fully inducible by PB in mouse primary hepatocytes.	Phenobarbital	52-54	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	111-118
9547348-1	1998	By extending previous studies of the phenobarbital (PB)-responsive 132-base pair (bp) enhancer sequence in the CYP2B10 gene, we have delimited a 51-bp enhancer element that is fully inducible by PB in mouse primary hepatocytes.	Phenobarbital	195-197	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	111-118
9563480-16	1998	This age-dependent nature of initiation, together with the differential responses of Bcl-2+ and Bcl-2- lesions, may be responsible for the apparently contradictory outcomes of PB treatment in infant and adult B6C3F1 mice.	Phenobarbital	176-178	BCL2 apoptosis regulator	Homo sapiens	85-90
9563480-16	1998	This age-dependent nature of initiation, together with the differential responses of Bcl-2+ and Bcl-2- lesions, may be responsible for the apparently contradictory outcomes of PB treatment in infant and adult B6C3F1 mice.	Phenobarbital	176-178	BCL2 apoptosis regulator	Homo sapiens	96-101
9545515-3	1998	By Northern blotting, using an oligonucleotide specific to CYP3A31, the mRNA for this isozyme was shown to be expressed constitutively in liver and induced by treatment with phenobarbital but repressed by 3-methylcholanthrene or dexamethasone treatments.	Phenobarbital	174-187	cytochrome P450 3A31	Mesocricetus auratus	59-66
9559668-3	1998	Using both wild type and aryl hydrocarbon receptor knock out C57BL/6J mice, we demonstrate that phenobarbital induced hnRNA, mRNA and protein for the cytochrome P-4501A2 gene in the presence or absence of the aryl hydrocarbon receptor.	Phenobarbital	96-109	aryl-hydrocarbon receptor	Mus musculus	25-50
9559668-3	1998	Using both wild type and aryl hydrocarbon receptor knock out C57BL/6J mice, we demonstrate that phenobarbital induced hnRNA, mRNA and protein for the cytochrome P-4501A2 gene in the presence or absence of the aryl hydrocarbon receptor.	Phenobarbital	96-109	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	150-169
9559668-3	1998	Using both wild type and aryl hydrocarbon receptor knock out C57BL/6J mice, we demonstrate that phenobarbital induced hnRNA, mRNA and protein for the cytochrome P-4501A2 gene in the presence or absence of the aryl hydrocarbon receptor.	Phenobarbital	96-109	aryl-hydrocarbon receptor	Mus musculus	209-234
9559668-4	1998	Using the DNA binding site for the aryl hydrocarbon receptor as a probe, gel retardation analyses showed that phenobarbital treatment induced protein binding, regardless of the presence of the aryl hydrocarbon receptor.	Phenobarbital	110-123	aryl-hydrocarbon receptor	Mus musculus	35-60
9480906-0	1998	Protein serine/threonine phosphatase inhibitors suppress phenobarbital-induced Cyp2b10 gene transcription in mouse primary hepatocytes.	Phenobarbital	57-70	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	79-86
9500848-9	1998	The testosterone 7 alpha-hydroxylase activity and the mRNA level in liver were both decreased moderately by administration of 3-methylcholanthrene and slightly by administration of phenobarbital.	Phenobarbital	181-194	cytochrome P450 2A9	Mesocricetus auratus	4-36
9537282-2	1998	DDT, DDE, and DDD were each found to be pure phenobarbital-type cytochrome P-450 inducers in the male F344/NCr rat, causing induction of hepatic CYP2B and CYP3A, but not CYP1A.	Phenobarbital	45-58	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	64-80
9537282-2	1998	DDT, DDE, and DDD were each found to be pure phenobarbital-type cytochrome P-450 inducers in the male F344/NCr rat, causing induction of hepatic CYP2B and CYP3A, but not CYP1A.	Phenobarbital	45-58	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	155-160
9480906-1	1998	Using a primary hepatocyte culture in which the mouse Cyp2b10 gene transcription is activated by phenobarbital (PB)-type inducers, we examined the cellular signalling mechanisms associated with PB induction.	Phenobarbital	97-110	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	54-61
9480906-1	1998	Using a primary hepatocyte culture in which the mouse Cyp2b10 gene transcription is activated by phenobarbital (PB)-type inducers, we examined the cellular signalling mechanisms associated with PB induction.	Phenobarbital	112-114	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	54-61
9480906-1	1998	Using a primary hepatocyte culture in which the mouse Cyp2b10 gene transcription is activated by phenobarbital (PB)-type inducers, we examined the cellular signalling mechanisms associated with PB induction.	Phenobarbital	194-196	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	54-61
9634719-1	1998	The transcription level of CYP2B1/2 gene in the liver of Sprague-Dawley (SD), Brattleboro (BL) and Wistar (W) rats treated with isosafrol (IS), Arochlor 1254 (AC), phenobarbital (PB) and triphenildioxane (TPD) was studied.	Phenobarbital	164-177	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	27-35
9547864-6	1998	The decreased level of Cx32 protein in plasma membranes was observed in the PB group.	Phenobarbital	76-78	gap junction protein, beta 1	Rattus norvegicus	23-27
9634719-1	1998	The transcription level of CYP2B1/2 gene in the liver of Sprague-Dawley (SD), Brattleboro (BL) and Wistar (W) rats treated with isosafrol (IS), Arochlor 1254 (AC), phenobarbital (PB) and triphenildioxane (TPD) was studied.	Phenobarbital	179-181	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	27-35
9472691-9	1998	When introduced into primary rat liver cell cultures by transient transfection, hPPAR alpha-6/29 prevented the suppression of hepatocyte apoptosis by the PP nafenopin, but not that seen in response to phenobarbitone (PB), a nongenotoxic carcinogen whose action does not involve PPAR alpha.	Phenobarbital	217-219	peroxisome proliferator activated receptor alpha	Homo sapiens	80-85
9448743-10	1998	Densitometric quantitation of immunoblots revealed that the hepatic CYP2B content was elevated by approximately 15-, 22-, and 25-fold, and the hepatic CYP3A content was increased by 2-, 2-, and 8-fold after treatment with zolazepam, Telazol, and PB, respectively.	Phenobarbital	246-248	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	151-156
9566755-4	1998	Similarly, HST-a and ASTIV mRNA levels become suppressed or induced, respectively, following in vivo treatment with phenobarbital (PB)-like CYP2B/3A inducers or prototypic CYP3A inducers such as glucocorticoid hormones.	Phenobarbital	116-129	fibroblast growth factor 4	Rattus norvegicus	11-14
9566755-4	1998	Similarly, HST-a and ASTIV mRNA levels become suppressed or induced, respectively, following in vivo treatment with phenobarbital (PB)-like CYP2B/3A inducers or prototypic CYP3A inducers such as glucocorticoid hormones.	Phenobarbital	116-129	sulfotransferase family 1A member 1	Rattus norvegicus	21-26
9566755-4	1998	Similarly, HST-a and ASTIV mRNA levels become suppressed or induced, respectively, following in vivo treatment with phenobarbital (PB)-like CYP2B/3A inducers or prototypic CYP3A inducers such as glucocorticoid hormones.	Phenobarbital	131-133	fibroblast growth factor 4	Rattus norvegicus	11-14
9566755-4	1998	Similarly, HST-a and ASTIV mRNA levels become suppressed or induced, respectively, following in vivo treatment with phenobarbital (PB)-like CYP2B/3A inducers or prototypic CYP3A inducers such as glucocorticoid hormones.	Phenobarbital	131-133	sulfotransferase family 1A member 1	Rattus norvegicus	21-26
9448747-0	1998	Effect of phenobarbital on hepatic CYP1A1 and CYP1A2 in the Ahr-null mouse.	Phenobarbital	10-23	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	35-41
9448747-0	1998	Effect of phenobarbital on hepatic CYP1A1 and CYP1A2 in the Ahr-null mouse.	Phenobarbital	10-23	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	46-52
9448747-2	1998	Using the Ahr -/- mice, we examined the induction of CYP1A1 and CYP1A2 by PB.	Phenobarbital	74-76	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	53-59
9448747-2	1998	Using the Ahr -/- mice, we examined the induction of CYP1A1 and CYP1A2 by PB.	Phenobarbital	74-76	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	64-70
9448747-3	1998	CYP1A2 mRNA and protein were induced by PB in the null mice, suggesting that CYP1A2 is regulated by PB by a mechanism independent of the aryl hydrocarbon receptor (AHR).	Phenobarbital	40-42	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	0-6
9448747-3	1998	CYP1A2 mRNA and protein were induced by PB in the null mice, suggesting that CYP1A2 is regulated by PB by a mechanism independent of the aryl hydrocarbon receptor (AHR).	Phenobarbital	40-42	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	77-83
9448747-3	1998	CYP1A2 mRNA and protein were induced by PB in the null mice, suggesting that CYP1A2 is regulated by PB by a mechanism independent of the aryl hydrocarbon receptor (AHR).	Phenobarbital	100-102	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	0-6
9448747-3	1998	CYP1A2 mRNA and protein were induced by PB in the null mice, suggesting that CYP1A2 is regulated by PB by a mechanism independent of the aryl hydrocarbon receptor (AHR).	Phenobarbital	100-102	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	77-83
9472691-9	1998	When introduced into primary rat liver cell cultures by transient transfection, hPPAR alpha-6/29 prevented the suppression of hepatocyte apoptosis by the PP nafenopin, but not that seen in response to phenobarbitone (PB), a nongenotoxic carcinogen whose action does not involve PPAR alpha.	Phenobarbital	217-219	peroxisome proliferator activated receptor alpha	Rattus norvegicus	81-91
9472709-5	1998	These results indicate that the inhibitory actions of TPA and PB on GJIC are cell-specific rather than connexin-specific and that TPA inhibits connexin43 and connexin32-mediated GJIC through a protein kinase C-dependent mechanism.	Phenobarbital	62-64	gap junction protein, alpha 1	Rattus norvegicus	143-153
9472709-5	1998	These results indicate that the inhibitory actions of TPA and PB on GJIC are cell-specific rather than connexin-specific and that TPA inhibits connexin43 and connexin32-mediated GJIC through a protein kinase C-dependent mechanism.	Phenobarbital	62-64	gap junction protein, beta 1	Rattus norvegicus	158-168
9441723-14	1997	While MX inhibited more than 90% of the PB-induced CYP2B activity in the microsomes, MK caused only a small (about 20%) reduction in PB-induced CYP2B enzyme activity.	Phenobarbital	40-42	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	51-56
9443857-7	1998	Antibody inhibition experiments demonstrated ethosuximide metabolite levels for PB microsomes were not affected by CYP2B1 antibodies, whereas CYP3A2 antibodies reduced metabolite levels for both PB and CTZ microsomes by over 80%.	Phenobarbital	195-197	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	142-148
10366993-10	1998	Both phenobarbital and DTZ decreased SBP and DBP significantly without affecting the HR.	Phenobarbital	5-18	sex hormone-binding globulin	Oryctolagus cuniculus	37-40
10366993-10	1998	Both phenobarbital and DTZ decreased SBP and DBP significantly without affecting the HR.	Phenobarbital	5-18	vitamin D-binding protein	Oryctolagus cuniculus	45-48
9414482-0	1998	Regulatory DNA elements of phenobarbital-responsive cytochrome P450 CYP2B genes.	Phenobarbital	27-40	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	68-73
9414482-1	1998	This article reviews recent progress in characterizing cis-acting DNA elements of the phenobarbital-inducible CYP2B genes.	Phenobarbital	86-99	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	110-115
9664231-4	1998	At equivalent 100 microM concentrations, the C6 and C8 MDB congeners were more effective than the prototypical inducer phenobarbital (PB) with respect to induction potency of CYP2B1, CYP2B2, and CYP3A1 gene expression.	Phenobarbital	119-132	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	175-181
9664231-4	1998	At equivalent 100 microM concentrations, the C6 and C8 MDB congeners were more effective than the prototypical inducer phenobarbital (PB) with respect to induction potency of CYP2B1, CYP2B2, and CYP3A1 gene expression.	Phenobarbital	119-132	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	195-201
9664231-4	1998	At equivalent 100 microM concentrations, the C6 and C8 MDB congeners were more effective than the prototypical inducer phenobarbital (PB) with respect to induction potency of CYP2B1, CYP2B2, and CYP3A1 gene expression.	Phenobarbital	134-136	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	175-181
9664231-4	1998	At equivalent 100 microM concentrations, the C6 and C8 MDB congeners were more effective than the prototypical inducer phenobarbital (PB) with respect to induction potency of CYP2B1, CYP2B2, and CYP3A1 gene expression.	Phenobarbital	134-136	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	183-189
9502574-2	1998	Two genes, the gene encoding the furosemide-sensitive apical Na-K-2Cl cotransporter (NKCC2) and the gene encoding the luminal inwardly-rectifying potassium channel Kir 1.1 (ROMK), have been reported to cause the neonatal subtype of Bartter syndrome.	Phenobarbital	118-125	potassium inwardly rectifying channel subfamily J member 1	Homo sapiens	173-177
9394036-5	1997	Administration of p-AZPB to rats increased hepatic CYP2B1/2 protein and testosterone 16beta-hydroxylase activity, although the effects were less than those of unmodified PB.	Phenobarbital	22-24	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	51-59
9394036-8	1997	The results showed that p-nitro-PB, m-amino-PB, and p-hydroxy-PB were also potent inducers for CYP2B1/2, with lower activity than that of unmodified PB, whereas the other three isomers had no effect.	Phenobarbital	32-34	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	95-101
9441723-13	1997	To evaluate the ability of MK to inhibit phenobarbital-induced CYP2B activity, mice were given 500 ppm phenobarbital (PB) in the drinking water for 5 days to induce CYP2B isozymes, followed by a single equimolar (0.67 mmol/kg) oral gavage dose of either MK (198 mg/kg) or MX (200 mg/kg), and microsomes were prepared 18 h later.	Phenobarbital	41-54	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	63-68
9441723-14	1997	While MX inhibited more than 90% of the PB-induced CYP2B activity in the microsomes, MK caused only a small (about 20%) reduction in PB-induced CYP2B enzyme activity.	Phenobarbital	133-135	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	144-149
9441723-16	1997	MK is a PB-type inducer of mouse liver CYP2B isozymes, but unlike MX, MK does not effectively inhibit PB-induced CYP2B enzyme activity.	Phenobarbital	8-10	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	39-44
9436821-7	1997	The IL-1beta-stimulated increase in nitrite formation, iNOS protein, and mRNA abundance in VSMCs was significantly augmented in the presence of thiopental (100 microM), whereas methohexital, hexobarbital, pentobarbital, and phenobarbital were without effect.	Phenobarbital	224-237	interleukin 1 beta	Homo sapiens	4-12
9506012-3	1997	The final model describing valproic acid relative clearance was CL (mL/hr/kg) = 15.6.TBW (kg)-0.252.DOSE (mg/kg/day)0.183.0.898GEN.COPB.COCBZ, where COPB equals 1.10 if the patient is treated with phenobarbital, a value of unity otherwise, and COCBZ equals 0.769.DOSE (mg/kg/day)0.179 if the patient is treated with carbamazepine, a value of unity otherwise.	Phenobarbital	197-210	COPI coat complex subunit beta 1	Homo sapiens	131-135
20654335-9	1997	After exposure of the collagen gel cultures to 3.2 mm phenobarbital, the mEH activity was increased to the same extent (factor 2 to 2.5) in both culture models.	Phenobarbital	54-67	epoxide hydrolase 1, microsomal	Mus musculus	73-76
9434138-5	1997	The level of cytochrome P-450 in freshly prepared hepatocytes from phenobarbital-treated rats was 2.5 times higher than that from the control rats, and remained about three times higher than the latter after 22 h of incubation with 2 mM hydrazine.	Phenobarbital	67-80	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
9347925-8	1997	PB treated rats had a higher cytochrome P450 2B1/2 activity over the entire course of feeding.	Phenobarbital	0-2	cytochrome P450 2B1	Rattus norvegicus	29-48
9367997-0	1997	Phenobarbital alters protein binding to the CYP2B1/2 phenobarbital-responsive unit in native chromatin.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	44-50
9367997-0	1997	Phenobarbital alters protein binding to the CYP2B1/2 phenobarbital-responsive unit in native chromatin.	Phenobarbital	53-66	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	44-50
9367997-2	1997	Functional analyses have identified a phenobarbital-responsive unit in the rat CYP2B1/2 and mouse Cyp2b10 genes about -2.3 kilobase pairs from the transcriptional start site, but little or no changes in protein binding to this region were observed in vitro.	Phenobarbital	38-51	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	79-85
9367997-2	1997	Functional analyses have identified a phenobarbital-responsive unit in the rat CYP2B1/2 and mouse Cyp2b10 genes about -2.3 kilobase pairs from the transcriptional start site, but little or no changes in protein binding to this region were observed in vitro.	Phenobarbital	38-51	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	98-105
9367997-3	1997	To examine the role of chromatin structure, protein binding to the phenobarbital-responsive unit assessed by in vitro DNase I footprinting was compared with that assessed by DNase I in vivo footprints in native chromatin.	Phenobarbital	67-80	deoxyribonuclease 1	Rattus norvegicus	118-125
9406998-1	1997	Human microsomal epoxide hydrolase (HYL1) plays an important role in the detoxification of environmental compounds and drugs, such as the aromatic anticonvulsants phenytoin, carbamazepine, and phenobarbital, by converting their P450-generated epoxide metabolites into nontoxic diols.	Phenobarbital	193-206	epoxide hydrolase 1	Homo sapiens	6-34
9407006-0	1997	The Drosophila cytochrome P450 gene Cyp6a2: structure, localization, heterologous expression, and induction by phenobarbital.	Phenobarbital	111-124	Cytochrome P450-6a2	Drosophila melanogaster	36-42
9407006-2	1997	Phenobarbital treatment of flies leads to a rapid increase in the level of CYP6A2 mRNA and to an increased production of the CYP6A2 protein.	Phenobarbital	0-13	Cytochrome P450-6a2	Drosophila melanogaster	75-81
9407006-2	1997	Phenobarbital treatment of flies leads to a rapid increase in the level of CYP6A2 mRNA and to an increased production of the CYP6A2 protein.	Phenobarbital	0-13	Cytochrome P450-6a2	Drosophila melanogaster	125-131
9407006-9	1997	The Cyp6a2 gene appears to be a suitable model for a genetic analysis of the phenobarbital induction process.	Phenobarbital	77-90	Cytochrome P450-6a2	Drosophila melanogaster	4-10
9327729-7	1997	The relatively infrequent basophilic tumors found with phenobarbital treatment, however, did express Bcl-2.	Phenobarbital	55-68	B cell leukemia/lymphoma 2	Mus musculus	101-106
9357489-2	1997	Phenobarbitone (inducer) treatment showed induced levels of hepatic mitochondrial and microsomal cytochrome P-450 and glutathione-S-transferase in normal as well as in infected mice.	Phenobarbital	0-14	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	97-143
9328175-3	1997	Studies undertaken at low substrate concentration (20 microM) with microsomes from livers of rats treated with the enzyme inducers phenobarbital, dexamethasone, isosafrole and isoniazid indicated that a number of cytochrome P450 isozymes can catalyze the high affinity component.	Phenobarbital	131-144	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	213-228
9314612-4	1997	Compounds which induce CYP3A4 (e.g. carbamazepine, phenytoin and phenobarbital) increase felbamate clearance.	Phenobarbital	65-78	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	23-29
9314612-6	1997	Felbamate has been shown in vitro to inhibit CYP2C19, which would account for its effect on phenytoin clearance, and it had been postulated that this could be the mechanism underlying the reduced clearance of phenobarbital by felbamate.	Phenobarbital	209-222	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	45-52
9262383-1	1997	We have previously demonstrated that specific activation of a cAMP-dependent protein kinase A (PKA) pathway resulted in complete repression of phenobarbital (PB)-inducible CYP gene expression in primary rat hepatocyte cultures.	Phenobarbital	143-156	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	172-175
9260906-9	1997	Phenobarbital slightly increased the CYP2B-mediated activities of pentoxyresorufin-O-depentylase, 2beta- and 16beta-testosterone hydroxylase.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	37-42
9280408-0	1997	Effect of ovariectomy and androgen on phenobarbital induction of hepatic CYP2B1 and CYP2B2 in Sprague-Dawley rats.	Phenobarbital	38-51	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	73-79
9280408-0	1997	Effect of ovariectomy and androgen on phenobarbital induction of hepatic CYP2B1 and CYP2B2 in Sprague-Dawley rats.	Phenobarbital	38-51	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	84-90
9280408-1	1997	The purpose of this study was to investigate the impact of prepubertal ovariectomy and postpubertal administration of testosterone on inducibility of rat hepatic CYP2B1 and CYP2B2 by phenobarbital.	Phenobarbital	183-196	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	162-168
9280408-1	1997	The purpose of this study was to investigate the impact of prepubertal ovariectomy and postpubertal administration of testosterone on inducibility of rat hepatic CYP2B1 and CYP2B2 by phenobarbital.	Phenobarbital	183-196	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	173-179
9280408-5	1997	The lesser inducibility of CYP2B1 in adult female rats was attributed to the presence of an intact ovary because prepubertal ovariectomy (day 25 of age) resulted in increased induction of CYP2B1 and its associated activities (androstenedione 16beta-hydroxylase, benzyloxyresorufin O-dealkylase and pentoxyresorufin O-dealkylase) by phenobarbital.	Phenobarbital	332-345	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	27-33
9280408-8	1997	Overall, the results show a sex difference in phenobarbital induction of hepatic CYP2B1 but not CYP2B2 in adult Sprague-Dawley rats.	Phenobarbital	46-59	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	81-87
9280408-9	1997	They also indicate that prepubertal ovariectomy enhances the effect of phenobarbital on CYP2B1, whereas administration of testosterone enanthate postpubertally does not influence the inducibility of either CYP2B1 or CYP2B2 in prepubertally ovariectomized adult rats.	Phenobarbital	71-84	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	88-94
9262383-1	1997	We have previously demonstrated that specific activation of a cAMP-dependent protein kinase A (PKA) pathway resulted in complete repression of phenobarbital (PB)-inducible CYP gene expression in primary rat hepatocyte cultures.	Phenobarbital	158-160	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	172-175
9262383-4	1997	PB induction responses were assessed by use of specific hybridization probes to CYP2B1 and CYP2B2 mRNAs.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	80-86
9262383-4	1997	PB induction responses were assessed by use of specific hybridization probes to CYP2B1 and CYP2B2 mRNAs.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	91-97
9230284-8	1997	Addition of the hepatocyte mitogen and autocrine growth factor, transforming growth factor-alpha (TGF-alpha), to culture medium lacking PB induced a dose-dependent increase in 6/27C1 hepatocyte colony formation.	Phenobarbital	136-138	transforming growth factor alpha	Rattus norvegicus	64-96
9298501-2	1997	Several drugs and other compounds, e.g. phenobarbital, gemfibrozil, fenofibrate, prednisone, estrogen and alcohol, induce apolipoprotein A-I synthesis.	Phenobarbital	40-53	apolipoprotein A1	Homo sapiens	122-140
9210976-13	1997	However, the content of hepatic cytochrome P-450 and the weight of liver increased significantly in PB pretreated rats, while the values were not significantly different between the control and CM pretreated rats.	Phenobarbital	100-102	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	32-48
9230198-4	1997	In the present study, using this in vitro model of hepatocarcinogenesis, we demonstrated that phenobarbital, a tumor promoter of rodent hepatocarcinogenesis, triggers remarkable apoptosis specifically in the c-myc-transfected CHST8 cells at 39 degrees C, which show abundant c-myc expression despite growth arrest.	Phenobarbital	94-107	carbohydrate sulfotransferase 8	Mus musculus	226-231
9230198-5	1997	Dissociation of p53 proteins from degrading T antigens followed by a phenobarbital and c-myc-dependent, 15-fold induction of Bax protein, known to activate the apoptotic pathway downstream of p53, occurred in association with this phenomenon.	Phenobarbital	69-82	transformation related protein 53, pseudogene	Mus musculus	16-19
9230198-5	1997	Dissociation of p53 proteins from degrading T antigens followed by a phenobarbital and c-myc-dependent, 15-fold induction of Bax protein, known to activate the apoptotic pathway downstream of p53, occurred in association with this phenomenon.	Phenobarbital	69-82	BCL2-associated X protein	Mus musculus	125-128
9230198-5	1997	Dissociation of p53 proteins from degrading T antigens followed by a phenobarbital and c-myc-dependent, 15-fold induction of Bax protein, known to activate the apoptotic pathway downstream of p53, occurred in association with this phenomenon.	Phenobarbital	69-82	transformation related protein 53, pseudogene	Mus musculus	192-195
9230198-6	1997	The effects of phenobarbital and c-myc in increasing Bax on shifting the temperature from 33 degrees C to 39 degrees C were additive, with both having similar degrees of influence on the protein level.	Phenobarbital	15-28	BCL2-associated X protein	Mus musculus	53-56
9230198-7	1997	Interestingly, subsequent introduction of an activated c-H-ras oncogene into the c-myc-transfected CHST8 cells resulted not only in escape from the growth arrest at 39 degrees C but also in complete inhibition of the phenobarbital-inducible apoptosis along with de novo induction of the Bax antagonist, Bcl-2.	Phenobarbital	217-230	Harvey rat sarcoma virus oncogene	Mus musculus	55-62
9230198-7	1997	Interestingly, subsequent introduction of an activated c-H-ras oncogene into the c-myc-transfected CHST8 cells resulted not only in escape from the growth arrest at 39 degrees C but also in complete inhibition of the phenobarbital-inducible apoptosis along with de novo induction of the Bax antagonist, Bcl-2.	Phenobarbital	217-230	carbohydrate sulfotransferase 8	Mus musculus	99-104
9230198-7	1997	Interestingly, subsequent introduction of an activated c-H-ras oncogene into the c-myc-transfected CHST8 cells resulted not only in escape from the growth arrest at 39 degrees C but also in complete inhibition of the phenobarbital-inducible apoptosis along with de novo induction of the Bax antagonist, Bcl-2.	Phenobarbital	217-230	BCL2-associated X protein	Mus musculus	287-290
9230198-7	1997	Interestingly, subsequent introduction of an activated c-H-ras oncogene into the c-myc-transfected CHST8 cells resulted not only in escape from the growth arrest at 39 degrees C but also in complete inhibition of the phenobarbital-inducible apoptosis along with de novo induction of the Bax antagonist, Bcl-2.	Phenobarbital	217-230	B cell leukemia/lymphoma 2	Mus musculus	303-308
9230198-8	1997	These findings strongly suggest that the phenobarbital-inducible apoptosis is mediated by Bax.	Phenobarbital	41-54	BCL2-associated X protein	Mus musculus	90-93
9230284-8	1997	Addition of the hepatocyte mitogen and autocrine growth factor, transforming growth factor-alpha (TGF-alpha), to culture medium lacking PB induced a dose-dependent increase in 6/27C1 hepatocyte colony formation.	Phenobarbital	136-138	transforming growth factor alpha	Rattus norvegicus	98-107
9230284-9	1997	At the optimal concentration of 3 ng/ml, TGF-alpha sustained hepatocyte clonal expansion at 84% of the level induced by 2 mM PB.	Phenobarbital	125-127	transforming growth factor alpha	Rattus norvegicus	41-50
9357164-9	1997	Again the sensitivity of the response to CCl4 was enhanced remarkably in hepatocytes isolated from phenobarbital- pretreated rats; LDH leakage increased by 3-fold and thio-barbituric acid reactive substances by 25-fold.	Phenobarbital	99-112	C-C motif chemokine ligand 4	Rattus norvegicus	41-45
9195908-6	1997	In addition, IL-1 strongly suppressed the induction of rGSTA2 by 3-methylcholanthrene, oltipraz (a synthetic derivative of 1, 2-dithiole-3-thione), and phenobarbital and that of rGSTM1 by oltipraz and phenobarbital, whereas it was ineffective on rGSTP1 induction by these compounds.	Phenobarbital	152-165	glutathione S-transferase alpha 2	Rattus norvegicus	55-61
9195908-6	1997	In addition, IL-1 strongly suppressed the induction of rGSTA2 by 3-methylcholanthrene, oltipraz (a synthetic derivative of 1, 2-dithiole-3-thione), and phenobarbital and that of rGSTM1 by oltipraz and phenobarbital, whereas it was ineffective on rGSTP1 induction by these compounds.	Phenobarbital	201-214	glutathione S-transferase alpha 2	Rattus norvegicus	55-61
9195908-6	1997	In addition, IL-1 strongly suppressed the induction of rGSTA2 by 3-methylcholanthrene, oltipraz (a synthetic derivative of 1, 2-dithiole-3-thione), and phenobarbital and that of rGSTM1 by oltipraz and phenobarbital, whereas it was ineffective on rGSTP1 induction by these compounds.	Phenobarbital	201-214	glutathione S-transferase mu 1	Rattus norvegicus	178-184
9169466-0	1997	Characterization of a phenobarbital-responsive enhancer module in mouse P450 Cyp2b10 gene.	Phenobarbital	22-35	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	77-84
9185622-1	1997	Our laboratory has proposed that phenobarbital (PB), a typical lipophilic agent that induces some members of the supergene family of liver microsomal cytochromes P450 (e.g., CYP2B1/2 and CYP3A23), acts through a complex process inhibitable by the presence of growth hormone (GH), the absence of some components of the extracellular matrix, or a disrupted cytoskeleton.	Phenobarbital	33-46	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	174-180
9185622-1	1997	Our laboratory has proposed that phenobarbital (PB), a typical lipophilic agent that induces some members of the supergene family of liver microsomal cytochromes P450 (e.g., CYP2B1/2 and CYP3A23), acts through a complex process inhibitable by the presence of growth hormone (GH), the absence of some components of the extracellular matrix, or a disrupted cytoskeleton.	Phenobarbital	33-46	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	187-194
9185622-1	1997	Our laboratory has proposed that phenobarbital (PB), a typical lipophilic agent that induces some members of the supergene family of liver microsomal cytochromes P450 (e.g., CYP2B1/2 and CYP3A23), acts through a complex process inhibitable by the presence of growth hormone (GH), the absence of some components of the extracellular matrix, or a disrupted cytoskeleton.	Phenobarbital	33-46	gonadotropin releasing hormone receptor	Rattus norvegicus	259-273
9185622-1	1997	Our laboratory has proposed that phenobarbital (PB), a typical lipophilic agent that induces some members of the supergene family of liver microsomal cytochromes P450 (e.g., CYP2B1/2 and CYP3A23), acts through a complex process inhibitable by the presence of growth hormone (GH), the absence of some components of the extracellular matrix, or a disrupted cytoskeleton.	Phenobarbital	33-46	gonadotropin releasing hormone receptor	Rattus norvegicus	275-277
9185622-1	1997	Our laboratory has proposed that phenobarbital (PB), a typical lipophilic agent that induces some members of the supergene family of liver microsomal cytochromes P450 (e.g., CYP2B1/2 and CYP3A23), acts through a complex process inhibitable by the presence of growth hormone (GH), the absence of some components of the extracellular matrix, or a disrupted cytoskeleton.	Phenobarbital	48-50	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	174-180
9185622-1	1997	Our laboratory has proposed that phenobarbital (PB), a typical lipophilic agent that induces some members of the supergene family of liver microsomal cytochromes P450 (e.g., CYP2B1/2 and CYP3A23), acts through a complex process inhibitable by the presence of growth hormone (GH), the absence of some components of the extracellular matrix, or a disrupted cytoskeleton.	Phenobarbital	48-50	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	187-194
9185622-1	1997	Our laboratory has proposed that phenobarbital (PB), a typical lipophilic agent that induces some members of the supergene family of liver microsomal cytochromes P450 (e.g., CYP2B1/2 and CYP3A23), acts through a complex process inhibitable by the presence of growth hormone (GH), the absence of some components of the extracellular matrix, or a disrupted cytoskeleton.	Phenobarbital	48-50	gonadotropin releasing hormone receptor	Rattus norvegicus	259-273
9185622-1	1997	Our laboratory has proposed that phenobarbital (PB), a typical lipophilic agent that induces some members of the supergene family of liver microsomal cytochromes P450 (e.g., CYP2B1/2 and CYP3A23), acts through a complex process inhibitable by the presence of growth hormone (GH), the absence of some components of the extracellular matrix, or a disrupted cytoskeleton.	Phenobarbital	48-50	gonadotropin releasing hormone receptor	Rattus norvegicus	275-277
9185622-2	1997	To verify that these manipulations of the culture environment block specific steps in the PB induction pathway rather than simply exerting nonspecific or toxic effects on CYP2B1/2 gene transcription, we have now examined PB induction of CYP3A23, a gene known to also be transcriptionally activated by dexamethasone (DEX) through a "nonclassical" pathway apparently involving the glucocorticoid receptor.	Phenobarbital	221-223	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	237-244
9185622-3	1997	We found that in primary cultures of adult rat hepatocytes treated with PB, induction of CYP3A23 mRNA, just as we reported for induction of CYP2B1/2 mRNA, required the use of Matrigel (a reconstituted basement membrane) and was blocked by the presence of cytoskeletal inhibitors (colchicine or cytochalasins) or of physiologic concentrations of GH in the culture medium.	Phenobarbital	72-74	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	89-96
9185622-3	1997	We found that in primary cultures of adult rat hepatocytes treated with PB, induction of CYP3A23 mRNA, just as we reported for induction of CYP2B1/2 mRNA, required the use of Matrigel (a reconstituted basement membrane) and was blocked by the presence of cytoskeletal inhibitors (colchicine or cytochalasins) or of physiologic concentrations of GH in the culture medium.	Phenobarbital	72-74	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	140-148
9185622-3	1997	We found that in primary cultures of adult rat hepatocytes treated with PB, induction of CYP3A23 mRNA, just as we reported for induction of CYP2B1/2 mRNA, required the use of Matrigel (a reconstituted basement membrane) and was blocked by the presence of cytoskeletal inhibitors (colchicine or cytochalasins) or of physiologic concentrations of GH in the culture medium.	Phenobarbital	72-74	gonadotropin releasing hormone receptor	Rattus norvegicus	345-347
9185622-4	1997	Moreover, PB induction of CYP3A23 and of CYP2B1/2 mRNAs was greatly diminished by inhibitors of cAMP-dependent protein kinase (PKA).	Phenobarbital	10-12	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	26-33
9185622-4	1997	Moreover, PB induction of CYP3A23 and of CYP2B1/2 mRNAs was greatly diminished by inhibitors of cAMP-dependent protein kinase (PKA).	Phenobarbital	10-12	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	41-47
9185622-6	1997	We conclude that the effects of extracellular matrix, GH, disruption of the cytoskeleton, and activation of cAMP-dependent protein kinase, pharmacologically define multiple, pretranscriptional steps in the pathway(s) for PB induction of liver cytochromes P450.	Phenobarbital	221-223	gonadotropin releasing hormone receptor	Rattus norvegicus	54-56
9202759-7	1997	Similarly, tumor promotion by phenobarbital was completely inhibited in the c-myc/HGF double transgenic mice whereas phenobarbital was an effective tumor promoter in the c-myc single transgenic mice.	Phenobarbital	30-43	hepatocyte growth factor	Mus musculus	82-85
9169013-2	1997	In rat hepatocytes, phenobarbital increases ALA-S gene transcription and dibutyryl cAMP potentiates this induction, whereas insulin and glucose have the opposite effect.	Phenobarbital	20-33	5'-aminolevulinate synthase 1	Rattus norvegicus	44-49
9187311-0	1997	Changes in glutamate receptors, c-fos mRNA expression and activator protein-1 (AP-1) DNA binding activity in the brain of phenobarbital-dependent and -withdrawn rats.	Phenobarbital	122-135	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	79-83
9187311-5	1997	PB withdrawal seizures were followed by increased expression of c-fos mRNA in the hippocampus and cerebral cortex and of c-jun mRNA in the cerebral cortex.	Phenobarbital	0-2	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	64-69
9187311-7	1997	Furthermore, PB withdrawal enhanced AP-1 DNA binding activity in the brain.	Phenobarbital	13-15	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-40
9168259-1	1997	The kinetics of inactivation of cytochrome P450 2B1, the major phenobarbital inducible rat hepatic P450, by N-benzyl-1-aminobenzotriazole (BBT) were characterized.	Phenobarbital	63-76	cytochrome P450 2B1	Rattus norvegicus	32-51
9283635-3	1997	Phenobarbital, a hepatic enzyme inducer, has been used in the treatment of patients with non-insulin-dependent diabetes mellitus (NIDDM), increasing the insulin-mediated glucose disposal.	Phenobarbital	0-13	insulin	Homo sapiens	93-100
9283635-11	1997	These data indicate that phenobarbital activated some of the insulin-stimulated glucose metabolism steps which were depressed in diabetic erythrocytes, supporting the view that erythrocytes participate in glucose homeostasis.	Phenobarbital	25-38	insulin	Homo sapiens	61-68
9140468-0	1997	Enhancing effects of phenobarbital and 3-methylcholanthrene on GST-P-positive liver cell foci development in a new medium-term rat liver bioassay using D-galactosamine.	Phenobarbital	21-34	glutathione S-transferase pi 1	Rattus norvegicus	63-68
9179985-5	1997	Cytochrome P450 oxidatively converted flupyrazofos to flupyrazofos oxon, a major metabolite and phenobarbital-induced microsomes increased this desulphuration by 8-fold.	Phenobarbital	96-109	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-15
9113263-4	1997	These effects were augmented in cells isolated from phenobarbital-treated rats, and the lag phase was reduced, implying that the effects of both drugs were dependent on their cytochrome P-450-mediated metabolism.	Phenobarbital	52-65	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	175-191
9128144-1	1997	Previous studies have revealed the functional importance of the negatively charged amino-acid residue Asp-290 of the phenobarbital-inducible dog liver cytochrome P-450 (P-450) 2B11 (Harlow, G.R.	Phenobarbital	117-130	Cytochrome P450 1A1	Canis lupus familiaris	151-167
9083008-1	1997	Heme deficiency precipitated by CoCl2 administration to rats leads to a striking decrease in the inducibility of CYP2B1/B2 mRNA levels and its transcription by phenobarbitone (PB), besides decreasing the basal levels.	Phenobarbital	160-174	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	113-119
9083008-1	1997	Heme deficiency precipitated by CoCl2 administration to rats leads to a striking decrease in the inducibility of CYP2B1/B2 mRNA levels and its transcription by phenobarbitone (PB), besides decreasing the basal levels.	Phenobarbital	176-178	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	113-119
9144458-0	1997	Cytochrome P450 inactivation during reductive metabolism of 1,1-dichloro-2,2,2-trifluoroethane (HCFC-123) by phenobarbital- and pyridine-induced rat liver microsomes.	Phenobarbital	109-122	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-15
9111218-3	1997	Pretreatment of rats with phenobarbital (PB) substantially increased the catalytic activity of pentoxyresorufin (PR) O-depentylase, an activity catalyzed by cytochrome P450 2B1, in rat hepatocytes.	Phenobarbital	26-39	cytochrome P450 2B1	Rattus norvegicus	157-176
9111218-3	1997	Pretreatment of rats with phenobarbital (PB) substantially increased the catalytic activity of pentoxyresorufin (PR) O-depentylase, an activity catalyzed by cytochrome P450 2B1, in rat hepatocytes.	Phenobarbital	41-43	cytochrome P450 2B1	Rattus norvegicus	157-176
9149374-11	1997	At 72 h, CYP2A5 (coumarin-7-hydroxylase) activity was not detected in rat liver slices but in mouse liver slices, 2A5 was induced 2-fold by beta NF, 11-fold by phenobarbital (PB) and 3-fold by TCDD.	Phenobarbital	160-173	cytochrome P450, family 2, subfamily a, polypeptide 3	Rattus norvegicus	17-39
9149374-11	1997	At 72 h, CYP2A5 (coumarin-7-hydroxylase) activity was not detected in rat liver slices but in mouse liver slices, 2A5 was induced 2-fold by beta NF, 11-fold by phenobarbital (PB) and 3-fold by TCDD.	Phenobarbital	175-177	cytochrome P450, family 2, subfamily a, polypeptide 3	Rattus norvegicus	17-39
9275273-3	1997	Phenobarbital treatment increased the cytochrome P-450 amount and the p-nitrophenol (p-NPh) formation rate in hepatocytes from female and male rats to the same extent.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	38-54
9029046-6	1997	Using isoform-specific antipeptide antibodies, both UGT1.1r and UGT2B1 in Wistar and Sprague-Dawley rats were inducible by PB treatment.	Phenobarbital	123-125	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	64-70
9231341-10	1997	Anti-CYP 2C11 also partially inhibited the N-demethylation of racemic chlorpheniramine in rat-liver microsomes exposed to phenobarbitone and 3-methylcholanthrene.	Phenobarbital	122-136	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	5-13
9231341-11	1997	That CYP 2B1 was involved in the N-demethylation of both enantiomers was also supported by results from an experiment using phenobarbitone-inducible rat-liver microsomes.	Phenobarbital	124-138	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	5-12
9063451-9	1997	A 2-3-fold increase over the basal level of chloramphenicol acetyltransferase activity was observed in phenobarbital-treated co-cultures transfected with the phenobarbital-responsive element construct, although phenobarbital had no effect on large CYP2B1 or CYP2B2 promoter fragments.	Phenobarbital	103-116	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	248-254
9063451-9	1997	A 2-3-fold increase over the basal level of chloramphenicol acetyltransferase activity was observed in phenobarbital-treated co-cultures transfected with the phenobarbital-responsive element construct, although phenobarbital had no effect on large CYP2B1 or CYP2B2 promoter fragments.	Phenobarbital	103-116	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	258-264
9063451-9	1997	A 2-3-fold increase over the basal level of chloramphenicol acetyltransferase activity was observed in phenobarbital-treated co-cultures transfected with the phenobarbital-responsive element construct, although phenobarbital had no effect on large CYP2B1 or CYP2B2 promoter fragments.	Phenobarbital	158-171	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	248-254
9063451-9	1997	A 2-3-fold increase over the basal level of chloramphenicol acetyltransferase activity was observed in phenobarbital-treated co-cultures transfected with the phenobarbital-responsive element construct, although phenobarbital had no effect on large CYP2B1 or CYP2B2 promoter fragments.	Phenobarbital	158-171	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	258-264
9063451-9	1997	A 2-3-fold increase over the basal level of chloramphenicol acetyltransferase activity was observed in phenobarbital-treated co-cultures transfected with the phenobarbital-responsive element construct, although phenobarbital had no effect on large CYP2B1 or CYP2B2 promoter fragments.	Phenobarbital	158-171	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	248-254
9063451-9	1997	A 2-3-fold increase over the basal level of chloramphenicol acetyltransferase activity was observed in phenobarbital-treated co-cultures transfected with the phenobarbital-responsive element construct, although phenobarbital had no effect on large CYP2B1 or CYP2B2 promoter fragments.	Phenobarbital	158-171	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	258-264
9029046-0	1997	Induction of two UDP-glucuronosyltransferase isoforms sensitive to phenobarbital that are involved in morphine glucuronidation: production of isoform-selective antipeptide antibodies toward UGT1.1r and UGT2B1.	Phenobarbital	67-80	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	17-44
9029046-0	1997	Induction of two UDP-glucuronosyltransferase isoforms sensitive to phenobarbital that are involved in morphine glucuronidation: production of isoform-selective antipeptide antibodies toward UGT1.1r and UGT2B1.	Phenobarbital	67-80	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	202-208
9029046-1	1997	We document here in that two UDP-glucuronosyltransferase (UGT) isoforms sensitive to phenobarbital are involved in morphine glucuronidation in Wistar and Sprague-Dawley rats.	Phenobarbital	85-98	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	29-56
9029046-1	1997	We document here in that two UDP-glucuronosyltransferase (UGT) isoforms sensitive to phenobarbital are involved in morphine glucuronidation in Wistar and Sprague-Dawley rats.	Phenobarbital	85-98	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	58-61
9029046-3	1997	Although the morphine UGT activity in the liver of Gunn rats was increased by phenobarbital (PB) treatment, this was significantly less than that in the liver of PB-treated Wistar rats.	Phenobarbital	78-91	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	22-25
9029046-3	1997	Although the morphine UGT activity in the liver of Gunn rats was increased by phenobarbital (PB) treatment, this was significantly less than that in the liver of PB-treated Wistar rats.	Phenobarbital	93-95	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	22-25
9084959-20	1997	Recognised enzyme inducers of CYP3A, which are likely to be prescribed for patients with HIV disease, include rifampicin (rifampin) [treatment of pulmonary tuberculosis], rifabutin (treatment and prophylaxis of Mycobacterium avium complex), phenobarbital (phenobarbitone), phenytoin and carbamazepine (treatment of seizures secondary to cerebral toxoplasmosis or cerebral lymphoma).	Phenobarbital	241-254	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	30-35
9084959-20	1997	Recognised enzyme inducers of CYP3A, which are likely to be prescribed for patients with HIV disease, include rifampicin (rifampin) [treatment of pulmonary tuberculosis], rifabutin (treatment and prophylaxis of Mycobacterium avium complex), phenobarbital (phenobarbitone), phenytoin and carbamazepine (treatment of seizures secondary to cerebral toxoplasmosis or cerebral lymphoma).	Phenobarbital	256-270	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	30-35
9206565-1	1997	It was shown on an experimental model of chronic gastric ulcer in rats that administration of microsomal oxidation inductors benzonal (benzobarbital) and phenobarbital in a dose of 50 mg/kg for 10 days significantly increases the content of cytochrome P-450 in the gastric mucosa.	Phenobarbital	154-167	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	241-257
9029046-8	1997	This study is the first demonstration that protein levels of two morphine UGT isoforms, UGT1.1r and UGT2B1, in the liver of Wistar and Sprague-Dawley rats are inducible by PB treatment.	Phenobarbital	172-174	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	74-77
9029046-8	1997	This study is the first demonstration that protein levels of two morphine UGT isoforms, UGT1.1r and UGT2B1, in the liver of Wistar and Sprague-Dawley rats are inducible by PB treatment.	Phenobarbital	172-174	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	100-106
9166105-0	1997	Reversal of phenobarbital-induced hyperplasia and hypertrophy in the livers of lpr mice.	Phenobarbital	12-25	Fas (TNF receptor superfamily member 6)	Mus musculus	79-82
9089811-1	1997	A three-dimensional structural model of rabbit phenobarbital-inducible cytochrome P450 2B4 (LM2) was constructed by homology modeling techniques previously developed for building and evaluating a 3D model of the cytochrome P450choP isozyme.	Phenobarbital	47-60	cytochrome P450 2B4	Oryctolagus cuniculus	71-90
9049185-9	1997	Increased expression of Ha-ras was evident in some spontaneous B6C3F1 liver tumors and in most of the PB-induced liver tumors.	Phenobarbital	102-104	Harvey rat sarcoma virus oncogene	Mus musculus	24-30
9101035-12	1997	The increase of bromide formation after CDBM administration in phenobarbital (PB)-pretreated rats indicated that cytochrome P-450 2B1 and 2B2 (CYP2B1 and CYP2B2) play a role as catalysts of the CDBM biotransformation.	Phenobarbital	63-76	cytochrome P450 2B1	Rattus norvegicus	113-141
9029169-0	1997	Induction of lung carcinogenesis in AKR-mice by N-nitrosodiethylamine/phenobarbitone, associated with high expression of c-myc and c-jun oncoproteins.	Phenobarbital	70-84	jun proto-oncogene	Mus musculus	131-136
8990265-6	1997	Phenobarbital-inducible CYP2B1 and CYP2B2 were constitutively expressed in dwarf rats, although substantially absent in normal SD rats.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	24-30
8990265-6	1997	Phenobarbital-inducible CYP2B1 and CYP2B2 were constitutively expressed in dwarf rats, although substantially absent in normal SD rats.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	35-41
8990268-4	1997	CYP3A9 induction was different from other CYP3A isoenzymes, since phenobarbital was a more effective inducer than dexamethasone and clotrimazole.	Phenobarbital	66-79	cytochrome P450, family 3, subfamily a, polypeptide 9	Rattus norvegicus	0-6
8990268-4	1997	CYP3A9 induction was different from other CYP3A isoenzymes, since phenobarbital was a more effective inducer than dexamethasone and clotrimazole.	Phenobarbital	66-79	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	0-5
9209687-4	1997	Maximum labelling indices of &gt; 5-fold the unstimulated control value were observed in hepatocytes isolated from control and 1 day PB pre-treated mice when cultured in the presence of 5 or 10 ng/ml EGF or HGF.	Phenobarbital	133-135	epidermal growth factor	Mus musculus	200-203
9209687-4	1997	Maximum labelling indices of &gt; 5-fold the unstimulated control value were observed in hepatocytes isolated from control and 1 day PB pre-treated mice when cultured in the presence of 5 or 10 ng/ml EGF or HGF.	Phenobarbital	133-135	hepatocyte growth factor	Mus musculus	207-210
9209685-0	1997	Changes in protein and mRNA levels of growth factor/growth factor receptors in rat livers after administration of phenobarbitone or methylclofenapate.	Phenobarbital	114-128	myotrophin	Rattus norvegicus	38-51
9209685-0	1997	Changes in protein and mRNA levels of growth factor/growth factor receptors in rat livers after administration of phenobarbitone or methylclofenapate.	Phenobarbital	114-128	myotrophin	Rattus norvegicus	52-65
9209685-1	1997	The effects of phenobarbitone and methylclofenapate were studied on the expression of growth factor and growth factor receptors in livers of male Wistar rats.	Phenobarbital	15-29	myotrophin	Rattus norvegicus	86-99
9209685-1	1997	The effects of phenobarbitone and methylclofenapate were studied on the expression of growth factor and growth factor receptors in livers of male Wistar rats.	Phenobarbital	15-29	myotrophin	Rattus norvegicus	104-117
9101035-12	1997	The increase of bromide formation after CDBM administration in phenobarbital (PB)-pretreated rats indicated that cytochrome P-450 2B1 and 2B2 (CYP2B1 and CYP2B2) play a role as catalysts of the CDBM biotransformation.	Phenobarbital	63-76	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	143-149
9101035-12	1997	The increase of bromide formation after CDBM administration in phenobarbital (PB)-pretreated rats indicated that cytochrome P-450 2B1 and 2B2 (CYP2B1 and CYP2B2) play a role as catalysts of the CDBM biotransformation.	Phenobarbital	63-76	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	154-160
9101035-12	1997	The increase of bromide formation after CDBM administration in phenobarbital (PB)-pretreated rats indicated that cytochrome P-450 2B1 and 2B2 (CYP2B1 and CYP2B2) play a role as catalysts of the CDBM biotransformation.	Phenobarbital	78-80	cytochrome P450 2B1	Rattus norvegicus	113-141
9101035-12	1997	The increase of bromide formation after CDBM administration in phenobarbital (PB)-pretreated rats indicated that cytochrome P-450 2B1 and 2B2 (CYP2B1 and CYP2B2) play a role as catalysts of the CDBM biotransformation.	Phenobarbital	78-80	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	143-149
9101035-12	1997	The increase of bromide formation after CDBM administration in phenobarbital (PB)-pretreated rats indicated that cytochrome P-450 2B1 and 2B2 (CYP2B1 and CYP2B2) play a role as catalysts of the CDBM biotransformation.	Phenobarbital	78-80	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	154-160
9217276-6	1997	Phenobarbital, a typical inducer of CYP3A2 and 2B1 increased CYP3A2 level as well, but had less potency in the induction of CYP2B1 in HSCs.	Phenobarbital	0-13	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	36-50
9279133-3	1997	NADPH dependent lipid peroxidation and cytosolic glutathione-s-transferase activity were also enhanced due to PB and 3-MC treatment but the magnitude of increase was less in FR animals.	Phenobarbital	110-112	hematopoietic prostaglandin D synthase	Rattus norvegicus	49-74
9080675-11	1997	Antibodies to phenobarbital-inducible rat CYP2B1 or to scup P450B, a putative CYP2B, detected one or more proteins in several species, suggesting that CYP2B-like proteins are highly expressed in some tropical fishes.	Phenobarbital	14-27	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	42-48
9217276-6	1997	Phenobarbital, a typical inducer of CYP3A2 and 2B1 increased CYP3A2 level as well, but had less potency in the induction of CYP2B1 in HSCs.	Phenobarbital	0-13	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	36-42
9217276-6	1997	Phenobarbital, a typical inducer of CYP3A2 and 2B1 increased CYP3A2 level as well, but had less potency in the induction of CYP2B1 in HSCs.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	124-130
9343833-1	1997	We investigated the effects of type of dietary fat and phenobarbital on gamma-glutamyl transpeptidase-positive foci development.	Phenobarbital	55-68	gamma-glutamyltransferase 1	Rattus norvegicus	72-101
9007836-4	1997	Phenobarbital increased hepatic CYP 2 A 5-mediated coumarin 7-hydroxylase (COH) activity (13.2-fold) and the amount of CYP 2 A 5 steady-state mRNA (10.6-fold).	Phenobarbital	0-13	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	32-41
9007836-4	1997	Phenobarbital increased hepatic CYP 2 A 5-mediated coumarin 7-hydroxylase (COH) activity (13.2-fold) and the amount of CYP 2 A 5 steady-state mRNA (10.6-fold).	Phenobarbital	0-13	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	51-73
9007836-4	1997	Phenobarbital increased hepatic CYP 2 A 5-mediated coumarin 7-hydroxylase (COH) activity (13.2-fold) and the amount of CYP 2 A 5 steady-state mRNA (10.6-fold).	Phenobarbital	0-13	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	119-128
9007836-6	1997	Of these inducers, only phenobarbital affected CYP 1 A 12 and CYP 2 B 10 expression.	Phenobarbital	24-37	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	62-72
9343833-8	1997	However, in the presence of phenobarbital, 15% corn oil significantly enhanced gamma-glutamyl transpeptidase-positive foci development compared with 10% fish oil (p &lt; 0.05).	Phenobarbital	28-41	gamma-glutamyltransferase 1	Rattus norvegicus	79-108
9343833-10	1997	In conclusion, there was an interaction between type of dietary fat and phenobarbital on gamma-glutamyl transpeptidase-positive foci development during hepatocarcinogenesis in rats.	Phenobarbital	72-85	gamma-glutamyltransferase 1	Rattus norvegicus	89-118
9018095-0	1996	Dose-related increases in quantitative values for altered hepatocytic foci and cytochrome P-450 levels in the livers of rats exposed to phenobarbital in a medium-term bioassay.	Phenobarbital	136-149	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	79-95
9007046-16	1997	These data indicate that MX is a PB-like inducer of cytochrome P-450 enzymes and may cause liver tumors in a manner analogous to PB.	Phenobarbital	33-35	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	52-68
9018095-1	1996	The dose-response relationship between liver tumor promoting activity and cytochrome P-450 (CYP) induction by phenobarbital sodium (PB) was investigated using the liver medium-term bioassay system of Ito.	Phenobarbital	110-130	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	74-90
9018095-1	1996	The dose-response relationship between liver tumor promoting activity and cytochrome P-450 (CYP) induction by phenobarbital sodium (PB) was investigated using the liver medium-term bioassay system of Ito.	Phenobarbital	110-130	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	92-95
9018095-1	1996	The dose-response relationship between liver tumor promoting activity and cytochrome P-450 (CYP) induction by phenobarbital sodium (PB) was investigated using the liver medium-term bioassay system of Ito.	Phenobarbital	132-134	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	74-90
9018095-1	1996	The dose-response relationship between liver tumor promoting activity and cytochrome P-450 (CYP) induction by phenobarbital sodium (PB) was investigated using the liver medium-term bioassay system of Ito.	Phenobarbital	132-134	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	92-95
8996092-9	1996	At least one cytochrome P450 gene (CYP6A1, phenobarbital-inducible gene from Musca domestica) was shown to contain Barbie box sequence in the coding part of the gene.	Phenobarbital	43-56	cytochrome P450 6A1	Musca domestica	35-41
8912644-1	1996	Phenobarbital (PB) is a potent inducer of cytochrome P450 enzymes, particularly CYP2B1/2B2.	Phenobarbital	15-17	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	80-90
8954103-5	1996	Since the PB-induced UDP-glucuronosyltransferase gene expression was not reduced by insulin, the suppressive effect of insulin was considered to be specific to the CYP2B1/2B2 gene.	Phenobarbital	10-12	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	21-48
8954103-5	1996	Since the PB-induced UDP-glucuronosyltransferase gene expression was not reduced by insulin, the suppressive effect of insulin was considered to be specific to the CYP2B1/2B2 gene.	Phenobarbital	10-12	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	164-174
8954103-6	1996	These results demonstrate that insulin in media masks the PB-induced expression of the CYP2B1/2B2 gene in conventional monolayer hepatocytes and that the use of insulin-free media with primary hepatocytes provides a useful tool for investigating the molecular mechanism of CYP2B1/2B2 gene expression.	Phenobarbital	58-60	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	87-97
8954103-6	1996	These results demonstrate that insulin in media masks the PB-induced expression of the CYP2B1/2B2 gene in conventional monolayer hepatocytes and that the use of insulin-free media with primary hepatocytes provides a useful tool for investigating the molecular mechanism of CYP2B1/2B2 gene expression.	Phenobarbital	58-60	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	273-283
9118895-3	1996	In rats, inhalation of benzene (4 mg/liter of air) caused a rapid destruction of CYP2B1 previously induced by phenobarbital.	Phenobarbital	110-123	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	81-87
8912644-0	1996	In vivo phenobarbital treatment increases protein binding to a putative AP-1 site in the CYP2B2 promoter.	Phenobarbital	8-21	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	89-95
8954103-0	1996	Insulin suppresses the induction of CYP2B1 and CYP2B2 gene expression by phenobarbital in adult rat cultured hepatocytes.	Phenobarbital	73-86	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	36-42
8954103-0	1996	Insulin suppresses the induction of CYP2B1 and CYP2B2 gene expression by phenobarbital in adult rat cultured hepatocytes.	Phenobarbital	73-86	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	47-53
8954103-1	1996	The effect of insulin on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes was investigated.	Phenobarbital	29-42	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	75-81
8954103-1	1996	The effect of insulin on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes was investigated.	Phenobarbital	29-42	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	86-92
8954103-1	1996	The effect of insulin on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes was investigated.	Phenobarbital	29-42	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	94-104
8954103-1	1996	The effect of insulin on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes was investigated.	Phenobarbital	44-46	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	75-81
8954103-1	1996	The effect of insulin on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes was investigated.	Phenobarbital	44-46	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	86-92
8954103-1	1996	The effect of insulin on the phenobarbital (PB)-induced gene expression of CYP2B1 and CYP2B2 (CYP2B1/2B2) in adult rat hepatocytes was investigated.	Phenobarbital	44-46	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	94-104
8954103-3	1996	Although the induction by PB was not seen in monolayer hepatocytes cultured on type I collagen under standard culture conditions, the induced expression of the CYP2B1/2B2 gene was observed in monolayer hepatocytes by removing insulin from the medium.	Phenobarbital	26-28	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	160-170
8954103-4	1996	Further, we succeeded in maintaining the prolonged induction of CYP2B1/2B2 by PB in monolayer hepatocytes by using a medium containing dexamethasone but not insulin.	Phenobarbital	78-80	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	64-74
8968658-4	1996	Phenobarbital, phenytoin, primidone and carbamazepine are potent inducers of cytochrome P450 (CYP), epoxide hydrolase and uridine diphosphate glucuronosyltransferase (UDPGT) enzyme systems; oxcarbazepine is a weak inducer of CYP enzymes, probably acting on a few specific isoforms only.	Phenobarbital	0-13	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	167-172
8912644-1	1996	Phenobarbital (PB) is a potent inducer of cytochrome P450 enzymes, particularly CYP2B1/2B2.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	80-90
8912644-5	1996	Likewise, a putative AP-1 site, identified at -1441 in the CYP2B2 5"-flanking region, also formed a sequence specific DNA/protein complex which was enhanced after PB exposure.	Phenobarbital	163-165	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	59-65
8912644-6	1996	These data may support a role of AP-1 in the PB induction mechanism of CYP2B1/2B2.	Phenobarbital	45-47	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	71-77
8937853-4	1996	The increases in CYP2B1/2 levels produced by 3 x 10(-5) M fluvastatin treatment were larger than those produced by lovastatin or simvastatin treatment or by treatment with 10(-4) M phenobarbital.	Phenobarbital	181-194	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	17-23
8937853-8	1996	Doses of 50 or 100 mg/ kg/day fluvastatin administered for 3 days to rats increased the hepatic levels of CYP2B1/2 and CYP4A mRNA and immunoreactive protein, although to much lower levels than those produced by treatment with phenobarbital or ciprofibrate, respectively.	Phenobarbital	226-239	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	106-112
8930209-0	1996	Imprinted overinduction of hepatic CYP2B1 and 2B2 in adult rats neonatally exposed to phenobarbital.	Phenobarbital	86-99	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	35-49
8930209-3	1996	However, early exposure to the barbiturate permanently alters (i.e., imprints) the inductive responsiveness of CYP2B1 and 2B2 to subsequent phenobarbital challenge in adulthood.	Phenobarbital	140-153	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	111-125
8930209-4	1996	That is, neonatal administration of therapeutic-like levels of phenobarbital causes an overinduction (approximately 30-40%) of CYP2B1 and 2B2 mRNAs, proteins and specific catalytic activity (androstenedione 16 beta-hydroxylase) levels when the rats are rechallenged as adults with as little as 1 mg or 10 mg/kg b.wt.	Phenobarbital	63-76	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	127-141
8930209-7	1996	Because endogenous growth hormone normally inhibits phenobarbital induction of CYP2B1 and 2B2, and the level of inhibition is directly related to the height of the secretory pulse, we have proposed that the overinduction of CYP2B1 and 2B2 in adult rats neonatally exposed to phenobarbital results, at least in part, from a "deinhibition" by the subnormal pulse amplitudes in the plasma growth hormone profiles.	Phenobarbital	52-65	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	79-93
8930209-7	1996	Because endogenous growth hormone normally inhibits phenobarbital induction of CYP2B1 and 2B2, and the level of inhibition is directly related to the height of the secretory pulse, we have proposed that the overinduction of CYP2B1 and 2B2 in adult rats neonatally exposed to phenobarbital results, at least in part, from a "deinhibition" by the subnormal pulse amplitudes in the plasma growth hormone profiles.	Phenobarbital	52-65	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	224-238
8930209-7	1996	Because endogenous growth hormone normally inhibits phenobarbital induction of CYP2B1 and 2B2, and the level of inhibition is directly related to the height of the secretory pulse, we have proposed that the overinduction of CYP2B1 and 2B2 in adult rats neonatally exposed to phenobarbital results, at least in part, from a "deinhibition" by the subnormal pulse amplitudes in the plasma growth hormone profiles.	Phenobarbital	275-288	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	224-238
8948090-7	1996	Treatment of rat with phenobarbital caused increases in both CYP2B1 and 3A1 levels and all of the N-demethylation activities examined.	Phenobarbital	22-35	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	61-67
8937440-0	1996	New proteins in the rat CYP2B subfamily: presence in liver microsomes of the constitutive CYP2B3 protein and the phenobarbital-inducible protein product of alternatively spliced CYP2B2 mRNA.	Phenobarbital	113-126	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	178-184
8948088-7	1996	Despite an apparent down-regulation of CYP2E1 expression occurring in all rats as a result of PB induction, P females maintained higher 2E1 levels and showed enhanced MEOS, 4-AOH and PNP-OH activities with respect to NP females.	Phenobarbital	94-96	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	39-45
8948089-19	1996	The microsomal testosterone 6 beta-hydroxylation rate (CYP3A) was increased after phenobarbital and triacetyloleandomycin treatment.	Phenobarbital	82-95	cytochrome P450 family 3 subfamily A member 28	Capra hircus	55-60
8957062-12	1996	DEN and PB exposure increased liver ornithine decarboxylase activity and this increase was significantly inhibited by feeding of CHL during the initiation phase (P&lt;0.001).	Phenobarbital	8-10	ornithine decarboxylase 1	Rattus norvegicus	36-59
8948014-4	1996	In hepatocytes treated with metyrapone or with phenobarbital, accumulation of CYP2B1 mRNA levels preceded an increase in CYP2B-associated, pentoxyresorufin O-depentylase activity.	Phenobarbital	47-60	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	78-84
8948014-5	1996	However, CYP2B1 mRNA levels were first detectable after 24 hours of treatment with phenobarbital, whereas metyrapone elicited a substantial increase in mRNA levels within 14 hours, suggesting differing mechanisms leading to accumulation of CYP2B1 mRNA under the two inducers.	Phenobarbital	83-96	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	9-15
8870689-8	1996	Pretreatment of rats with P450 inducers (beta-naphthoflavone, phenobarbital, acetone and dexamethasone) increased PL N-dealkylase activity in liver microsomes.	Phenobarbital	62-75	phospholamban	Rattus norvegicus	114-118
8790372-4	1996	Furthermore, tumor promotion by phenobarbital was completely inhibited in the c-myc/HGF double transgenic mice, whereas phenobarbital was an effective tumor promoter in the c-myc single transgenic mice.	Phenobarbital	32-45	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	78-83
8790372-4	1996	Furthermore, tumor promotion by phenobarbital was completely inhibited in the c-myc/HGF double transgenic mice, whereas phenobarbital was an effective tumor promoter in the c-myc single transgenic mice.	Phenobarbital	32-45	hepatocyte growth factor	Mus musculus	84-87
8790372-4	1996	Furthermore, tumor promotion by phenobarbital was completely inhibited in the c-myc/HGF double transgenic mice, whereas phenobarbital was an effective tumor promoter in the c-myc single transgenic mice.	Phenobarbital	120-133	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	173-178
8798596-0	1996	Phenobarbital induction mediated by a distal CYP2B2 sequence in rat liver transiently transfected in situ.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	45-51
8798596-12	1996	In this system, a distal CYP2B2 element mediates a response to phenobarbital, and proximal elements, including the Barbie box, are not required for the induction.	Phenobarbital	63-76	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	25-31
8807143-13	1996	Similarly, tumour promotion by phenobarbitone was completely inhibited in the c-myc/HGF double transgenic mice whereas phenobarbitone was an effective tumour promoter in the c-myc single transgenic mice.	Phenobarbital	119-133	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	174-179
8824533-0	1996	Effect of the separate and combined administration of mestranol and phenobarbital on the development of altered hepatic foci expressing placental form of glutathione S-transferase in the rat.	Phenobarbital	68-81	hematopoietic prostaglandin D synthase	Rattus norvegicus	154-179
8769571-1	1996	Cytochromes P450 2B1 and 2B2 (CYP2B1 and CYP2B2) are well-known phenobarbital-inducible genes in rat liver.	Phenobarbital	64-77	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	30-36
8769571-1	1996	Cytochromes P450 2B1 and 2B2 (CYP2B1 and CYP2B2) are well-known phenobarbital-inducible genes in rat liver.	Phenobarbital	64-77	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	41-47
8713075-0	1996	Genetic analysis of the phenobarbital regulation of the cytochrome P-450 2b-9 and aldehyde dehydrogenase type 2 mRNAs in mouse liver.	Phenobarbital	24-37	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	56-77
8713075-1	1996	The aim of this study was to investigate the effect of the genetic background on the phenobarbital inducibility of cytochrome P-450 2b-9, cytochrome P-450 2b-10 and aldehyde dehydrogenase type 2 mRNAs in mice.	Phenobarbital	85-98	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	115-136
8713075-1	1996	The aim of this study was to investigate the effect of the genetic background on the phenobarbital inducibility of cytochrome P-450 2b-9, cytochrome P-450 2b-10 and aldehyde dehydrogenase type 2 mRNAs in mice.	Phenobarbital	85-98	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	138-160
8713075-2	1996	We analysed the basal expression and the phenobarbital inducibility of both cytochrome P-450 mRNAs by semi-quantitative specific reverse transcription-PCR analyses in five inbred mouse strains (A/J,BALB/cByJ,C57BL/6J, DBA/2J and SWR/J).	Phenobarbital	41-54	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	76-92
8713075-4	1996	In all these mouse strains, phenobarbital induced cytochrome P-450 2b-10 mRNA whereas it could have either a positive or a negative effect on cytochrome P-450 2b-9 expression, depending on the strain and the sex of the mice.	Phenobarbital	28-41	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	50-72
8713075-4	1996	In all these mouse strains, phenobarbital induced cytochrome P-450 2b-10 mRNA whereas it could have either a positive or a negative effect on cytochrome P-450 2b-9 expression, depending on the strain and the sex of the mice.	Phenobarbital	28-41	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	142-163
8713075-5	1996	Specifically, phenobarbital increased cytochrome P-450 2b-9 expression in C57BL/6J males while it decreased it in DBA/2J mice.	Phenobarbital	14-27	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	38-59
8713075-8	1996	Genetic analysis revealed that the phenobarbital-inducible phenotype was either a semi-dominant or a recessive trait in F1 animals from a C57BL/6J x DBA/2J cross for the cytochrome P-450 2b-9 and the aldehyde dehydrogenase type 2 genes, respectively.	Phenobarbital	35-48	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	170-191
8807143-13	1996	Similarly, tumour promotion by phenobarbitone was completely inhibited in the c-myc/HGF double transgenic mice whereas phenobarbitone was an effective tumour promoter in the c-myc single transgenic mice.	Phenobarbital	31-45	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	78-83
8807143-13	1996	Similarly, tumour promotion by phenobarbitone was completely inhibited in the c-myc/HGF double transgenic mice whereas phenobarbitone was an effective tumour promoter in the c-myc single transgenic mice.	Phenobarbital	31-45	hepatocyte growth factor	Mus musculus	84-87
8706011-15	1996	Tamoxifen also produced a dose-dependent increase in UGT2B1 mRNA, a phenobarbital-inducible enzyme; mRNA levels reached 210 and 420% of control in females and males, respectively.	Phenobarbital	68-81	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	53-59
8761421-6	1996	We found that ALDH-3 and p21 expression were significantly enhanced in rats receiving PB after DEN initiation at 26 weeks and that the incidence of hepatocellular carcinomas was likewise increased compared to control or DEN only treated animals.	Phenobarbital	86-88	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	14-20
8761421-6	1996	We found that ALDH-3 and p21 expression were significantly enhanced in rats receiving PB after DEN initiation at 26 weeks and that the incidence of hepatocellular carcinomas was likewise increased compared to control or DEN only treated animals.	Phenobarbital	86-88	KRAS proto-oncogene, GTPase	Rattus norvegicus	25-28
8761421-7	1996	DEN initiation followed by a combination of PB and either 0.1 or 0.5% DEHP significantly reduced ALDH-3 but not p21 Ras expression at 26 weeks compared to DEN plus PB only.	Phenobarbital	44-46	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	97-103
8761421-9	1996	DEN followed by any of the three doses of DEHP without PB resulted in ALDH-3 expression similar to DEN alone.	Phenobarbital	55-57	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	70-76
8690406-8	1996	In both control and phenobarbital-treated hepatocytes, rat recombinant IFN-gamma (33 U/mL) reduced mRNA for 3A2 and 3A1-like CYPs, as well as 3A protein and testosterone 6 beta-hydroxylase activity.	Phenobarbital	20-33	interferon gamma	Rattus norvegicus	71-80
8690406-8	1996	In both control and phenobarbital-treated hepatocytes, rat recombinant IFN-gamma (33 U/mL) reduced mRNA for 3A2 and 3A1-like CYPs, as well as 3A protein and testosterone 6 beta-hydroxylase activity.	Phenobarbital	20-33	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	157-188
8660686-0	1996	Involvement of synthesis and phosphorylation of nuclear protein factors that bind to the positive cis-acting element in the transcriptional activation of the CYP2B1/B2 gene by phenobarbitone in vivo.	Phenobarbital	176-190	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	158-164
8660686-2	1996	Treatment of rats with cycloheximide, a protein synthetic inhibitor, suppresses basal as well as phenobarbitone-induced levels of CYP2B1/B2 mRNA and its run-on transcription.	Phenobarbital	97-111	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	130-136
8660686-4	1996	Treatment of rats with 2-aminopurine, a general protein kinase inhibitor, blocks the phenobarbitone-mediated increase in CYP2B1/B2 mRNA, cell-free transcription of a minigene construct containing the positive element, pP450e179DNA, and binding of nuclear proteins to the positive element.	Phenobarbital	85-99	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	121-127
8660686-11	1996	It is concluded that phenobarbitone treatment enhances in vivo the synthesis and phosphorylation of protein factors binding to the positive element and these constitute a minimal requirement for the transcriptional activation of the CYP2B1/B2 gene.	Phenobarbital	21-35	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	233-239
8819303-7	1996	The oral treatment of male dogs with phenobarbital (PB), rifampicin (Rif) or beta-naphthoflavone (beta-NF) induced significant increases in the contents of CYP1A1/2 (12-fold by beta-NF), 2B11 (16-fold by PB), 2C21 (2-fold by PB) and 3A12 (5-fold by PB and Rif), resulting in marked proportional alterations of the P450 enzymes in dog liver microsomes.	Phenobarbital	37-50	Cytochrome P450 1A1	Canis lupus familiaris	156-162
8995791-0	1996	Inducibility of the Drosophila melanogaster cytochrome P450 gene, CYP6A2, by phenobarbital in insecticide susceptible or resistant strains.	Phenobarbital	77-90	Cytochrome P450-6a2	Drosophila melanogaster	66-72
8819303-7	1996	The oral treatment of male dogs with phenobarbital (PB), rifampicin (Rif) or beta-naphthoflavone (beta-NF) induced significant increases in the contents of CYP1A1/2 (12-fold by beta-NF), 2B11 (16-fold by PB), 2C21 (2-fold by PB) and 3A12 (5-fold by PB and Rif), resulting in marked proportional alterations of the P450 enzymes in dog liver microsomes.	Phenobarbital	204-206	Cytochrome P450 1A1	Canis lupus familiaris	156-162
8656450-4	1996	Pyridine, phenobarbital, and beta-naphthoflavone, inducers of CYP2E1, CYP2B, and CYP1A, respectively, increased the toxicity of styrene.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily e, polypeptide 1	Mus musculus	62-68
8819303-7	1996	The oral treatment of male dogs with phenobarbital (PB), rifampicin (Rif) or beta-naphthoflavone (beta-NF) induced significant increases in the contents of CYP1A1/2 (12-fold by beta-NF), 2B11 (16-fold by PB), 2C21 (2-fold by PB) and 3A12 (5-fold by PB and Rif), resulting in marked proportional alterations of the P450 enzymes in dog liver microsomes.	Phenobarbital	52-54	Cytochrome P450 1A1	Canis lupus familiaris	156-162
8656450-4	1996	Pyridine, phenobarbital, and beta-naphthoflavone, inducers of CYP2E1, CYP2B, and CYP1A, respectively, increased the toxicity of styrene.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	70-75
8819303-7	1996	The oral treatment of male dogs with phenobarbital (PB), rifampicin (Rif) or beta-naphthoflavone (beta-NF) induced significant increases in the contents of CYP1A1/2 (12-fold by beta-NF), 2B11 (16-fold by PB), 2C21 (2-fold by PB) and 3A12 (5-fold by PB and Rif), resulting in marked proportional alterations of the P450 enzymes in dog liver microsomes.	Phenobarbital	204-206	Cytochrome P450 1A1	Canis lupus familiaris	156-162
8819303-7	1996	The oral treatment of male dogs with phenobarbital (PB), rifampicin (Rif) or beta-naphthoflavone (beta-NF) induced significant increases in the contents of CYP1A1/2 (12-fold by beta-NF), 2B11 (16-fold by PB), 2C21 (2-fold by PB) and 3A12 (5-fold by PB and Rif), resulting in marked proportional alterations of the P450 enzymes in dog liver microsomes.	Phenobarbital	204-206	Cytochrome P450 1A1	Canis lupus familiaris	156-162
8661355-5	1996	That is, neonatal exposure to phenobarbital enhanced the responsiveness to exogenous hCG as measured by an above-normal increase in testosterone concentration.	Phenobarbital	30-43	hypertrichosis 2 (generalised, congenital)	Homo sapiens	85-88
8640740-0	1996	Low expression of the WAF1/CIP1 gene product, p21, in enzyme-altered foci induced in rat liver by diethylnitrosamine or phenobarbital.	Phenobarbital	120-133	cyclin-dependent kinase inhibitor 1A	Rattus norvegicus	22-26
8640740-0	1996	Low expression of the WAF1/CIP1 gene product, p21, in enzyme-altered foci induced in rat liver by diethylnitrosamine or phenobarbital.	Phenobarbital	120-133	cyclin-dependent kinase inhibitor 1A	Rattus norvegicus	27-31
8640740-0	1996	Low expression of the WAF1/CIP1 gene product, p21, in enzyme-altered foci induced in rat liver by diethylnitrosamine or phenobarbital.	Phenobarbital	120-133	KRAS proto-oncogene, GTPase	Rattus norvegicus	46-49
8640740-1	1996	The expression of the WAF1/CIP1 gene product, p21, in enzyme-altered foci (EAF) induced by diethylnitrosamine (DEN) and phenobarbital (PB) was examined.	Phenobarbital	120-133	cyclin-dependent kinase inhibitor 1A	Rattus norvegicus	22-26
8640740-1	1996	The expression of the WAF1/CIP1 gene product, p21, in enzyme-altered foci (EAF) induced by diethylnitrosamine (DEN) and phenobarbital (PB) was examined.	Phenobarbital	120-133	cyclin-dependent kinase inhibitor 1A	Rattus norvegicus	27-31
8640740-1	1996	The expression of the WAF1/CIP1 gene product, p21, in enzyme-altered foci (EAF) induced by diethylnitrosamine (DEN) and phenobarbital (PB) was examined.	Phenobarbital	120-133	KRAS proto-oncogene, GTPase	Rattus norvegicus	46-49
8640740-1	1996	The expression of the WAF1/CIP1 gene product, p21, in enzyme-altered foci (EAF) induced by diethylnitrosamine (DEN) and phenobarbital (PB) was examined.	Phenobarbital	135-137	cyclin-dependent kinase inhibitor 1A	Rattus norvegicus	22-26
8640740-1	1996	The expression of the WAF1/CIP1 gene product, p21, in enzyme-altered foci (EAF) induced by diethylnitrosamine (DEN) and phenobarbital (PB) was examined.	Phenobarbital	135-137	KRAS proto-oncogene, GTPase	Rattus norvegicus	46-49
8665510-2	1996	By contrast, treatment of rats with either of the inducing agents phenobarbital or 3-methylcholanthrene results in an approximate increase of only 1.4-fold in the amount of AFAR in rat liver.	Phenobarbital	66-79	aldo-keto reductase family 7 member A3	Rattus norvegicus	173-177
8627517-7	1996	Pyridine or phenobarbital potentiation of CCl4-induced increases in ALT activity implys that cytochrome P450 2E1 (P450 2E1) and P450 2B expression may be associated with the increased toxicity.	Phenobarbital	12-25	C-C motif chemokine ligand 4	Rattus norvegicus	42-46
8627517-7	1996	Pyridine or phenobarbital potentiation of CCl4-induced increases in ALT activity implys that cytochrome P450 2E1 (P450 2E1) and P450 2B expression may be associated with the increased toxicity.	Phenobarbital	12-25	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	93-112
21781672-11	1996	In mice pretreated with phenobarbital, CCl(4) also attenuated the increase in content of P450 in the small intestine, which appeared to be a result of induction by phenobarbital of CYP2E1.	Phenobarbital	24-37	cytochrome P450, family 2, subfamily e, polypeptide 1	Mus musculus	181-187
21781672-11	1996	In mice pretreated with phenobarbital, CCl(4) also attenuated the increase in content of P450 in the small intestine, which appeared to be a result of induction by phenobarbital of CYP2E1.	Phenobarbital	164-177	cytochrome P450, family 2, subfamily e, polypeptide 1	Mus musculus	181-187
8614014-5	1996	At a dose of 25 micrograms/plate, BaP produced 55, 83, 217, and 161 net revertants per plate with UI-, PB-, AR-, and TCDD-induced S9, respectively.	Phenobarbital	103-105	prohibitin 2	Rattus norvegicus	34-37
8638929-7	1996	In addition, N-methyl-PB was found to suppress PB-mediated induction of CYP2B1.	Phenobarbital	22-24	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	72-78
8638929-8	1996	Hepatic levels of CYP2B1 mRNA and protein were increased by treatment with PB or N-methyl-PB alone, but decreased by cotreatment with 1 mM PB and N-methyl-PB.	Phenobarbital	75-77	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	18-24
8638929-8	1996	Hepatic levels of CYP2B1 mRNA and protein were increased by treatment with PB or N-methyl-PB alone, but decreased by cotreatment with 1 mM PB and N-methyl-PB.	Phenobarbital	90-92	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	18-24
8625499-14	1996	With microsomes from PB-pretreated rats, inhibition by mAb-2B1 indicated a 62% contribution by cytochrome P450 2B1 to debutylation of NDBA and 65% to depropylation of NDPA.	Phenobarbital	21-23	cytochrome P450 2B1	Rattus norvegicus	95-114
8797068-3	1996	PBR levels were 50% to 80% higher in patients treated with carbamazepine, phenobarbital and valproic acid than in controls and untreated epileptics.	Phenobarbital	74-87	translocator protein	Homo sapiens	0-3
8667238-0	1996	Suppressed expression of phenobarbital-inducible hepatic cytochrome P-450s in Eisai-hyperbilirubinuria rats (EHBR/Eis).	Phenobarbital	25-38	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	57-73
8667238-11	1996	Although PB expressed CYP2B1/2 apoprotein and mRNA to a similar extent in both homozygous and heterozygous EHBR/Eis livers, CYP3A2 and CYP2C6 were less responsive to PB in homozygous EHBR/Eis.	Phenobarbital	9-11	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	22-28
8621653-0	1996	Characterization of phenobarbital-inducible mouse Cyp2b10 gene transcription in primary hepatocytes.	Phenobarbital	20-33	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	50-57
8621653-1	1996	The mouse phenobarbital (PB)-inducible Cyp2b10 gene promoter has been isolated and sequenced, and control of its expression has been characterized.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	39-46
8621653-1	1996	The mouse phenobarbital (PB)-inducible Cyp2b10 gene promoter has been isolated and sequenced, and control of its expression has been characterized.	Phenobarbital	25-27	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	39-46
8621653-4	1996	In this report, we have developed a primary mouse hepatocyte culture system in which endogenous 2B10 mRNA as well as Cyp2b10-driven CAT activity were induced by PB and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP), but not by the 3-chloro derivative of TCPOBOP.	Phenobarbital	161-163	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	117-124
8621653-9	1996	Our results indicate that sequences important for PB-induced transcription of Cyp2b10 gene are located in the distal promoter.	Phenobarbital	50-52	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	78-85
8801059-4	1996	An elevation of GST activities by 45 to 100% was observed after pretreatment of rats with phenobarbital (PB).	Phenobarbital	90-103	hematopoietic prostaglandin D synthase	Rattus norvegicus	16-19
8801059-4	1996	An elevation of GST activities by 45 to 100% was observed after pretreatment of rats with phenobarbital (PB).	Phenobarbital	105-107	hematopoietic prostaglandin D synthase	Rattus norvegicus	16-19
8795461-1	1996	Rapid-onset cataracts were induced in SPF C57 bl/6 mice by intraperitoneal administration of naphthalene following cytochrome P-450 isozyme induction with phenobarbital.	Phenobarbital	155-168	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	115-131
8619256-5	1996	mEH activity was increased by beta-naphthoflavone, isosafrole, phenobarbital and clofibric acid.	Phenobarbital	63-76	epoxide hydrolase 1, microsomal	Mus musculus	0-3
8619614-0	1996	Phenobarbital-induced activation of CYP2H1 and 5-aminolevulinate synthase genes in chick embryo hepatocytes is blocked by an inhibitor of protein phosphorylation.	Phenobarbital	0-13	cytochrome P450 2H1	Gallus gallus	36-42
8646785-2	1996	Pretreating mice with three inducers of cytochrome P-450 (phenobarbital, clophen A50 and butylated hydroxytoluene (BHT)) increased the yield of the nitrosyl complex which correlated with a rise in the cytochrome P-450 content of mouse liver microsomes.	Phenobarbital	58-71	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	40-56
8646785-2	1996	Pretreating mice with three inducers of cytochrome P-450 (phenobarbital, clophen A50 and butylated hydroxytoluene (BHT)) increased the yield of the nitrosyl complex which correlated with a rise in the cytochrome P-450 content of mouse liver microsomes.	Phenobarbital	58-71	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	201-217
8600980-12	1996	In microsomes from phenobarbital-treated rats, anti-CYP2B1/B2 IgG completely prevented the NADPH- and NADH-dependent increases in reactive oxygen formation produced by ferritin.	Phenobarbital	19-32	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	52-58
8619614-1	1996	The phenobarbital-induced activation of cytochrome P4502H1 (CYP2H1) and 5-aminolevulinate synthase (ALAS-1) genes in chick embryo hepatocytes occurs at the level of gene transcription, but the molecular mechanism underlying this induction is not understood in detail.	Phenobarbital	4-17	cytochrome P450 2H1	Gallus gallus	40-58
8619614-1	1996	The phenobarbital-induced activation of cytochrome P4502H1 (CYP2H1) and 5-aminolevulinate synthase (ALAS-1) genes in chick embryo hepatocytes occurs at the level of gene transcription, but the molecular mechanism underlying this induction is not understood in detail.	Phenobarbital	4-17	cytochrome P450 2H1	Gallus gallus	60-66
8619614-1	1996	The phenobarbital-induced activation of cytochrome P4502H1 (CYP2H1) and 5-aminolevulinate synthase (ALAS-1) genes in chick embryo hepatocytes occurs at the level of gene transcription, but the molecular mechanism underlying this induction is not understood in detail.	Phenobarbital	4-17	5'-aminolevulinate synthase 1	Gallus gallus	100-106
8619614-2	1996	In the present study, we report that the protein kinase inhibitor 2-aminopurine markedly inhibits the phenobarbital-induced activation of CYP2H1 and ALAS-1 genes as measured by Northern blot analysis, but does not alter the basal expression of these genes in the absence of drug.	Phenobarbital	102-115	cytochrome P450 2H1	Gallus gallus	138-144
8619614-2	1996	In the present study, we report that the protein kinase inhibitor 2-aminopurine markedly inhibits the phenobarbital-induced activation of CYP2H1 and ALAS-1 genes as measured by Northern blot analysis, but does not alter the basal expression of these genes in the absence of drug.	Phenobarbital	102-115	5'-aminolevulinate synthase 1	Gallus gallus	149-155
8619614-7	1996	The induction of the CYP2H1 gene by phenobarbital was not altered by treating cells with the specific inhibitors for protein kinase C (GF 109203X and Ro 31-8220) or prolonged exposure to 12-O-tetradecanoyl-phorbol 13-acetate (TPA) or treatment with the specific inhibitors for tyrosine kinase (genistein and tyrphostin A25).	Phenobarbital	36-49	cytochrome P450 2H1	Gallus gallus	21-27
8615908-1	1996	The objectives of this study were to characterize further the effects of phenobarbital (PB) on cytochrome P4502B1 and 2B2 (P4502B1/2) enzyme activity and immunoreactivity in rat hepatocytes and to investigate the mechanism(s) mediating the ability of interleukin-6 (IL-6) to inhibit this induction.	Phenobarbital	88-90	interleukin 6	Rattus norvegicus	251-264
8615908-1	1996	The objectives of this study were to characterize further the effects of phenobarbital (PB) on cytochrome P4502B1 and 2B2 (P4502B1/2) enzyme activity and immunoreactivity in rat hepatocytes and to investigate the mechanism(s) mediating the ability of interleukin-6 (IL-6) to inhibit this induction.	Phenobarbital	88-90	interleukin 6	Rattus norvegicus	266-270
8615908-6	1996	When IL-6 was added concomitantly with or up to 12 hr after the addition of PB, the PB induction of BROD activity and immunoreactivity was inhibited significantly.	Phenobarbital	76-78	interleukin 6	Rattus norvegicus	5-9
8615908-6	1996	When IL-6 was added concomitantly with or up to 12 hr after the addition of PB, the PB induction of BROD activity and immunoreactivity was inhibited significantly.	Phenobarbital	84-86	interleukin 6	Rattus norvegicus	5-9
8615908-7	1996	When 18 hr elapsed between the time of addition of PB and IL-6, the inhibitory effects of IL-6 were no longer apparent, suggesting that the actions of IL-6 were mediated by early events in the induction process.	Phenobarbital	51-53	interleukin 6	Rattus norvegicus	90-94
8615908-7	1996	When 18 hr elapsed between the time of addition of PB and IL-6, the inhibitory effects of IL-6 were no longer apparent, suggesting that the actions of IL-6 were mediated by early events in the induction process.	Phenobarbital	51-53	interleukin 6	Rattus norvegicus	90-94
8615908-11	1996	Results suggest that the inhibition of PB-induced BROD activity by IL-6 is due to an action on early cellular and molecular events in the induction process.	Phenobarbital	39-41	interleukin 6	Rattus norvegicus	67-71
8643092-0	1996	Phenobarbital induction of hepatic CYP2B1 and CYP2B2: pretranscriptional and post-transcriptional effects of gender, adult age, and phenobarbital dose.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	35-41
8786535-10	1996	In contrast to the opposing action of volatile anesthetics, pentobarbital and phenobarbital inhibited GluR3 and GluR6 kainate responses and had a much greater effect on GluR6 receptors.	Phenobarbital	78-91	glutamate receptor, ionotropic, AMPA 3 L homeolog	Xenopus laevis	102-107
8786535-10	1996	In contrast to the opposing action of volatile anesthetics, pentobarbital and phenobarbital inhibited GluR3 and GluR6 kainate responses and had a much greater effect on GluR6 receptors.	Phenobarbital	78-91	glutamate receptor, ionotropic, kainate 2 S homeolog	Xenopus laevis	112-117
8786535-10	1996	In contrast to the opposing action of volatile anesthetics, pentobarbital and phenobarbital inhibited GluR3 and GluR6 kainate responses and had a much greater effect on GluR6 receptors.	Phenobarbital	78-91	glutamate receptor, ionotropic, kainate 2 S homeolog	Xenopus laevis	169-174
8643092-0	1996	Phenobarbital induction of hepatic CYP2B1 and CYP2B2: pretranscriptional and post-transcriptional effects of gender, adult age, and phenobarbital dose.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	46-52
8643092-2	1996	In this regard, we examined the interactions of gender, adult age, and barbiturate dose on the course of phenobarbital induction of hepatic CYP2B1 and CYP2B2.	Phenobarbital	105-118	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	140-146
8643092-2	1996	In this regard, we examined the interactions of gender, adult age, and barbiturate dose on the course of phenobarbital induction of hepatic CYP2B1 and CYP2B2.	Phenobarbital	105-118	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	151-157
8643092-3	1996	We observed that femaleness and youth were associated with the greatest inhibition, so that both the rate and initiation of CYP2B1 and CYP2B2 induction were suppressed most in the young adult (65 days of age) females, followed by the mature adult (150 days of age) females and then by the young adult males, with the mature adult males exhibiting the least suppression of phenobarbital induction.	Phenobarbital	372-385	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	124-130
8643092-3	1996	We observed that femaleness and youth were associated with the greatest inhibition, so that both the rate and initiation of CYP2B1 and CYP2B2 induction were suppressed most in the young adult (65 days of age) females, followed by the mature adult (150 days of age) females and then by the young adult males, with the mature adult males exhibiting the least suppression of phenobarbital induction.	Phenobarbital	372-385	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	135-141
8643092-9	1996	The considerably elevated growth hormone pulse amplitudes observed in the young rats of both genders seem to be an additional inhibitory signal antagonizing phenobarbital induction of CYP2B1 and CYP2B2.	Phenobarbital	157-170	gonadotropin releasing hormone receptor	Rattus norvegicus	26-40
8643092-9	1996	The considerably elevated growth hormone pulse amplitudes observed in the young rats of both genders seem to be an additional inhibitory signal antagonizing phenobarbital induction of CYP2B1 and CYP2B2.	Phenobarbital	157-170	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	184-190
8643092-9	1996	The considerably elevated growth hormone pulse amplitudes observed in the young rats of both genders seem to be an additional inhibitory signal antagonizing phenobarbital induction of CYP2B1 and CYP2B2.	Phenobarbital	157-170	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	195-201
8643092-11	1996	Last, although as little as 1 mg/kg phenobarbital increased CYP2B1 mRNA concentrations by 100%, there was no translation into detectable levels of protein.	Phenobarbital	36-49	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	60-66
8643092-13	1996	Unlike use of the 10 mg/kg dose, CYP2B1 and CYP2B2 induction by phenobarbital at 1 mg/kg was unaffected by age or gender.	Phenobarbital	64-77	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	33-39
8643092-13	1996	Unlike use of the 10 mg/kg dose, CYP2B1 and CYP2B2 induction by phenobarbital at 1 mg/kg was unaffected by age or gender.	Phenobarbital	64-77	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	44-50
8573202-1	1996	Cytochrome P450 (CYP) 2B1 and 2B2 are encoded by two closely related genes, CYP2B1 and CYP2B2, that are expressed at low levels in adult rat liver but are induced markedly by the administration of the drug phenobarbital (PB) or other structurally unrelated hydrophobic compounds to animals.	Phenobarbital	206-219	cytochrome P450 2B1	Rattus norvegicus	0-33
8730921-6	1996	Compared with 72-h control (dimethyl sulphoxide only treated) rat liver slice microsomes, PB induced CYP2B1/2 and 3A, BNF induced CYP1A2, and ARO induced CYP1A2, 2B1/2, and 3A.	Phenobarbital	90-92	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	101-107
8730921-6	1996	Compared with 72-h control (dimethyl sulphoxide only treated) rat liver slice microsomes, PB induced CYP2B1/2 and 3A, BNF induced CYP1A2, and ARO induced CYP1A2, 2B1/2, and 3A.	Phenobarbital	90-92	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	154-160
8730921-6	1996	Compared with 72-h control (dimethyl sulphoxide only treated) rat liver slice microsomes, PB induced CYP2B1/2 and 3A, BNF induced CYP1A2, and ARO induced CYP1A2, 2B1/2, and 3A.	Phenobarbital	90-92	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	104-109
8573185-9	1996	Using urinary excretion of the enzymes alkaline phosphatase and gamma-glutamyl transferase as an index of renal damage, we observed that pretreatment of rats with PB, which induced hepatic P450 (P450II2B1), protected against OTA nephrotoxicity, whereas cobalt-protoporphyrin IX pretreatment, which decreased P450 levels, exacerbated OTA nephrotoxicity.	Phenobarbital	163-165	gamma-glutamyltransferase 1	Rattus norvegicus	64-90
8573202-1	1996	Cytochrome P450 (CYP) 2B1 and 2B2 are encoded by two closely related genes, CYP2B1 and CYP2B2, that are expressed at low levels in adult rat liver but are induced markedly by the administration of the drug phenobarbital (PB) or other structurally unrelated hydrophobic compounds to animals.	Phenobarbital	206-219	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	76-82
8573202-1	1996	Cytochrome P450 (CYP) 2B1 and 2B2 are encoded by two closely related genes, CYP2B1 and CYP2B2, that are expressed at low levels in adult rat liver but are induced markedly by the administration of the drug phenobarbital (PB) or other structurally unrelated hydrophobic compounds to animals.	Phenobarbital	221-223	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	87-93
8573202-1	1996	Cytochrome P450 (CYP) 2B1 and 2B2 are encoded by two closely related genes, CYP2B1 and CYP2B2, that are expressed at low levels in adult rat liver but are induced markedly by the administration of the drug phenobarbital (PB) or other structurally unrelated hydrophobic compounds to animals.	Phenobarbital	206-219	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	87-93
8573202-1	1996	Cytochrome P450 (CYP) 2B1 and 2B2 are encoded by two closely related genes, CYP2B1 and CYP2B2, that are expressed at low levels in adult rat liver but are induced markedly by the administration of the drug phenobarbital (PB) or other structurally unrelated hydrophobic compounds to animals.	Phenobarbital	221-223	cytochrome P450 2B1	Rattus norvegicus	0-33
8573202-1	1996	Cytochrome P450 (CYP) 2B1 and 2B2 are encoded by two closely related genes, CYP2B1 and CYP2B2, that are expressed at low levels in adult rat liver but are induced markedly by the administration of the drug phenobarbital (PB) or other structurally unrelated hydrophobic compounds to animals.	Phenobarbital	221-223	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	76-82
8579377-1	1996	Asp-290 of the phenobarbital-inducible dog liver cytochrome P450 (P450) 2B11 was mutated to nine other amino acid residues by site-directed mutagenesis, and the functional significance of the unique negative charge in P450 2B11 at that position was studied.	Phenobarbital	15-28	Cytochrome P450 1A1	Canis lupus familiaris	49-76
8907578-5	1996	In phenobarbital-treated mice, interferon beta reduced the induction of total cytochrome P-450 (22%), the activities of pentoxyresorufin O-dealkylase (38%), benzyloxyresorufin O-dealkylase (30%), erythromycin N-demethylase (30%), 7-ethoxycoumarin O-deethylase (16%) and cytochrome P-450 2B1 (33%) and 3A (45%) proteins.	Phenobarbital	3-16	interferon beta 1, fibroblast	Mus musculus	31-46
8593816-5	1996	Monoclonal antibody directed toward CYP2B1/2B2 completely inhibited the 6 alpha- and 6 beta-hydroxylation of E2 and partially inhibited the 2-hydroxylation of E2 by liver microsomes from phenobarbital-treated adult female rats.	Phenobarbital	187-200	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	36-46
8907578-5	1996	In phenobarbital-treated mice, interferon beta reduced the induction of total cytochrome P-450 (22%), the activities of pentoxyresorufin O-dealkylase (38%), benzyloxyresorufin O-dealkylase (30%), erythromycin N-demethylase (30%), 7-ethoxycoumarin O-deethylase (16%) and cytochrome P-450 2B1 (33%) and 3A (45%) proteins.	Phenobarbital	3-16	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	78-94
8907578-5	1996	In phenobarbital-treated mice, interferon beta reduced the induction of total cytochrome P-450 (22%), the activities of pentoxyresorufin O-dealkylase (38%), benzyloxyresorufin O-dealkylase (30%), erythromycin N-demethylase (30%), 7-ethoxycoumarin O-deethylase (16%) and cytochrome P-450 2B1 (33%) and 3A (45%) proteins.	Phenobarbital	3-16	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	270-286
8632764-3	1996	P-glycoprotein and CYP3A4 were constitutively expressed in both LS180/AD50 and LS180/WT cells, and both proteins were up-regulated after treatment with many drugs, including rifampicin, phenobarbital, clotrimazole, reserpine, and isosafrole.	Phenobarbital	186-199	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
8632764-3	1996	P-glycoprotein and CYP3A4 were constitutively expressed in both LS180/AD50 and LS180/WT cells, and both proteins were up-regulated after treatment with many drugs, including rifampicin, phenobarbital, clotrimazole, reserpine, and isosafrole.	Phenobarbital	186-199	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	19-25
8561493-0	1996	Purification of a phenobarbital-inducible UDP-glucuronosyltransferase isoform from dog liver which catalyzes morphine and testosterone glucuronidation.	Phenobarbital	18-31	UDP-glucuronosyltransferase 1-6	Canis lupus familiaris	42-69
8848823-6	1996	These results suggest that PB is an inducer of the 2-hydroxylation of DMI, a reaction primarily catalyzed by CYP2D6, but do not provide further information on the specific P450 isoenzyme(s) being induced.	Phenobarbital	27-29	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	109-115
8561506-1	1996	We have been able to demonstrate that cytochrome b4 interacts closely with cytochrome P450 in the microsomal membrane, and that substrates can serve to order the interaction: Using the water-soluble carbodiimide EDC we could crosslink cytochrome b5 and CYP2B4 in microsomes from phenobarbital-treated rabbits and cytochrome b5 and CYP1A2 in microsomes from beta-naphthoflavone-treated animals.	Phenobarbital	279-292	cytochrome b5	Oryctolagus cuniculus	235-248
8561493-1	1996	A morphine UDP-glucuronosyltransferase (UGT) which could belong to the UGT2B subfamily was isolated from liver microsomes of a male beagle dog treated with phenobarbital.	Phenobarbital	156-169	UDP-glucuronosyltransferase 1-6	Canis lupus familiaris	11-38
8561493-1	1996	A morphine UDP-glucuronosyltransferase (UGT) which could belong to the UGT2B subfamily was isolated from liver microsomes of a male beagle dog treated with phenobarbital.	Phenobarbital	156-169	UDP-glucuronosyltransferase 1-6	Canis lupus familiaris	40-43
8561493-7	1996	The substrate specificity of UGTDOG-PB is similar to that of stably expressed UGT2B1 which is considered a phenobarbital-inducible morphine UGT in the rat except that UGTDOG-PB is capable of glucuronidating 4-nitrophenol but not chloramphenicol.	Phenobarbital	107-120	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	78-84
8561493-7	1996	The substrate specificity of UGTDOG-PB is similar to that of stably expressed UGT2B1 which is considered a phenobarbital-inducible morphine UGT in the rat except that UGTDOG-PB is capable of glucuronidating 4-nitrophenol but not chloramphenicol.	Phenobarbital	107-120	UDP-glucuronosyltransferase 1-6	Canis lupus familiaris	29-32
8534266-7	1996	Curcumin was also a potent inhibitor of glutathione S-transferase (GST) activity in cytosol from liver of rats treated with phenobarbital (PB), beta-naphthoflavone (beta NF) and pyrazole (Pyr), when measured towards 1-chloro-2,4-dinitrobenzene (CDNB) as substrate.	Phenobarbital	124-137	hematopoietic prostaglandin D synthase	Rattus norvegicus	40-65
9328629-3	1996	Also the potentiation of the anticonvulsive effect of diazepam, phenobarbital and valproic acid (VPA) was observed in BCCA and AOAA (CD97, 150 mg/kg) treated animals.	Phenobarbital	64-77	adhesion G protein-coupled receptor E5	Mus musculus	133-137
8534266-7	1996	Curcumin was also a potent inhibitor of glutathione S-transferase (GST) activity in cytosol from liver of rats treated with phenobarbital (PB), beta-naphthoflavone (beta NF) and pyrazole (Pyr), when measured towards 1-chloro-2,4-dinitrobenzene (CDNB) as substrate.	Phenobarbital	124-137	hematopoietic prostaglandin D synthase	Rattus norvegicus	67-70
8534266-7	1996	Curcumin was also a potent inhibitor of glutathione S-transferase (GST) activity in cytosol from liver of rats treated with phenobarbital (PB), beta-naphthoflavone (beta NF) and pyrazole (Pyr), when measured towards 1-chloro-2,4-dinitrobenzene (CDNB) as substrate.	Phenobarbital	139-141	hematopoietic prostaglandin D synthase	Rattus norvegicus	40-65
8534266-7	1996	Curcumin was also a potent inhibitor of glutathione S-transferase (GST) activity in cytosol from liver of rats treated with phenobarbital (PB), beta-naphthoflavone (beta NF) and pyrazole (Pyr), when measured towards 1-chloro-2,4-dinitrobenzene (CDNB) as substrate.	Phenobarbital	139-141	hematopoietic prostaglandin D synthase	Rattus norvegicus	67-70
8534266-8	1996	In liver cytosol from rats treated with phenobarbital (PB), curcumin inhibited GST activity in a mixed-type manner with a Ki of 5.75 microM and Ki of 12.5 microM.	Phenobarbital	40-53	hematopoietic prostaglandin D synthase	Rattus norvegicus	79-82
8534266-8	1996	In liver cytosol from rats treated with phenobarbital (PB), curcumin inhibited GST activity in a mixed-type manner with a Ki of 5.75 microM and Ki of 12.5 microM.	Phenobarbital	55-57	hematopoietic prostaglandin D synthase	Rattus norvegicus	79-82
8869742-3	1996	Treatment of humans or hepatoma cell lines with drugs such as phenobarbital causes the induction of hepatic bilirubin UGT by increased transcription from the UGT1 gene.	Phenobarbital	62-75	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	118-121
8869742-3	1996	Treatment of humans or hepatoma cell lines with drugs such as phenobarbital causes the induction of hepatic bilirubin UGT by increased transcription from the UGT1 gene.	Phenobarbital	62-75	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	158-162
8884465-0	1996	Changes in chromatin structure and nuclear matrix association of the rat cytochrome P450 2B1/2 (CYP2B1/2) gene following induction with phenobarbital.	Phenobarbital	136-149	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	73-94
8726684-12	1996	In a separate group of obese and lean rats, regulation of the AII receptor by phenobarbital (PB) was examined.	Phenobarbital	78-91	angiotensinogen	Rattus norvegicus	62-65
8726684-12	1996	In a separate group of obese and lean rats, regulation of the AII receptor by phenobarbital (PB) was examined.	Phenobarbital	93-95	angiotensinogen	Rattus norvegicus	62-65
8726684-13	1996	Administration of PB restored AII receptor density in liver from obese rats to levels obtained in lean rats.	Phenobarbital	18-20	angiotensinogen	Rattus norvegicus	30-33
9037862-2	1996	Although the number of GST-P positive foci in the liver was significantly increased in the PB group as compared to the control group, there were no significant fluctuations in the SDM, PTU and PB groups.	Phenobarbital	91-93	glutathione S-transferase pi 1	Rattus norvegicus	23-28
8923030-5	1996	However, western blotting suggests that these enzymes are not always coordinately regulated, as treatment with phenobarbital and beta-naphthoflavone results in differences in the relative increase in hepatic GST Yc2 and AFAR.	Phenobarbital	111-124	glutathione S-transferase alpha 3	Rattus norvegicus	208-215
8923030-5	1996	However, western blotting suggests that these enzymes are not always coordinately regulated, as treatment with phenobarbital and beta-naphthoflavone results in differences in the relative increase in hepatic GST Yc2 and AFAR.	Phenobarbital	111-124	aldo-keto reductase family 7 member A3	Rattus norvegicus	220-224
8565130-0	1996	Phenobarbital selectively promotes initiated cells with reduced TGF beta receptor levels.	Phenobarbital	0-13	transforming growth factor, beta 1	Rattus norvegicus	64-72
8565130-2	1996	In this study we investigated whether PB selectively promotes a population of initiated cells with reduced levels of transforming growth factor-beta (TGF beta) receptors types I, II and III.	Phenobarbital	38-40	transforming growth factor, beta 1	Rattus norvegicus	150-158
8565130-10	1996	These results demonstrate that PB selectively promotes initiated cells with reduced levels of TGF beta types I-III receptors and suggests a mechanistic role for TGF beta in PB-induced liver tumor promotion.	Phenobarbital	31-33	transforming growth factor, beta 1	Rattus norvegicus	94-102
8565130-10	1996	These results demonstrate that PB selectively promotes initiated cells with reduced levels of TGF beta types I-III receptors and suggests a mechanistic role for TGF beta in PB-induced liver tumor promotion.	Phenobarbital	31-33	transforming growth factor, beta 1	Rattus norvegicus	161-169
8565130-10	1996	These results demonstrate that PB selectively promotes initiated cells with reduced levels of TGF beta types I-III receptors and suggests a mechanistic role for TGF beta in PB-induced liver tumor promotion.	Phenobarbital	173-175	transforming growth factor, beta 1	Rattus norvegicus	161-169
8825185-15	1996	Whereas phenobarbital treatment alone enhanced c-fos expression only marginally, CCI4 treatment of phenobarbital-pretreated animals increased c-fos expression by up to an additional approximately 8-fold and c-jun mRNA levels by up to an additional approximately 5-fold over the respective levels monitored in the hepatic tissue of CCI4-treated animals.	Phenobarbital	8-21	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	47-52
8825185-15	1996	Whereas phenobarbital treatment alone enhanced c-fos expression only marginally, CCI4 treatment of phenobarbital-pretreated animals increased c-fos expression by up to an additional approximately 8-fold and c-jun mRNA levels by up to an additional approximately 5-fold over the respective levels monitored in the hepatic tissue of CCI4-treated animals.	Phenobarbital	99-112	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	142-147
8825185-16	1996	Enhanced CYP2E1 or CYP2B1/2B2 levels after treatment with pyridine or phenobarbital elevated c-fos mRNA over untreated controls.	Phenobarbital	70-83	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	9-15
8825185-16	1996	Enhanced CYP2E1 or CYP2B1/2B2 levels after treatment with pyridine or phenobarbital elevated c-fos mRNA over untreated controls.	Phenobarbital	70-83	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	19-25
8825185-16	1996	Enhanced CYP2E1 or CYP2B1/2B2 levels after treatment with pyridine or phenobarbital elevated c-fos mRNA over untreated controls.	Phenobarbital	70-83	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
9176742-6	1996	Consistently, at this chloroform concentration, the effect of phenobarbital (CYP2B1/2 inducer) was maximal, producing very high levels of adducts.	Phenobarbital	62-75	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	77-83
8884465-0	1996	Changes in chromatin structure and nuclear matrix association of the rat cytochrome P450 2B1/2 (CYP2B1/2) gene following induction with phenobarbital.	Phenobarbital	136-149	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	96-104
8884465-1	1996	Treatment of rats with phenobarbital has been shown to result in an enormous increase in CYP2B1/2 mRNA levels in the liver.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	89-95
8884465-2	1996	This study was performed in order to relate this effect of phenobarbital treatment to changes in the chromatin structure of the CYP2B1/2 gene.	Phenobarbital	59-72	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	128-136
8884465-3	1996	Phenobarbital treatment was shown to be associated with a twofold increase in DNase I sensitivity of the CYP2B1/2 gene in the liver.	Phenobarbital	0-13	deoxyribonuclease 1	Rattus norvegicus	78-85
8884465-3	1996	Phenobarbital treatment was shown to be associated with a twofold increase in DNase I sensitivity of the CYP2B1/2 gene in the liver.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	105-113
8884465-4	1996	In addition, induction of the CYP2B1/2 gene transcription by phenobarbital resulted in a marked enrichment in the liver of CYP2B1/2 sequences in the nuclear matrix as compared to the matrix-free fraction.	Phenobarbital	61-74	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	30-38
8884465-4	1996	In addition, induction of the CYP2B1/2 gene transcription by phenobarbital resulted in a marked enrichment in the liver of CYP2B1/2 sequences in the nuclear matrix as compared to the matrix-free fraction.	Phenobarbital	61-74	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	30-36
8571362-5	1995	Phenobarbital-potentiated CCl4 injury does not lead to animal mortality in spite of much higher liver injury in comparison to the chlordecone+CCl4 model.	Phenobarbital	0-13	C-C motif chemokine ligand 4	Homo sapiens	26-30
8558437-2	1996	Although CYP3A1 induction by PB was similarly repressed by most of the cAMP-enhancing strategies, forskolin additions in particular resulted in marked stimulation of CYP3A1 expression.	Phenobarbital	29-31	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	9-15
8560502-8	1995	Induction of CYP2E1 and CYP2B1/2 with pyridine and phenobarbital, respectively, did not alter this lack of effect.	Phenobarbital	51-64	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	13-19
8560502-8	1995	Induction of CYP2E1 and CYP2B1/2 with pyridine and phenobarbital, respectively, did not alter this lack of effect.	Phenobarbital	51-64	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	24-30
8591727-9	1995	Treatment of cells with inducers of CYP1A (beta-naphthoflavone) and CYP3A (rifampicin and phenobarbital) greatly increased the rate of production of this metabolite.	Phenobarbital	90-103	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	68-73
7488175-4	1995	The CYP2B1 antipeptide IgG inhibited pentoxyresorufin O-dealkylase activity of microsomes obtained from phenobarbital-treated rats in a dose-dependent manner, whereas it did not inhibit ethoxyresorufin O-deethylase activity of microsomes obtained from 3-methylcholanthrene-treated rats.	Phenobarbital	104-117	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	4-10
8558843-0	1995	Critical role of extracellular matrix on induction by phenobarbital of cytochrome P450 2B1/2 in primary cultures of adult rat hepatocytes.	Phenobarbital	54-67	cytochrome P450 2B1	Rattus norvegicus	71-90
8558843-1	1995	BACKGROUND: Although it has been known for more than three decades that administration of lipophilic chemicals, including phenobarbital, produces liver hypertrophy, proliferation of smooth endoplasmic reticulum, and induction of liver microsomal enzymes such as cytochromes P450 (CYP) 2B1 and 2B2, the mechanism of this adaptive response remains largely unknown.	Phenobarbital	122-135	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	274-296
8558843-4	1995	Subsequent incubation in medium containing Matrigel as a soluble component, fully restored, in a dose-dependent manner, the ability to respond to phenobarbital with induction of CYP 2B1/2 mRNAs.	Phenobarbital	146-159	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	178-187
8558843-9	1995	CONCLUSIONS: We conclude that the process by which phenobarbital induced 2B1/2 mRNAs in hepatocytes appears to require highly concerted effects of specific extracellular components prominently involving laminin.	Phenobarbital	51-64	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	73-78
8615872-10	1995	In parallel experiments, western blot analysis of immunoreactive CYP2B1 and CYP2B2 protein showed that PB, the PCB mixtures, and congeners induced both proteins.	Phenobarbital	103-105	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	65-71
8615872-10	1995	In parallel experiments, western blot analysis of immunoreactive CYP2B1 and CYP2B2 protein showed that PB, the PCB mixtures, and congeners induced both proteins.	Phenobarbital	103-105	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	76-82
8615872-11	1995	Previous studies have identified a cis-acting DNA element that plays a role in regulating CYP2B1/B2 gene expression and binds nuclear trans-acting factor(s) induced by PB.	Phenobarbital	168-170	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	90-96
8615872-13	1995	Both PB and PCBs appear to induce CYP2B1/B2 via a common mechanism.	Phenobarbital	5-7	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	34-40
7576107-0	1995	Expression of c-myc in altered hepatic foci induced in rats by various single doses of diethylnitrosamine and promotion by 0.05% phenobarbital.	Phenobarbital	129-142	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	14-19
7574722-0	1995	Cloning and expression of a rat liver phenobarbital-inducible UDP-glucuronosyltransferase (2B12) with specificity for monoterpenoid alcohols.	Phenobarbital	38-51	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	62-89
7568186-1	1995	The phenobarbitone-responsive minimal promoter has been shown to lie between nt -179 and nt + 1 in the 5" (upstream) region of the CYP2B1/B2 gene in rat liver, on the basis of the drug responsiveness of the sequence linked to human growth hormone gene as reporter and targeted to liver as an asialoglycoprotein-DNA complex in vivo.	Phenobarbital	4-18	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	131-137
7568186-1	1995	The phenobarbitone-responsive minimal promoter has been shown to lie between nt -179 and nt + 1 in the 5" (upstream) region of the CYP2B1/B2 gene in rat liver, on the basis of the drug responsiveness of the sequence linked to human growth hormone gene as reporter and targeted to liver as an asialoglycoprotein-DNA complex in vivo.	Phenobarbital	4-18	growth hormone 1	Homo sapiens	232-246
7487997-0	1995	Nuclear matrix condensation and c-myc and c-fos expression are specifically altered in culture rat hepatocytes after exposure to cyproterone acetate and phenobarbital.	Phenobarbital	153-166	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	32-37
7487997-0	1995	Nuclear matrix condensation and c-myc and c-fos expression are specifically altered in culture rat hepatocytes after exposure to cyproterone acetate and phenobarbital.	Phenobarbital	153-166	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	42-47
7487997-4	1995	C-fos expression and decrease in nuclear fluorescence could be induced by both chemicals, phenobarbital being the lesser potent, whereas c-myc expression was only inducible by cyproterone acetate.	Phenobarbital	90-103	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	0-5
7574722-6	1995	Northern blot analysis showed that treatment of rats with phenobarbital increased hepatic mRNA levels for UGT2B12 approximately twofold.	Phenobarbital	58-71	UDP glucuronosyltransferase 2 family, polypeptide B35	Rattus norvegicus	106-113
8593453-2	1995	When different types of tumor promotors, phenobarbital (PB) and deoxycholic acid (DCA), were administered for 5 weeks after initiation by 3"-MeDAB, preneoplastic alterations in the liver, determined by glutathione S-transferase placental form (GST-P), were markedly increased.	Phenobarbital	41-54	glutathione S-transferase pi 1	Rattus norvegicus	202-249
7575638-1	1995	Phenobarbital-dependent induction of mouse cytochrome P-450 (Cyp) orthologous to rat CYP2B1 and its modulation by hepatotrophic growth factors were examined in primary hepatocyte cultures.	Phenobarbital	0-13	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	43-59
8847705-2	1995	gamma-Glutamyltranspeptidase (GGT), a biochemical marker for identifying putative preneoplastic lesions in the liver, is highly expressed in phenobarbital (PB)-promoted altered hepatic foci but not in those promoted by peroxisome proliferators.	Phenobarbital	141-154	gamma-glutamyltransferase 1	Rattus norvegicus	0-28
8847705-2	1995	gamma-Glutamyltranspeptidase (GGT), a biochemical marker for identifying putative preneoplastic lesions in the liver, is highly expressed in phenobarbital (PB)-promoted altered hepatic foci but not in those promoted by peroxisome proliferators.	Phenobarbital	141-154	gamma-glutamyltransferase 1	Rattus norvegicus	30-33
8847705-2	1995	gamma-Glutamyltranspeptidase (GGT), a biochemical marker for identifying putative preneoplastic lesions in the liver, is highly expressed in phenobarbital (PB)-promoted altered hepatic foci but not in those promoted by peroxisome proliferators.	Phenobarbital	156-158	gamma-glutamyltransferase 1	Rattus norvegicus	0-28
8847705-2	1995	gamma-Glutamyltranspeptidase (GGT), a biochemical marker for identifying putative preneoplastic lesions in the liver, is highly expressed in phenobarbital (PB)-promoted altered hepatic foci but not in those promoted by peroxisome proliferators.	Phenobarbital	156-158	gamma-glutamyltransferase 1	Rattus norvegicus	30-33
8847705-8	1995	Both doses of CIP significantly inhibited the induction of GGT activity at 48 and 72 hours, whereas PB enhanced GGT activity.	Phenobarbital	100-102	gamma-glutamyltransferase 1	Rattus norvegicus	112-115
8847705-11	1995	The results of this experiment show that CIP and PB have different effects on GGT activity and LTC4 concentration.	Phenobarbital	49-51	gamma-glutamyltransferase 1	Rattus norvegicus	78-81
8577819-7	1995	Based on relative levels of immunoreactive protein, the phenobarbital-inducible isoforms, CYP2B1 and CYP2B2, are most susceptible to T3-mediated suppression.	Phenobarbital	56-69	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	90-96
8577819-7	1995	Based on relative levels of immunoreactive protein, the phenobarbital-inducible isoforms, CYP2B1 and CYP2B2, are most susceptible to T3-mediated suppression.	Phenobarbital	56-69	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	101-107
7575638-1	1995	Phenobarbital-dependent induction of mouse cytochrome P-450 (Cyp) orthologous to rat CYP2B1 and its modulation by hepatotrophic growth factors were examined in primary hepatocyte cultures.	Phenobarbital	0-13	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	61-64
7575638-1	1995	Phenobarbital-dependent induction of mouse cytochrome P-450 (Cyp) orthologous to rat CYP2B1 and its modulation by hepatotrophic growth factors were examined in primary hepatocyte cultures.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	85-91
7575638-4	1995	Furthermore, EGF led to repression of accumulation of corresponding mRNA under phenobarbital, an effect not blocked by inhibition of protein synthesis under cycloheximide.	Phenobarbital	79-92	epidermal growth factor	Mus musculus	13-16
7554701-5	1995	Because felbamate inhibits the S-mephenytoin hydroxylase (CYP2C19) isozyme in vitro, it appears that phenobarbital hydroxylation is mediated in part by this isozyme.	Phenobarbital	101-114	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	58-65
8565792-7	1995	These results indicate that imipramine has two actions on the liver CYP system (i.e. as an inhibitor of the CYP2D enzyme and as a phenobarbital-type inducer).	Phenobarbital	130-143	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	68-71
8553686-11	1995	P4502B, along with flavin-containing monooxygenase, also contributed to the detoxification of SN in both the untreated (34%) and PB-treated (40%) guinea pig.	Phenobarbital	129-131	flavin-containing monooxygenase	Cavia porcellus	19-50
7477969-6	1995	The spinal cord microsomes also cross-reacted with the antiserum to the phenobarbital-inducible form of rat brain cytochrome P450.	Phenobarbital	72-85	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	114-129
7482557-3	1995	Transforming growth factor beta 1 (TGF-beta), a potent mitoinhibitory growth factor for hepatocytes, has been associated with the mitosuppression caused by PB and certain peroxisomal proliferators.	Phenobarbital	156-158	transforming growth factor beta 1	Homo sapiens	0-33
7541730-5	1995	PB and DEX increased NADPH cytochrome c reductase activity but had no effect on either DT-diaphorase or cytochrome P450 dependent activities.	Phenobarbital	0-2	cytochrome c, somatic	Homo sapiens	27-39
7482557-3	1995	Transforming growth factor beta 1 (TGF-beta), a potent mitoinhibitory growth factor for hepatocytes, has been associated with the mitosuppression caused by PB and certain peroxisomal proliferators.	Phenobarbital	156-158	transforming growth factor beta 1	Homo sapiens	35-43
7624894-8	1995	The mouse liver GST activity toward AFB1-epoxide was 3-fold greater than that of phenobarbital-induced rats, 4.5-fold greater than DR rats, and 14.7-fold greater than the GST activity of AL rats.	Phenobarbital	81-94	hematopoietic prostaglandin D synthase	Rattus norvegicus	16-19
7646073-0	1995	Phenobarbital induction of CYP2B1, CYP2B2, and CYP3A1 in rat liver: genetic differences in a common regulatory mechanism.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	27-33
7646073-0	1995	Phenobarbital induction of CYP2B1, CYP2B2, and CYP3A1 in rat liver: genetic differences in a common regulatory mechanism.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	35-41
7646073-0	1995	Phenobarbital induction of CYP2B1, CYP2B2, and CYP3A1 in rat liver: genetic differences in a common regulatory mechanism.	Phenobarbital	0-13	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	47-53
7646073-3	1995	Immunoblot analysis revealed that the strain-specific differences of phenobarbital responsiveness (10-fold for CYP2B1, CYP2B2, and CYP3A1 in females) are much smaller in male animals and are also greatly diminished by hypophysectomy.	Phenobarbital	69-82	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	111-117
7646073-3	1995	Immunoblot analysis revealed that the strain-specific differences of phenobarbital responsiveness (10-fold for CYP2B1, CYP2B2, and CYP3A1 in females) are much smaller in male animals and are also greatly diminished by hypophysectomy.	Phenobarbital	69-82	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	119-125
7646073-3	1995	Immunoblot analysis revealed that the strain-specific differences of phenobarbital responsiveness (10-fold for CYP2B1, CYP2B2, and CYP3A1 in females) are much smaller in male animals and are also greatly diminished by hypophysectomy.	Phenobarbital	69-82	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	131-137
7646073-4	1995	Partial depletion of thyroid hormone and growth hormone levels by methimazole treatment was equally as effective as hypophysectomy in elevating phenobarbital-induced levels of CYP2B1, CYP2B2, and CYP3A1 in Wistar Furth rats, while the Fischer strain was unaffected.	Phenobarbital	144-157	gonadotropin releasing hormone receptor	Rattus norvegicus	41-55
7646073-4	1995	Partial depletion of thyroid hormone and growth hormone levels by methimazole treatment was equally as effective as hypophysectomy in elevating phenobarbital-induced levels of CYP2B1, CYP2B2, and CYP3A1 in Wistar Furth rats, while the Fischer strain was unaffected.	Phenobarbital	144-157	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	176-182
7646073-4	1995	Partial depletion of thyroid hormone and growth hormone levels by methimazole treatment was equally as effective as hypophysectomy in elevating phenobarbital-induced levels of CYP2B1, CYP2B2, and CYP3A1 in Wistar Furth rats, while the Fischer strain was unaffected.	Phenobarbital	144-157	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	184-190
7646073-4	1995	Partial depletion of thyroid hormone and growth hormone levels by methimazole treatment was equally as effective as hypophysectomy in elevating phenobarbital-induced levels of CYP2B1, CYP2B2, and CYP3A1 in Wistar Furth rats, while the Fischer strain was unaffected.	Phenobarbital	144-157	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	196-202
7646073-10	1995	We conclude that multiple cytochrome P450 genes share a common phenobarbital induction pathway that, in part, alleviates the suppressive effects of thyroid hormone and growth hormone which are far greater in female Wistar Furth rats.	Phenobarbital	63-76	gonadotropin releasing hormone receptor	Rattus norvegicus	168-182
7601424-9	1995	Although proliferation of hepatocytes in low-serum decreased by 75%, the appearance of apoptosis in the presence of PB was associated with increased expression of the c-myc gene.	Phenobarbital	116-118	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	167-172
7587963-1	1995	The aim of this study was to determine whether treatment of cynomolgus monkeys (Macaca fasicularis) with phenobarbital, beta-naphthoflavone, or dexamethasone causes an induction of microsomal crytochrome P450 (CYP) enzymes that are structurally and functionally related to rat enzymes belonging to the CYP1A, CYP2B, and CYP3A gene families.	Phenobarbital	105-118	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	320-325
7587963-2	1995	Oral treatment of male and female monkeys with phenobarbital resulted in a marked induction of a protein recognized by antibody against rat CYP2B1, as determined by Western immunoblotting.	Phenobarbital	47-60	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	140-146
7587963-5	1995	Antibody, against rat CYP2B1 markedly inhibited this reaction in liver microsomes from phenobarbital-treated monkeys, but not from control monkeys.	Phenobarbital	87-100	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	22-28
7587963-12	1995	Treatment of monkeys with phenobarbital resulted in a 2- to 3-fold induction of a protein recognized by antibody against rat CYP3A1.	Phenobarbital	26-39	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	125-131
7616408-2	1995	The present study investigates the potential for modulating the cytotoxicity and antitumor activity of thiotepa by prior treatment of tumor-bearing rats with the CYP2B1 inducer phenobarbital or the CYP2C11 inhibitor 2-diethylaminoethyl-2,2-diphenylvalerate hydrochloride (SKF-525A) and examines the role of TEPA in the cytotoxicity of thiotepa in vivo.	Phenobarbital	177-190	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	162-168
7789536-0	1995	Interleukin-1 beta antagonizes phenobarbital induction of several major cytochromes P450 in adult rat hepatocytes in primary culture.	Phenobarbital	31-44	interleukin 1 beta	Rattus norvegicus	0-18
7607552-1	1995	Cytochrome P450 2B1, encoded by CYP2B1, and cytochrome P450 2B2, encoded by CYP2B2, are inducible in rat liver by phenobarbital (PB).	Phenobarbital	114-127	cytochrome P450 2B1	Rattus norvegicus	0-19
7607552-1	1995	Cytochrome P450 2B1, encoded by CYP2B1, and cytochrome P450 2B2, encoded by CYP2B2, are inducible in rat liver by phenobarbital (PB).	Phenobarbital	114-127	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	32-38
7607552-1	1995	Cytochrome P450 2B1, encoded by CYP2B1, and cytochrome P450 2B2, encoded by CYP2B2, are inducible in rat liver by phenobarbital (PB).	Phenobarbital	114-127	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	44-63
7607552-1	1995	Cytochrome P450 2B1, encoded by CYP2B1, and cytochrome P450 2B2, encoded by CYP2B2, are inducible in rat liver by phenobarbital (PB).	Phenobarbital	114-127	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	76-82
7607552-1	1995	Cytochrome P450 2B1, encoded by CYP2B1, and cytochrome P450 2B2, encoded by CYP2B2, are inducible in rat liver by phenobarbital (PB).	Phenobarbital	129-131	cytochrome P450 2B1	Rattus norvegicus	0-19
7616408-1	1995	The anticancer drug and alkylating agent thiotepa is metabolized by oxidative desulfuration to yield the alkylating metabolite N,N",N"-triethylenephosphoramide (TEPA) in a reaction that is catalyzed by specific liver cytochrome P450 (CYP) enzymes, including CYP2B1, the major phenobarbital-inducible P450 of rat liver, and CYP2C11, a constitutively expressed, male-specific form.	Phenobarbital	276-289	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	217-232
7616408-1	1995	The anticancer drug and alkylating agent thiotepa is metabolized by oxidative desulfuration to yield the alkylating metabolite N,N",N"-triethylenephosphoramide (TEPA) in a reaction that is catalyzed by specific liver cytochrome P450 (CYP) enzymes, including CYP2B1, the major phenobarbital-inducible P450 of rat liver, and CYP2C11, a constitutively expressed, male-specific form.	Phenobarbital	276-289	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	234-237
7616408-1	1995	The anticancer drug and alkylating agent thiotepa is metabolized by oxidative desulfuration to yield the alkylating metabolite N,N",N"-triethylenephosphoramide (TEPA) in a reaction that is catalyzed by specific liver cytochrome P450 (CYP) enzymes, including CYP2B1, the major phenobarbital-inducible P450 of rat liver, and CYP2C11, a constitutively expressed, male-specific form.	Phenobarbital	276-289	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	258-264
7616408-1	1995	The anticancer drug and alkylating agent thiotepa is metabolized by oxidative desulfuration to yield the alkylating metabolite N,N",N"-triethylenephosphoramide (TEPA) in a reaction that is catalyzed by specific liver cytochrome P450 (CYP) enzymes, including CYP2B1, the major phenobarbital-inducible P450 of rat liver, and CYP2C11, a constitutively expressed, male-specific form.	Phenobarbital	276-289	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	323-330
7607552-1	1995	Cytochrome P450 2B1, encoded by CYP2B1, and cytochrome P450 2B2, encoded by CYP2B2, are inducible in rat liver by phenobarbital (PB).	Phenobarbital	129-131	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	32-38
7607552-1	1995	Cytochrome P450 2B1, encoded by CYP2B1, and cytochrome P450 2B2, encoded by CYP2B2, are inducible in rat liver by phenobarbital (PB).	Phenobarbital	129-131	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	44-63
7789536-1	1995	We have investigated the effects of interleukin (IL)-1 beta and IL6 on expression and phenobarbital (PB) induction of ethoxyresorufin O-deethylase (EROD) and pentoxyresorufin O-deethylase (PROD) activities, as well as on mRNA levels of cytochromes P450 (CYP) 1A, 2B, 2C, 2E and 3A, in rat hepatocytes in primary culture.	Phenobarbital	86-99	interleukin 6	Rattus norvegicus	64-67
7607552-1	1995	Cytochrome P450 2B1, encoded by CYP2B1, and cytochrome P450 2B2, encoded by CYP2B2, are inducible in rat liver by phenobarbital (PB).	Phenobarbital	129-131	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	76-82
7789536-2	1995	IL6 slightly antagonized PB-induced PROD activity.	Phenobarbital	25-27	interleukin 6	Rattus norvegicus	0-3
7789536-3	1995	Strikingly, IL1 beta strongly inhibited basal EROD and PROD activities, and fully blocked their induction by PB in a dose-dependent fashion.	Phenobarbital	109-111	interleukin 1 beta	Rattus norvegicus	12-20
7789536-5	1995	Our results demonstrate that IL1 beta can suppress basal CYP activities, as well as PB-inducible expression of five CYP mRNAs in rat hepatocytes in primary culture.	Phenobarbital	84-86	interleukin 1 beta	Rattus norvegicus	29-37
7783881-3	1995	In the groups receiving carbamazepine or phenobarbital, mean TC, HDL-C, and LDL-C levels were higher than in the control group, the differences being statistically significant for all except LDL-C in the phenobarbital group.	Phenobarbital	41-54	component of oligomeric golgi complex 2	Homo sapiens	191-196
7603447-1	1995	A chicken anti-rat polyclonal antibody to a purified rat liver UDP-glucuronosyltransferase (UGT) with catalytic activity toward opioid substrates was used to screen a liver cDNA library prepared from phenobarbital-treated Wistar rats.	Phenobarbital	200-213	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	63-90
7603447-1	1995	A chicken anti-rat polyclonal antibody to a purified rat liver UDP-glucuronosyltransferase (UGT) with catalytic activity toward opioid substrates was used to screen a liver cDNA library prepared from phenobarbital-treated Wistar rats.	Phenobarbital	200-213	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	92-95
7783881-3	1995	In the groups receiving carbamazepine or phenobarbital, mean TC, HDL-C, and LDL-C levels were higher than in the control group, the differences being statistically significant for all except LDL-C in the phenobarbital group.	Phenobarbital	204-217	component of oligomeric golgi complex 2	Homo sapiens	76-81
7783881-3	1995	In the groups receiving carbamazepine or phenobarbital, mean TC, HDL-C, and LDL-C levels were higher than in the control group, the differences being statistically significant for all except LDL-C in the phenobarbital group.	Phenobarbital	204-217	component of oligomeric golgi complex 2	Homo sapiens	191-196
7587934-1	1995	The kinetics of mechanism-based inactivation of phenobarbital-inducible rabbit hepatic cytochromes P450 2B4 and 2B5 by N-benzyl-(BBT) and N-alpha-methylbenzyl (alpha MB) 1-aminobenzotriazole were investigated using reconstituted P450 2B4, a stable heterologous expression system, and hepatic microsomes.	Phenobarbital	48-61	cytochrome P450 2B4	Oryctolagus cuniculus	99-115
7759530-0	1995	cAMP-associated inhibition of phenobarbital-inducible cytochrome P450 gene expression in primary rat hepatocyte cultures.	Phenobarbital	30-43	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	54-69
7759530-4	1995	PB-inducible responses were measured in hepatocytes by hybridization to cytochrome P450 (CYP) CYP2B1, CYP2B2, and CYP3A1 mRNAs.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	72-87
7759530-4	1995	PB-inducible responses were measured in hepatocytes by hybridization to cytochrome P450 (CYP) CYP2B1, CYP2B2, and CYP3A1 mRNAs.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	89-92
7759530-4	1995	PB-inducible responses were measured in hepatocytes by hybridization to cytochrome P450 (CYP) CYP2B1, CYP2B2, and CYP3A1 mRNAs.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	94-100
7759530-4	1995	PB-inducible responses were measured in hepatocytes by hybridization to cytochrome P450 (CYP) CYP2B1, CYP2B2, and CYP3A1 mRNAs.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	102-108
7759530-4	1995	PB-inducible responses were measured in hepatocytes by hybridization to cytochrome P450 (CYP) CYP2B1, CYP2B2, and CYP3A1 mRNAs.	Phenobarbital	0-2	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	114-120
7759530-6	1995	A similar inhibition of PB-induced CYP3A1 mRNA levels was effected by the cAMP analogs and glucagon.	Phenobarbital	24-26	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	35-41
7759530-9	1995	A requirement for protein kinase A (PKA) was demonstrated by the use of (Sp)-cAMPS, a highly specific activator of PKA, whereas the inactive diastereoisomer, (Rp)-cAMPS, was ineffective in modulating PB induction.	Phenobarbital	200-202	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	18-34
7759530-9	1995	A requirement for protein kinase A (PKA) was demonstrated by the use of (Sp)-cAMPS, a highly specific activator of PKA, whereas the inactive diastereoisomer, (Rp)-cAMPS, was ineffective in modulating PB induction.	Phenobarbital	200-202	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	36-39
7771797-4	1995	Phenobarbital increased Cyp2b-10 expression more than that of Cyp2b-9 in both sexes.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	24-32
7771797-9	1995	The expression level of Cyp2b-10 mRNA by phenobarbital or beta-estradiol was higher than that of Cyp2b-9, as observed in vivo, and &gt; 10(-7) M beta-estradiol induced both in vitro.	Phenobarbital	41-54	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	24-32
7587934-4	1995	Preincubation of phenobarbital-induced hepatic microsomes with BBT and alpha MB resulted in concentration-dependent decreases in marker activities of P450 2B4 and 2B5, benzyloxyresorufin O-debenzylase and androstenedione 15 alpha-hydroxylase, respectively.	Phenobarbital	17-30	cytochrome P450 2B4	Oryctolagus cuniculus	150-166
7752288-6	1995	Western blot analyses indicated that cytosolic PKC alpha levels in male rats neonatally exposed to PB were decreased by approximately 63% relative to the vehicle control group but were not significantly altered in the DES males.	Phenobarbital	99-101	protein kinase C, alpha	Rattus norvegicus	47-56
7752288-8	1995	These results show that neonatal treatment with DES or PB differentially alters hepatic monooxygenase enzyme activities and PKC alpha levels in adult rats.	Phenobarbital	55-57	protein kinase C, alpha	Rattus norvegicus	124-133
7727516-4	1995	In reconstituted vesicular systems composed of phospholipids, NADPH cytochrome P-450 reductase and P-450, the intensities of EPR signals produced by the formation of the methyl-, ethyl- and isopropyl-free radicals, were 3- to 5-fold more intense in membrane vesicles containing ethanol-inducible CYP2E1 than phenobarbital-inducible CYP2B1.	Phenobarbital	308-321	cytochrome p450 oxidoreductase	Rattus norvegicus	62-94
7748182-9	1995	Pretreatment of female rats with phenobarbitone or dexamethasone resulted in a 4- to 5-fold increase in [14C]tamoxifen binding, relative to controls, consistent with the involvement of CYP2B1 and CYP3A1 in the metabolic activation.	Phenobarbital	33-47	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	185-191
7748182-9	1995	Pretreatment of female rats with phenobarbitone or dexamethasone resulted in a 4- to 5-fold increase in [14C]tamoxifen binding, relative to controls, consistent with the involvement of CYP2B1 and CYP3A1 in the metabolic activation.	Phenobarbital	33-47	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	196-202
7728897-6	1995	On the other hand, four PB-inducible forms of cytochrome P-450 were not induced with the 4-MeSO2 isomers.	Phenobarbital	24-26	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	46-62
7728897-7	1995	The relation between liver concentrations of the corresponding 3-MeSO2 derivatives and induction of four PB-inducible forms of cytochrome P-450 after administration of four PCBs and their 3-MeSO2 derivatives further confirmed that the 3-MeSO2 metabolites played an important role in the induction which parent PCB congeners caused on the hepatic drug-metabolizing enzyme system.	Phenobarbital	105-107	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	127-143
7728897-7	1995	The relation between liver concentrations of the corresponding 3-MeSO2 derivatives and induction of four PB-inducible forms of cytochrome P-450 after administration of four PCBs and their 3-MeSO2 derivatives further confirmed that the 3-MeSO2 metabolites played an important role in the induction which parent PCB congeners caused on the hepatic drug-metabolizing enzyme system.	Phenobarbital	105-107	pyruvate carboxylase	Rattus norvegicus	173-176
7607117-5	1995	Significantly greater IL-2 production was observed in PBMC from carbamazepine (CBZ)-treated patients as compared with both the control group or with valproate and phenobarbital (PB)-treated patients.	Phenobarbital	54-56	interleukin 2	Homo sapiens	22-26
7697745-3	1995	Induction by sodium phenobarbital (NaPB) led to a conspicuous increase in all situations, up to approximately 38-fold in female rat and mouse liver, with the exception of hamster kidney where PROD activity was only slightly affected.	Phenobarbital	13-33	NSF attachment protein beta	Rattus norvegicus	35-39
7566474-4	1995	At normal therapeutic concentrations, diazepam, carbamazepine and phenobarbital occupy respectively 70, 30 and 10% of PBR sites in human lymphocytes.	Phenobarbital	66-79	translocator protein	Homo sapiens	118-121
7900791-0	1995	Neonatal phenobarbital-induced defects in age- and sex-specific growth hormone profiles regulating monooxygenases.	Phenobarbital	9-22	gonadotropin releasing hormone receptor	Rattus norvegicus	64-78
7900791-2	1995	Neonatal exposure to phenobarbital at anticonvulsant therapeutic doses for the rat reduced the pulse amplitudes of circulating growth hormone in both the 65- and 150-day-old males but only in the 65-day-old females.	Phenobarbital	21-34	gonadotropin releasing hormone receptor	Rattus norvegicus	127-141
7900791-5	1995	Because growth hormone is the primary regulator of sex-dependent hepatic monooxygenases, we have proposed that the abnormal plasma growth hormone profiles produced by neonatal phenobarbital are responsible for the permanent induction of hepatic monooxygenases.	Phenobarbital	176-189	gonadotropin releasing hormone receptor	Rattus norvegicus	8-22
7900791-5	1995	Because growth hormone is the primary regulator of sex-dependent hepatic monooxygenases, we have proposed that the abnormal plasma growth hormone profiles produced by neonatal phenobarbital are responsible for the permanent induction of hepatic monooxygenases.	Phenobarbital	176-189	gonadotropin releasing hormone receptor	Rattus norvegicus	131-145
7628308-5	1995	SMX N-hydroxylation in phenobarbital-treated rat hepatic microsomes was inhibited 70% by anti-CYP2C6 antisera.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	94-100
7628308-10	1995	CYP-mediated reduction of SMX-HA to SMX was markedly induced in dexamethasone and phenobarbital-treated rat hepatic microsomes, and was attributed to CYP3A and CYP2B forms.	Phenobarbital	82-95	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-3
7628309-6	1995	Additions of phenobarbital to the cultures induced CYP3A mRNA and CYP3A immunoreactive protein to a greater extent in rabbit hepatocytes (94-108% of the dexamethasone response) than in rat hepatocytes (38-57% of the dexamethasone response).	Phenobarbital	13-26	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	51-56
7628309-6	1995	Additions of phenobarbital to the cultures induced CYP3A mRNA and CYP3A immunoreactive protein to a greater extent in rabbit hepatocytes (94-108% of the dexamethasone response) than in rat hepatocytes (38-57% of the dexamethasone response).	Phenobarbital	13-26	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	66-71
7628308-10	1995	CYP-mediated reduction of SMX-HA to SMX was markedly induced in dexamethasone and phenobarbital-treated rat hepatic microsomes, and was attributed to CYP3A and CYP2B forms.	Phenobarbital	82-95	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	150-155
7628309-7	1995	In primary cultures of human hepatocytes, dexamethasone and phenobarbital treatments induced CYP3A mRNA (&gt; or = 4.4- and 1.9-fold, respectively, over the amounts of CYP3A mRNA in incubated control cultures).	Phenobarbital	60-73	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	93-98
7628309-7	1995	In primary cultures of human hepatocytes, dexamethasone and phenobarbital treatments induced CYP3A mRNA (&gt; or = 4.4- and 1.9-fold, respectively, over the amounts of CYP3A mRNA in incubated control cultures).	Phenobarbital	60-73	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	168-173
7732053-0	1995	Circadian-time rhythm of hepatic protein kinase C of rats pretreated with phenobarbital.	Phenobarbital	74-87	protein kinase C, gamma	Rattus norvegicus	33-49
7732053-2	1995	for 3 days) were studied in outbred male Wistar rats weighing 280-360 g. The well-known phenobarbital induction of cytochrome P-450 and 7-pentylresorufin-O-depentylase (PROD) was associated with inhibition of the hepatic PKC.	Phenobarbital	88-101	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	115-131
7732053-6	1995	Furthermore, phenobarbital inhibited the enzyme more strongly at 19.00 h than at 07.00 h. Our results suggest that increase of hepatic cytochrome P-450 content as well as induction of PROD are inversely related with the function of PKC.	Phenobarbital	13-26	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	135-151
7732053-6	1995	Furthermore, phenobarbital inhibited the enzyme more strongly at 19.00 h than at 07.00 h. Our results suggest that increase of hepatic cytochrome P-450 content as well as induction of PROD are inversely related with the function of PKC.	Phenobarbital	13-26	protein kinase C, gamma	Rattus norvegicus	232-235
7773543-9	1995	These results suggest that pilocarpine has (i) a high affinity towards phenobarbitone-inducible CYP2A4/5 and CYP2B activities in mouse liver, (ii) a high affinity towards CYP2A6 in human liver microsomes and (iii) a moderate affinity towards CYP3A enzyme(s) in both microsomal preparations.	Phenobarbital	71-85	cytochrome P450, family 2, subfamily a, polypeptide 4	Mus musculus	96-102
7873612-6	1995	The transcription of the new gene is enhanced in either sex by pregnenolone-alpha-carbonitrile, dexamethasone, phenobarbital, and triacetyloleandomycin, known inducers of CYP3A gene expression.	Phenobarbital	111-124	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	171-176
7886683-6	1995	Phenobarbital increased GST activity in the liver but not in lung or pancreas.	Phenobarbital	0-13	hematopoietic prostaglandin D synthase	Rattus norvegicus	24-27
7853177-5	1995	At low concentration, parathion was a competitive inhibitor of 2B1-mediated androstenedione 16 beta-hydroxylation (Ki = 0.44 +/- 0.07 microM) and of 7-pentylresorufin O-depentylation (Ki = 0.40 +/- 0.03 microM) in microsomes from PB-pretreated rats and was similarly effective against androstenedione 16 alpha- and 16 beta-hydroxylation catalyzed by purified 2B1.	Phenobarbital	230-232	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	63-66
7768670-7	1995	Furthermore, a significant suppression was observed when splenocytes were preincubated for 1 h with 1 mM cocaine in the presence of liver S-9 fractions isolated from phenobarbital-induced mice.	Phenobarbital	166-179	proteasome (prosome, macropain) 26S subunit, non-ATPase, 11	Mus musculus	138-141
7540119-3	1995	It was also demonstrated that tumor promoter phenobarbital influenced c-fos and c-myc expressions and decreased alpha 1I3 mRNA level in rat liver during a long term experiment.	Phenobarbital	45-58	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
7853177-2	1995	In the present study, two distinct components of the inhibition of the phenobarbital (PB)-inducible P450 2B1 by parathion were characterized.	Phenobarbital	71-84	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	105-108
7853177-2	1995	In the present study, two distinct components of the inhibition of the phenobarbital (PB)-inducible P450 2B1 by parathion were characterized.	Phenobarbital	86-88	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	105-108
7773300-4	1995	In the present report, we have characterized culture conditions further by examining individual and interactive effects of dexamethasone (Dex) and PB on CYP2B1, CYP2B2, and CYP3A1 expression.	Phenobarbital	147-149	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	153-159
7773300-4	1995	In the present report, we have characterized culture conditions further by examining individual and interactive effects of dexamethasone (Dex) and PB on CYP2B1, CYP2B2, and CYP3A1 expression.	Phenobarbital	147-149	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	161-167
7773300-4	1995	In the present report, we have characterized culture conditions further by examining individual and interactive effects of dexamethasone (Dex) and PB on CYP2B1, CYP2B2, and CYP3A1 expression.	Phenobarbital	147-149	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	173-179
7773300-7	1995	In contrast, at levels &gt; 10(-7) M, Dex profoundly inhibited PB induction of the CYP2B1 and CYP2B2 genes.	Phenobarbital	63-65	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	83-89
7773300-7	1995	In contrast, at levels &gt; 10(-7) M, Dex profoundly inhibited PB induction of the CYP2B1 and CYP2B2 genes.	Phenobarbital	63-65	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	94-100
7773300-9	1995	Similarly, concentrations of PB &gt; 0.5 mM resulted in substantially reduced levels of CYP2B1 and CYP2B2 induction than those attainable at lower PB concentrations.	Phenobarbital	29-31	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	88-94
7773300-9	1995	Similarly, concentrations of PB &gt; 0.5 mM resulted in substantially reduced levels of CYP2B1 and CYP2B2 induction than those attainable at lower PB concentrations.	Phenobarbital	29-31	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	99-105
7773300-10	1995	These results suggest that Dex and PB function cooperatively to regulate the CYP2B1 and CYP2B2 genes, and that composite interactions may either negatively or positively regulate expression, in a concentration-dependent manner.	Phenobarbital	35-37	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	77-83
7773300-10	1995	These results suggest that Dex and PB function cooperatively to regulate the CYP2B1 and CYP2B2 genes, and that composite interactions may either negatively or positively regulate expression, in a concentration-dependent manner.	Phenobarbital	35-37	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	88-94
7773300-11	1995	CYP3A1 was not regulated in a similar biphasic fashion, as this gene was fully responsive even at high dose levels of PB or Dex.	Phenobarbital	118-120	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	0-6
7540119-3	1995	It was also demonstrated that tumor promoter phenobarbital influenced c-fos and c-myc expressions and decreased alpha 1I3 mRNA level in rat liver during a long term experiment.	Phenobarbital	45-58	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	80-85
7540119-3	1995	It was also demonstrated that tumor promoter phenobarbital influenced c-fos and c-myc expressions and decreased alpha 1I3 mRNA level in rat liver during a long term experiment.	Phenobarbital	45-58	alpha-1-inhibitor III	Rattus norvegicus	112-121
7840637-0	1995	Maintenance of phenobarbital-inducible Cyp2b gene expression in C57BL/6 mouse hepatocytes in primary culture as spheroids.	Phenobarbital	15-28	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	39-44
7827137-10	1995	The tumor promoter phenobarbital induced MGMT, but not MPG mRNA in hepatocytes.	Phenobarbital	19-32	O-6-methylguanine-DNA methyltransferase	Rattus norvegicus	41-45
7827108-4	1995	Vmax values of G6PDH for glucose-6-phosphate decreased mainly in intermediate and pericentral zones after partial hepatectomy, whereas they increased after PB treatment.	Phenobarbital	156-158	glucose-6-phosphate dehydrogenase	Rattus norvegicus	15-20
7827108-6	1995	The affinity of G6PDH for glucose-6-phosphate was similar in all zones and it was decreased 2-3 fold by PB and 3-MC treatment.	Phenobarbital	104-106	glucose-6-phosphate dehydrogenase	Rattus norvegicus	16-21
7840628-1	1995	At low levels of phenobarbital induction two forms of isoenzyme 2 (LM2; CYP2B4) were obtained during purification of cytochrome P450 from rabbit liver microsomes.	Phenobarbital	17-30	cytochrome P450 2B4	Oryctolagus cuniculus	72-78
7840637-2	1995	Both the constitutive and phenobarbital-inducible expression of Cyp2b-9 and Cyp2b-10 mRNA decreased rapidly after transferring the hepatocytes to monolayer culture.	Phenobarbital	26-39	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	64-71
7840637-2	1995	Both the constitutive and phenobarbital-inducible expression of Cyp2b-9 and Cyp2b-10 mRNA decreased rapidly after transferring the hepatocytes to monolayer culture.	Phenobarbital	26-39	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	76-84
7840637-4	1995	However, in spheroid culture, the Cyp2b-9 and Cyp2b-10 mRNAs were induced by phenobarbital at high levels for at least 4 days either with continuous exposure from the start of cultivation or for 24 h before harvesting.	Phenobarbital	77-90	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	34-41
7840637-4	1995	However, in spheroid culture, the Cyp2b-9 and Cyp2b-10 mRNAs were induced by phenobarbital at high levels for at least 4 days either with continuous exposure from the start of cultivation or for 24 h before harvesting.	Phenobarbital	77-90	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	46-54
7840637-8	1995	There was more Cyp2b-10 species than those of Cyp2b-9 after exposure to phenobarbital both in vivo and in vitro.	Phenobarbital	72-85	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	15-23
7840637-8	1995	There was more Cyp2b-10 species than those of Cyp2b-9 after exposure to phenobarbital both in vivo and in vitro.	Phenobarbital	72-85	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	46-53
7840637-9	1995	Phenobarbital also induced CYP1A2 mRNA, which was again peculiar to spheroid culture.	Phenobarbital	0-13	cytochrome P450, family 1, subfamily a, polypeptide 2	Mus musculus	27-33
7840637-10	1995	Although the expression levels of both Cyp2b-9 and Cyp2b-10 species was very low in hepatocytes cultured without dexamethasone even in the presence of phenobarbital, the addition of 10(-7) or 10(-6) M dexamethasone caused an increase in the mRNA.	Phenobarbital	151-164	cytochrome P450, family 2, subfamily b, polypeptide 9	Mus musculus	39-46
7840637-10	1995	Although the expression levels of both Cyp2b-9 and Cyp2b-10 species was very low in hepatocytes cultured without dexamethasone even in the presence of phenobarbital, the addition of 10(-7) or 10(-6) M dexamethasone caused an increase in the mRNA.	Phenobarbital	151-164	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	51-59
7713363-11	1995	DL decreased the PB-induced BND activity and cytochrome P-450 and cytochrome b5 content.	Phenobarbital	17-19	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	45-79
7840789-10	1995	IL-1 beta and IL-6, at 50 U/mL culture medium, inhibited EROD induction by only 35% compared with the greater than 90% inhibitory effect on the PB induction of BROD activity.	Phenobarbital	144-146	interleukin 6	Rattus norvegicus	14-18
7756127-3	1995	This study has shown that the expression of CYP1A1 and UGT is concomitantly induced by 3-methylcholanthrene, dimethylbenz[a]anthracene, and RA, and that of NADPH reductase is only enhanced by phenobarbital and RA.	Phenobarbital	192-205	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	44-50
7756127-3	1995	This study has shown that the expression of CYP1A1 and UGT is concomitantly induced by 3-methylcholanthrene, dimethylbenz[a]anthracene, and RA, and that of NADPH reductase is only enhanced by phenobarbital and RA.	Phenobarbital	192-205	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	55-58
7986077-9	1994	Present results suggest that an isoform of morphine UDP-glucuronyltransferase belongs to the UGT1 family and is phenobarbital-inducible.	Phenobarbital	112-125	UDP glycosyltransferase 1 family, polypeptide A4, pseudogene	Rattus norvegicus	93-97
7877604-4	1994	The hepatic regucalcin mRNA levels were markedly reduced by phenobarbital administration.	Phenobarbital	60-73	regucalcin	Rattus norvegicus	12-22
7877604-6	1994	Moreover, the hepatic regucalcin concentration was significantly decreased by the administration of phenobarbital (12 mg/100 g), although the serum regucalcin concentration was not altered appreciably.	Phenobarbital	100-113	regucalcin	Rattus norvegicus	22-32
7877604-8	1994	The present study demonstrates that the expression of hepatic regucalcin mRNA is decreased by phenobarbital administration in rats, suggesting that regucalcin does not have a role in drug metabolism related to phenobarbital.	Phenobarbital	94-107	regucalcin	Rattus norvegicus	62-72
7877603-1	1994	Cytochrome P450 LM2 (CYPIIB4) from phenobarbital-induced rabbit liver microsomes, purified to only one band in SDS-PAGE, was further resolved in five peaks by cation exchange HPLC.	Phenobarbital	35-48	cytochrome P450 2B4	Oryctolagus cuniculus	0-19
7877603-1	1994	Cytochrome P450 LM2 (CYPIIB4) from phenobarbital-induced rabbit liver microsomes, purified to only one band in SDS-PAGE, was further resolved in five peaks by cation exchange HPLC.	Phenobarbital	35-48	cytochrome P450 2B4	Oryctolagus cuniculus	21-28
7877604-0	1994	Expression of hepatic calcium-binding protein regucalcin mRNA is decreased by phenobarbital administration in rats.	Phenobarbital	78-91	regucalcin	Rattus norvegicus	46-56
7877604-1	1994	The effect of phenobarbital on the expression of calcium-binding protein regucalcin mRNA in rat liver was investigated.	Phenobarbital	14-27	regucalcin	Rattus norvegicus	73-83
7528014-2	1994	CYP2A5-mediated coumarin 7-hydroxylase (COH) activity was retained in simple culture conditions for at least 96 hours and the activity was inducible up to 33-fold by phenobarbital (PB).	Phenobarbital	166-179	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	0-6
8001232-0	1994	Transforming growth factor-beta receptors type I, II and III in phenobarbital-promoted rat liver tumors.	Phenobarbital	64-77	transforming growth factor, beta receptor 1	Rattus norvegicus	0-60
8001232-5	1994	However, type I, II and III TGF beta receptor mRNA and protein levels were decreased by approximately 50% in the DEN-initiated/PB-promoted liver tumors as compared to the receptor levels in normal liver tissue surrounding the tumors.	Phenobarbital	127-129	transforming growth factor, beta 1	Rattus norvegicus	28-36
8001232-7	1994	These data demonstrate that PB promotes the formation of a tumor phenotype that is characterized by a significantly reduced number of TGF beta type I, II and III receptors.	Phenobarbital	28-30	transforming growth factor, beta 1	Rattus norvegicus	134-142
7808429-2	1994	In this investigation, we examined the frequency of the P450 2B5-null phenotype and the functional consequences of polymorphic P450 2B5 expression in hepatic microsomes from phenobarbital-treated rabbits.	Phenobarbital	174-187	cytochrome P450 2B4	Oryctolagus cuniculus	127-135
7528014-3	1994	The constitutive activity and inducibility of COH was totally blocked by treatment of hepatocytes with actinomycin D, and short initial treatment with cycloheximide caused superinducibility when co-administered with PB.	Phenobarbital	216-218	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	46-49
7528014-5	1994	Administration of dibutyryl cAMP, forskolin, and 3-isobutyl-1-methylxanthine (IBMX) enhanced both basal and PB-induced COH activities and CYP2A5 mRNA levels, indicating that cAMP plays a major role in CYP2A5 expression.	Phenobarbital	108-110	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	119-122
7528014-5	1994	Administration of dibutyryl cAMP, forskolin, and 3-isobutyl-1-methylxanthine (IBMX) enhanced both basal and PB-induced COH activities and CYP2A5 mRNA levels, indicating that cAMP plays a major role in CYP2A5 expression.	Phenobarbital	108-110	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	138-144
8001226-11	1994	Alternate substrates of CYP3A, cortisol and erythromycin, inhibited tamoxifen binding in liver microsomes from PCN- and phenobarbital-treated rats.	Phenobarbital	120-133	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	24-29
8001226-13	1994	Antibodies against rat CYP3A1 strongly inhibited tamoxifen binding to liver microsomes from PCN- and phenobarbital-treated rats, whereas the antibodies anti-CYP2B1/2B2 did not inhibit binding.	Phenobarbital	101-114	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	23-29
7982658-3	1994	Phenobarbital increased both alpha 1 acid glycoprotein secretion and corresponding mRNA levels in primary rat hepatocytes cultured on matrigel.	Phenobarbital	0-13	orosomucoid 1	Rattus norvegicus	29-54
7982658-5	1994	These results show that (a) phenobarbital acts directly on hepatocytes by increasing alpha 1-acid glycoprotein gene expression and (b) this effect is mediated by a specific mechanism independent of pathways involved in alpha 1-acid glycoprotein induction by interleukin-1, interleukin-6 and glucocorticoids.	Phenobarbital	28-41	interleukin 6	Rattus norvegicus	273-286
20693085-10	1994	In cultured rat hepatocytes treated with phenobarbital, significant EROD activity was detected in the absence of immunoreactive CYP1A1 induction.	Phenobarbital	41-54	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	128-134
7528014-5	1994	Administration of dibutyryl cAMP, forskolin, and 3-isobutyl-1-methylxanthine (IBMX) enhanced both basal and PB-induced COH activities and CYP2A5 mRNA levels, indicating that cAMP plays a major role in CYP2A5 expression.	Phenobarbital	108-110	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	201-207
7528014-2	1994	CYP2A5-mediated coumarin 7-hydroxylase (COH) activity was retained in simple culture conditions for at least 96 hours and the activity was inducible up to 33-fold by phenobarbital (PB).	Phenobarbital	166-179	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	16-38
7528014-2	1994	CYP2A5-mediated coumarin 7-hydroxylase (COH) activity was retained in simple culture conditions for at least 96 hours and the activity was inducible up to 33-fold by phenobarbital (PB).	Phenobarbital	166-179	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	40-43
7528014-2	1994	CYP2A5-mediated coumarin 7-hydroxylase (COH) activity was retained in simple culture conditions for at least 96 hours and the activity was inducible up to 33-fold by phenobarbital (PB).	Phenobarbital	181-183	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	0-6
7528014-2	1994	CYP2A5-mediated coumarin 7-hydroxylase (COH) activity was retained in simple culture conditions for at least 96 hours and the activity was inducible up to 33-fold by phenobarbital (PB).	Phenobarbital	181-183	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	16-38
7528014-2	1994	CYP2A5-mediated coumarin 7-hydroxylase (COH) activity was retained in simple culture conditions for at least 96 hours and the activity was inducible up to 33-fold by phenobarbital (PB).	Phenobarbital	181-183	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	40-43
7535226-6	1994	Exposure to PB + CCl4 results in enhanced liver injury similar to that observed with CD, but the animals recover and survive in contrast to the greatly amplified lethality of CD + CCl4.	Phenobarbital	12-14	C-C motif chemokine ligand 4	Rattus norvegicus	180-184
7980651-5	1994	In contrast to the suppressive effects on the spontaneous increases in 2B1/2 mRNA, low doses of DEX (10(-8) to 10(-7) M) enhanced the induction of 2B1/2 mRNA by phenobarbital (2.5-fold at 10(-7) M DEX).	Phenobarbital	161-174	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	147-152
7696542-4	1994	Pretreatment of mice with the P450 inducer phenobarbital enhanced the hepatotoxic response, as indicated by an increase in plasma alanine aminotransferase (ALT) levels and hepatic necrosis, while pretreatment with the P450 inhibitor piperonyl butoxide markedly attenuated the toxic response.	Phenobarbital	43-56	glutamic pyruvic transaminase, soluble	Mus musculus	130-154
7696542-4	1994	Pretreatment of mice with the P450 inducer phenobarbital enhanced the hepatotoxic response, as indicated by an increase in plasma alanine aminotransferase (ALT) levels and hepatic necrosis, while pretreatment with the P450 inhibitor piperonyl butoxide markedly attenuated the toxic response.	Phenobarbital	43-56	glutamic pyruvic transaminase, soluble	Mus musculus	156-159
7979401-1	1994	The phenobarbital (PB)-mediated expression of five forms of cytochrome P450 (CYP2A1, CYP2B1, CYP2B2, CYP2C6, and CYP3A1) and epoxide hydrolase has been examined in male and female rats from three inbred strains [Fischer (F344), Wistar Furth (WF), and Wistar Kyoto (WK)].	Phenobarbital	4-17	cytochrome P450, family 2, subfamily a, polypeptide 1	Rattus norvegicus	77-83
7979401-1	1994	The phenobarbital (PB)-mediated expression of five forms of cytochrome P450 (CYP2A1, CYP2B1, CYP2B2, CYP2C6, and CYP3A1) and epoxide hydrolase has been examined in male and female rats from three inbred strains [Fischer (F344), Wistar Furth (WF), and Wistar Kyoto (WK)].	Phenobarbital	4-17	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	85-91
7979401-1	1994	The phenobarbital (PB)-mediated expression of five forms of cytochrome P450 (CYP2A1, CYP2B1, CYP2B2, CYP2C6, and CYP3A1) and epoxide hydrolase has been examined in male and female rats from three inbred strains [Fischer (F344), Wistar Furth (WF), and Wistar Kyoto (WK)].	Phenobarbital	4-17	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	93-99
7979401-1	1994	The phenobarbital (PB)-mediated expression of five forms of cytochrome P450 (CYP2A1, CYP2B1, CYP2B2, CYP2C6, and CYP3A1) and epoxide hydrolase has been examined in male and female rats from three inbred strains [Fischer (F344), Wistar Furth (WF), and Wistar Kyoto (WK)].	Phenobarbital	4-17	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	101-107
7979401-1	1994	The phenobarbital (PB)-mediated expression of five forms of cytochrome P450 (CYP2A1, CYP2B1, CYP2B2, CYP2C6, and CYP3A1) and epoxide hydrolase has been examined in male and female rats from three inbred strains [Fischer (F344), Wistar Furth (WF), and Wistar Kyoto (WK)].	Phenobarbital	4-17	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	113-119
7979401-1	1994	The phenobarbital (PB)-mediated expression of five forms of cytochrome P450 (CYP2A1, CYP2B1, CYP2B2, CYP2C6, and CYP3A1) and epoxide hydrolase has been examined in male and female rats from three inbred strains [Fischer (F344), Wistar Furth (WF), and Wistar Kyoto (WK)].	Phenobarbital	19-21	cytochrome P450, family 2, subfamily a, polypeptide 1	Rattus norvegicus	77-83
7979401-1	1994	The phenobarbital (PB)-mediated expression of five forms of cytochrome P450 (CYP2A1, CYP2B1, CYP2B2, CYP2C6, and CYP3A1) and epoxide hydrolase has been examined in male and female rats from three inbred strains [Fischer (F344), Wistar Furth (WF), and Wistar Kyoto (WK)].	Phenobarbital	19-21	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	85-91
7979401-1	1994	The phenobarbital (PB)-mediated expression of five forms of cytochrome P450 (CYP2A1, CYP2B1, CYP2B2, CYP2C6, and CYP3A1) and epoxide hydrolase has been examined in male and female rats from three inbred strains [Fischer (F344), Wistar Furth (WF), and Wistar Kyoto (WK)].	Phenobarbital	19-21	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	93-99
7979401-1	1994	The phenobarbital (PB)-mediated expression of five forms of cytochrome P450 (CYP2A1, CYP2B1, CYP2B2, CYP2C6, and CYP3A1) and epoxide hydrolase has been examined in male and female rats from three inbred strains [Fischer (F344), Wistar Furth (WF), and Wistar Kyoto (WK)].	Phenobarbital	19-21	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	101-107
7979401-1	1994	The phenobarbital (PB)-mediated expression of five forms of cytochrome P450 (CYP2A1, CYP2B1, CYP2B2, CYP2C6, and CYP3A1) and epoxide hydrolase has been examined in male and female rats from three inbred strains [Fischer (F344), Wistar Furth (WF), and Wistar Kyoto (WK)].	Phenobarbital	19-21	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	113-119
7945456-1	1994	Phenobarbital (PB) induces transcription of the alpha 1-acid glycoprotein (AGP) gene, one of the major positive acute-phase proteins, the expression of which is controlled by a specific combination of glucocorticoids and cytokines.	Phenobarbital	0-13	orosomucoid 1	Rattus norvegicus	75-78
7945456-1	1994	Phenobarbital (PB) induces transcription of the alpha 1-acid glycoprotein (AGP) gene, one of the major positive acute-phase proteins, the expression of which is controlled by a specific combination of glucocorticoids and cytokines.	Phenobarbital	15-17	orosomucoid 1	Rattus norvegicus	75-78
7945456-3	1994	We found that the pattern of whole-serum proteins in PB-treated rats differed markedly from that observed during a typical acute inflammatory response (in turpentine-treated rats): levels of some positive acute-phase proteins (APP) increased slightly (alpha 1-acid glycoprotein, haptoglobin, hemopexin and T-kininogen), while levels of alpha 2 macroglobulin, the most sensitive marker of the acute-phase reaction, decreased.	Phenobarbital	53-55	haptoglobin	Rattus norvegicus	279-290
7945456-3	1994	We found that the pattern of whole-serum proteins in PB-treated rats differed markedly from that observed during a typical acute inflammatory response (in turpentine-treated rats): levels of some positive acute-phase proteins (APP) increased slightly (alpha 1-acid glycoprotein, haptoglobin, hemopexin and T-kininogen), while levels of alpha 2 macroglobulin, the most sensitive marker of the acute-phase reaction, decreased.	Phenobarbital	53-55	hemopexin	Rattus norvegicus	292-301
7945456-3	1994	We found that the pattern of whole-serum proteins in PB-treated rats differed markedly from that observed during a typical acute inflammatory response (in turpentine-treated rats): levels of some positive acute-phase proteins (APP) increased slightly (alpha 1-acid glycoprotein, haptoglobin, hemopexin and T-kininogen), while levels of alpha 2 macroglobulin, the most sensitive marker of the acute-phase reaction, decreased.	Phenobarbital	53-55	alpha-2-macroglobulin	Rattus norvegicus	336-357
7945456-6	1994	Glucocorticoid involvement is also ruled out by the observed enhancement of the effect of PB on AGP expression in adrenalectomized animals.	Phenobarbital	90-92	orosomucoid 1	Rattus norvegicus	96-99
7945456-7	1994	Our results suggest that phenobarbital acts on AGP expression by a mechanism independent of the inflammatory pathway.	Phenobarbital	25-38	orosomucoid 1	Rattus norvegicus	47-50
8055622-4	1994	Since the M6P/IGF-II receptor facilitates the proteolytic activation of TGF-beta 1, this suggests that PB increases the capacity of normal hepatocytes to activate TGF-beta 1.	Phenobarbital	103-105	transforming growth factor, beta 1	Rattus norvegicus	72-82
8069948-2	1994	CYP2A5 antibody inhibited AFB1 and NDEA metabolism by 40-60% in untreated hamsters and after treatment with phenobarbital (PB) or 3-methylcholanthrene (MC).	Phenobarbital	108-121	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	0-6
8069948-2	1994	CYP2A5 antibody inhibited AFB1 and NDEA metabolism by 40-60% in untreated hamsters and after treatment with phenobarbital (PB) or 3-methylcholanthrene (MC).	Phenobarbital	123-125	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	0-6
7853362-0	1994	Hepatic cytochrome P450 2B induction by ethyl/phenyl-substituted congeners of phenobarbital in the B6C3F1 mouse.	Phenobarbital	78-91	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	8-26
7853362-1	1994	The abilities of structural congeners of phenobarbital to induce immunoreactive hepatic cytochrome P450 2B (CYP2B) protein and associated catalytic activity (benzyloxyresorufin O-dealkylation) in the male B6C3F1 mouse were examined.	Phenobarbital	41-54	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	88-106
7853362-1	1994	The abilities of structural congeners of phenobarbital to induce immunoreactive hepatic cytochrome P450 2B (CYP2B) protein and associated catalytic activity (benzyloxyresorufin O-dealkylation) in the male B6C3F1 mouse were examined.	Phenobarbital	41-54	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	108-113
7853362-3	1994	The congeners were administered in the diet for 2 weeks at concentrations equimolar to 500 ppm of the prototype CYP2B inducer, phenobarbital.	Phenobarbital	127-140	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	112-117
7853362-4	1994	Of the series of compounds tested, phenobarbital was the most effective inducer of benzyloxyresorufin O-dealkylation and immunoreactive CYP2B protein, with 2-ethyl-2-phenylsuccinimide, 5-ethyl-5-phenylhydantoin, primidone, and glutethimide being only 19-42% as effective.	Phenobarbital	35-48	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	136-141
7853362-6	1994	Dose-response experiments performed with 5-ethyl-5-phenylhydantoin indicated that the intrinsic CYP2B-inducing activity of this congener was as great as that of phenobarbital in the mouse, although a fourfold greater dietary concentration of this hydantoin (2000 ppm) was required to elicit a response equivalent to that caused by 500 ppm phenobarbital.	Phenobarbital	339-352	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	96-101
7526150-1	1994	Previous studies have shown that exposure of phenobarbital-pretreated rats to halothane in 10% O2 causes centrilobular necrosis, induces expression of the 72-kDa heat shock protein (HSP72), and produces several trifluoroacetylated adducts.	Phenobarbital	45-58	selenoprotein K	Rattus norvegicus	162-180
7526150-1	1994	Previous studies have shown that exposure of phenobarbital-pretreated rats to halothane in 10% O2 causes centrilobular necrosis, induces expression of the 72-kDa heat shock protein (HSP72), and produces several trifluoroacetylated adducts.	Phenobarbital	45-58	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	182-187
7526150-9	1994	In contrast, HSP72 was induced only in the rats pretreated with phenobarbital and exposed to 1% halothane in 10% O2.	Phenobarbital	64-77	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	13-18
7894498-8	1994	In rabbit liver, CYP4B1 was induced by phenobarbital primarily in zone 1 hepatocytes (periportal).	Phenobarbital	39-52	cytochrome P450 4B1	Oryctolagus cuniculus	17-23
7923571-0	1994	Rapid development of hepatic tumors in transforming growth factor alpha transgenic mice associated with increased cell proliferation in precancerous hepatocellular lesions initiated by N-nitrosodiethylamine and promoted by phenobarbital.	Phenobarbital	223-236	transforming growth factor alpha	Mus musculus	39-71
7923571-12	1994	Proliferating cell nuclear antigen (PCNA) labeling indices of hepatocellular foci and adenomas in DEN- or DEN/PB-treated MT42 mice were significantly higher than those of CD-1 mice.	Phenobarbital	110-112	proliferating cell nuclear antigen	Mus musculus	0-34
7923571-12	1994	Proliferating cell nuclear antigen (PCNA) labeling indices of hepatocellular foci and adenomas in DEN- or DEN/PB-treated MT42 mice were significantly higher than those of CD-1 mice.	Phenobarbital	110-112	proliferating cell nuclear antigen	Mus musculus	36-40
7923571-14	1994	In conclusion, TGF-alpha transgenic mice clearly demonstrated enhanced sensitivity to the development of hepatocellular carcinoma in the DEN initiation and PB promotion regime, possibly through a mechanism of increased hepatocyte proliferation in precancerous lesions (foci and adenomas), driven by high expression of the mitogen TGF-alpha in these lesions.	Phenobarbital	156-158	transforming growth factor alpha	Mus musculus	15-24
7836507-3	1994	Spontaneous luteinizing hormone (LH) surges were measured as well as GnRH-induced LH surges on the day of pro-oestrus during infusions with 100-4000 pmol GnRH/rat/10 h, in phenobarbital blocked rats.	Phenobarbital	172-185	gonadotropin releasing hormone 1	Rattus norvegicus	154-158
7837047-6	1994	This was evidenced by the lower CSF phenobarbitone concentration, at the onset of the hypnotic effect, in the cyclosporin-treated group vs control values (115 +/- 4 vs 93 +/- 7 mg L-1, P = 0.01).	Phenobarbital	36-50	colony stimulating factor 2	Rattus norvegicus	32-35
8068731-2	1994	Cholestyramine and phenobarbital induced primarily the cytosolic farnesyl pyrophosphate synthase, whereas clofibrate and phthalates elevated the corresponding peroxisomal activity.	Phenobarbital	19-32	farnesyl diphosphate synthase	Rattus norvegicus	65-96
8093105-10	1994	Pentoxyresorufin and benzyloxyresorufin were metabolised by several different P450 forms in non-induced rat liver microsomes but mainly by the CYP1A subfamily in 3MC-induced microsomes and by CYP2B1 in PB- and ISF-induced microsomes.	Phenobarbital	202-204	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	192-198
8080449-7	1994	Glutathione-S-transferase (GST) activities against 1-chloro-2, 4-dinitrobenzene (CDNB) were higher in PC hepatocytes and remained so after induction with PB.	Phenobarbital	154-156	glutathione S-transferase kappa 1	Homo sapiens	0-25
8080449-7	1994	Glutathione-S-transferase (GST) activities against 1-chloro-2, 4-dinitrobenzene (CDNB) were higher in PC hepatocytes and remained so after induction with PB.	Phenobarbital	154-156	glutathione S-transferase kappa 1	Homo sapiens	27-30
20693081-4	1994	Furthermore, GalN treatment resulted in an increase in the activity of the PB-induced forms of CYP (namely CYP 2B1/2) as measured by 7-pentoxyresorufin O-depentylase (PROD) activity.	Phenobarbital	75-77	cytochrome P450, family 2, subfamily b, polypeptide 12	Rattus norvegicus	107-116
8093105-4	1994	Purified phenobarbitone (PB)-induced CYP2B1 was selective for benzyloxyresorufin and pentoxyresorufin.	Phenobarbital	9-23	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	37-43
8093105-4	1994	Purified phenobarbitone (PB)-induced CYP2B1 was selective for benzyloxyresorufin and pentoxyresorufin.	Phenobarbital	25-27	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	37-43
8080435-4	1994	Anti-CYP2B1/2 and anti-CYP1A1/2 inhibited the formation only in phenobarbital (PB)- and 3-methylcholanthrene (MC)-induced microsomes, respectively.	Phenobarbital	64-77	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	5-11
8080435-4	1994	Anti-CYP2B1/2 and anti-CYP1A1/2 inhibited the formation only in phenobarbital (PB)- and 3-methylcholanthrene (MC)-induced microsomes, respectively.	Phenobarbital	64-77	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	23-29
8080435-4	1994	Anti-CYP2B1/2 and anti-CYP1A1/2 inhibited the formation only in phenobarbital (PB)- and 3-methylcholanthrene (MC)-induced microsomes, respectively.	Phenobarbital	79-81	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	5-11
8080435-4	1994	Anti-CYP2B1/2 and anti-CYP1A1/2 inhibited the formation only in phenobarbital (PB)- and 3-methylcholanthrene (MC)-induced microsomes, respectively.	Phenobarbital	79-81	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	23-29
8068203-2	1994	Synthesis in the liver of the prototypic forms P450 2B1 and P450 2B2 is dramatically induced by phenobarbital.	Phenobarbital	96-109	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	52-55
8068204-0	1994	Interaction of proteins with a cytochrome P450 2B2 gene promoter: identification of two DNA sequences that bind proteins that are enriched or activated in response to phenobarbital.	Phenobarbital	167-180	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	31-50
8068204-8	1994	These two DNA sequences and their cognate binding proteins may play a role in the induction of CYP2B2 gene expression in response to phenobarbital.	Phenobarbital	133-146	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	95-101
8055622-4	1994	Since the M6P/IGF-II receptor facilitates the proteolytic activation of TGF-beta 1, this suggests that PB increases the capacity of normal hepatocytes to activate TGF-beta 1.	Phenobarbital	103-105	transforming growth factor, beta 1	Rattus norvegicus	163-173
7528203-18	1994	P450 RL33/cDEX mRNA represented over 70% of the total P450 3A mRNA from untreated, PB-, and DEX-treated rat liver.	Phenobarbital	83-85	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	5-9
8053924-8	1994	Formation of AMT, as measured by intrinsic clearance (Clint), was significantly increased in microsomes from rats pre-treated with phenobarbitone, dexamethasone and clofibrate (inducers of CYP2B, CYP3A and CYP4A, respectively).	Phenobarbital	131-145	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	196-201
8053925-6	1994	As expected, PB and MC increased GST activity together with the concentration of subunits 1 and 3 in rats.	Phenobarbital	13-15	hematopoietic prostaglandin D synthase	Rattus norvegicus	33-36
7928610-0	1994	Effects of short- and long-term administration of phenobarbital on endogenous ACTH concentration and results of ACTH stimulation tests in dogs.	Phenobarbital	50-63	proopiomelanocortin	Canis lupus familiaris	78-82
8031839-5	1994	The administration of phenobarbital and dexamethasone affected the expression of Cyp4a proteins in the liver, but not in the kidney, where testosterone was the key regulatory factor, demonstrating interesting tissue-specific effects in the regulation of these enzymes.	Phenobarbital	22-35	cytochrome P450, family 4, subfamily a, polypeptide 10	Mus musculus	81-86
7893187-1	1994	This paper presents a study of the action of phenobarbital (anticonvulsant barbituric acid with pK1 = 7.3 and pK2 = 11.8) on the short-circuit current and on the transepithelial conductance of the frog isolated skin.	Phenobarbital	45-58	prokineticin 1	Homo sapiens	96-99
7893187-1	1994	This paper presents a study of the action of phenobarbital (anticonvulsant barbituric acid with pK1 = 7.3 and pK2 = 11.8) on the short-circuit current and on the transepithelial conductance of the frog isolated skin.	Phenobarbital	45-58	prokineticin 2	Homo sapiens	110-113
7528203-15	1994	Northern blot analysis using an oligonucleotide probe specific for P450 RL33/cDEX revealed that P450 RL33/cDEX mRNA was induced strongly by pregnenolone 16 alpha-carbonitrile and DEX and weakly by phenobarbital (PB) and triacetyloleandomycin.	Phenobarbital	197-210	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	72-76
7528203-15	1994	Northern blot analysis using an oligonucleotide probe specific for P450 RL33/cDEX revealed that P450 RL33/cDEX mRNA was induced strongly by pregnenolone 16 alpha-carbonitrile and DEX and weakly by phenobarbital (PB) and triacetyloleandomycin.	Phenobarbital	197-210	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	77-81
7848579-4	1994	PB combination showed an increased incidence of GST-P+ foci in gamma ray irradiated groups.	Phenobarbital	0-2	glutathione S-transferase pi 1	Rattus norvegicus	48-53
8031133-0	1994	Growth hormone-dependent and -independent sexually dimorphic regulation of phenobarbital-induced hepatic cytochromes P450 2B1 and 2B2.	Phenobarbital	75-88	gonadotropin releasing hormone receptor	Rattus norvegicus	0-14
8031133-1	1994	Sexually dimorphic regulation of phenobarbital-induced cytochromes P450 2B1 and 2B2 (collectively referred to as P450 2B) as well as P450 2B-dependent monooxygenase activities was studied in multi-hormone-depleted hypophysectomized rats and in growth hormone (GH)-deficient monosodium glutamate (MSG)-treated rats.	Phenobarbital	33-46	gonadotropin releasing hormone receptor	Rattus norvegicus	244-258
8031133-1	1994	Sexually dimorphic regulation of phenobarbital-induced cytochromes P450 2B1 and 2B2 (collectively referred to as P450 2B) as well as P450 2B-dependent monooxygenase activities was studied in multi-hormone-depleted hypophysectomized rats and in growth hormone (GH)-deficient monosodium glutamate (MSG)-treated rats.	Phenobarbital	33-46	gonadotropin releasing hormone receptor	Rattus norvegicus	260-262
8031133-2	1994	Our results indicate that endogenous GH suppresses phenobarbital induction of P450 2B and that the feminine pattern of continuous GH secretion is more suppressive than the masculine profile of episodic secretion.	Phenobarbital	51-64	gonadotropin releasing hormone receptor	Rattus norvegicus	37-39
8031133-4	1994	Last, irrespective of the presence or absence of circulating GH, the magnitude of phenobarbital induction of P450 2B and associated monooxygenases was consistently lower in female rats, suggesting the presence of some degree of sex-dependent, but GH-independent regulation.	Phenobarbital	82-95	gonadotropin releasing hormone receptor	Rattus norvegicus	247-249
7528203-15	1994	Northern blot analysis using an oligonucleotide probe specific for P450 RL33/cDEX revealed that P450 RL33/cDEX mRNA was induced strongly by pregnenolone 16 alpha-carbonitrile and DEX and weakly by phenobarbital (PB) and triacetyloleandomycin.	Phenobarbital	197-210	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	101-105
7528203-15	1994	Northern blot analysis using an oligonucleotide probe specific for P450 RL33/cDEX revealed that P450 RL33/cDEX mRNA was induced strongly by pregnenolone 16 alpha-carbonitrile and DEX and weakly by phenobarbital (PB) and triacetyloleandomycin.	Phenobarbital	197-210	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	106-110
7528203-18	1994	P450 RL33/cDEX mRNA represented over 70% of the total P450 3A mRNA from untreated, PB-, and DEX-treated rat liver.	Phenobarbital	83-85	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	10-14
7528203-15	1994	Northern blot analysis using an oligonucleotide probe specific for P450 RL33/cDEX revealed that P450 RL33/cDEX mRNA was induced strongly by pregnenolone 16 alpha-carbonitrile and DEX and weakly by phenobarbital (PB) and triacetyloleandomycin.	Phenobarbital	212-214	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	72-76
8058060-1	1994	Cytochrome P450 2C6 (CYP2C6) is a developmentally regulated, constitutively expressed form of rat liver microsomal cytochrome P450 that in the liver of adult male rats is induced to a limited extent by phenobarbital.	Phenobarbital	202-215	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	0-19
7528203-15	1994	Northern blot analysis using an oligonucleotide probe specific for P450 RL33/cDEX revealed that P450 RL33/cDEX mRNA was induced strongly by pregnenolone 16 alpha-carbonitrile and DEX and weakly by phenobarbital (PB) and triacetyloleandomycin.	Phenobarbital	212-214	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	77-81
7528203-15	1994	Northern blot analysis using an oligonucleotide probe specific for P450 RL33/cDEX revealed that P450 RL33/cDEX mRNA was induced strongly by pregnenolone 16 alpha-carbonitrile and DEX and weakly by phenobarbital (PB) and triacetyloleandomycin.	Phenobarbital	212-214	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	101-105
7528203-15	1994	Northern blot analysis using an oligonucleotide probe specific for P450 RL33/cDEX revealed that P450 RL33/cDEX mRNA was induced strongly by pregnenolone 16 alpha-carbonitrile and DEX and weakly by phenobarbital (PB) and triacetyloleandomycin.	Phenobarbital	212-214	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	106-110
8058060-1	1994	Cytochrome P450 2C6 (CYP2C6) is a developmentally regulated, constitutively expressed form of rat liver microsomal cytochrome P450 that in the liver of adult male rats is induced to a limited extent by phenobarbital.	Phenobarbital	202-215	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	21-27
8031317-2	1994	Exposure to benzene was reported to lower the cytochrome P450 (CYP; EC 1.14.14.1) content in phenobarbital-pretreated (PB) rats in vivo (Gut I, Zbl Pharm 122: 1139-1161, 1983).	Phenobarbital	93-106	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	46-61
8003039-4	1994	The microsomal binding of dexamethasone is antagonised by several transcriptional and/or post-transcriptional CYP3A inducers with decreasing potency pregnenolone 16 alpha carbonitrile &gt; metyrapone &gt; phenobarbitone.	Phenobarbital	205-219	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	110-115
8031317-2	1994	Exposure to benzene was reported to lower the cytochrome P450 (CYP; EC 1.14.14.1) content in phenobarbital-pretreated (PB) rats in vivo (Gut I, Zbl Pharm 122: 1139-1161, 1983).	Phenobarbital	93-106	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	63-66
8081427-0	1994	Expression of the CYP3A and CYP2C11 enzymes in a nutritionally obese rodent model: response to phenobarbital treatment.	Phenobarbital	95-108	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	18-23
8195225-5	1994	Increase in the ionic strength also enhanced the rate of cytochrome P450 reduction in control and phenobarbital-induced rat liver microsomes and in reconstituted systems containing purified rat liver CYP2C6, CYP2C12, CYP2C13, and CYP2E1, and rat reductase.	Phenobarbital	98-111	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	57-72
8195225-5	1994	Increase in the ionic strength also enhanced the rate of cytochrome P450 reduction in control and phenobarbital-induced rat liver microsomes and in reconstituted systems containing purified rat liver CYP2C6, CYP2C12, CYP2C13, and CYP2E1, and rat reductase.	Phenobarbital	98-111	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	200-206
8195225-5	1994	Increase in the ionic strength also enhanced the rate of cytochrome P450 reduction in control and phenobarbital-induced rat liver microsomes and in reconstituted systems containing purified rat liver CYP2C6, CYP2C12, CYP2C13, and CYP2E1, and rat reductase.	Phenobarbital	98-111	cytochrome P450, family 2, subfamily c, polypeptide 13	Rattus norvegicus	217-224
8195225-5	1994	Increase in the ionic strength also enhanced the rate of cytochrome P450 reduction in control and phenobarbital-induced rat liver microsomes and in reconstituted systems containing purified rat liver CYP2C6, CYP2C12, CYP2C13, and CYP2E1, and rat reductase.	Phenobarbital	98-111	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	230-236
8205532-11	1994	In PB-treated livers, a P450 fraction containing CYP2H1/H2, the major PB-induced P450s, had the highest tamoxifen 4-hydroxylase and N-demethylase activities, a finding compatible with one or both of those P450s being responsible for the PB-induced tamoxifen 4-hydroxylation and N-demethylation.	Phenobarbital	3-5	cytochrome P450 2H1	Gallus gallus	49-55
8205532-11	1994	In PB-treated livers, a P450 fraction containing CYP2H1/H2, the major PB-induced P450s, had the highest tamoxifen 4-hydroxylase and N-demethylase activities, a finding compatible with one or both of those P450s being responsible for the PB-induced tamoxifen 4-hydroxylation and N-demethylation.	Phenobarbital	70-72	cytochrome P450 2H1	Gallus gallus	49-55
8205532-11	1994	In PB-treated livers, a P450 fraction containing CYP2H1/H2, the major PB-induced P450s, had the highest tamoxifen 4-hydroxylase and N-demethylase activities, a finding compatible with one or both of those P450s being responsible for the PB-induced tamoxifen 4-hydroxylation and N-demethylation.	Phenobarbital	70-72	cytochrome P450 2H1	Gallus gallus	49-55
8205533-0	1994	Colocalized alterations in connexin32 and cytochrome P450IIB1/2 by phenobarbital and related liver tumor promoters.	Phenobarbital	67-80	gap junction protein, beta 1	Rattus norvegicus	27-37
8205533-2	1994	Previous studies in our laboratory showed that the liver tumor promoter phenobarbital (PB) reversibly decreases the abundance of the GJ protein connexin32 (Cx32) in both preneoplastic-altered hepatic foci and centrolobular hepatocytes (M. J. Neveu et al., Cancer Commun., 2: 21-31, 1990).	Phenobarbital	72-85	gap junction protein, beta 1	Rattus norvegicus	144-154
8205533-2	1994	Previous studies in our laboratory showed that the liver tumor promoter phenobarbital (PB) reversibly decreases the abundance of the GJ protein connexin32 (Cx32) in both preneoplastic-altered hepatic foci and centrolobular hepatocytes (M. J. Neveu et al., Cancer Commun., 2: 21-31, 1990).	Phenobarbital	72-85	gap junction protein, beta 1	Rattus norvegicus	156-160
8205533-2	1994	Previous studies in our laboratory showed that the liver tumor promoter phenobarbital (PB) reversibly decreases the abundance of the GJ protein connexin32 (Cx32) in both preneoplastic-altered hepatic foci and centrolobular hepatocytes (M. J. Neveu et al., Cancer Commun., 2: 21-31, 1990).	Phenobarbital	87-89	gap junction protein, beta 1	Rattus norvegicus	144-154
8205533-2	1994	Previous studies in our laboratory showed that the liver tumor promoter phenobarbital (PB) reversibly decreases the abundance of the GJ protein connexin32 (Cx32) in both preneoplastic-altered hepatic foci and centrolobular hepatocytes (M. J. Neveu et al., Cancer Commun., 2: 21-31, 1990).	Phenobarbital	87-89	gap junction protein, beta 1	Rattus norvegicus	156-160
8205533-3	1994	Because the inhibitory effects of PB on GJ intercellular communication are prevented by the nonspecific cytochrome P-450 inhibitor SKF-525A (J. E. Klauning, et al., Toxicol.	Phenobarbital	34-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	104-120
8205533-5	1994	Pharmacol., 102: 533-563, 1990), we investigated whether alterations in Cx32 are coincident with changes in the major PB-inducible cytochrome P-450, termed b/e or IIB1/2.	Phenobarbital	118-120	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	131-147
8205533-6	1994	Immunostaining of liver cryosections from rats fed dietary PB demonstrated that centrolobular hepatocytes that exhibit reduced Cx32 express enhanced cytochrome P450IIB1/2 protein.	Phenobarbital	59-61	gap junction protein, beta 1	Rattus norvegicus	127-131
8205533-10	1994	To determine the molecular mechanisms responsible for the modification in Cx32 staining, we examined the mRNA and protein levels of Cx32 and P450IIB1/2 in total-tissue homogenates from PB-treated rats.	Phenobarbital	185-187	gap junction protein, beta 1	Rattus norvegicus	132-136
8205533-13	1994	Examination of Cx32 solubility in 20 mM NaOH demonstrated that PB treatment results in the generation of a NaOH-soluble form of Cx32 (i.e., 47 kDa).	Phenobarbital	63-65	gap junction protein, beta 1	Rattus norvegicus	15-19
8205533-13	1994	Examination of Cx32 solubility in 20 mM NaOH demonstrated that PB treatment results in the generation of a NaOH-soluble form of Cx32 (i.e., 47 kDa).	Phenobarbital	63-65	gap junction protein, beta 1	Rattus norvegicus	128-132
8205533-14	1994	In addition, trypsinized paraffin-embedded liver sections from PB-treated rats exhibited diffuse cytoplasmic Cx32 staining that was restricted to centrolobular cells.	Phenobarbital	63-65	gap junction protein, beta 1	Rattus norvegicus	109-113
8081427-0	1994	Expression of the CYP3A and CYP2C11 enzymes in a nutritionally obese rodent model: response to phenobarbital treatment.	Phenobarbital	95-108	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	28-35
7526561-0	1994	C-raf expression in early rat liver tumorigenesis after promotion with polychlorinated biphenyls or phenobarbital.	Phenobarbital	100-113	Raf-1 proto-oncogene, serine/threonine kinase	Rattus norvegicus	0-5
7983678-9	1994	Studies have shown that pretreatment with phenobarbital results in postponed low-dose CCl4-stimulated cell division by 24 hours, which accordingly postpones the optimal autoprotection.	Phenobarbital	42-55	C-C motif chemokine ligand 4	Homo sapiens	86-90
8209390-4	1994	The maximal induction of P450 isoenzymes CYP2B1/2B2 (20- to 25-fold) and CYP2C6 (6-fold) were found at 0.75 mM PB at both oxygen tensions.	Phenobarbital	111-113	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	41-51
8209390-4	1994	The maximal induction of P450 isoenzymes CYP2B1/2B2 (20- to 25-fold) and CYP2C6 (6-fold) were found at 0.75 mM PB at both oxygen tensions.	Phenobarbital	111-113	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	73-79
8209390-5	1994	In contrast, the highest induction of CYP1A1/1A2 (3-fold), of CYP3A (2-fold), and EROD activity were found with 3 mM PB in 4% O2 cultures.	Phenobarbital	117-119	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	38-44
8209390-5	1994	In contrast, the highest induction of CYP1A1/1A2 (3-fold), of CYP3A (2-fold), and EROD activity were found with 3 mM PB in 4% O2 cultures.	Phenobarbital	117-119	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	62-67
7909493-9	1994	PB treatment increased both the average number of persistent GGT-positive nodules and the ratio of persistent GGT-positive to rGSTP1-1-positive nodules/cm2.	Phenobarbital	0-2	glutathione S-transferase pi 1	Rattus norvegicus	126-132
8198522-12	1994	Both BHA and BHT were also able to induce this enzyme but, by contrast, PB was found to be a poor inducer of AFB1-AR.	Phenobarbital	72-74	aldo-keto reductase family 7 member A3	Rattus norvegicus	109-116
7920410-1	1994	We have studied lysosomal proteases capable of degrading a major form of cytochrome P450 (CYP2B1) which was purified from the liver microsomes of phenobarbital-treated rats.	Phenobarbital	146-159	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	90-96
8198522-8	1994	Administration of the antioxidants EQ, BHA or BHT, as well as PB, led to a marked increase in levels of the GST Yc2 subunit in rat liver, and this increase coincided with a substantial rise in the GST activity towards AFB1-8,9-epoxide; neither AFB1, 3-MC nor clofibrate caused induction of Yc2 or any of the GST subunits examined.	Phenobarbital	62-64	glutathione S-transferase alpha 3	Rattus norvegicus	108-115
8198522-8	1994	Administration of the antioxidants EQ, BHA or BHT, as well as PB, led to a marked increase in levels of the GST Yc2 subunit in rat liver, and this increase coincided with a substantial rise in the GST activity towards AFB1-8,9-epoxide; neither AFB1, 3-MC nor clofibrate caused induction of Yc2 or any of the GST subunits examined.	Phenobarbital	62-64	hematopoietic prostaglandin D synthase	Rattus norvegicus	108-111
8198522-8	1994	Administration of the antioxidants EQ, BHA or BHT, as well as PB, led to a marked increase in levels of the GST Yc2 subunit in rat liver, and this increase coincided with a substantial rise in the GST activity towards AFB1-8,9-epoxide; neither AFB1, 3-MC nor clofibrate caused induction of Yc2 or any of the GST subunits examined.	Phenobarbital	62-64	glutathione S-transferase alpha 3	Rattus norvegicus	112-115
8198522-8	1994	Administration of the antioxidants EQ, BHA or BHT, as well as PB, led to a marked increase in levels of the GST Yc2 subunit in rat liver, and this increase coincided with a substantial rise in the GST activity towards AFB1-8,9-epoxide; neither AFB1, 3-MC nor clofibrate caused induction of Yc2 or any of the GST subunits examined.	Phenobarbital	62-64	hematopoietic prostaglandin D synthase	Rattus norvegicus	197-200
7958191-0	1994	Cell systems capable of sustaining phenobarbital induction by CYP2B genes.	Phenobarbital	35-48	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	62-67
7920427-1	1994	Primary cultures of dog hepatocytes sensitivity responded to various inducers of cytochrome P-450; phenobarbital (PB) significantly elevated the activity of 7-ethoxycoumarin O-deethylase (ECOD) and progesterone 6 beta-hydroxylase (6 beta-OHP).	Phenobarbital	99-112	Cytochrome P450 1A1	Canis lupus familiaris	81-97
7920427-1	1994	Primary cultures of dog hepatocytes sensitivity responded to various inducers of cytochrome P-450; phenobarbital (PB) significantly elevated the activity of 7-ethoxycoumarin O-deethylase (ECOD) and progesterone 6 beta-hydroxylase (6 beta-OHP).	Phenobarbital	114-116	Cytochrome P450 1A1	Canis lupus familiaris	81-97
7920427-4	1994	Pretreatment of the cultures with PB enhanced GSH depletion by bromobenzene, while beta-NF and Rif had little effect, suggesting that the 2B type cytochrome P-450 is responsible for the primary oxidation of bromobenzene to GSH-reactive metabolite(s).	Phenobarbital	34-36	Cytochrome P450 1A1	Canis lupus familiaris	146-162
8197589-4	1994	Pretreatment of rats with phenobarbital (PB) prior to menthofuran treatment potentiated hepatotoxicity suggesting that a PB-induced cytochrome P-450 catalyzed the formation of reactive metabolite(s) responsible for the hepatotoxicity.	Phenobarbital	26-39	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	132-148
7961616-1	1994	An epoxide hydrolase (mEH) in liver microsomes was purified to apparent homogeneity from a dog treated with phenobarbital.	Phenobarbital	108-121	epoxide hydrolase 1, microsomal	Mus musculus	22-25
7817119-0	1994	Effect of phenobarbital and mirex pretreatments on CCl4 autoprotection.	Phenobarbital	10-23	C-C motif chemokine ligand 4	Rattus norvegicus	51-55
8197589-4	1994	Pretreatment of rats with phenobarbital (PB) prior to menthofuran treatment potentiated hepatotoxicity suggesting that a PB-induced cytochrome P-450 catalyzed the formation of reactive metabolite(s) responsible for the hepatotoxicity.	Phenobarbital	41-43	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	132-148
8197589-4	1994	Pretreatment of rats with phenobarbital (PB) prior to menthofuran treatment potentiated hepatotoxicity suggesting that a PB-induced cytochrome P-450 catalyzed the formation of reactive metabolite(s) responsible for the hepatotoxicity.	Phenobarbital	121-123	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	132-148
8135806-1	1994	Immunocytochemical studies have revealed that one of the major heat shock proteins, HSP72, is induced in livers of rats that have been pretreated with phenobarbital and then administered halothane in a hypoxic gas mixture of 10% oxygen.	Phenobarbital	151-164	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	84-89
8018775-10	1994	After treatment of rats with PB both CYP2B1 and CYP2B2 were observed in the liver, while only the former was found in the lung and kidney.	Phenobarbital	29-31	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	37-43
8018775-10	1994	After treatment of rats with PB both CYP2B1 and CYP2B2 were observed in the liver, while only the former was found in the lung and kidney.	Phenobarbital	29-31	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	48-54
8025560-3	1994	In both strains, CYP6A1 was inducible by phenobarbital treatment of the flies.	Phenobarbital	41-54	cytochrome P450 6A1	Musca domestica	17-23
7513451-1	1994	We previously reported that when primary cultures of rat hepatocytes were treated with phenobarbital (PB) or one of several organochlorine pesticides, including Mirex, there was co-induction of cytochrome P450 2B1 and 2B2 mRNAs and immunoreactive proteins, whereas Kepone selectively induced 2B2 (Kocarek et al.	Phenobarbital	87-100	cytochrome P450 2B1	Rattus norvegicus	194-221
7513451-1	1994	We previously reported that when primary cultures of rat hepatocytes were treated with phenobarbital (PB) or one of several organochlorine pesticides, including Mirex, there was co-induction of cytochrome P450 2B1 and 2B2 mRNAs and immunoreactive proteins, whereas Kepone selectively induced 2B2 (Kocarek et al.	Phenobarbital	102-104	cytochrome P450 2B1	Rattus norvegicus	194-221
7513451-5	1994	Indeed, Kepone treatment actively suppressed induction of 2B1 and 2B2 mRNAs in hepatocytes cotreated with phenobarbital.	Phenobarbital	106-119	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	58-69
7513451-12	1994	Treatment with chloral hydrate (3 x 10(-3) M), like Kepone (10(-5) M), suppressed 2B1/2 mRNA induction following phenobarbital (10(-4) M) treatment, while Kepone alcohol (10(-5) M), which is not a gem-diol, produced less suppression.	Phenobarbital	113-126	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	82-85
7513451-13	1994	Our results suggest that selective induction by Kepone of 2B2 is unlikely related to its effects as a weak classical estrogen, while the ability of Kepone to suppress induction of 2B1 and 2B2 by PB may be related to its properties as a gem-diol.	Phenobarbital	195-197	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	180-183
8135806-3	1994	Western blotting with a mouse monoclonal anti-HSP70 IgG antibody, which recognizes both the constitutive (HSP73) and inducible (HSP72) forms, revealed that HSP72 was induced and translocated into the nucleus in only those rats exposed to halothane under hypoxia following phenobarbital pretreatment.	Phenobarbital	272-285	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	46-51
8135806-3	1994	Western blotting with a mouse monoclonal anti-HSP70 IgG antibody, which recognizes both the constitutive (HSP73) and inducible (HSP72) forms, revealed that HSP72 was induced and translocated into the nucleus in only those rats exposed to halothane under hypoxia following phenobarbital pretreatment.	Phenobarbital	272-285	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	128-133
8135806-3	1994	Western blotting with a mouse monoclonal anti-HSP70 IgG antibody, which recognizes both the constitutive (HSP73) and inducible (HSP72) forms, revealed that HSP72 was induced and translocated into the nucleus in only those rats exposed to halothane under hypoxia following phenobarbital pretreatment.	Phenobarbital	272-285	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	156-161
8135852-10	1994	PB also induced non-constitutive CYP2A/CYP2B protein bands at 49 and 52 kDa in some monkeys.	Phenobarbital	0-2	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	33-38
8135852-10	1994	PB also induced non-constitutive CYP2A/CYP2B protein bands at 49 and 52 kDa in some monkeys.	Phenobarbital	0-2	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	39-44
7517894-2	1994	Expression of hepatic NADPH cytochrome P450 reductase, phenobarbital-induced CYP2B1&amp;2, and the polymeric immunoglobulin receptor (pIgR) decline as a function of aging.	Phenobarbital	55-68	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	77-83
8118938-2	1994	Pretreatment of rats with phenobarbital increased DNA adduct formation by microsomal activation of TMX 3- to 6-fold, depending on the cofactors used.	Phenobarbital	26-39	thioredoxin-related transmembrane protein 3	Rattus norvegicus	99-104
7516854-12	1994	In PB-treated rats, CYP2B1/2 was involved in the increased formation of M1 and M4, whereas CYP3A was partly involved in the enhanced M2 and M4 formation, and primarily responsible for the increased M5 formation.	Phenobarbital	3-5	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	20-26
7517894-5	1994	On the other hand, the expression of phenobarbital-induced microsomal CYP2B1&amp;2 and the steady state level of its mRNA exhibit parallel age-dependent shifts.	Phenobarbital	37-50	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	70-76
28921207-2	1994	Inhalation of halothane under a hypoxic condition significantly increased serum glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) levels in rats pretreated with phenobarbital compared with rats pretreated without phenobarbital.	Phenobarbital	191-204	glutamic--pyruvic transaminase	Rattus norvegicus	124-153
28921207-3	1994	Pretreatment with saikosaponin (especially-a and-d) and with phenobarbital suppressed the increase in serum GOT and GPT levels in comparison with the rats treated with phenobarbital, halothane, and hypoxia.	Phenobarbital	61-74	glutamic--pyruvic transaminase	Rattus norvegicus	116-119
8139483-3	1994	In control rats receiving PB in drinking water (0.5 mg/mL), serum insulin and triglyceride levels were diminished without any change in glucose and cholesterol concentrations in the fed state.	Phenobarbital	26-28	insulin	Homo sapiens	66-73
8138968-1	1994	The present study describes the effects of 2,2",4,4",5,5"-hexachlorobiphenyl, a "phenobarbital-like" inducer of hepatic cytochrome P450, on the CYP2B1 and CYP2B2 enzymes in the phenotypically obese fa/fa Zucker rat.	Phenobarbital	81-94	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	144-150
8138968-1	1994	The present study describes the effects of 2,2",4,4",5,5"-hexachlorobiphenyl, a "phenobarbital-like" inducer of hepatic cytochrome P450, on the CYP2B1 and CYP2B2 enzymes in the phenotypically obese fa/fa Zucker rat.	Phenobarbital	81-94	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	155-161
8138968-6	1994	These data are similar to those reported earlier that demonstrate resistance of the CYP2B1/2B2 genes to the inductive effects of phenobarbital in fa/fa Zucker rats.	Phenobarbital	129-142	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	84-90
8138968-7	1994	Apparently a genetic defect in obese Zucker rats impairs the increase in CYP2B1/2B2 gene transcription after treatment with phenobarbital as well as 2,2",4,4",5,5"-hexachlorobiphenyl.	Phenobarbital	124-137	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	73-79
8138968-8	1994	This study provides evidence that phenobarbital and "phenobarbital-like" inducers share a common cellular element(s) in the induction process of the CYP2B1/2B2 enzymes.	Phenobarbital	34-47	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	149-159
8138968-8	1994	This study provides evidence that phenobarbital and "phenobarbital-like" inducers share a common cellular element(s) in the induction process of the CYP2B1/2B2 enzymes.	Phenobarbital	53-66	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	149-159
7908202-0	1994	Alterations in the methylation status and expression of the raf oncogene in phenobarbital-induced and spontaneous B6C3F1 mouse liver tumors.	Phenobarbital	76-89	zinc fingers and homeoboxes 2	Mus musculus	60-63
7908202-3	1994	Seven days after partial hepatectomy or after administration of a promoting dose of phenobarbital (PB) for 14 d; raf in B6C3F1 mouse liver was hypomethylated.	Phenobarbital	84-97	zinc fingers and homeoboxes 2	Mus musculus	113-116
7908202-3	1994	Seven days after partial hepatectomy or after administration of a promoting dose of phenobarbital (PB) for 14 d; raf in B6C3F1 mouse liver was hypomethylated.	Phenobarbital	99-101	zinc fingers and homeoboxes 2	Mus musculus	113-116
7908202-7	1994	In both PB-induced and spontaneous B6C3F1 liver tumors, raf was hypomethylated in a nonrandom fashion.	Phenobarbital	8-10	zinc fingers and homeoboxes 2	Mus musculus	56-59
8139483-4	1994	Administration of PB in drinking water (0.25 mg/mL) to both groups of diabetic rats decreased their water intake and serum triglyceride levels in the absence of an effect on glucose, insulin, and cholesterol concentrations in the fed state.	Phenobarbital	18-20	insulin	Homo sapiens	183-190
8139483-6	1994	PB treatment increased the heparin-releasable lipoprotein lipase (LPL) activity of epididymal fat in both control and low-dose diabetic groups; this was not assessed in the high-dose diabetic group.	Phenobarbital	0-2	lipoprotein lipase	Rattus norvegicus	66-69
8139483-8	1994	In contrast, PB administration enhanced insulin-mediated peripheral glucose utilization, as well as suppression of hepatic glucose production, in both low-dose and high-dose diabetic groups.	Phenobarbital	13-15	insulin	Homo sapiens	40-47
8003099-0	1994	Regulation of apolipoprotein A-I gene expression by phenobarbital in the human hepatocarcinoma cell line, Hep3B.	Phenobarbital	52-65	apolipoprotein A1	Homo sapiens	14-32
8117097-0	1994	Characterization of a phenobarbital-inducible Ah receptor-like protein in the Sprague-Dawley rat.	Phenobarbital	22-35	aryl hydrocarbon receptor	Rattus norvegicus	46-57
8003099-2	1994	The effect of phenobarbital on apo A-I mRNA and protein levels was studied in the human hepatoma cell line, Hep3B.	Phenobarbital	14-27	apolipoprotein A1	Homo sapiens	31-38
8003099-4	1994	The induction of apo A-I mRNA level caused by phenobarbital could be due to increased rates of transcription and/or alteration in mRNA stability.	Phenobarbital	46-59	apolipoprotein A1	Homo sapiens	17-24
8003099-6	1994	We have demonstrated that phenobarbital treatment is associated with a 2-fold induction in apo A-I transcriptional activity.	Phenobarbital	26-39	apolipoprotein A1	Homo sapiens	91-98
8003099-7	1994	The estimated half-lives for apo A-I mRNA are 2 h and 3.6 h in the absence or presence of phenobarbital, respectively.	Phenobarbital	90-103	apolipoprotein A1	Homo sapiens	29-36
8003099-8	1994	The combination of increase in apo A-I transcription rate and mRNA stabilization could explain the 4-fold induction in apo A-I mRNA levels caused by phenobarbital treatment.	Phenobarbital	149-162	apolipoprotein A1	Homo sapiens	31-38
8003099-8	1994	The combination of increase in apo A-I transcription rate and mRNA stabilization could explain the 4-fold induction in apo A-I mRNA levels caused by phenobarbital treatment.	Phenobarbital	149-162	apolipoprotein A1	Homo sapiens	119-126
8003099-10	1994	The results suggest that the mechanism(s) by which phenobarbital induces apo A-I production operate at both pre- and either co- or post-translational mechanisms.	Phenobarbital	51-64	apolipoprotein A1	Homo sapiens	73-80
7906730-0	1994	Strychnine and brucine as the potent inducers of drug metabolizing enzymes in rat liver: different profiles from phenobarbital on the induction of cytochrome P450 and UDP-glucuronosyltransferase.	Phenobarbital	113-126	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	167-194
7513337-0	1994	Stimulation of HMG-CoA reductase as a consequence of phenobarbital-induced primary stimulation of cholesterol 7 alpha-hydroxylase in rat liver.	Phenobarbital	53-66	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	98-129
7513337-1	1994	Among nine strains of rat, two were found that responded to phenobarbital treatment with increased activity of hepatic cholesterol 7 alpha-hydroxylase.	Phenobarbital	60-73	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	119-150
7513337-6	1994	The phenobarbital treatment resulted in decreased content of free cholesterol in liver microsomes in a strain of rat that responded with increased cholesterol 7 alpha-hydroxylase activity.	Phenobarbital	4-17	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	147-178
7513337-9	1994	A primary upregulation of the cholesterol 7 alpha-hydroxylase by the cytochrome P450 inducer phenobarbital can be expected to lead to increased consumption of cholesterol substrate.	Phenobarbital	93-106	cytochrome P450 family 7 subfamily A member 1	Rattus norvegicus	30-61
7906857-7	1994	The higg-Km demethylation activity was induced by phenobarbital and pregnenolone-16 alpha-carbonitrile and the activity in both untreated and phenobarbital-induced microsomes was suppressed by anti-CYP2B1 IgG.	Phenobarbital	50-63	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	198-204
7906730-10	1994	These results indicated that strychnine and brucine cause phenobarbital-like induction of the P450 enzyme, but show a different profile from phenobarbital in the induction of UDP-glucuronosyltransferase.	Phenobarbital	141-154	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	175-202
7906857-7	1994	The higg-Km demethylation activity was induced by phenobarbital and pregnenolone-16 alpha-carbonitrile and the activity in both untreated and phenobarbital-induced microsomes was suppressed by anti-CYP2B1 IgG.	Phenobarbital	142-155	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	198-204
8293312-8	1994	Their Bmax was also reduced from early phenobarbital exposed animals" levels by 15% for PreB and by 25% for NeoB (p &lt; 0.001).	Phenobarbital	39-52	prolactin regulatory element binding	Mus musculus	88-92
8297392-0	1994	New cytochrome P450-dependent reactions from wheat: terminal and sub-terminal hydroxylation of oleic acid by microsomes from naphthalic acid anhydride and phenobarbital induced wheat seedlings.	Phenobarbital	155-168	cytochrome P450 709B1	Triticum aestivum	4-19
8297392-3	1994	Terminal and sub-terminal hydroxylation of oleic acid and the cytochrome P450 content were strongly enhanced in microsomes from wheat shoots treated with naphthalic acid anhydride and phenobarbital.	Phenobarbital	184-197	cytochrome P450 709B1	Triticum aestivum	62-77
8124661-4	1994	But phenobarbital increased the level of GST-P and the number and size of GST-P positive foci with little affect on the ploidy population changed by 3"-MeDAB.	Phenobarbital	4-17	glutathione S-transferase pi 1	Rattus norvegicus	41-46
8124661-4	1994	But phenobarbital increased the level of GST-P and the number and size of GST-P positive foci with little affect on the ploidy population changed by 3"-MeDAB.	Phenobarbital	4-17	glutathione S-transferase pi 1	Rattus norvegicus	74-79
8142011-0	1994	Screening for p53 mutations in C3H/He mouse liver tumors derived spontaneously or induced with diethylnitrosamine or phenobarbitone.	Phenobarbital	117-131	transformation related protein 53, pseudogene	Mus musculus	14-17
8142011-1	1994	Distinct differences have been described in the development of C3H/He mouse liver tumors induced by the genotoxic carcinogen diethylnitrosamine (DEN) and by the nongenotoxic agent phenobarbitone (PB) in terms of pathology and the frequency of mutation at codon 61 of the Ha-ras oncogene.	Phenobarbital	180-194	Harvey rat sarcoma virus oncogene	Mus musculus	271-277
8290267-1	1994	A regulatory element, EpRE, was found to be responsible for the induction of mouse glutathione S-transferase (GST) Ya gene expression by a variety of chemical agents such as planar aromatic hydrocarbons, diphenols, phorbol ester, phenobarbital and electrophilic compounds.	Phenobarbital	230-243	glutathione S-transferase, alpha 1 (Ya)	Mus musculus	83-117
8304968-4	1994	Antibodies raised to CYP2C11 and 2B1/2 inhibited TMO N-demethylation in hepatic microsomes of untreated and phenobarbital-treated rats, respectively.	Phenobarbital	108-121	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	21-28
8082573-7	1994	Considering the selective prerequisites for oxidative attack by cytochrome P-450 at vulnerable nitrogen centers, many cytotoxic amines belonging to the category of relatively rigid, planar molecules undergo N-oxidative activation by the cytochrome P-450IA subfamily, while more bulky amines with flexible conformation are N-oxygenated preferentially by phenobarbital-inducible cytochromes P-450.	Phenobarbital	353-366	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	64-80
8301593-9	1994	In rats treated with phenobarbital for 4 days, IL-2 coadministration decreased immunoreactive cytochromes P-450 2B1/2 29%, whereas cytochromes P-450 1A2, 2C11 and 3A decreased 38, 63 and 67%, respectively.	Phenobarbital	21-34	interleukin 2	Rattus norvegicus	47-51
8149892-4	1994	Linopirdine also increased the rates of reactions selectively catalyzed by CYP2B and 3A (pentoxyresorufin O-dealkylation, benzphetamine N-demethylation, erythromycin N-demethylation, and testosterone 2 beta-, 6 beta-, 16 beta-hydroxylation), 1.7- to 3.0-fold vs. control, similar to increases produced by the prototypical CYP2B and 3A inducers phenobarbital and dexamethasone.	Phenobarbital	344-357	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	75-87
8149892-4	1994	Linopirdine also increased the rates of reactions selectively catalyzed by CYP2B and 3A (pentoxyresorufin O-dealkylation, benzphetamine N-demethylation, erythromycin N-demethylation, and testosterone 2 beta-, 6 beta-, 16 beta-hydroxylation), 1.7- to 3.0-fold vs. control, similar to increases produced by the prototypical CYP2B and 3A inducers phenobarbital and dexamethasone.	Phenobarbital	344-357	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	75-80
8039532-2	1994	The mean serum activity of gamma-glutamyl transpeptidase (gamma-GTP), an indicator of enzyme induction, in the groups of patients receiving enzyme inducers such as CBZ, DPH, and/or PB was at least some 5-fold higher than in patients receiving VPA alone, which is well known to be a non-inducer.	Phenobarbital	181-183	inactive glutathione hydrolase 2	Homo sapiens	27-56
8039532-2	1994	The mean serum activity of gamma-glutamyl transpeptidase (gamma-GTP), an indicator of enzyme induction, in the groups of patients receiving enzyme inducers such as CBZ, DPH, and/or PB was at least some 5-fold higher than in patients receiving VPA alone, which is well known to be a non-inducer.	Phenobarbital	181-183	inactive glutathione hydrolase 2	Homo sapiens	58-67
8175925-7	1994	In the majority of PB-promoted foci, Cx32 immunoreactivity decreased independently of changes in mRNA abundance.	Phenobarbital	19-21	gap junction protein, beta 1	Rattus norvegicus	37-41
8175925-8	1994	Continuous thymidine labeling, following cessation of PB promotion, showed that downregulation of Cx32 staining is reversible in foci that are promoter-dependent for growth, but irreversible in lesions that are promoter-independent for growth.	Phenobarbital	54-56	gap junction protein, beta 1	Rattus norvegicus	98-102
8302279-0	1994	A recombinant phenobarbital-inducible rat liver UDP-glucuronosyltransferase (UDP-glucuronosyltransferase 2B1) stably expressed in V79 cells catalyzes the glucuronidation of morphine, phenols, and carboxylic acids.	Phenobarbital	14-27	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	48-75
8297481-3	1994	When hepatic AST IV activity was assessed, N-hydroxy-2AAF sulfotransferase activity was found to decrease 80-90% in response to 2AAF feeding, but activity recovered to essentially normal levels in the livers of rats subsequently placed on either control diets or diets with phenobarbital, suggesting a reversible cytotoxic mechanism for loss of AST IV activity.	Phenobarbital	274-287	sulfotransferase family 1A member 1	Rattus norvegicus	13-19
8297481-6	1994	In tissue sections from rats initially fed 2AAF and then placed on a control diet (group 2) or a diet with phenobarbital (group 3), the nodules continued to show low levels of AST IV expression, while expression in the areas surrounding nodules returned to the normal, high levels.	Phenobarbital	107-120	sulfotransferase family 1A member 1	Rattus norvegicus	176-182
8297481-7	1994	In addition, among those rats fed 2AAF for just 3 wk and then control diet or diet containing phenobarbital for 6 wk, only rats fed phenobarbital developed altered foci that stained weakly for AST IV expression.	Phenobarbital	94-107	sulfotransferase family 1A member 1	Rattus norvegicus	193-199
8208127-3	1994	Using the standard induction procedures [Aroclor 1254 or a combination of phenobarbitone (PB) and beta-naphthoflavone (beta-NF)] the level of CYP2E1 in rat liver is actually suppressed and it has been suggested that this may account for the negative findings with these compounds in the Ames test.	Phenobarbital	74-88	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	142-148
8208127-3	1994	Using the standard induction procedures [Aroclor 1254 or a combination of phenobarbitone (PB) and beta-naphthoflavone (beta-NF)] the level of CYP2E1 in rat liver is actually suppressed and it has been suggested that this may account for the negative findings with these compounds in the Ames test.	Phenobarbital	90-92	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	142-148
8297481-7	1994	In addition, among those rats fed 2AAF for just 3 wk and then control diet or diet containing phenobarbital for 6 wk, only rats fed phenobarbital developed altered foci that stained weakly for AST IV expression.	Phenobarbital	132-145	sulfotransferase family 1A member 1	Rattus norvegicus	193-199
8302279-0	1994	A recombinant phenobarbital-inducible rat liver UDP-glucuronosyltransferase (UDP-glucuronosyltransferase 2B1) stably expressed in V79 cells catalyzes the glucuronidation of morphine, phenols, and carboxylic acids.	Phenobarbital	14-27	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	77-108
8302279-1	1994	V79 (Chinese hamster lung fibroblast) cell lines expressing a functional recombinant phenobarbital-inducible rat liver UDP-glucuronosyltransferase (UGT), i.e., UGT2B1, were established.	Phenobarbital	85-98	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	119-146
8302279-1	1994	V79 (Chinese hamster lung fibroblast) cell lines expressing a functional recombinant phenobarbital-inducible rat liver UDP-glucuronosyltransferase (UGT), i.e., UGT2B1, were established.	Phenobarbital	85-98	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	148-151
8302279-1	1994	V79 (Chinese hamster lung fibroblast) cell lines expressing a functional recombinant phenobarbital-inducible rat liver UDP-glucuronosyltransferase (UGT), i.e., UGT2B1, were established.	Phenobarbital	85-98	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	160-166
8263600-7	1993	In rats of both genotypes, the activity and hepatic concentration of chloramphenicol-UDPGT mRNA and liver and urine ascorbic acid concentration were increased by sodium phenobarbital.	Phenobarbital	162-182	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	85-90
8274163-11	1993	Antibodies to CYP2B1 caused a 60% inhibition of DETC-MeSO formation by liver microsomes from phenobarbital-treated rats.	Phenobarbital	93-106	cytochrome P450 2B1	Rattus norvegicus	14-20
8274163-13	1993	Also, in liver microsomes from phenobarbital-treated rats, CYP2B1 is the major catalyst for the sulfoxidation of DETC-Me.	Phenobarbital	31-44	cytochrome P450 2B1	Rattus norvegicus	59-65
8267646-3	1993	Cytochrome P450 induction by phenobarbital potentiated the in vitro cytotoxicity of cocaine by a factor of 13 (IC50 = 84 microM in induced cells vs 1100 microM in non-induced cells).	Phenobarbital	29-42	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-15
8129853-3	1993	Using triacetyloleandomycin-metabolite complex formation, testosterone hydroxylase assays and immunoblots from peptide maps, we obtained results suggesting that in liver microsomes from mature rats, at least three, possibly four CYP3A proteins are expressed: one is present in females, another is male-specific, and one or two additional CYP3A proteins are inducible by phenobarbital, steroids, and triacetyloleandomycin.	Phenobarbital	370-383	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	229-234
8013408-0	1993	Association between responsiveness to phenobarbital induction of CYP2B1/2 and 3A1 in rat hepatic hyperplastic nodules and their zonal origin.	Phenobarbital	38-51	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	65-71
8013408-5	1993	As phenobarbital-induced expression of both CYP2B1/2 and 3A1 in normal liver is heavily localized to the centrilobular zone, these observations suggest that the ability of preneoplastic nodules to respond to induction of these P450 proteins is determined primarily from the zonal origin of the precursor hepatocytes.	Phenobarbital	3-16	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	44-50
7969856-6	1994	The LH response to LHRH was lower in PB-treated PE than in IGE subjects on the same drug regimen.	Phenobarbital	37-39	gonadotropin releasing hormone 1	Homo sapiens	19-23
7969856-9	1994	PB and CBZ, but not PHT, blunt the LH response to exogenous LHRH in PE.	Phenobarbital	0-2	gonadotropin releasing hormone 1	Homo sapiens	60-64
8268200-5	1993	Phenobarbital treatment increased the levels of microsomal proteins recognized by antibody to cytochrome P4502B, as well as dealkylases of pentoxyresorufin, but decreased the level of proteins recognized by anti-cytochrome P450C11 or cytochrome P4502E.	Phenobarbital	0-13	cytochrome P450 family 11 subfamily B member 1	Homo sapiens	212-230
8274026-0	1993	Expression of a male-specific cytochrome P450 isozyme (CYP2C11) in fa/fa Zucker rats: effect of phenobarbital treatment.	Phenobarbital	96-109	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	55-62
8274026-1	1993	The present study determined the effect of genetic obesity and phenobarbital (PB) treatment on the expression and regulation of the hepatic cytochrome P450 enzyme (CYP2C11) in Fa/?	Phenobarbital	63-76	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	164-171
8274026-1	1993	The present study determined the effect of genetic obesity and phenobarbital (PB) treatment on the expression and regulation of the hepatic cytochrome P450 enzyme (CYP2C11) in Fa/?	Phenobarbital	78-80	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	164-171
8274026-8	1993	Treatment with PB further suppressed hepatic CYP2C11 protein levels and activities in both fa/fa and Fa/?	Phenobarbital	15-17	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	45-52
8274026-10	1993	The level of CYP2C11 steady-state mRNA was significantly higher after treatment with PB in Fa/?	Phenobarbital	85-87	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	13-20
8263600-8	1993	The data indicate that the stimulation of the expression of both the 4-nitrophenol and chloramphenicol UDPGT genes plays a key role in the ascorbic acid biosynthesis induced by 3MC and sodium phenobarbital.	Phenobarbital	185-205	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	103-108
8246922-9	1993	At 18 hr post-treatment with phenobarbital, an optimal time period for hepatic induction, brain expression was characterized by a complex pattern of effects, with increased levels noted for CYP2B1 mRNA content in the medulla oblongata, midbrain, and cortex, but decreased contents measured in the cerebellum, the hypothalamus, and the striatum.	Phenobarbital	29-42	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	190-196
8242872-0	1993	Glutathione S-transferase isoenzyme patterns in different subtypes of enzyme-altered rat liver foci treated with the peroxisome proliferator nafenopin or with phenobarbital.	Phenobarbital	159-172	hematopoietic prostaglandin D synthase	Rattus norvegicus	0-25
8242872-9	1993	Upon PB treatment expression of the GST subunits Yb1 and Yb2 was frequently elevated in ECF, while Ya and Yc remained more or less unchanged.	Phenobarbital	5-7	hematopoietic prostaglandin D synthase	Rattus norvegicus	36-39
8242872-9	1993	Upon PB treatment expression of the GST subunits Yb1 and Yb2 was frequently elevated in ECF, while Ya and Yc remained more or less unchanged.	Phenobarbital	5-7	Y box binding protein 1	Rattus norvegicus	49-52
8242872-9	1993	Upon PB treatment expression of the GST subunits Yb1 and Yb2 was frequently elevated in ECF, while Ya and Yc remained more or less unchanged.	Phenobarbital	5-7	Y box binding protein 3	Rattus norvegicus	57-60
8408026-5	1993	These results demonstrate that, in vivo, phenobarbital induction and tissue-specific control requires interaction of regulatory elements far upstream of the core CYP2B2 promoter region and upstream of motifs indicated previously as determinants of phenobarbital responsiveness.	Phenobarbital	41-54	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	162-168
8091338-11	1993	Some P450 (3A, 1A, 2E, ...) are inducible by compounds such as phenobarbital, rifampicin, aromatic hydrocarbon, ethanol, or omeprazole.	Phenobarbital	63-76	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	5-9
8408026-5	1993	These results demonstrate that, in vivo, phenobarbital induction and tissue-specific control requires interaction of regulatory elements far upstream of the core CYP2B2 promoter region and upstream of motifs indicated previously as determinants of phenobarbital responsiveness.	Phenobarbital	248-261	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	162-168
8408026-0	1993	Phenobarbital induction and tissue-specific expression of the rat CYP2B2 gene in transgenic mice.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	66-72
8232228-2	1993	Rat hepatoma cells (Fao and its derivatives) respond to phenobarbital or dexamethasone treatment with an increased accumulation of CYP2C6 mRNA and thus provide a culture system to investigate the mechanisms involved.	Phenobarbital	56-69	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	131-137
8399210-18	1993	Each of the liver mRNA species encoding udpgth-3, udpgth-2, or udpgth-1 was induced 2.5-3-fold by phenobarbital treatment of the Erythrocebus patas monkey.	Phenobarbital	98-111	UDP glucuronosyltransferase family 2 member B15	Homo sapiens	40-48
8399210-18	1993	Each of the liver mRNA species encoding udpgth-3, udpgth-2, or udpgth-1 was induced 2.5-3-fold by phenobarbital treatment of the Erythrocebus patas monkey.	Phenobarbital	98-111	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	50-58
8399210-18	1993	Each of the liver mRNA species encoding udpgth-3, udpgth-2, or udpgth-1 was induced 2.5-3-fold by phenobarbital treatment of the Erythrocebus patas monkey.	Phenobarbital	98-111	UDP glucuronosyltransferase family 2 member B4	Homo sapiens	63-71
7692844-10	1993	Pretreating rats with the mono-oxygenase inducers phenobarbitone, 3-methylcholanthrene or Aroclor 1254 showed the last-named to be the most potent inducer of CYP1A1.	Phenobarbital	50-64	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	158-164
8232228-4	1993	Run-on transcription measurements demonstrated that phenobarbital treatment led to a 3-4-fold increase in CYP2C6 gene transcription.	Phenobarbital	52-65	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	106-112
8232228-5	1993	Surprisingly, induction by phenobarbital of both accumulation of CYP2C6 mRNA and transcription of the gene was blocked by the antiprogestin-antiglucocorticoid RU486, suggesting the involvement of a steroid receptor in the induction process.	Phenobarbital	27-40	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	65-71
8232228-6	1993	Transfection of promoter constructs containing a reporter gene whose expression is driven by a 1.4-kilobase 5" flanking segment of the CYP2B1 or CYP2B2 genes, which are highly inducible by phenobarbital in rat liver, led to &gt; 3-fold increases in reporter gene activity in the presence of the drug.	Phenobarbital	189-202	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	135-141
8232228-6	1993	Transfection of promoter constructs containing a reporter gene whose expression is driven by a 1.4-kilobase 5" flanking segment of the CYP2B1 or CYP2B2 genes, which are highly inducible by phenobarbital in rat liver, led to &gt; 3-fold increases in reporter gene activity in the presence of the drug.	Phenobarbital	189-202	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	145-151
8232228-8	1993	The RU486 inhibition of the phenobarbital induction of both the endogenous CPY2C6 gene and the transfected CYP2B1 and CYP2B2 promoter constructs leads us to propose a model whereby the drug acts indirectly to cause the accumulation of an endogenous steroid, and this molecule, acting via its receptor, would be the direct inducer of cytochromes P450.	Phenobarbital	28-41	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	107-113
8232228-8	1993	The RU486 inhibition of the phenobarbital induction of both the endogenous CPY2C6 gene and the transfected CYP2B1 and CYP2B2 promoter constructs leads us to propose a model whereby the drug acts indirectly to cause the accumulation of an endogenous steroid, and this molecule, acting via its receptor, would be the direct inducer of cytochromes P450.	Phenobarbital	28-41	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	118-124
8395842-3	1993	Antibody inhibition experiments indicated that ethoxyresorufin and methoxyresorufin O-dealkylations were catalysed mainly by the P450 1A subfamily in untreated and BA-induced HepG2 cells, that additional unidentified P450 forms were considerably involved in methoxyresorufin and benzyloxyresorufin O-dealkylations and that the P450 2B subfamily was partially responsible for pentoxyresorufin O-dealkylation in PB-induced cells.	Phenobarbital	410-412	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	129-133
8249615-1	1993	Phenobarbital and dexamethasone are potent inducers of the same cytochrome P450 form, CYP3A1, but the mechanism of action is not quite clear.	Phenobarbital	0-13	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	86-92
8249615-2	1993	If the mechanism of induction by phenobarbital and dexamethasone is different, additive effect may be observed in the specific activities of CYP3A1: ethylmorphine or aminopyrine N-demethylation of liver microsomes from rats treated with phenobarbital and dexamethasone in combination.	Phenobarbital	33-46	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	141-147
8249615-2	1993	If the mechanism of induction by phenobarbital and dexamethasone is different, additive effect may be observed in the specific activities of CYP3A1: ethylmorphine or aminopyrine N-demethylation of liver microsomes from rats treated with phenobarbital and dexamethasone in combination.	Phenobarbital	237-250	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	141-147
7509649-2	1993	Liver cytosolic RNA of phenobarbital-treated donors was found to reproduce completely the effect of phenobarbital-induced resistance to barbiturates in recipient rats: the reduction of hexenal-induced sleep and the increase of cytochrome P450 content in hepatic microsomes.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	227-242
7509649-2	1993	Liver cytosolic RNA of phenobarbital-treated donors was found to reproduce completely the effect of phenobarbital-induced resistance to barbiturates in recipient rats: the reduction of hexenal-induced sleep and the increase of cytochrome P450 content in hepatic microsomes.	Phenobarbital	100-113	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	227-242
8364928-7	1993	These results demonstrate that chemical agents as diverse as nitrosamines and phenobarbital act as cocarcinogens with TGF-alpha in the livers of these transgenic mice, indicating that TGF-alpha possesses the unique ability to complement both initiation and promotion in hepatocarcinogenesis.	Phenobarbital	78-91	transforming growth factor alpha	Mus musculus	118-127
8364928-7	1993	These results demonstrate that chemical agents as diverse as nitrosamines and phenobarbital act as cocarcinogens with TGF-alpha in the livers of these transgenic mice, indicating that TGF-alpha possesses the unique ability to complement both initiation and promotion in hepatocarcinogenesis.	Phenobarbital	78-91	transforming growth factor alpha	Mus musculus	184-193
7902236-10	1993	Phenobarbital treatment increased the concentrations of cytochrome P-450 in both groups to the same extent.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	56-72
7902236-11	1993	However, greater CYP2B1/2B2 activity was found in control rats following phenobarbital administration, whereas the amount of protein and mRNA was similar in each treated group.	Phenobarbital	73-86	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	17-23
8353528-0	1993	Tissue distribution of microsomal cytochrome P-450 monooxygenases and their inducibility by phenobarbital in the insecticide resistant LPR strain of house fly, Musca domestica L. Cytochrome P-450s, cytochrome b5, P-450 reductase, and four P-450 monooxygenase activities were abundant in proximal intestine (PI), Malpighian tubules (MT), and fat bodies (FB) in the insecticide resistant (LPR) strain of house fly.	Phenobarbital	92-105	cytochrome p-450	None	34-50
8212068-4	1993	Results suggest that atrazine behaves like a relatively weak inducer of phenobarbital-inducible families of cytochrome P-450.	Phenobarbital	72-85	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	108-124
8228727-7	1993	Endogenous GnRH release was suppressed with phenobarbital.	Phenobarbital	44-57	gonadotropin releasing hormone 1	Rattus norvegicus	11-15
8364903-1	1993	The fate of placental glutathione S-transferase (GST-P)-immunoreactive hepatocytes, detectable in livers of rats soon after treatment with N-nitrosodiethylamine (DEN), was examined sequentially with or without phenobarbital (PB) promotion.	Phenobarbital	210-223	glutathione S-transferase pi 1	Rattus norvegicus	49-54
8364903-1	1993	The fate of placental glutathione S-transferase (GST-P)-immunoreactive hepatocytes, detectable in livers of rats soon after treatment with N-nitrosodiethylamine (DEN), was examined sequentially with or without phenobarbital (PB) promotion.	Phenobarbital	225-227	glutathione S-transferase pi 1	Rattus norvegicus	49-54
8364903-13	1993	Almost all GST-P+ foci identifiable in H&amp;E stained sections were larger than ten cells, consisted of clear cells (in both groups) or mixed (clear-eosinophilic) cells in PB-exposed rats, and appeared to be evenly distributed throughout the three zones of the liver.	Phenobarbital	173-175	glutathione S-transferase pi 1	Homo sapiens	11-16
8285945-1	1993	Mice were exposed to phenobarbital (PhB) prenatally (PreB offspring) by feeding their mothers 3 g/kg PhB in milled food on gestation days 9-18, or neonatally by directly injecting pups of intact mothers with daily dose of 50 mg PhB on postnatal days 2-21 (NeoB offspring).	Phenobarbital	21-34	prolactin regulatory element binding	Mus musculus	53-57
8364903-14	1993	These results suggest that the promotive effect of PB is most evident as an increase in larger hepatocyte populations composed of more than three GST-P+ hepatocytes, rather than in increasing the populations of single GST-P immunoreactive cells.	Phenobarbital	51-53	glutathione S-transferase pi 1	Rattus norvegicus	146-151
8364903-14	1993	These results suggest that the promotive effect of PB is most evident as an increase in larger hepatocyte populations composed of more than three GST-P+ hepatocytes, rather than in increasing the populations of single GST-P immunoreactive cells.	Phenobarbital	51-53	glutathione S-transferase pi 1	Rattus norvegicus	218-223
8364903-15	1993	PB may cause clonal expansion of these single GST-P reactive hepatocytes.	Phenobarbital	0-2	glutathione S-transferase pi 1	Rattus norvegicus	46-51
8285945-1	1993	Mice were exposed to phenobarbital (PhB) prenatally (PreB offspring) by feeding their mothers 3 g/kg PhB in milled food on gestation days 9-18, or neonatally by directly injecting pups of intact mothers with daily dose of 50 mg PhB on postnatal days 2-21 (NeoB offspring).	Phenobarbital	36-39	prolactin regulatory element binding	Mus musculus	53-57
8334163-7	1993	Treatment of the hepatocyte cultures with phenobarbital (2 mM) or 3-methylcholanthene (5 microM) for 24, 48, or 72 h, beginning 24 h after plating, resulted in significant increases in glutathione S-transferase activity relative to control, with maximal increases of 158 and 164% measured at 72 h following phenobarbital or 3-methylcholanthrene treatment, respectively.	Phenobarbital	307-320	hematopoietic prostaglandin D synthase	Rattus norvegicus	185-210
8334163-7	1993	Treatment of the hepatocyte cultures with phenobarbital (2 mM) or 3-methylcholanthene (5 microM) for 24, 48, or 72 h, beginning 24 h after plating, resulted in significant increases in glutathione S-transferase activity relative to control, with maximal increases of 158 and 164% measured at 72 h following phenobarbital or 3-methylcholanthrene treatment, respectively.	Phenobarbital	42-55	hematopoietic prostaglandin D synthase	Rattus norvegicus	185-210
8101867-1	1993	Block of a voltage-activated Ca2+ channel current by phenobarbital (PHB), 5-(2-cyclohexylideneethyl)-5-ethyl barbituric acid (CHEB), and the optical R(-)- and S(+)-enantiomers of pentobarbital (PB) was examined in freshly dissociated adult guinea pig hippocampal CA1 neurons; the effects of the barbiturates on GABA-activated Cl- current were also characterized in the same preparation.	Phenobarbital	53-66	LOW QUALITY PROTEIN: carbonic anhydrase 2	Cavia porcellus	29-32
8101867-1	1993	Block of a voltage-activated Ca2+ channel current by phenobarbital (PHB), 5-(2-cyclohexylideneethyl)-5-ethyl barbituric acid (CHEB), and the optical R(-)- and S(+)-enantiomers of pentobarbital (PB) was examined in freshly dissociated adult guinea pig hippocampal CA1 neurons; the effects of the barbiturates on GABA-activated Cl- current were also characterized in the same preparation.	Phenobarbital	68-71	LOW QUALITY PROTEIN: carbonic anhydrase 2	Cavia porcellus	29-32
8101867-2	1993	(-)-PB, PHB, and CHEB produced a reversible, concentration-dependent block of the peak Ca2+ channel current (3 mM Ba2+ as the charge carrier) evoked by depolarization from -80 to -10 mV (IC50 values, 3.5, 72, and 118 microM, respectively).	Phenobarbital	8-11	LOW QUALITY PROTEIN: carbonic anhydrase 2	Cavia porcellus	87-90
8101867-12	1993	In contrast, PHB was more potent as a GABA enhancer than as blocker of Ca2+ current, but the maximal potentiation of GABA responses was 40% of that obtained with (-)-PB.	Phenobarbital	13-16	LOW QUALITY PROTEIN: carbonic anhydrase 2	Cavia porcellus	71-74
8104124-13	1993	Although we were unable to reconstitute the N-demethylation activity with purified CYP3A1, which is difficult to reconstitute, collectively the evidence demonstrated that CYP3A enzymes catalyze N-demethylation in PB and PCN microsomes.	Phenobarbital	213-215	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	83-89
8330366-0	1993	Modulation of aflatoxin B1-induced glutathione S-transferase placental form positive hepatic foci by pretreatment of rats with phenobarbital and buthionine sulfoximine.	Phenobarbital	127-140	hematopoietic prostaglandin D synthase	Rattus norvegicus	35-60
8104124-13	1993	Although we were unable to reconstitute the N-demethylation activity with purified CYP3A1, which is difficult to reconstitute, collectively the evidence demonstrated that CYP3A enzymes catalyze N-demethylation in PB and PCN microsomes.	Phenobarbital	213-215	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	83-88
8104124-18	1993	Mab anti-CYP2C11/2C6 (P-450h/k) inhibited N-demethylation in PB, PCN, and control male rat liver microsomes, suggesting that CYP2C11 and/or CYP2C6 catalyze this reaction to some extent.	Phenobarbital	61-63	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	9-16
8355263-1	1993	D. melanogaster development was markedly retarded and its survival decreased by larvae treatment with compounds being strong inducers of the cytochrome P-450 2B in mammals--phenobarbital (PB*), perfluorodecaline (PFD), transtilbene oxide (TSO), and triphenyldioxane (TPD).	Phenobarbital	173-186	Cytochrome P450-9b2	Drosophila melanogaster	141-157
8508509-7	1993	Both terpene diets significantly increased the activity of the methylcholanthrene-inducible and the phenobarbital-inducible UDPGT isozymes.	Phenobarbital	100-113	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	124-129
8512318-1	1993	The present study describes the mechanism of the dampened induction of the CYP2B1 and CYP2B2 genes following phenobarbital treatment in the phenotypically obese fa/fa Zucker rat.	Phenobarbital	109-122	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	75-81
8512318-1	1993	The present study describes the mechanism of the dampened induction of the CYP2B1 and CYP2B2 genes following phenobarbital treatment in the phenotypically obese fa/fa Zucker rat.	Phenobarbital	109-122	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	86-92
8512318-2	1993	The fa/fa Zucker rat demonstrated a threefold lower level of CYP2B1/2B2 enzyme induction, as indicated by reduced testosterone oxidation at the 16 beta position and resorufin formation from pentoxy- and benzyloxyresorufin, protein concentration (Western blot analysis), and steady-state mRNA levels (Northern and slot blot analyses) following in vivo treatment with phenobarbital than the Fa/?	Phenobarbital	366-379	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	61-67
8512318-5	1993	Phenobarbital-treated (0.75 mM) hepatocytes from fa/fa Zucker rats showed approximately a three-fold lower induction response based on measurements of CYP2B1/2B2 (R-17 cDNA probe) and CYP2B1 (oligo probe) mRNAs.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	151-157
8512318-5	1993	Phenobarbital-treated (0.75 mM) hepatocytes from fa/fa Zucker rats showed approximately a three-fold lower induction response based on measurements of CYP2B1/2B2 (R-17 cDNA probe) and CYP2B1 (oligo probe) mRNAs.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	184-190
8508186-1	1993	Antisera to purified house fly NADPH-cytochrome P450 reductase were used to select cDNA clones from an expression library of abdomens of phenobarbital-treated house flies.	Phenobarbital	137-150	NADPH--cytochrome P450 reductase	Musca domestica	31-62
8355263-4	1993	The toxicity of phenobarbital was shown to be decreased by the cytochrome P-450 inhibitor piperonyl butoxide by adding 20-hydroxyecdysone or by treatment with aminophylline--the indirect enhancer of ecdysone production in the larval prothoracic gland.	Phenobarbital	16-29	Cytochrome P450-9b2	Drosophila melanogaster	63-79
8510012-9	1993	Similar increases in glutathione transferase activities were observed in animals of both phenotypes after phenobarbital treatment.	Phenobarbital	106-119	glutathione S-transferase alpha 4	Rattus norvegicus	21-44
8316947-5	1993	Pretreatment with PB, BNF or PB pretreatment prior to 1,2-DCB administration increased hepatic toxicity within 24 h. Toxicity was characterized by increased ALT/GPT activity and increased liver weight.	Phenobarbital	29-31	glutamic--pyruvic transaminase	Rattus norvegicus	161-164
8212741-20	1993	In a similar manner, induction of cytochrome P450 PBD-1 (CYP 3A12) by PB was confirmed.	Phenobarbital	50-52	cytochrome P450 3A12	Canis lupus familiaris	57-65
8511800-0	1993	Regulation of phenobarbital-inducible cytochrome P450 2B1/2 mRNA by lovastatin and oxysterols in primary cultures of adult rat hepatocytes.	Phenobarbital	14-27	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	54-59
8511800-5	1993	In contrast to the potentiation of 2B1/2 mRNA induction produced by treatments with LOVA in combination with PB or CTZ, cotreatment of hepatocytes with PB and CTZ did not result in increased induction relative to that seen in cells treated with either agent alone.	Phenobarbital	109-111	UDP glucuronosyltransferase family 2 member B17	Rattus norvegicus	35-40
8257941-8	1993	These results indicate that MYR interferes with the in vivo barbiturate metabolism and support the view that MYR induces the phenobarbital-inducible cytochrome P-450 (P-450 2B subfamily) enzymes in the rat.	Phenobarbital	125-138	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	149-165
8496149-9	1993	Phenobarbital treatment increased the electrogenic transport of [35S]sulfobromophthalein (BSP) (5 and 50 microM) but not the electrogenic uptake of [14C] glycocholic acid (10 and 200 microM).	Phenobarbital	0-13	integrin-binding sialoprotein	Rattus norvegicus	90-93
8316947-5	1993	Pretreatment with PB, BNF or PB pretreatment prior to 1,2-DCB administration increased hepatic toxicity within 24 h. Toxicity was characterized by increased ALT/GPT activity and increased liver weight.	Phenobarbital	18-20	glutamic--pyruvic transaminase	Rattus norvegicus	161-164
8477751-9	1993	Similarly, hepatocytes from phenobarbital-treated rats preserved the contents of barbiturate-inducible CYP2B1/2 and CYP3A proteins best when cultured on CMF/COL.	Phenobarbital	28-41	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	103-109
8477751-9	1993	Similarly, hepatocytes from phenobarbital-treated rats preserved the contents of barbiturate-inducible CYP2B1/2 and CYP3A proteins best when cultured on CMF/COL.	Phenobarbital	28-41	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	116-121
8477751-10	1993	After exposure of hepatocytes cultured on CMF/COL to phenobarbital from days 3-6, CYP3A proteins were enhanced more than twofold and CYP2B1/2, depending on the exposure level, increased 1.3-6-fold.	Phenobarbital	53-66	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	82-87
8477751-10	1993	After exposure of hepatocytes cultured on CMF/COL to phenobarbital from days 3-6, CYP3A proteins were enhanced more than twofold and CYP2B1/2, depending on the exposure level, increased 1.3-6-fold.	Phenobarbital	53-66	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	133-139
8457584-0	1993	Inactivation of phenobarbital-inducible rabbit-liver microsomal cytochrome P-450 by allylisopropylacetamide: impact on electron transfer.	Phenobarbital	16-29	cytochrome P-450	Oryctolagus cuniculus	64-80
8468368-8	1993	By contrast, the skin tumor-promoting phorbol ester, TPA, or liver tumor promoter, phenobarbital, were without effect or inhibitory at low [Ca2+]o but in combination with EGF, stimulated DNA synthesis at [Ca2+]o &gt; 0.4 mM, suggesting that Ca2+ may have some role in mediating or modulating the stimulatory effects of these agents.	Phenobarbital	83-96	carbonic anhydrase 2	Rattus norvegicus	140-143
8457584-1	1993	Application of a single dose of allylisopropylacetamide (AIA) to phenobarbital-pretreated rabbits resulted in partial destruction of the heme moiety of liver microsomal cytochrome P-450.	Phenobarbital	65-78	cytochrome P-450	Oryctolagus cuniculus	169-185
8457584-9	1993	These findings were interpreted to mean that there exist multiple reductase- and cytochrome-b5-binding domains in phenobarbital-inducible cytochrome P-450, some of which seem to be common to the two redox proteins.	Phenobarbital	114-127	cytochrome P-450	Oryctolagus cuniculus	138-154
7682481-6	1993	Phenobarbital administration caused a gradual decrease in responsiveness to the growth factors: after 10 days, hepatocytes became insensitive to the mitogenic effects of HGF, EGF and aFGF.	Phenobarbital	0-13	fibroblast growth factor 1	Rattus norvegicus	183-187
7682481-7	1993	However, an early increase in responsiveness to HGF and aFGF occurred in phenobarbital-exposed hepatocytes.	Phenobarbital	73-86	hepatocyte growth factor	Rattus norvegicus	48-51
7682481-7	1993	However, an early increase in responsiveness to HGF and aFGF occurred in phenobarbital-exposed hepatocytes.	Phenobarbital	73-86	fibroblast growth factor 1	Rattus norvegicus	56-60
8468368-8	1993	By contrast, the skin tumor-promoting phorbol ester, TPA, or liver tumor promoter, phenobarbital, were without effect or inhibitory at low [Ca2+]o but in combination with EGF, stimulated DNA synthesis at [Ca2+]o &gt; 0.4 mM, suggesting that Ca2+ may have some role in mediating or modulating the stimulatory effects of these agents.	Phenobarbital	83-96	carbonic anhydrase 2	Rattus norvegicus	205-208
8468368-8	1993	By contrast, the skin tumor-promoting phorbol ester, TPA, or liver tumor promoter, phenobarbital, were without effect or inhibitory at low [Ca2+]o but in combination with EGF, stimulated DNA synthesis at [Ca2+]o &gt; 0.4 mM, suggesting that Ca2+ may have some role in mediating or modulating the stimulatory effects of these agents.	Phenobarbital	83-96	carbonic anhydrase 2	Rattus norvegicus	205-208
8461036-13	1993	Immunoinhibition studies with epitope specific monoclonal antibodies were consistent with the major involvement of phenobarbitone- and steroid-inducible products of the Cyp2b and Cyp2c subfamilies.	Phenobarbital	115-129	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	169-174
8457190-0	1993	Phenobarbital induction of AP-1 binding activity mediates activation of glutathione S-transferase and quinone reductase gene expression.	Phenobarbital	0-13	glutathione S-transferase kappa 1	Homo sapiens	72-97
8457190-1	1993	Phenobarbital is an inducer of xenobiotic-metabolizing enzymes, such as cytochrome P-450, glutathione S-transferases (GSTs) and NAD(P)H:quinone reductase, as well as being a promoter of hepatocarcinogenesis.	Phenobarbital	0-13	glutathione S-transferase kappa 1	Homo sapiens	118-122
8461038-3	1993	The prototype cytochrome P450 inducers, 3-methylcholanthrene (3-MC) and phenobarbital (PB), increased ECOD and GST activities reaching an optimum 7 days after culturing, followed by a decline in activity.	Phenobarbital	72-85	glutathione S-transferase kappa 1	Homo sapiens	111-114
8461038-3	1993	The prototype cytochrome P450 inducers, 3-methylcholanthrene (3-MC) and phenobarbital (PB), increased ECOD and GST activities reaching an optimum 7 days after culturing, followed by a decline in activity.	Phenobarbital	87-89	glutathione S-transferase kappa 1	Homo sapiens	111-114
8461036-13	1993	Immunoinhibition studies with epitope specific monoclonal antibodies were consistent with the major involvement of phenobarbitone- and steroid-inducible products of the Cyp2b and Cyp2c subfamilies.	Phenobarbital	115-129	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	179-184
8440422-4	1993	Phenobarbital caused an induction of GST activity in culture at 72 and 168 hr.	Phenobarbital	0-13	hematopoietic prostaglandin D synthase	Rattus norvegicus	37-40
8054610-2	1993	It has been established that this medicines do not influence at ASPOL in LL in concentration range of 10-10 M. Phenobarbital (10 M) and Na-valproate (10 M) inhibit ASPOL and PhPOL in HRB in 20-25%.	Phenobarbital	111-124	ArfGAP with FG repeats 1, pseudogene 1	Rattus norvegicus	183-186
8095861-8	1993	This was, in part, owing to enhanced GGT expression in AHF with PB administration.	Phenobarbital	64-66	gamma-glutamyltransferase 1	Rattus norvegicus	37-40
8452565-0	1993	Cytochrome P450 isoforms in human fetal tissues related to phenobarbital-inducible forms in the mouse.	Phenobarbital	59-72	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	0-15
8442654-0	1993	Influence of extracellular matrix overlay on phenobarbital-mediated induction of CYP2B1, 2B2, and 3A1 genes in primary adult rat hepatocyte culture.	Phenobarbital	45-58	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	81-87
8442654-2	1993	In the present study, we have reexamined a variety of hepatocyte culture conditions and their relative abilities in preserving the PB-induction response within the CYP2B and 3A gene subfamilies.	Phenobarbital	131-133	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	164-176
8442654-6	1993	Induction in culture by 1 mM PB of CYP2B1, 2B2, and 3A1 mRNA levels was highly dependent on a variety of factors, including medium formulation and 0.1 microM dexamethasone addition.	Phenobarbital	29-31	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	35-41
8442654-11	1993	However, Chee"s formulation produced an abnormal PB-induced expression of CYP1A1, as determined by mRNA analysis, high rates of O-dealkylation of 7-ethoxyresorufin, and inhibition of enzymatic activity by 1 microM alpha-naphthoflavone.	Phenobarbital	49-51	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	74-80
8453930-8	1993	Qualitative and quantitative similar findings were observed during perfusion with PB 0.1 mg/ml, (i.e., a concentration 20 times higher than that of 3 alpha-OH-DHP).	Phenobarbital	82-84	dihydropyrimidinase	Rattus norvegicus	159-162
8382483-0	1993	Regulation of fibronectin mRNA expression in primary hepatocytes in response to EGF and phenobarbital.	Phenobarbital	88-101	fibronectin 1	Rattus norvegicus	14-25
8382483-3	1993	However, the presence of phenobarbital (PB) in the culture medium led to a dose-dependent decrease in fibronectin mRNA levels concomitant to an increase of cytochrome P450-2B1 (CYP2B1) mRNA, whereas the coaddition of EGF reversed the suppressive effect of PB in a similar dose-dependent manner.	Phenobarbital	25-38	fibronectin 1	Rattus norvegicus	102-113
8382483-3	1993	However, the presence of phenobarbital (PB) in the culture medium led to a dose-dependent decrease in fibronectin mRNA levels concomitant to an increase of cytochrome P450-2B1 (CYP2B1) mRNA, whereas the coaddition of EGF reversed the suppressive effect of PB in a similar dose-dependent manner.	Phenobarbital	25-38	cytochrome P450 2B1	Rattus norvegicus	156-175
8382483-3	1993	However, the presence of phenobarbital (PB) in the culture medium led to a dose-dependent decrease in fibronectin mRNA levels concomitant to an increase of cytochrome P450-2B1 (CYP2B1) mRNA, whereas the coaddition of EGF reversed the suppressive effect of PB in a similar dose-dependent manner.	Phenobarbital	25-38	cytochrome P450 2B1	Rattus norvegicus	177-183
8382483-3	1993	However, the presence of phenobarbital (PB) in the culture medium led to a dose-dependent decrease in fibronectin mRNA levels concomitant to an increase of cytochrome P450-2B1 (CYP2B1) mRNA, whereas the coaddition of EGF reversed the suppressive effect of PB in a similar dose-dependent manner.	Phenobarbital	40-42	fibronectin 1	Rattus norvegicus	102-113
8382483-3	1993	However, the presence of phenobarbital (PB) in the culture medium led to a dose-dependent decrease in fibronectin mRNA levels concomitant to an increase of cytochrome P450-2B1 (CYP2B1) mRNA, whereas the coaddition of EGF reversed the suppressive effect of PB in a similar dose-dependent manner.	Phenobarbital	40-42	cytochrome P450 2B1	Rattus norvegicus	156-175
8382483-3	1993	However, the presence of phenobarbital (PB) in the culture medium led to a dose-dependent decrease in fibronectin mRNA levels concomitant to an increase of cytochrome P450-2B1 (CYP2B1) mRNA, whereas the coaddition of EGF reversed the suppressive effect of PB in a similar dose-dependent manner.	Phenobarbital	40-42	cytochrome P450 2B1	Rattus norvegicus	177-183
8382483-3	1993	However, the presence of phenobarbital (PB) in the culture medium led to a dose-dependent decrease in fibronectin mRNA levels concomitant to an increase of cytochrome P450-2B1 (CYP2B1) mRNA, whereas the coaddition of EGF reversed the suppressive effect of PB in a similar dose-dependent manner.	Phenobarbital	256-258	cytochrome P450 2B1	Rattus norvegicus	177-183
8441997-5	1993	Studies with deuterated analogs of Tris-BP implicate oxidation at C-2 of the propyl group as a major pathway that leads to protein binding which is enhanced by phenobarbital pretreatment of rats.	Phenobarbital	160-173	complement C2	Rattus norvegicus	66-69
8509896-2	1993	In this study, we examined the effects of phenobarbital (PB) and 3-methylcholanthrene (MC), both of which are known to stimulate AsA biosynthesis in rats, on the hepatic levels of GLO activity, GLO mRNA, and AsA.	Phenobarbital	42-55	gulonolactone (L-) oxidase	Rattus norvegicus	180-183
8509896-2	1993	In this study, we examined the effects of phenobarbital (PB) and 3-methylcholanthrene (MC), both of which are known to stimulate AsA biosynthesis in rats, on the hepatic levels of GLO activity, GLO mRNA, and AsA.	Phenobarbital	57-59	gulonolactone (L-) oxidase	Rattus norvegicus	180-183
8509896-6	1993	However, the level of GLO mRNA and the activity of GLO in the liver tended to be slightly decreased by the administration of PB or MC, though the differences were not significant.	Phenobarbital	125-127	gulonolactone (L-) oxidase	Rattus norvegicus	22-25
8509896-6	1993	However, the level of GLO mRNA and the activity of GLO in the liver tended to be slightly decreased by the administration of PB or MC, though the differences were not significant.	Phenobarbital	125-127	gulonolactone (L-) oxidase	Rattus norvegicus	51-54
8509896-7	1993	Thus it is clear that the treatment with PB or MC stimulates the biosynthesis of AsA by increasing the activity of some enzyme(s) participating in the synthesis prior to GLO.	Phenobarbital	41-43	gulonolactone (L-) oxidase	Rattus norvegicus	170-173
8417813-0	1993	Preferential increase of glutathione S-transferase class alpha transcripts in cultured human hepatocytes by phenobarbital, 3-methylcholanthrene, and dithiolethiones.	Phenobarbital	108-121	glutathione S-transferase kappa 1	Homo sapiens	25-50
8435089-5	1993	Bilirubin UGT HP3 was induced 2-3-fold in the livers from patients treated with phenytoin and phenobarbital.	Phenobarbital	94-107	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	10-13
8435089-5	1993	Bilirubin UGT HP3 was induced 2-3-fold in the livers from patients treated with phenytoin and phenobarbital.	Phenobarbital	94-107	defensin alpha 3	Homo sapiens	14-17
8417813-8	1993	These results clearly indicate that phenobarbital, 3-methylcholanthrene, and dithiolethiones are able to markedly increase mRNA levels of GST in human hepatocytes and that the GST alpha class is preferentially involved.	Phenobarbital	36-49	glutathione S-transferase kappa 1	Homo sapiens	138-141
8417813-8	1993	These results clearly indicate that phenobarbital, 3-methylcholanthrene, and dithiolethiones are able to markedly increase mRNA levels of GST in human hepatocytes and that the GST alpha class is preferentially involved.	Phenobarbital	36-49	glutathione S-transferase kappa 1	Homo sapiens	176-179
8380963-4	1993	3-Methylcholanthrene, beta-naphthoflavone, and benz[alpha]anthracene were strong inducers of CYP1A1, benzo[alpha]pyrene induced CYP1A1 activity only weakly, while benzo[e]pyrene and phenobarbital were essentially inactive as inducers.	Phenobarbital	182-195	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	93-99
8447722-6	1993	A participation of those isoenzymes of the cytochrome P-450 enzyme system which can be induced by phenobarbital is assumed.	Phenobarbital	98-111	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	43-59
7678728-1	1993	The present study examines the effect of inhibiting protein synthesis with cycloheximide on the induction of the genes for cytochrome P4502H1 (CYP2H1) and 5-aminolevulinate synthase (ALAS) in phenobarbital-treated chick embryo livers.	Phenobarbital	192-205	cytochrome P450 2H1	Gallus gallus	143-149
7678728-2	1993	Phenobarbital administration caused a 10- to 15-fold increase in the levels of mRNAs for both CYP2H1 and ALAS.	Phenobarbital	0-13	cytochrome P450 2H1	Gallus gallus	94-100
7678728-3	1993	Cycloheximide treatment alone also induced the levels of mRNA for CYP2H1 and ALAS by 7- and 3-fold, respectively, but in combination, cycloheximide and phenobarbital elicited an additional effect resulting in a 33- and 40-fold increase, respectively.	Phenobarbital	152-165	cytochrome P450 2H1	Gallus gallus	66-72
8425266-0	1993	Different inhibition of DNA synthesis by transforming growth factor beta and phenobarbital on GST-P-positive and GST-P-negative hepatocytes.	Phenobarbital	77-90	glutathione S-transferase pi 1	Rattus norvegicus	94-99
8425266-0	1993	Different inhibition of DNA synthesis by transforming growth factor beta and phenobarbital on GST-P-positive and GST-P-negative hepatocytes.	Phenobarbital	77-90	glutathione S-transferase pi 1	Rattus norvegicus	113-118
8425275-2	1993	Redox-enzyme modulation, which included increased cytochrome P450 reductase activity induced by phenobarbital-Na (100 mg/kg, i.p.	Phenobarbital	96-112	cytochrome p450 oxidoreductase	Rattus norvegicus	50-75
22358698-0	1993	Thein utero initiation with DMN alters the complement of cytosolic glutathione S-transferases and the phenobarbital-induced expression ofc-jun andc-myc oncogenes in primary neonatal rat hepatocytes.	Phenobarbital	102-115	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	148-151
1417000-0	1992	Effect of dexamethasone and phenobarbital on run-on transcription rate and CYP3A mRNA concentration in rat liver: changes during development.	Phenobarbital	28-41	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	75-80
7924770-2	1993	The inhibition of these enzyme activities by monoclonal antibodies raised against 3-methyl-cholanthrene-induced (MAb 1-7-1) and phenobarbital-induced (MAb 2-66-3) rat hepatic cytochrome P-450 was used to measure the contribution of the MAb-defined, epitope-specific P-450 to the total activities during these ages of goat development.	Phenobarbital	128-141	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	175-191
8093255-0	1993	Phenobarbital-induced hepatocellular proliferation: anti-bromodeoxyuridine and anti-proliferating cell nuclear antigen immunocytochemistry.	Phenobarbital	0-13	proliferating cell nuclear antigen	Homo sapiens	84-118
8421322-2	1993	Previously, we have observed changes in adult testosterone metabolism and in cytochrome P-450 (P-450) mRNA levels in animals neonatally exposed to phenobarbital (PB) or diethylstilbestrol (DES).	Phenobarbital	147-160	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	77-93
8421322-2	1993	Previously, we have observed changes in adult testosterone metabolism and in cytochrome P-450 (P-450) mRNA levels in animals neonatally exposed to phenobarbital (PB) or diethylstilbestrol (DES).	Phenobarbital	162-164	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	77-93
8421322-8	1993	The results confirm that neonatal exposure to DES or PB can cause alterations in adult hepatic cytochrome P-450 levels but show that these chemicals act on different enzymes.	Phenobarbital	53-55	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	95-111
1463452-0	1992	Characterization of a phenobarbital-inducible cytochrome P-450, NADPH-cytochrome P-450 reductase and reconstituted cytochrome P-450 mono-oxygenase system from rat brain.	Phenobarbital	22-35	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	46-62
1463452-0	1992	Characterization of a phenobarbital-inducible cytochrome P-450, NADPH-cytochrome P-450 reductase and reconstituted cytochrome P-450 mono-oxygenase system from rat brain.	Phenobarbital	22-35	cytochrome p450 oxidoreductase	Rattus norvegicus	64-96
1463452-0	1992	Characterization of a phenobarbital-inducible cytochrome P-450, NADPH-cytochrome P-450 reductase and reconstituted cytochrome P-450 mono-oxygenase system from rat brain.	Phenobarbital	22-35	cytochrome P450, family 2, subfamily j, polypeptide 3	Rattus norvegicus	115-146
1463452-2	1992	Cytochrome P-450 was purified to apparent homogeneity from the brain microsomes of phenobarbital-treated rats.	Phenobarbital	83-96	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
7763748-0	1993	The in utero initiation with DMN alters the complement of cytosolic glutathione S-transferases and the phenobarbital-induced expression of c-jun and c-myc oncogenes in primary neonatal rat hepatocytes.	Phenobarbital	103-116	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	149-154
7680337-7	1993	Exposure to phenobarbital on Days 3 to 6 increased the total cytochrome P-450 content twofold; exposure to 3-methylcholanthrene increased the activity of the corresponding cytochrome P-450 isoforms to 20 times that observed in untreated cultures and 6 times that observed in freshly isolated cells.	Phenobarbital	12-25	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	61-77
8255142-2	1993	This oxidation is inversely influenced by cytochrome P-450 inducers in the rat such as 3-methylcholantrene (3-MC) and phenobarbital (PB).	Phenobarbital	118-131	cytochrome P-450	Oryctolagus cuniculus	42-58
8255142-2	1993	This oxidation is inversely influenced by cytochrome P-450 inducers in the rat such as 3-methylcholantrene (3-MC) and phenobarbital (PB).	Phenobarbital	133-135	cytochrome P-450	Oryctolagus cuniculus	42-58
1469101-6	1992	Pretreatment of rats with isonicotinic acid hydrazide and phenobarbital to induce cytochrome P-450 enhanced the production of F2-isoprostanes after CCl4 administration eightfold and fivefold, respectively, whereas inhibition of the cytochrome P-450 system with SKF-525A and 4-methylpyrazole decreased formation of F2-isoprostanes after CCl4 by 55 and 82%, respectively.	Phenobarbital	58-71	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	82-98
1469101-6	1992	Pretreatment of rats with isonicotinic acid hydrazide and phenobarbital to induce cytochrome P-450 enhanced the production of F2-isoprostanes after CCl4 administration eightfold and fivefold, respectively, whereas inhibition of the cytochrome P-450 system with SKF-525A and 4-methylpyrazole decreased formation of F2-isoprostanes after CCl4 by 55 and 82%, respectively.	Phenobarbital	58-71	C-C motif chemokine ligand 4	Rattus norvegicus	148-152
1469101-6	1992	Pretreatment of rats with isonicotinic acid hydrazide and phenobarbital to induce cytochrome P-450 enhanced the production of F2-isoprostanes after CCl4 administration eightfold and fivefold, respectively, whereas inhibition of the cytochrome P-450 system with SKF-525A and 4-methylpyrazole decreased formation of F2-isoprostanes after CCl4 by 55 and 82%, respectively.	Phenobarbital	58-71	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	232-248
1469101-6	1992	Pretreatment of rats with isonicotinic acid hydrazide and phenobarbital to induce cytochrome P-450 enhanced the production of F2-isoprostanes after CCl4 administration eightfold and fivefold, respectively, whereas inhibition of the cytochrome P-450 system with SKF-525A and 4-methylpyrazole decreased formation of F2-isoprostanes after CCl4 by 55 and 82%, respectively.	Phenobarbital	58-71	C-C motif chemokine ligand 4	Rattus norvegicus	336-340
1416970-3	1992	Oligomers and monomers of NADPH-cytochrome P450 reductase and cytochrome P450 LM2 (2B4) isolated from the liver microsomes of phenobarbital-treated rabbits were examined for physicochemical properties and catalytic activities.	Phenobarbital	126-139	NADPH--cytochrome P450 reductase	Oryctolagus cuniculus	26-57
1445240-1	1992	The major phenobarbital-inducible rat hepatic cytochromes P-450, CYP2B1 and CYP2B2, are the paradigmatic members of a cytochrome P-450 gene subfamily that contains at least seven additional members.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	65-71
1445240-1	1992	The major phenobarbital-inducible rat hepatic cytochromes P-450, CYP2B1 and CYP2B2, are the paradigmatic members of a cytochrome P-450 gene subfamily that contains at least seven additional members.	Phenobarbital	10-23	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	76-82
1417000-1	1992	Modulation of CYP3A1 and CYP3A2 mRNA expression by dexamethasone and by phenobarbital has been studied in immature (21-day-old) and adult (90-day-old) rat liver.	Phenobarbital	72-85	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	14-20
1417000-1	1992	Modulation of CYP3A1 and CYP3A2 mRNA expression by dexamethasone and by phenobarbital has been studied in immature (21-day-old) and adult (90-day-old) rat liver.	Phenobarbital	72-85	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	25-31
1381906-12	1992	Treatment of monkeys with phenobarbital or dexamethasone increased coumarin 7-hydroxylase activity, whereas treatment with beta-naphthoflavone caused a slight decrease.	Phenobarbital	26-39	cytochrome P450 family 2 subfamily A member 6	Homo sapiens	67-89
1417986-3	1992	PB induced similar drug-metabolizing enzymes (CYP2B, CYP3A, and epoxide hydrolase) in rats, mice, rabbits and hamsters.	Phenobarbital	0-2	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	53-58
1417986-4	1992	PB and two structural analogues (ethylphenylhydantoin and barbital) induced a variety of drug-metabolizing enzymes (CYP2B, CYP3A, CYP2A, epoxide hydrolase) in a series of inbred strains of rats.	Phenobarbital	0-2	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	123-128
1417986-5	1992	In contrast, levels of aldehyde dehydrogenase (ALDH) (propionaldehyde, NAD+) which were expressed constitutively in all strains of rats were induced by PB in only two of the eight strains (ACI, Copenhagen).	Phenobarbital	152-154	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	23-45
1417986-5	1992	In contrast, levels of aldehyde dehydrogenase (ALDH) (propionaldehyde, NAD+) which were expressed constitutively in all strains of rats were induced by PB in only two of the eight strains (ACI, Copenhagen).	Phenobarbital	152-154	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	47-51
1417986-7	1992	These results imply that induction of ALDH (propionaldehyde, NAD+) is associated with the PB pleiotropic response in Copenhagen rats.	Phenobarbital	90-92	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	38-42
1524447-0	1992	Inhibition of protein synthesis increases the transcription of the phenobarbital-inducible CYP2H1 and CYP2H2 genes in chick embryo hepatocytes.	Phenobarbital	67-80	cytochrome P450 2H1	Gallus gallus	91-97
16653069-5	1992	Seed treatment with the safener naphthalic acid anhydride or treatment of seedlings with phenobarbital increased cytochrome P-450 content and lauric acid hydroxylase (LAH) activity of the microsomes.	Phenobarbital	89-102	cytochrome P450 709B1	Triticum aestivum	113-129
1524447-0	1992	Inhibition of protein synthesis increases the transcription of the phenobarbital-inducible CYP2H1 and CYP2H2 genes in chick embryo hepatocytes.	Phenobarbital	67-80	cytochrome P450 family 2 subfamily C member 23b	Gallus gallus	102-108
1524447-12	1992	It is also possible that this factor is involved in regulating the phenobarbital response of CYP2H1/2.	Phenobarbital	67-80	cytochrome P450 2H1	Gallus gallus	93-101
1435745-3	1992	Formation of catechol and sesamol from MDB in microsomal incubation mixtures was enhanced about 5- and 3-fold, respectively, by pretreatment of the rabbits with phenobarbital, which induced CYP2B4 and CYP4B1.	Phenobarbital	161-174	cytochrome P450 2B4	Oryctolagus cuniculus	190-196
1435745-3	1992	Formation of catechol and sesamol from MDB in microsomal incubation mixtures was enhanced about 5- and 3-fold, respectively, by pretreatment of the rabbits with phenobarbital, which induced CYP2B4 and CYP4B1.	Phenobarbital	161-174	cytochrome P450 4B1	Oryctolagus cuniculus	201-207
1435745-10	1992	Reconstitution experiments with CYP2B4 suggested that phenobarbital-inducible complex formation from MDA was not due to the carbene pathway involving the methylenedioxy group but was due to oxidation of the amino group.	Phenobarbital	54-67	cytochrome P450 2B4	Oryctolagus cuniculus	32-38
16653070-6	1992	Treatments of wheat seedlings with phenobarbital or the safener naphthalic acid anhydride enhanced the cytochrome P-450 content of the microsomes and all related activities except that of cinnamic acid 4-hydroxylase, which was reduced.	Phenobarbital	35-48	cytochrome P450 709B1	Triticum aestivum	103-119
1390673-1	1992	A monoclonal antibody (MAb) to phenobarbital-induced rat cytochrome P450b was used to study the interaction of the substrate benzphetamine (Bz) with cytochromes P450 in liver microsomes.	Phenobarbital	31-44	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	57-73
1426026-1	1992	The identity of the sigma receptor as a form of cytochrome P-450 was investigated in rats treated with 3-methylcholanthrene or phenobarbital.	Phenobarbital	127-140	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	48-64
1520280-0	1992	Effect of pyrazole, cobalt and phenobarbital on mouse liver cytochrome P-450 2a-4/5 (Cyp2a-4/5) expression.	Phenobarbital	31-44	cytochrome P450, family 2, subfamily a, polypeptide 4	Mus musculus	60-83
1520280-0	1992	Effect of pyrazole, cobalt and phenobarbital on mouse liver cytochrome P-450 2a-4/5 (Cyp2a-4/5) expression.	Phenobarbital	31-44	cytochrome P450, family 2, subfamily a, polypeptide 4	Mus musculus	85-92
1520280-1	1992	Pyrazole, cobalt and phenobarbital increase the activity of coumarin 7-hydroxylase (COH) in mouse liver.	Phenobarbital	21-34	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	60-82
1520280-1	1992	Pyrazole, cobalt and phenobarbital increase the activity of coumarin 7-hydroxylase (COH) in mouse liver.	Phenobarbital	21-34	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	84-87
1639811-1	1992	We have examined differences in post-translational regulation between rat liver ethanol-inducible cytochrome P450 2E1 (CYP2E1) and phenobarbital-inducible CYP2B1 using hepatocyte cultures and subcellular fractions, prepared from starved and acetone-treated rats.	Phenobarbital	131-144	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	155-161
1354082-5	1992	Moreover, phenobarbital (PB) also enhanced the induction of GGT-positive hepatocellular lesions only in the CCl4-induced liver cirrhosis model, no promotion influence being exerted after treatment with the non-carcinogenic furfural.	Phenobarbital	10-23	C-C motif chemokine ligand 4	Rattus norvegicus	108-112
1354082-5	1992	Moreover, phenobarbital (PB) also enhanced the induction of GGT-positive hepatocellular lesions only in the CCl4-induced liver cirrhosis model, no promotion influence being exerted after treatment with the non-carcinogenic furfural.	Phenobarbital	25-27	C-C motif chemokine ligand 4	Rattus norvegicus	108-112
1530140-7	1992	Comparison of the CCl4-phenobarbital group with pair-fed controls (n = 8) showed: increased serum vitamin A, decreased hepatic vitamin A, increased cytochrome P450, marked hepatic fat accumulation, hepatic cell necrosis, and early cirrhosis.	Phenobarbital	23-36	C-C motif chemokine ligand 4	Rattus norvegicus	18-22
1530140-8	1992	Thus, CCl4 (with phenobarbitol), which is a more potent hepatotoxin as evidenced by a more elevated cytochrome P450 and distorted liver morphology, not only reduced liver vitamin A, but also increased serum vitamin A.	Phenobarbital	17-30	C-C motif chemokine ligand 4	Rattus norvegicus	6-10
1473038-8	1992	The ability of 4-nonyl DDC to lower ferrochelatase activity was attributed to the formation of N-nonylprotoporphyrin IX following the administration of 4-nonyl DDC to phenobarbital-treated rats.	Phenobarbital	167-180	ferrochelatase	Rattus norvegicus	36-50
1352315-0	1992	Quantitative image cytometry of hepatocytes expressing gamma-glutamyl transpeptidase and glutathione S-transferase in diethylnitrosamine-initiated rats treated with phenobarbital and/or phthalate esters.	Phenobarbital	165-178	gamma-glutamyltransferase 1	Rattus norvegicus	55-84
1513322-1	1992	The absence of phenobarbital (PB)-inducible cytochrome P450 2B2 (CYP2B2) in hepatic microsomes from Marshall 520 (M520) and Wistar Munich (WM) inbred strains of rat was previously reported [Biochem.	Phenobarbital	30-32	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	65-71
1513322-4	1992	In the present study, solution hybridization was used to quantify PB-induced CYP2B2 and CYP2B1 mRNAs in livers from M520, WM, and outbred Sprague-Dawley rats, as well as additional inbred strains that express all known electrophoretic phenotypes for both of these closely related isozymes.	Phenobarbital	66-68	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	77-83
1513322-4	1992	In the present study, solution hybridization was used to quantify PB-induced CYP2B2 and CYP2B1 mRNAs in livers from M520, WM, and outbred Sprague-Dawley rats, as well as additional inbred strains that express all known electrophoretic phenotypes for both of these closely related isozymes.	Phenobarbital	66-68	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	88-94
1641859-7	1992	T4 UDP-GT activity was increased by PB, 3MC, PCN, and CLO 88, 150, 100, and 160%, respectively on a per-milligram-microsomal-protein basis and 138, 125, 100, and 145% on a per-kilogram-body-weight basis, respectively.	Phenobarbital	36-38	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	3-9
1306117-0	1992	Induction of various cytochromes CYP2B, CYP2C and CYP3A by phenobarbitone in non-human primates.	Phenobarbital	59-73	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	33-38
1306117-0	1992	Induction of various cytochromes CYP2B, CYP2C and CYP3A by phenobarbitone in non-human primates.	Phenobarbital	59-73	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	40-45
1306117-0	1992	Induction of various cytochromes CYP2B, CYP2C and CYP3A by phenobarbitone in non-human primates.	Phenobarbital	59-73	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	50-55
1306117-2	1992	Hydroxylation of testosterone at the 6 beta, 2 beta, and 15 beta positions, metabolites normally associated with CYP3A P450s increased 2- to 5-fold in PB-treated animals.	Phenobarbital	151-153	cytochrome P450, family 2, subfamily c, polypeptide 12	Rattus norvegicus	39-64
1306117-2	1992	Hydroxylation of testosterone at the 6 beta, 2 beta, and 15 beta positions, metabolites normally associated with CYP3A P450s increased 2- to 5-fold in PB-treated animals.	Phenobarbital	151-153	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	113-118
1306117-10	1992	However, high concentrations of polyclonal antiserum directed against rat CYP2B inhibited all three activities in PB-induced patas monkeys.	Phenobarbital	114-116	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	74-79
1509508-0	1992	Modification by phenobarbital of decreased glutathione content and glutathione S-transferase activity in livers of lead-treated mice.	Phenobarbital	16-29	hematopoietic prostaglandin D synthase	Mus musculus	67-92
1638686-6	1992	Total liver and kidney microsomal cytochrome P450 content and activities of representative drug-metabolizing enzymes for PB, MC and PCN, i.e. benzphetamine N-demethylase, ethoxycoumarin O-deethylase (ECD) and erythromycin N-demethylase, were also determined in all groups.	Phenobarbital	121-123	ecdysoneless cell cycle regulator	Rattus norvegicus	171-198
1391210-2	1992	The K(app) values for the perfluorodecalin binding to cytochrome P-450 in microsomes isolated from the livers of control and phenobarbital-treated rats are 5 x 10(-5) M and 2.3 x 10(-6) M, respectively.	Phenobarbital	125-138	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	54-70
1451030-3	1992	In this study the activity of 17-day-old chick embryo hepatic UROG-D was determined by measuring the conversion of pentacarboxylporphyrinogen I to coproporphyrinogen I, and it was shown that a UROG-D inhibitor, previously reported to accumulate in TCBP-treated and PB-treated chick embryo hepatocytes in culture, also accumulates in OX-DDC-treated and nifedipine-treated chick embryo hepatocytes in culture.	Phenobarbital	265-267	uroporphyrinogen decarboxylase	Gallus gallus	62-68
1451030-3	1992	In this study the activity of 17-day-old chick embryo hepatic UROG-D was determined by measuring the conversion of pentacarboxylporphyrinogen I to coproporphyrinogen I, and it was shown that a UROG-D inhibitor, previously reported to accumulate in TCBP-treated and PB-treated chick embryo hepatocytes in culture, also accumulates in OX-DDC-treated and nifedipine-treated chick embryo hepatocytes in culture.	Phenobarbital	265-267	uroporphyrinogen decarboxylase	Gallus gallus	193-199
1568734-1	1992	Experiments performed in different models of hepatic regeneration at the time of maximal DNA synthesis, determined by thymidine kinase activity assay, demonstrated that spermidine N8-acetyltransferase activity increased 48 hr after CCl4 administration (2-fold), 72 hr after CCl4 plus phenobarbital (3-fold) and 24 hr after partial hepatectomy (4.5-fold).	Phenobarbital	284-297	C-C motif chemokine ligand 4	Rattus norvegicus	232-236
1439179-7	1992	These results suggest that phenobarbital- and pregnenolone 16 alpha-carbonitrile-inducible form(s) of cytochrome P-450 is responsible for the reductive metabolism of zonisamide to 2-sulfamoylacetylphenol in rat liver microsomes.	Phenobarbital	27-40	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	102-118
1413866-2	1992	The content and specific activities of inducible cytochrome P-450 enzymes were determined in liver microsomes of rats of various ages after maximal induction with phenobarbital, isosafrole of 3-methylcholanthrene, and in untreated animals.	Phenobarbital	163-176	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	49-65
1585371-6	1992	The ability of microsomes from fluorocarbon-exposed animals to metabolize (R)- and (S)-warfarin indicates that TFE exposure inactivated the phenobarbital-inducible isozymes P450IIB1, P450IIC6, and P450IIIA to approximately equal degrees (21-35%).	Phenobarbital	140-153	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	197-205
1413874-5	1992	Injection of As3+ to rats treated with phenobarbital and isosafrole significantly decreases the total content of hepatic cytochrome P-450 and various mixed function oxidase (MFO) activities, with the exception of ECOD which appears to be insensitive to As3+.	Phenobarbital	39-52	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	121-137
1506922-4	1992	The cytochrome P-450 content plateaued even at 5% level of dietary protein in experiment 1 and in the PB-untreated groups of experiment 2.	Phenobarbital	102-104	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	4-20
1349513-0	1992	Association between growth stimulation by phenobarbital and expression of cytochromes P450 1A1, 1A2, 2B1/2 and 3A1 in hepatic hyperplastic nodules in male F344 rats.	Phenobarbital	42-55	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	74-104
1349513-5	1992	PB treatment resulted in a 89% increase in the number of persistent gamma-glutamyl transpeptidase (GTT) nodules per cm2 section, a 278% increase in the area of persistent GGT nodules per cm2 section, and a 116% increase in the average area per persistent nodule.	Phenobarbital	0-2	gamma-glutamyltransferase 1	Rattus norvegicus	68-97
1349513-7	1992	A slight but uniform increase in CYP1A2 expression (relative to surrounding, non-nodular tissue) was observed in 50% (23/46) and 59% (60/102) of persistent nodules in control and PB-treated animals respectively.	Phenobarbital	179-181	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	33-39
1349513-8	1992	In contrast, for nodules undergoing remodeling, CYP1A2 expression was elevated in only 9% (2/22) and 0% (0/24) in control and PB groups respectively.	Phenobarbital	126-128	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	48-54
1349513-9	1992	In the PB group, CYP2B1/2 was underexpressed in 53% (54/102) of persistent GGT nodules and in 0% (0/24) of the remodeling nodules.	Phenobarbital	7-9	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	17-23
1567478-6	1992	The results thus extend evidence that both 3-MC and PB induce the synthesis of UGT protein(s) involved in the glucuronidation of T4, 3-MC being a strong and PB a weak inducer.	Phenobarbital	52-54	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	79-82
1567478-6	1992	The results thus extend evidence that both 3-MC and PB induce the synthesis of UGT protein(s) involved in the glucuronidation of T4, 3-MC being a strong and PB a weak inducer.	Phenobarbital	157-159	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	79-82
1587338-2	1992	Both pituitary and serum concentrations of growth hormone were significantly reduced in cirrhotic rats compared with age-related untreated rats or those treated only with phenobarbitone.	Phenobarbital	171-185	gonadotropin releasing hormone receptor	Rattus norvegicus	43-57
1494976-5	1992	Carrageenan also depressed the induction of hepatic S-9 cytochrome P-450 content caused by PB treatment, and suppressed the induction of AM, BenzP, MP, arylhydrocarbon and 7-ethoxycoumarine metabolism by PB treatment.	Phenobarbital	91-93	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	56-72
1372805-8	1992	When male F344/NCr rats were administered various doses of phenobarbital or dichlorodiphenyltrichloroethane (DDT), strong correlations between the induction of CYP2B1 and the induction of epoxide hydrolase or UDP-glucuronyltransferase activities were observed.	Phenobarbital	59-72	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	160-166
1552174-0	1992	Relation between cytochrome P-450 increase and endoplasmic reticulum proliferation in hepatocytes of mice treated with phenobarbital: a microphotometric and morphometric study.	Phenobarbital	119-132	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	17-33
1554380-3	1992	In contrast, outbred female lean and obese Zucker rats showed markedly reduced CYP2B1 responses (less than 15% and less than 5% of those observed in the female DA or F344/NCr rat) to PB (doses less than or equal to 300 ppm), BB (1500 ppm) or EPH (500 ppm).	Phenobarbital	183-185	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	79-85
1554380-4	1992	In parallel studies, profound increases in RNA levels coding for CYP2B1, glutathione S-transferases Ya/Yc (alpha subclass), or epoxide hydrolase were detected in the female F344/NCr rat following treatment with PB (300 ppm), BB (1500 ppm) or EPH (500 ppm).	Phenobarbital	211-213	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	65-71
1554380-9	1992	This decreased responsiveness of female lean Zucker rats to induction of CYP2B1, relative to that of F344/NCr rats, was also observed with the structurally-diverse PB-type inducers clonazepam, clotrimazole and 2-hexanone.	Phenobarbital	164-166	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	73-79
1312398-0	1992	The tumour promoters dieldrin and phenobarbital increase the frequency of c-Ha-ras wild-type, but not of c-Ha-ras mutated focal liver lesions in male C3H/He mice.	Phenobarbital	34-47	Harvey rat sarcoma virus oncogene	Mus musculus	74-82
1553754-6	1992	UDP-GT activity toward T4 was increased by PB, 3MC, PCN, and PCB 270, 400, 570, and 660%, respectively, and was found to correlate with serum T4 levels (total and free).	Phenobarbital	43-45	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	0-6
1553756-1	1992	Glutathione S-transferase (GST) expression was examined in hepatic cytosol from rats and rabbits treated with 4-picoline, pyrrole, pyridine, pyrazine, imidazole, or piperidine using enzymatic activity, SDS-PAGE, and immunoblot analyses and the results were compared to those obtained with phenobarbital and 3-methylcholanthrene.	Phenobarbital	289-302	hematopoietic prostaglandin D synthase	Rattus norvegicus	0-25
1553756-5	1992	While phenobarbital and 3-methylcholanthrene induce class alpha and mu GST expression in rat hepatic cytosol, one of the most interesting observations was that neither of these agents stimulated GST expression in the rabbit.	Phenobarbital	6-19	hematopoietic prostaglandin D synthase	Rattus norvegicus	71-74
1553756-1	1992	Glutathione S-transferase (GST) expression was examined in hepatic cytosol from rats and rabbits treated with 4-picoline, pyrrole, pyridine, pyrazine, imidazole, or piperidine using enzymatic activity, SDS-PAGE, and immunoblot analyses and the results were compared to those obtained with phenobarbital and 3-methylcholanthrene.	Phenobarbital	289-302	hematopoietic prostaglandin D synthase	Rattus norvegicus	27-30
1731631-1	1992	A clone was isolated from a cDNA library constructed from phenobarbital-treated Wistar rat liver and proven to correspond to the full-length mRNA of a polymorphic variant of Sprague-Dawley CYP3A1.	Phenobarbital	58-71	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	189-195
1740154-7	1992	The relative induction of CYP2B1/2, CYP3A1 and CYPEtOH2 after treatment with phenobarbital was stronger in periportal hepatocytes, resulting in levelling out of the initial perivenous dominance of CYP2B1/2 and CYP3A1, whereas CYPEtOH2 became periportal-dominated.	Phenobarbital	77-90	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	26-32
1740154-7	1992	The relative induction of CYP2B1/2, CYP3A1 and CYPEtOH2 after treatment with phenobarbital was stronger in periportal hepatocytes, resulting in levelling out of the initial perivenous dominance of CYP2B1/2 and CYP3A1, whereas CYPEtOH2 became periportal-dominated.	Phenobarbital	77-90	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	36-42
1740154-7	1992	The relative induction of CYP2B1/2, CYP3A1 and CYPEtOH2 after treatment with phenobarbital was stronger in periportal hepatocytes, resulting in levelling out of the initial perivenous dominance of CYP2B1/2 and CYP3A1, whereas CYPEtOH2 became periportal-dominated.	Phenobarbital	77-90	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	197-203
1740154-7	1992	The relative induction of CYP2B1/2, CYP3A1 and CYPEtOH2 after treatment with phenobarbital was stronger in periportal hepatocytes, resulting in levelling out of the initial perivenous dominance of CYP2B1/2 and CYP3A1, whereas CYPEtOH2 became periportal-dominated.	Phenobarbital	77-90	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	210-216
1735448-1	1992	The serum level of alpha 1-acid glycoprotein (alpha 1-AGP) is significantly increased in various animal species by treatment with cytokines, glucocorticoids and phenobarbital.	Phenobarbital	161-174	orosomucoid 1	Rattus norvegicus	19-44
1741290-7	1992	It is therefore, concluded that the region -69 to -98 nt acts as a positive cis-acting element in the transcription of the CYP2B1/B2 genes and in mediating the inductive effects of phenobarbitone.	Phenobarbital	181-195	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	123-129
1735448-1	1992	The serum level of alpha 1-acid glycoprotein (alpha 1-AGP) is significantly increased in various animal species by treatment with cytokines, glucocorticoids and phenobarbital.	Phenobarbital	161-174	orosomucoid 1	Rattus norvegicus	46-57
1735448-3	1992	The main purpose of this study was to assess whether phenobarbital acts on alpha 1-AGP synthesis in the liver at the transcriptional or translational level.	Phenobarbital	53-66	orosomucoid 1	Rattus norvegicus	75-86
1536639-0	1992	Phenobarbital induction of cytochrome P-450 gene expression.	Phenobarbital	0-13	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	27-43
1606640-4	1992	The microsomes from rats treated with phenobarbital, an inducer of cytochrome P-450 reductase, greatly stimulated both the AH.generation and the NADPH oxidation.	Phenobarbital	38-51	cytochrome p450 oxidoreductase	Rattus norvegicus	67-93
1514921-2	1992	Microsomal mixtures were prepared from control, 3-methylcholanthrene and phenobarbital pretreated animals, resulting in different levels of cytochrome P-450 isozymes.	Phenobarbital	73-86	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	140-156
1538719-5	1992	Phenobarbital-inducible P-450 2B4 also had high activity in the 4-hydroxylation reaction of retinoids, and cytochrome b5 was found to increase the activity of P-450 2B4 with each substrate but to increase the activity of P-450 1A2 only with retinoic acid.	Phenobarbital	0-13	cytochrome b5	Oryctolagus cuniculus	107-120
1735448-5	1992	The analysis of total hepatic RNA showed that a single injection of phenobarbital induced an 11-fold increase in phenobarbital-dependent cytochrome P450IIB mRNA, whereas seven injections of phenobarbital were required to induce a maximum 5.5-fold increase in alpha 1-AGP mRNA.	Phenobarbital	68-81	orosomucoid 1	Rattus norvegicus	259-270
1735448-5	1992	The analysis of total hepatic RNA showed that a single injection of phenobarbital induced an 11-fold increase in phenobarbital-dependent cytochrome P450IIB mRNA, whereas seven injections of phenobarbital were required to induce a maximum 5.5-fold increase in alpha 1-AGP mRNA.	Phenobarbital	113-126	orosomucoid 1	Rattus norvegicus	259-270
1735448-5	1992	The analysis of total hepatic RNA showed that a single injection of phenobarbital induced an 11-fold increase in phenobarbital-dependent cytochrome P450IIB mRNA, whereas seven injections of phenobarbital were required to induce a maximum 5.5-fold increase in alpha 1-AGP mRNA.	Phenobarbital	113-126	orosomucoid 1	Rattus norvegicus	259-270
1735448-7	1992	Hepatocytes isolated after the seventh injection of phenobarbital showed a threefold increased capacity to secrete alpha 1-AGP, corresponding to a 3.2-fold increased alpha 1-AGP mRNA content in the liver.	Phenobarbital	52-65	orosomucoid 1	Rattus norvegicus	115-126
1735448-7	1992	Hepatocytes isolated after the seventh injection of phenobarbital showed a threefold increased capacity to secrete alpha 1-AGP, corresponding to a 3.2-fold increased alpha 1-AGP mRNA content in the liver.	Phenobarbital	52-65	orosomucoid 1	Rattus norvegicus	166-177
1735448-8	1992	In conditions in which its effect on the induction of alpha 1-AGP synthesis was maximum, phenobarbital caused a 30% reduction in liver albumin mRNA and in albumin secretion by isolated hepatocytes, resulting from a 60-70% reduction in the rate of transcription of the albumin gene measured in isolated nuclei.	Phenobarbital	89-102	orosomucoid 1	Rattus norvegicus	54-65
1735448-9	1992	We conclude that the effect of phenobarbital on alpha 1-AGP and albumin gene expression occurs at the transcriptional rather than the translational level.	Phenobarbital	31-44	orosomucoid 1	Rattus norvegicus	48-59
1316128-0	1992	Regulation of phenobarbital-induced ferrochelatase mRNA activity by dibutyryl cAMP and glucose in normal and diabetic rat hepatocytes.	Phenobarbital	14-27	ferrochelatase	Rattus norvegicus	36-50
1316128-1	1992	The induction of ferrochelatase activity by phenobarbital and its potentiation by dibutyryl cAMP assayed in normal rat hepatocytes are associated with increased activity of ferrochelatase mRNA.	Phenobarbital	44-57	ferrochelatase	Rattus norvegicus	17-31
1316128-1	1992	The induction of ferrochelatase activity by phenobarbital and its potentiation by dibutyryl cAMP assayed in normal rat hepatocytes are associated with increased activity of ferrochelatase mRNA.	Phenobarbital	44-57	ferrochelatase	Rattus norvegicus	173-187
1370768-7	1992	We have shown that during augmentative hyperplasia caused by the tumor promoters alpha-hexachlorocyclohexane, phenobarbital and ciprofibrate, plasma levels of HGF also increase.	Phenobarbital	110-123	hepatocyte growth factor	Rattus norvegicus	159-162
1316128-4	1992	The inducing effect exerted by phenobarbital on the activity of ferrochelatase mRNA in diabetic hepatocytes is greater than that observed in normal cells.	Phenobarbital	31-44	ferrochelatase	Rattus norvegicus	64-78
1316128-9	1992	The results obtained suggest that ferrochelatase is more susceptible to induction with phenobarbital in diabetic rat hepatocytes than in normal rat hepatocytes.	Phenobarbital	87-100	ferrochelatase	Rattus norvegicus	34-48
1391424-6	1992	3-Hydroxymethyl antipyrine ClF (phenobarbital inducible microsomal cytochrome P-450 isoenzymes) increased 300% only at 48 hours.	Phenobarbital	32-45	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	67-83
1347004-1	1992	Induction of cytochrome P-450-dependent monooxygenases with phenobarbital (PB) or other hepatic drug-metabolizing enzyme inducers in the rat is associated with enhanced cocaine hepatotoxicity both in vivo and in cultured rat hepatocytes.	Phenobarbital	60-73	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
1347004-1	1992	Induction of cytochrome P-450-dependent monooxygenases with phenobarbital (PB) or other hepatic drug-metabolizing enzyme inducers in the rat is associated with enhanced cocaine hepatotoxicity both in vivo and in cultured rat hepatocytes.	Phenobarbital	75-77	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	13-29
1348223-8	1992	Phenobarbital treatment greatly enhanced bromobenzene-induced GGT and LDH release into the lavage fluid in a dose-dependent manner.	Phenobarbital	0-13	gamma-glutamyltransferase 1	Rattus norvegicus	62-65
1342996-5	1992	Both cytochrome P-450 and NADPH-cytochrome P-450 reductase activity was induced by phenobarbital in all animals.	Phenobarbital	83-96	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	5-21
1397146-6	1992	Under the control condition, the postsynaptic Nut cell exhibits dendritic dominance with rho = 2.52, normalized equivalent cable length L = 1.08, and a membrane time constant tau o = 52 ms. With phenobarbital application, changes in the geometrical parameters consistent with a decrease in the specific membrane resistance Rm are observed.	Phenobarbital	195-208	NUT midline carcinoma family member 1	Homo sapiens	46-49
1342996-5	1992	Both cytochrome P-450 and NADPH-cytochrome P-450 reductase activity was induced by phenobarbital in all animals.	Phenobarbital	83-96	cytochrome p450 oxidoreductase	Rattus norvegicus	26-58
1342996-7	1992	On the contrary, cytochrome b5 and NADH-cytochrome b5 reductase activity was inhibited after phenobarbital injection.	Phenobarbital	93-106	cytochrome b5 type A	Rattus norvegicus	17-30
1342996-7	1992	On the contrary, cytochrome b5 and NADH-cytochrome b5 reductase activity was inhibited after phenobarbital injection.	Phenobarbital	93-106	cytochrome b5 type A	Rattus norvegicus	40-53
1542250-1	1992	Liver sections removed from phenobarbital induced rats 24 to 48 hours after a 2 hour exposure to 1.0% halothane with 10% oxygen and subjected to immunocytochemical treatment showed evidence of centrilobular damage as well as evidence of the production of a protein which has immunoreactivity with anti HSP 72 antibodies.	Phenobarbital	28-41	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	302-308
1433423-3	1992	By comparison, it was found that PB could induce MFO activities in kidney cortex microsomes and liver microsomes, both hepatic and renal microsomal MFO were decreased by the ip injection of CdCl2, and Cd2+ could markedly decrease the phenobarbital induction to hepatic and renal microsomal MFO activities with the exception of NADPH-cytochrome c reductase in kidney cortex microsomes.	Phenobarbital	33-35	Cd2 molecule	Rattus norvegicus	201-204
1433423-3	1992	By comparison, it was found that PB could induce MFO activities in kidney cortex microsomes and liver microsomes, both hepatic and renal microsomal MFO were decreased by the ip injection of CdCl2, and Cd2+ could markedly decrease the phenobarbital induction to hepatic and renal microsomal MFO activities with the exception of NADPH-cytochrome c reductase in kidney cortex microsomes.	Phenobarbital	234-247	Cd2 molecule	Rattus norvegicus	201-204
1284994-0	1992	Pivotal role of hepatocellular regeneration in the ultimate hepatotoxicity of CCl4 in chlordecone-, mirex-, or phenobarbital-pretreated rats.	Phenobarbital	111-124	C-C motif chemokine ligand 4	Rattus norvegicus	78-82
1284994-9	1992	Actual liver injury by CCl4 was greater in PB- than in CD-pretreated rats, as evidenced by histopathological observations.	Phenobarbital	43-45	C-C motif chemokine ligand 4	Rattus norvegicus	23-27
1284994-14	1992	These findings suggest that there is recovery in N-, PB-, or M-pretreated rats from CCl4-induced injury by virtue of the stimulated hepatocellular regeneration and tissue repair.	Phenobarbital	53-55	C-C motif chemokine ligand 4	Rattus norvegicus	84-88
12671788-8	1992	Diseases associated with serum lipase activity within the reference range or elevated less than twofold included gastritis, gastric ulcer, cholestasis, phenobarbital-induced hepatopathy, colitis, copper hepatopathy, abdominal hematoma, apocrine gland adenocarcinoma, and thrombocytopenia with pneumonia.	Phenobarbital	152-165	pancreatic lipase related protein 1	Canis lupus familiaris	31-37
1757130-1	1991	Enzyme-inducing drugs such as phenobarbital (PB) increase serum concentrations of an acute-phase protein, alpha 1-acid glycoprotein (AGP), in man, dogs, and rats via an unknown mechanism.	Phenobarbital	30-43	orosomucoid 1	Rattus norvegicus	133-136
1733051-2	1992	Pretreatment of animals with 80 mg/kg phenobarbital for the site-specific enzyme studies enhanced and accelerated CCl4 toxicity in slices resulting from increased radical formation.	Phenobarbital	38-51	C-C motif chemokine ligand 4	Rattus norvegicus	114-118
1747936-0	1991	Analysis of the Ha-ras oncogene in C3H/He mouse liver tumours derived spontaneously or induced with diethylnitrosamine or phenobarbitone.	Phenobarbital	122-136	Harvey rat sarcoma virus oncogene	Mus musculus	16-22
1747936-1	1991	In a study of the mechanisms involved in the induction of tumours by chemicals, the Ha-ras oncogene was analysed in liver tumours induced by the genotoxic carcinogen diethylnitrosamine (DEN), or the non-genotoxic agent phenobarbitone (PB) in C3H/He mice.	Phenobarbital	219-233	Harvey rat sarcoma virus oncogene	Mus musculus	84-90
1747936-1	1991	In a study of the mechanisms involved in the induction of tumours by chemicals, the Ha-ras oncogene was analysed in liver tumours induced by the genotoxic carcinogen diethylnitrosamine (DEN), or the non-genotoxic agent phenobarbitone (PB) in C3H/He mice.	Phenobarbital	235-237	Harvey rat sarcoma virus oncogene	Mus musculus	84-90
1747936-6	1991	Low and variable expression of the Ha-ras gene was detected in all liver tissues with moderately raised levels (175-200%) in spontaneous, DEN and PB-induced tumours as compared to normal liver tissue.	Phenobarbital	146-148	Harvey rat sarcoma virus oncogene	Mus musculus	35-41
1778655-1	1991	Temporal variations in cytochrome P-450 isozymes of rat testis, PB-P-450 (forms of cytochrome P-450 strongly induced by phenobarbital) and MC-P-448 (forms of cytochrome P-450 strongly induced by 3-methylcholanthrene), were investigated immunohistochemically by the avidin-biotin-complex method using specific antibodies against PB-P-450 and MC-P-448 isozymes.	Phenobarbital	120-133	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	23-39
1778655-1	1991	Temporal variations in cytochrome P-450 isozymes of rat testis, PB-P-450 (forms of cytochrome P-450 strongly induced by phenobarbital) and MC-P-448 (forms of cytochrome P-450 strongly induced by 3-methylcholanthrene), were investigated immunohistochemically by the avidin-biotin-complex method using specific antibodies against PB-P-450 and MC-P-448 isozymes.	Phenobarbital	120-133	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	83-99
1778655-1	1991	Temporal variations in cytochrome P-450 isozymes of rat testis, PB-P-450 (forms of cytochrome P-450 strongly induced by phenobarbital) and MC-P-448 (forms of cytochrome P-450 strongly induced by 3-methylcholanthrene), were investigated immunohistochemically by the avidin-biotin-complex method using specific antibodies against PB-P-450 and MC-P-448 isozymes.	Phenobarbital	120-133	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	83-99
1757130-1	1991	Enzyme-inducing drugs such as phenobarbital (PB) increase serum concentrations of an acute-phase protein, alpha 1-acid glycoprotein (AGP), in man, dogs, and rats via an unknown mechanism.	Phenobarbital	45-47	orosomucoid 1	Rattus norvegicus	133-136
1757130-4	1991	Pretreatment with PB for seven days modified neither parameter in SD rats while plantar edema was aggravated and serum AGP levels were increased in DA rats.	Phenobarbital	18-20	orosomucoid 1	Rattus norvegicus	119-122
1957312-8	1991	PB, a microsomal enzyme inducer, increased the cytochrome b5 and P450 content as well as the cytochrome P450-dependent O-depentylation of pentoxyresorufin.	Phenobarbital	0-2	cytochrome b5 type A	Rattus norvegicus	47-60
1800893-3	1991	In the genetically engineered cell lines, benzo[a]pyrene was metabolized specifically by the 3-methylcholanthrene inducible rat liver CYP1A1 (cell line XEM2) whereas cyclophosphamide increased the micronucleus frequency only in cultures expressing the phenobarbital inducible CYP2B1 (SD1).	Phenobarbital	252-265	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	134-140
1659407-2	1991	In mice, during liver cell proliferation induced by 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene and phenobarbital, pp63 transcript levels had a decrease of 40-50%.	Phenobarbital	99-112	alpha-2-HS-glycoprotein	Rattus norvegicus	114-118
1800796-3	1991	The level of P-450Md mRNA in female rats was increased by phenobarbital or dexamethasone treatment, whereas the level in the males was depressed by methylcholanthrene.	Phenobarbital	58-71	cytochrome P450, family 2, subfamily c, polypeptide 22	Rattus norvegicus	13-20
1717467-5	1991	Comparison of the amino acid sequence of rat liver msALDH with those of rat other class ALDHs showed that msALDH was 24.2, 24.0, and 65.5% identical to phenobarbital-inducible ALDH (variant class 1), mitochondrial ALDH (class 2), and tumor-associated ALDH (class 3), respectively.	Phenobarbital	152-165	aldehyde dehydrogenase 3 family, member A2	Rattus norvegicus	51-57
1717467-5	1991	Comparison of the amino acid sequence of rat liver msALDH with those of rat other class ALDHs showed that msALDH was 24.2, 24.0, and 65.5% identical to phenobarbital-inducible ALDH (variant class 1), mitochondrial ALDH (class 2), and tumor-associated ALDH (class 3), respectively.	Phenobarbital	152-165	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	53-57
1717467-5	1991	Comparison of the amino acid sequence of rat liver msALDH with those of rat other class ALDHs showed that msALDH was 24.2, 24.0, and 65.5% identical to phenobarbital-inducible ALDH (variant class 1), mitochondrial ALDH (class 2), and tumor-associated ALDH (class 3), respectively.	Phenobarbital	152-165	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	88-92
1717467-5	1991	Comparison of the amino acid sequence of rat liver msALDH with those of rat other class ALDHs showed that msALDH was 24.2, 24.0, and 65.5% identical to phenobarbital-inducible ALDH (variant class 1), mitochondrial ALDH (class 2), and tumor-associated ALDH (class 3), respectively.	Phenobarbital	152-165	aldehyde dehydrogenase 3 family, member A1	Rattus norvegicus	88-92
1898087-0	1991	Involvement of heme in the transcriptional activation of CYPIIB1/B2 gene by phenobarbitone in rat liver--studies with succinylacetone.	Phenobarbital	76-90	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	57-64
1898087-1	1991	Earlier studies in this laboratory had implicated heme to function as a positive modulator of phenobarbitone-mediated activation of CYPIIB1/B2 gene transcription in rat liver.	Phenobarbital	94-108	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	132-139
1898087-3	1991	The present studies indicate that succinylacetone does inhibit the phenobarbitone-mediated increase in CYPIIB1/B2 mRNAs and their transcription in rat liver at early time points (45 min to 3 h), but the inhibition is not pronounced at later time points (16 h).	Phenobarbital	67-81	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	103-110
1898087-6	1991	There is a good correlation between the amount of freshly synthesized nuclear heme pool and the activation of CYPIIB1/B2 transcription by phenobarbitone.	Phenobarbital	138-152	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	110-117
1930280-4	1991	However, adduct formation was significantly increased in microsomes from Sudan III-, phenobarbital- and dexamethasone-treated rats, suggesting the involvement of the CYP1A, CYP2B and CYP3A subfamilies, respectively.	Phenobarbital	85-98	cytochrome P450, family 3, subfamily a, polypeptide 62	Rattus norvegicus	183-188
1681808-9	1991	Phenobarbital, methylcholanthrene and dexamethasone were found to increase significantly gamma-glutamyltransferase while tyrosine aminotransferase activity was enhanced by dexamethasone.	Phenobarbital	0-13	gamma-glutamyltransferase 1	Rattus norvegicus	89-114
1777369-12	1991	The revised estimate of peak steady-state plasma phenobarbitone concentration utilising the 96 h post-single dose concentration (356 ng ml-1) was least biased (mean prediction error +/- 95% CI = 10.6 +/- 19.8 ng ml-1) and most precise (root mean square error +/- 95% CI = 28.3 +/- 19.0 ng ml-1).	Phenobarbital	49-63	interleukin 17F	Homo sapiens	136-140
1777369-12	1991	The revised estimate of peak steady-state plasma phenobarbitone concentration utilising the 96 h post-single dose concentration (356 ng ml-1) was least biased (mean prediction error +/- 95% CI = 10.6 +/- 19.8 ng ml-1) and most precise (root mean square error +/- 95% CI = 28.3 +/- 19.0 ng ml-1).	Phenobarbital	49-63	interleukin 17F	Homo sapiens	212-216
1777369-12	1991	The revised estimate of peak steady-state plasma phenobarbitone concentration utilising the 96 h post-single dose concentration (356 ng ml-1) was least biased (mean prediction error +/- 95% CI = 10.6 +/- 19.8 ng ml-1) and most precise (root mean square error +/- 95% CI = 28.3 +/- 19.0 ng ml-1).	Phenobarbital	49-63	interleukin 17F	Homo sapiens	212-216
1921373-1	1991	A common model for producing experimental liver cirrhosis is the administration of CCl4 to phenobarbital (PhB)-stimulated rats.	Phenobarbital	91-104	C-C motif chemokine ligand 4	Rattus norvegicus	83-87
1921373-1	1991	A common model for producing experimental liver cirrhosis is the administration of CCl4 to phenobarbital (PhB)-stimulated rats.	Phenobarbital	106-109	C-C motif chemokine ligand 4	Rattus norvegicus	83-87
1949030-10	1991	Short-term treatment (5 days) with PB produced a 2-fold increase in the number and total area of GGT-positive nodules in the DEN/AAF group, but it had no significant effect on the number, size distribution, or total area of GGT-positive nodules in the AFB group.	Phenobarbital	35-37	gamma-glutamyltransferase 1	Rattus norvegicus	97-100
1949030-10	1991	Short-term treatment (5 days) with PB produced a 2-fold increase in the number and total area of GGT-positive nodules in the DEN/AAF group, but it had no significant effect on the number, size distribution, or total area of GGT-positive nodules in the AFB group.	Phenobarbital	35-37	gamma-glutamyltransferase 1	Rattus norvegicus	224-227
1714717-0	1991	Effect of interleukin 6 on phenobarbital induction of cytochrome P-450IIB in cultured rat hepatocytes.	Phenobarbital	27-40	interleukin 6	Rattus norvegicus	10-23
1788981-2	1991	N-Methyl-N-alkyl-p-chlorobenzamides (alkyl = Me, Et, nPr, nBu, PhCH2, isoPr and cylcoPr) underwent mono-N-dealkylation exclusively with phenobarbital-induced rat liver microsomes; with each compound both demethylation and dealkylation occurred.	Phenobarbital	136-149	neuronal pentraxin receptor	Rattus norvegicus	53-56
1714717-1	1991	Human recombinant interleukin 6 (rhIL-6) caused a dose dependent decrease in the phenobarbital induction of benzyloxyresorufin O-deethylase activity in cultured rat hepatocytes.	Phenobarbital	81-94	interleukin 6	Rattus norvegicus	18-31
1933335-9	1991	MPTP toxicity was potentiated significantly in brain slices prepared from mice pretreated with phenobarbital, an inducer of cytochrome P-450.	Phenobarbital	95-108	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	124-140
1868078-1	1991	The induction mechanism by pyrazole or phenobarbital of coumarin 7-hydroxylase (cytochrome P450coh) was investigated in DBA/2J male mice.	Phenobarbital	39-52	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	56-78
1678603-9	1991	These results indicate that the PB-inducible isozymes such as CYP2B4 appear to play an important role in MDB demethylenation, whereas MDA and MDMA oxidation is mediated mainly by constitutive isozymes.	Phenobarbital	32-34	cytochrome P450 2B4	Oryctolagus cuniculus	62-68
1715015-1	1991	Cytochromes P450b and P450e (IIB1 and IIB2, respectively) are two remarkably similar microsomal hemoproteins whose inductions in rat liver are generally believed to be coordinately controlled by such xenobiotics as phenobarbital.	Phenobarbital	215-228	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	12-17
1914510-0	1991	Immunocytochemical study of phenobarbital- and 3-methylcholanthrene-inducible cytochrome P450 isozymes in primary cultures of porcine ciliary epithelium.	Phenobarbital	28-41	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	78-93
1715015-5	1991	Kepone also resembled phenobarbital in these experiments, in that there were dose-dependent increases in the amounts of hepatocellular P450p, P450pcn2, P450PB-1, P450f, and NADPH-cytochrome P450 oxidoreductase mRNAs.	Phenobarbital	22-35	cytochrome P450, family 2, subfamily c, polypeptide 12	Rattus norvegicus	152-160
1723229-4	1991	PB pretreatment produced a 50% increase in lipid peroxidation (TBAR) by liver homogenates and microsomes, an effect accompanied by increases in cytochrome P-450, NADPH-cytochrome P-450 reductase, NADPH oxidase and microsomal superoxide anion production, MC pretreatment resulted in increases in liver cytochrome P-450 and NADPH oxidase only.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	144-160
1723229-4	1991	PB pretreatment produced a 50% increase in lipid peroxidation (TBAR) by liver homogenates and microsomes, an effect accompanied by increases in cytochrome P-450, NADPH-cytochrome P-450 reductase, NADPH oxidase and microsomal superoxide anion production, MC pretreatment resulted in increases in liver cytochrome P-450 and NADPH oxidase only.	Phenobarbital	0-2	cytochrome p450 oxidoreductase	Rattus norvegicus	162-194
1723229-4	1991	PB pretreatment produced a 50% increase in lipid peroxidation (TBAR) by liver homogenates and microsomes, an effect accompanied by increases in cytochrome P-450, NADPH-cytochrome P-450 reductase, NADPH oxidase and microsomal superoxide anion production, MC pretreatment resulted in increases in liver cytochrome P-450 and NADPH oxidase only.	Phenobarbital	0-2	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	168-184
1859462-0	1991	Effect of the aging process on the gender and phenobarbital dependent expression of glutathione S-transferase subunits in brown Norway rat liver.	Phenobarbital	46-59	hematopoietic prostaglandin D synthase	Rattus norvegicus	84-109
1859462-1	1991	The effect of age, gender and phenobarbital treatment on the hepatic cytosolic glutathione S-transferase subunit composition was studied in Brown Norway rats.	Phenobarbital	30-43	hematopoietic prostaglandin D synthase	Rattus norvegicus	79-104
1859462-7	1991	In all the age groups studied phenobarbital administration (45 mg/kg body weight, i.p., once a day for 7 days) doubled total glutathione S-transferase protein in both genders and affected the subunit composition in a significant way, emphasizing the already existing differences between genders.	Phenobarbital	30-43	hematopoietic prostaglandin D synthase	Rattus norvegicus	125-150
2043158-0	1991	Evidence for the stability and cytochrome P450 specificity of the phenobarbital-induced reductive halothane-cytochrome P450 complex formed in rat hepatic microsomes.	Phenobarbital	66-79	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	31-46
1859452-8	1991	The induction of P450IIIA due to both phenobarbital and dexamethasone, as mirrored by 6 beta- and 15 beta-hydroxylation of testosterone, was the same in cultured hepatocytes and in vivo.	Phenobarbital	38-51	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	17-25
1941559-5	1991	The contents of hepatic cytochrome P-450 (1.29 versus 2.15 nmol/mg protein) and the weights of liver and stomach increased significantly in PB-treated rats, suggesting that the metabolizing enzymes for furosemide are induced by pretreatment with PB.	Phenobarbital	140-142	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	24-40
1906977-0	1991	Purification and properties of a rat liver phenobarbital-inducible 4-hydroxybiphenyl UDP-glucuronosyltransferase.	Phenobarbital	43-56	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	85-112
1906977-1	1991	A phenobarbital-inducible rat hepatic microsomal UDP-glucuronosyltransferase (UDPGT) that catalyzes the glucuronidation of 4-hydroxybiphenyl (4-HBP) has been purified to homogeneity.	Phenobarbital	2-15	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	49-76
1906977-1	1991	A phenobarbital-inducible rat hepatic microsomal UDP-glucuronosyltransferase (UDPGT) that catalyzes the glucuronidation of 4-hydroxybiphenyl (4-HBP) has been purified to homogeneity.	Phenobarbital	2-15	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	78-83
1898024-3	1991	Treatment of rats with phenobarbital (PB) or 3-methylcholanthrene (MC) caused a slight reduction or less than a twofold increase, respectively, in the rate of total metabolism (per nanomole of cytochrome P450) of the enantiomeric dihydrodiols compared to microsomes from control rats.	Phenobarbital	23-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	193-208
1898024-3	1991	Treatment of rats with phenobarbital (PB) or 3-methylcholanthrene (MC) caused a slight reduction or less than a twofold increase, respectively, in the rate of total metabolism (per nanomole of cytochrome P450) of the enantiomeric dihydrodiols compared to microsomes from control rats.	Phenobarbital	38-40	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	193-208
1898024-12	1991	Experiments with antibodies indicate that a large percentage of the metabolism by microsomes from control and PB-treated rats is catalyzed by cytochrome P450p (P450IIIA1), resulting in the altered stereoselectivity of these microsomes compared to that of the liver microsomes from MC-treated rats.	Phenobarbital	110-112	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	142-158
2060617-0	1991	Regulation of glutathione S-transferase gene expression by phenobarbital in cultured adult rat hepatocytes.	Phenobarbital	59-72	hematopoietic prostaglandin D synthase	Rattus norvegicus	14-39
2060617-1	1991	Previous studies, by using Northern blotting analyses, showed that phenobarbital (PB) affects the steady-state mRNA levels of glutathione S-transferase (GST) subunits 1/2, 3/4 and 7 in both conventional cultures of adult rat hepatocytes and co-cultures, with rat liver epithelial cells [Vandenberghe et al., 1989, FEBS Lett.	Phenobarbital	67-80	hematopoietic prostaglandin D synthase	Rattus norvegicus	126-151
2060617-1	1991	Previous studies, by using Northern blotting analyses, showed that phenobarbital (PB) affects the steady-state mRNA levels of glutathione S-transferase (GST) subunits 1/2, 3/4 and 7 in both conventional cultures of adult rat hepatocytes and co-cultures, with rat liver epithelial cells [Vandenberghe et al., 1989, FEBS Lett.	Phenobarbital	67-80	hematopoietic prostaglandin D synthase	Rattus norvegicus	153-156
2060617-1	1991	Previous studies, by using Northern blotting analyses, showed that phenobarbital (PB) affects the steady-state mRNA levels of glutathione S-transferase (GST) subunits 1/2, 3/4 and 7 in both conventional cultures of adult rat hepatocytes and co-cultures, with rat liver epithelial cells [Vandenberghe et al., 1989, FEBS Lett.	Phenobarbital	82-84	hematopoietic prostaglandin D synthase	Rattus norvegicus	126-151
2060617-1	1991	Previous studies, by using Northern blotting analyses, showed that phenobarbital (PB) affects the steady-state mRNA levels of glutathione S-transferase (GST) subunits 1/2, 3/4 and 7 in both conventional cultures of adult rat hepatocytes and co-cultures, with rat liver epithelial cells [Vandenberghe et al., 1989, FEBS Lett.	Phenobarbital	82-84	hematopoietic prostaglandin D synthase	Rattus norvegicus	153-156
2043158-0	1991	Evidence for the stability and cytochrome P450 specificity of the phenobarbital-induced reductive halothane-cytochrome P450 complex formed in rat hepatic microsomes.	Phenobarbital	66-79	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	108-123
2060617-5	1991	Data from this study demonstrate that the increase in steady-state mRNA levels observed in both conventional culture and co-culture after 4 days PB exposure results from an increased transcriptional activity of the GST genes.	Phenobarbital	145-147	hematopoietic prostaglandin D synthase	Rattus norvegicus	215-218
2043158-4	1991	A large portion of total microsomal cytochrome P450 was destroyed upon halothane reduction (up to 39%), yet the complexed cytochrome P450, particularly in microsomes from PB-treated animals, was resistant to the irreversible inactivation mechanisms of halothane reduction.	Phenobarbital	171-173	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	122-137
2051993-0	1991	Difference in the susceptibility of two phenobarbital-inducible forms, P450IIB1 and P450IIB2, to thyroid hormone- and growth hormone-induced suppression in rat liver: phenobarbital-inducible P450IIB2 suppression by thyroid hormone acting directly, but not through the pituitary system.	Phenobarbital	40-53	gonadotropin releasing hormone receptor	Rattus norvegicus	118-132
2051993-0	1991	Difference in the susceptibility of two phenobarbital-inducible forms, P450IIB1 and P450IIB2, to thyroid hormone- and growth hormone-induced suppression in rat liver: phenobarbital-inducible P450IIB2 suppression by thyroid hormone acting directly, but not through the pituitary system.	Phenobarbital	167-180	gonadotropin releasing hormone receptor	Rattus norvegicus	118-132
1897986-0	1991	A constitutive form of guinea pig liver cytochrome P450 closely related to phenobarbital inducible P450b(e).	Phenobarbital	75-88	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	99-104
1949908-15	1991	Moreover, both these pathways involve the cytochrome P-450 system and can be induced with phenobarbital.	Phenobarbital	90-103	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	42-58
2022168-11	1991	PB significantly increases the intracellular concentration of TGF-beta 1 in periportal hepatocytes but not in putative preneoplastic cells.	Phenobarbital	0-2	transforming growth factor, beta 1	Rattus norvegicus	62-72
1873508-4	1991	The contents of hepatic cytochrome P-450 (1.29 vs 2.15 nmol mg-1 protein) and the weights of liver and stomach increased significantly in PB treated rats, suggesting that the metabolizing enzymes for bumetanide are induced by pretreatment with PB.	Phenobarbital	138-140	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	24-40
2039754-8	1991	Anti-P450 IIIA isolated from phenobarbital-induced rat liver effectively inhibited TEST hydroxylation at the 2 beta-, 6 beta-, 15 alpha- and 15 beta-positions (by 31-56% when incubated with microsomes at a ratio of 5 mg IgG/mg protein).	Phenobarbital	29-42	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	5-14
2012803-1	1991	Flash photolysis of cytochrome P-450 in phenobarbital-induced rat liver microsomes was examined by observing the decay of absorbance change, A(t), at 450 nm after photolysis of the heme.CO complex by a depolarized laser flash.	Phenobarbital	40-53	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	20-36
1707352-9	1991	Subsequent feeding with a 0.05% PB diet for 64 weeks resulted in slightly increased development of GGT-positive foci but not GST-P positive lesions or hyperplastic nodules, suggesting a lack of tumor-initiating activity of the oxidative DNA damage associated with redox enzyme modulations with or without menadione.	Phenobarbital	32-34	gamma-glutamyltransferase 1	Rattus norvegicus	99-102
2048399-0	1991	Serum lipids, lipoproteins and apolipoproteins A and B in epileptic patients treated with valproic acid, carbamazepine or phenobarbital.	Phenobarbital	122-135	lipoprotein(a)	Homo sapiens	31-54
2061553-0	1991	A CCl4/CHCl3 interaction study in isolated hepatocytes: non-induced and phenobarbital-pretreated cells.	Phenobarbital	72-85	C-C motif chemokine ligand 4	Homo sapiens	2-6
2025880-3	1991	The role of cytochrome P-450 in the activation of 2-NP is indicated by the increase of liver DNA damage in rats pretreated with phenobarbital or beta-naphtoflavone, and by its reduction produced by methoxsalen.	Phenobarbital	128-141	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	12-28
2061553-8	1991	Phenobarbital pretreatment enhanced the toxicity of both CCl4 and CHCl3, alone and in combination.	Phenobarbital	0-13	C-C motif chemokine ligand 4	Homo sapiens	57-61
1819909-7	1991	The three-day administration of nifedipine plus phenobarbital resulted in a further increase in the BND activity and the cytochrome P-450 content.	Phenobarbital	48-61	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	121-137
2018490-2	1991	Partially purified P450F1 exhibited absorption spectra similar to those of P450(1), the major phenobarbital-inducible form in rabbit liver.	Phenobarbital	94-107	cytochrome P450 2C5	Oryctolagus cuniculus	75-82
1880703-5	1991	Carrageenan also suppressed induction of hexobarbital, aminopyrine and ethylmorphine metabolism by phenobarbital treatment, and depressed the induction of hepatic S-9 cytochrome P-450 content caused by phenobarbital treatment.	Phenobarbital	202-215	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	167-183
1854958-1	1991	It has been found that the Soviet anticonvulsant drug Benzonal is an inducer of the liver cytochrome P-450 of the phenobarbital type.	Phenobarbital	114-127	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	90-106
1854958-2	1991	The drug causes formation of the cytochrome P-450 form which is immunologically identical to the phenobarbital inducible form of the hemoprotein with identical molecular mass determined with the SDS-gel electrophoresis method in PAAG.	Phenobarbital	97-110	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	33-49
1877388-0	1991	The biological significance of lipoprotein lipase modulation by phenobarbital and heparin.	Phenobarbital	64-77	lipoprotein lipase	Rattus norvegicus	31-49
1882464-3	1991	The content of cytochrome b5 increases only after 4 administrations of phenobarbital and after 5th one it returns to the initial level.	Phenobarbital	71-84	cytochrome b5 type A	Rattus norvegicus	15-28
1882464-5	1991	Activity of glucose-6-phosphate dehydrogenase increases after a single administration of phenobarbital, that of malate dehydrogenase--after 3 administrations, 6--phosphogluconate-dehydrogenase--after 4 administrations of the preparation.	Phenobarbital	89-102	glucose-6-phosphate dehydrogenase	Rattus norvegicus	12-45
1900006-0	1991	Induction of alkoxyresorufin O-dealkylases and UDP-glucuronosyl transferase by phenobarbital and 3-methylcholanthrene in primary cultures of porcine ciliary epithelial cells.	Phenobarbital	79-92	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	47-75
1900006-7	1991	UDP-GT activity increased about 5-fold in PB-treated PE cells and about 4-fold in PB-treated NPE cells in 48 hr.	Phenobarbital	42-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
1900006-7	1991	UDP-GT activity increased about 5-fold in PB-treated PE cells and about 4-fold in PB-treated NPE cells in 48 hr.	Phenobarbital	82-84	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	0-6
1900006-9	1991	Induction by PB and MC of ER O-dealkylase, PR O-dealkylase and UDP-GT activities in ciliary NPE and PE cells was inhibited almost completely by 3.5 microM cyclohexamide and 40 nM actinomycin D.	Phenobarbital	13-15	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	63-69
1989519-9	1991	Ethanol and phenobarbital treatments both increased P450IIIA, as determined immunologically and by the amount of propoxycoumarin depropylase activity that is inhibited by triacetyloleandomycin.	Phenobarbital	12-25	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	52-60
2004789-3	1991	Comparison of the segregation patterns of these alleles in three sets of recombinant inbred strains with allele segregation patterns of previously characterized loci shows that the Rbp-4 locus is closely linked to the locus for phenobarbital-inducible cytochrome P450-2c (Cyp-2c) that has been shown by in situ hybridization to lie on chromosome 19, bands D1-D2.	Phenobarbital	228-241	retinol binding protein 4, plasma	Mus musculus	181-186
2004789-3	1991	Comparison of the segregation patterns of these alleles in three sets of recombinant inbred strains with allele segregation patterns of previously characterized loci shows that the Rbp-4 locus is closely linked to the locus for phenobarbital-inducible cytochrome P450-2c (Cyp-2c) that has been shown by in situ hybridization to lie on chromosome 19, bands D1-D2.	Phenobarbital	228-241	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	252-270
2004789-3	1991	Comparison of the segregation patterns of these alleles in three sets of recombinant inbred strains with allele segregation patterns of previously characterized loci shows that the Rbp-4 locus is closely linked to the locus for phenobarbital-inducible cytochrome P450-2c (Cyp-2c) that has been shown by in situ hybridization to lie on chromosome 19, bands D1-D2.	Phenobarbital	228-241	cytochrome P450, family 2, subfamily c, polypeptide 29	Mus musculus	272-278
1751755-0	1991	The effect of tryptophan on the phenobarbital-mediated induction of cytochrome P-450 in rat liver.	Phenobarbital	32-45	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	68-84
2053846-5	1991	A partition ratio, between metabolic turnover of the substrate and enzyme inactivation, of about 121 was found with microsomes from phenobarbital-treated rats, indicating that halothane is rather efficient as a suicide substrate of cytochrome P-450.	Phenobarbital	132-145	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	232-248
1751755-2	1991	The effect of intraperitoneal administration of phenobarbital (80 mg kg-1 body weight) and tryptophan (200 mg kg-1 body weight), separately or in combination, on the microsomal content of cytochrome P-450 and the activity of tryptophan 2,3-dioxygenase (EC 1.13.11.11) in Wistar rat liver was determined at different time intervals after injection.	Phenobarbital	48-61	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	188-204
1751755-3	1991	There was an increase in the amount of cytochrome P-450 within 12 h of administration of a single dose of phenobarbital which was maintained over the next 12 h. Tryptophan had no effect on the amount of cytochrome P-450, but administration of tryptophan in combination with phenobarbital blocked the increase that was found after administration of phenobarbital alone.	Phenobarbital	106-119	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-55
1751755-3	1991	There was an increase in the amount of cytochrome P-450 within 12 h of administration of a single dose of phenobarbital which was maintained over the next 12 h. Tryptophan had no effect on the amount of cytochrome P-450, but administration of tryptophan in combination with phenobarbital blocked the increase that was found after administration of phenobarbital alone.	Phenobarbital	274-287	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-55
1751755-3	1991	There was an increase in the amount of cytochrome P-450 within 12 h of administration of a single dose of phenobarbital which was maintained over the next 12 h. Tryptophan had no effect on the amount of cytochrome P-450, but administration of tryptophan in combination with phenobarbital blocked the increase that was found after administration of phenobarbital alone.	Phenobarbital	274-287	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	39-55
1751755-4	1991	Both phenobarbital and tryptophan increased tryptophan 2,3-dioxygenase activity (total enzyme and holoenzyme) but had different effects on the rate of activation and the degree of saturation of the enzyme with haem.	Phenobarbital	5-18	tryptophan 2,3-dioxygenase	Rattus norvegicus	44-70
1751755-7	1991	It is proposed that combined administration of phenobarbital and tryptophan leads to substrate stabilisation of tryptophan 2,3-dioxygenase, and that this is accompanied by the binding of the newly synthesised haem, thus making haem unavailable for formation of cytochrome P-450.	Phenobarbital	47-60	tryptophan 2,3-dioxygenase	Rattus norvegicus	112-138
1751755-7	1991	It is proposed that combined administration of phenobarbital and tryptophan leads to substrate stabilisation of tryptophan 2,3-dioxygenase, and that this is accompanied by the binding of the newly synthesised haem, thus making haem unavailable for formation of cytochrome P-450.	Phenobarbital	47-60	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	261-277
1988078-0	1991	Reversible and phorbol ester-specific defect of protein kinase C translocation in hepatocytes isolated from phenobarbital-treated rats.	Phenobarbital	108-121	protein kinase C, gamma	Rattus norvegicus	48-64
1988078-7	1991	However, both the diminished epidermal growth factor receptor response and the inhibition of TPA-induced PKC translocation were reversed by withdrawal of PB for 2 to 4 weeks.	Phenobarbital	154-156	protein kinase C, gamma	Rattus norvegicus	105-108
1988078-12	1991	These data demonstrate reversible inhibition of phorbol ester-induced PKC activation by the liver tumor promoter, PB, and suggest that PB alters a component of the PKC-signaling pathway other than the expression of PKC isozymes.	Phenobarbital	114-116	protein kinase C, gamma	Rattus norvegicus	70-73
1988078-1	1991	Phorbol ester-induced translocation of the calcium/phospholipid-dependent protein kinase, protein kinase C (PKC), from soluble to particulate cell fractions was inhibited in primary cultures of hepatocytes isolated from rats chronically exposed to the liver tumor promoter phenobarbital (PB).	Phenobarbital	273-286	protein kinase C, gamma	Rattus norvegicus	90-106
1988078-1	1991	Phorbol ester-induced translocation of the calcium/phospholipid-dependent protein kinase, protein kinase C (PKC), from soluble to particulate cell fractions was inhibited in primary cultures of hepatocytes isolated from rats chronically exposed to the liver tumor promoter phenobarbital (PB).	Phenobarbital	273-286	protein kinase C, gamma	Rattus norvegicus	108-111
1988078-1	1991	Phorbol ester-induced translocation of the calcium/phospholipid-dependent protein kinase, protein kinase C (PKC), from soluble to particulate cell fractions was inhibited in primary cultures of hepatocytes isolated from rats chronically exposed to the liver tumor promoter phenobarbital (PB).	Phenobarbital	288-290	protein kinase C, gamma	Rattus norvegicus	90-106
1988078-1	1991	Phorbol ester-induced translocation of the calcium/phospholipid-dependent protein kinase, protein kinase C (PKC), from soluble to particulate cell fractions was inhibited in primary cultures of hepatocytes isolated from rats chronically exposed to the liver tumor promoter phenobarbital (PB).	Phenobarbital	288-290	protein kinase C, gamma	Rattus norvegicus	108-111
1988078-7	1991	However, both the diminished epidermal growth factor receptor response and the inhibition of TPA-induced PKC translocation were reversed by withdrawal of PB for 2 to 4 weeks.	Phenobarbital	154-156	epidermal growth factor receptor	Rattus norvegicus	29-61
1914788-6	1991	In a parallel study, a gene for an inducible mouse UDPGT, designated UDPGTm-1, was shown by Northern blotting to be expressed in fetal liver by day 18 of gestation at low levels relative to adults, but was not induced transplacentally by MC, beta NF or phenobarbital (PB).	Phenobarbital	253-266	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	51-56
1914788-6	1991	In a parallel study, a gene for an inducible mouse UDPGT, designated UDPGTm-1, was shown by Northern blotting to be expressed in fetal liver by day 18 of gestation at low levels relative to adults, but was not induced transplacentally by MC, beta NF or phenobarbital (PB).	Phenobarbital	268-270	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	51-56
1914791-3	1991	Phenobarbital markedly increased cytochrome P-450 levels and the cytochrome-P-450-mediated formation of 4-hydroxybiphenyl whereas YZH had a slightly depressive effect on this enzyme system.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	33-49
1364405-4	1991	The numbers or areas of gamma-GTP or GST-P positive foci of the liver were increased in the DEN+PB groups treated with 38 ppm PB or above.	Phenobarbital	96-98	glutathione S-transferase pi 1	Rattus norvegicus	37-42
1808966-1	1991	Caffeine is mainly metabolized by 3-methylcholanthreneinducible cytochrome P-450, whereas metamizol (Analgin) is probably mainly metabolized by the phenobarbital inducible cytochrome P-450 family.	Phenobarbital	148-161	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	172-188
1832886-7	1991	Induction of P450 isoenzymes IA, IIB and IIE1 by pretreatment of mice with phenobarbitone, 3-methylcholanthrene or acetone had no significant effect on the toxicity of 4-HA towards hepatocytes.	Phenobarbital	75-89	ATPase, class II, type 9B	Mus musculus	33-36
1783050-4	1991	Phenobarbital treatment (60 mg/kg b. m. at 3 consecutive days each) increases the concentration and the monooxygenase activities of some cytochrome P-450 forms.	Phenobarbital	0-13	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	137-153
1781304-3	1991	Phenobarbital treatment induced a decrease in cerebral arteriovenous difference of glucose at P14 and no change at P10 and P21.	Phenobarbital	0-13	S100 calcium binding protein A9	Rattus norvegicus	94-97
1781304-5	1991	Cerebral uptake of beta-hydroxybutyrate was unchanged at P10 and increased by two-fold at P14 and by threefold at P21 by phenobarbital.	Phenobarbital	121-134	KRAS proto-oncogene, GTPase	Rattus norvegicus	114-117
1839629-6	1991	Among the ten drugs, CCl4, alcohol, paraquat, phenobarbital, thiopental and methylcholanthrene caused the TBA values to increase, and the phosphoglucomutase activity to decrease, in the liver 24 h after the doses.	Phenobarbital	46-59	C-C motif chemokine ligand 4	Rattus norvegicus	21-25
1780643-1	1991	Male Fischer 344 (F344) rats were treated with phenobarbital + carbon tetrachloride (CCl4) for 16 weeks to induce liver cirrhosis.	Phenobarbital	47-60	C-C motif chemokine ligand 4	Rattus norvegicus	85-89
2009865-4	1991	1,1-Dichloro-2,2-bis(p-chlorophenyl) ethylene (DDE) was used as an inducer of phenobarbital inducible cytochrome P-450, and beta-naphthoflavone (beta NF) was used as an inducer of 3-methylcholanthrene inducible cytochrome P-448.	Phenobarbital	78-91	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	211-227
2019352-10	1991	Induction of cytochrome P450 enzymes by administration of phenobarbital (100 mg/kg/day/3 days) resulted in a significant (p less than 0.05) increase in MOCA-globin adduct formation detected with 33.5 pmol/mg globin for induced rats versus 13.6 pmol/mg globin for control rats.	Phenobarbital	58-71	dedicator of cytokinesis 3	Homo sapiens	152-156
2011611-0	1991	Phenobarbital increases rat hepatic prostaglandin F2 alpha, glutathione S-transferase activity and oxidative stress.	Phenobarbital	0-13	hematopoietic prostaglandin D synthase	Rattus norvegicus	60-85
2011611-2	1991	PB treatment increased glutathione S-transferase (GST) activity by 80% and prostaglandin (PG) F2 alpha levels 4-fold (p less than 0.05).	Phenobarbital	0-2	hematopoietic prostaglandin D synthase	Rattus norvegicus	23-48
2011611-2	1991	PB treatment increased glutathione S-transferase (GST) activity by 80% and prostaglandin (PG) F2 alpha levels 4-fold (p less than 0.05).	Phenobarbital	0-2	hematopoietic prostaglandin D synthase	Rattus norvegicus	50-53
2011611-7	1991	PB"s effect on PGF2 alpha could be a result of both GST-mediated prostaglandin synthesis and oxidative stress.	Phenobarbital	0-2	hematopoietic prostaglandin D synthase	Rattus norvegicus	52-55
2086563-3	1990	Daily administration of PB, TP, TA, or PT induced cytochrome P-450, NADPH-cytochrome P-450 reductase and/or cytochrome b5.	Phenobarbital	24-26	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	50-66
2268369-0	1990	Immunochemical detection of human liver cytochrome P450 forms related to phenobarbital-inducible forms in the mouse.	Phenobarbital	73-86	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	40-55
2268369-1	1990	Polyclonal antibodies generated to four distinct mouse liver phenobarbital-inducible cytochrome P450 isoforms were used to analyse related forms in human liver.	Phenobarbital	61-74	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	85-100
2086563-3	1990	Daily administration of PB, TP, TA, or PT induced cytochrome P-450, NADPH-cytochrome P-450 reductase and/or cytochrome b5.	Phenobarbital	24-26	cytochrome p450 oxidoreductase	Rattus norvegicus	68-100
2086563-3	1990	Daily administration of PB, TP, TA, or PT induced cytochrome P-450, NADPH-cytochrome P-450 reductase and/or cytochrome b5.	Phenobarbital	24-26	cytochrome b5 type A	Rattus norvegicus	108-121
2212619-0	1990	Microphotometric analysis of cytochrome P-450 in periportal, midzonal, and perivenular hepatocytes of mice treated with phenobarbital.	Phenobarbital	120-133	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	29-45
2241158-0	1990	Role of heme in phenobarbital induction of cytochromes P450 and 5-aminolevulinate synthase in cultured rat hepatocytes maintained on an extracellular matrix.	Phenobarbital	16-29	5'-aminolevulinate synthase 1	Rattus norvegicus	64-90
2241158-3	1990	Phenobarbital treatment of rat cultures increased the total amount of cytochrome P450, activities catalyzed by IIB1/2 (benzyloxy- and pentoxyresorufin O-dealkylases) and ALA-S activity, and ALA-S mRNA.	Phenobarbital	0-13	5'-aminolevulinate synthase 1	Rattus norvegicus	170-175
2241158-3	1990	Phenobarbital treatment of rat cultures increased the total amount of cytochrome P450, activities catalyzed by IIB1/2 (benzyloxy- and pentoxyresorufin O-dealkylases) and ALA-S activity, and ALA-S mRNA.	Phenobarbital	0-13	5'-aminolevulinate synthase 1	Rattus norvegicus	190-195
2241158-6	1990	Lack of effect on the cytochrome P450 mRNAs was selective inasmuch as treatment with phenobarbital combined with succinyl acetone synergistically increased both ALA-S activity and ALA-S mRNA, presumably by blocking formation of heme, the feedback repressor of ALA-S.	Phenobarbital	85-98	5'-aminolevulinate synthase 1	Rattus norvegicus	161-166
2241158-6	1990	Lack of effect on the cytochrome P450 mRNAs was selective inasmuch as treatment with phenobarbital combined with succinyl acetone synergistically increased both ALA-S activity and ALA-S mRNA, presumably by blocking formation of heme, the feedback repressor of ALA-S.	Phenobarbital	85-98	5'-aminolevulinate synthase 1	Rattus norvegicus	180-185
2241158-6	1990	Lack of effect on the cytochrome P450 mRNAs was selective inasmuch as treatment with phenobarbital combined with succinyl acetone synergistically increased both ALA-S activity and ALA-S mRNA, presumably by blocking formation of heme, the feedback repressor of ALA-S.	Phenobarbital	85-98	5'-aminolevulinate synthase 1	Rattus norvegicus	180-185
1981550-6	1990	Microsomes from phenobarbital- or Aroclor 1254-treated rats produced greater amounts of F- per mg protein from high concentrations of R-134a than did microsomes from untreated rats, but when normalized for microsomal cytochrome P-450 content both phenobarbital and Aroclor treatment decreased the specific activity (nmol F-/nmol cytochrome P-450) of R-134a metabolism.	Phenobarbital	16-29	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	217-233
1981550-6	1990	Microsomes from phenobarbital- or Aroclor 1254-treated rats produced greater amounts of F- per mg protein from high concentrations of R-134a than did microsomes from untreated rats, but when normalized for microsomal cytochrome P-450 content both phenobarbital and Aroclor treatment decreased the specific activity (nmol F-/nmol cytochrome P-450) of R-134a metabolism.	Phenobarbital	16-29	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	329-345
2262816-9	1990	Nevertheless, it was important for the induction of both GST-A and GST-B by PB treatment.	Phenobarbital	76-78	hematopoietic prostaglandin D synthase	Rattus norvegicus	57-60
2262816-9	1990	Nevertheless, it was important for the induction of both GST-A and GST-B by PB treatment.	Phenobarbital	76-78	glutathione S-transferase alpha 2	Rattus norvegicus	67-72
2124384-3	1990	Antibody raised against cytochrome P-450b, which is the main isozyme of liver obtained from phenobarbital-treated rats, cross-reacted with pulmonary cytochrome P-450FII, but not with cytochrome P-450FI.	Phenobarbital	92-105	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	24-41
1977543-5	1990	Antipyrine and phenobarbital increased antipyrine elimination, serum gamma-glutamyltransferase, and the urinary excretion of renal gamma-glutamyltransferase, whereas urinary beta-N-acetylglucosaminidase, beta-glucuronidase, and total protein and glucose excretion were unchanged.	Phenobarbital	15-28	glucuronidase beta	Homo sapiens	204-222
2212619-1	1990	To obtain detailed information on the increase of cytochrome P-450 (P-450) content in periportal, midzonal, and perivenular hepatocytes after phenobarbital (PB) administration, and to study the mechanism of increased P-450 in the endoplasmic reticulum (ER), we estimated microphotometrically the P-450 content and morphometrically the area of ER in hepatocytes of three zones from mice injected with 35, 50, 100, or 150 mg/kg of PB for 3 days.	Phenobarbital	157-159	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	50-66
2212619-1	1990	To obtain detailed information on the increase of cytochrome P-450 (P-450) content in periportal, midzonal, and perivenular hepatocytes after phenobarbital (PB) administration, and to study the mechanism of increased P-450 in the endoplasmic reticulum (ER), we estimated microphotometrically the P-450 content and morphometrically the area of ER in hepatocytes of three zones from mice injected with 35, 50, 100, or 150 mg/kg of PB for 3 days.	Phenobarbital	142-155	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	50-66
2125771-2	1990	Isozymes of the cytochromes P-450, UDP-glucuronosyl transferases (UDPGT) and glutathione S-transferases appear to be differentially inducible by prototype inducers, such as 3-methylcholanthrene (MC), phenobarbital, pregnenolone 16 alpha-carbonitrile and clofibrate.	Phenobarbital	200-213	beta-1,3-glucuronyltransferase 2	Rattus norvegicus	35-64
2125771-2	1990	Isozymes of the cytochromes P-450, UDP-glucuronosyl transferases (UDPGT) and glutathione S-transferases appear to be differentially inducible by prototype inducers, such as 3-methylcholanthrene (MC), phenobarbital, pregnenolone 16 alpha-carbonitrile and clofibrate.	Phenobarbital	200-213	beta-1,3-glucuronyltransferase 2	Rattus norvegicus	66-71
1978678-0	1990	Effect of phenobarbital on the glucocorticoid receptor in rat hepatoma cells.	Phenobarbital	10-23	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	31-54
1978678-3	1990	Since both, phenobarbital and glucocorticoids, are capable of inducing the same cytochrome P450 species, we asked whether the glucocorticoid receptor could participate to the phenobarbital induced responses.	Phenobarbital	12-25	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	126-149
1978678-3	1990	Since both, phenobarbital and glucocorticoids, are capable of inducing the same cytochrome P450 species, we asked whether the glucocorticoid receptor could participate to the phenobarbital induced responses.	Phenobarbital	175-188	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	126-149
1978678-4	1990	The results presented here show that phenobarbital was able to induce a two-fold increase in the affinity of the glucocorticoid receptor for the binding of dexamethasone, as well as a 30% increase of the receptor number in Reuber rat hepatoma cells of the Fao line.	Phenobarbital	37-50	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	113-136
1978678-6	1990	To our knowledge, phenobarbital is the first compound shown to be able to induce, in intact cells, an increase in the affinity of the glucocorticoid receptor for the binding of its ligand.	Phenobarbital	18-31	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	134-157
2171427-4	1990	The cytochromes beta NF-A1 and beta NF-A2 were induced by both phenobarbital and beta-naphthoflavone treatment and were similar to P450 PB-A (previously purified from phenobarbital-induced hen livers) in molecular weights, isoelectric pH, spectral properties, behavior on chromatography columns, catalysis of substrates, immunological cross-reactivity on Ouchterlony plates and by immunoblotting, and NH2-terminal amino acid sequence.	Phenobarbital	63-76	POU class 2 homeobox 1	Gallus gallus	21-26
2171427-4	1990	The cytochromes beta NF-A1 and beta NF-A2 were induced by both phenobarbital and beta-naphthoflavone treatment and were similar to P450 PB-A (previously purified from phenobarbital-induced hen livers) in molecular weights, isoelectric pH, spectral properties, behavior on chromatography columns, catalysis of substrates, immunological cross-reactivity on Ouchterlony plates and by immunoblotting, and NH2-terminal amino acid sequence.	Phenobarbital	167-180	POU class 2 homeobox 1	Gallus gallus	21-26
2119910-6	1990	In total, 6 out of 35 liver tumours of male CF1 mice, two of them occurring after treatment with the tumour promoter phenobarbital solely, contained mutations at either the first or second base of codon 61 of the Ha-ras gene.	Phenobarbital	117-130	Harvey rat sarcoma virus oncogene	Mus musculus	213-219
2128752-4	1990	Inducibility of liver microsomal codeine UDPGT activity in rats was examined by pretreatment with phenobarbital and 3-methylcholanthrene and compared with those of other UDPGT activities.	Phenobarbital	98-111	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	41-46
2128752-6	1990	The inducibility of codeine UDPGT activity by phenobarbital pretreatment was not as high as that of morphine UDPGT activity.	Phenobarbital	46-59	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	28-33
2222405-4	1990	The newly synthesized cytochrome P-450 was enzymically active, as shown by the major induction of the P-450 PB4-dependent steroid 16 beta-hydroxylase and pentoxyresorufin O-dealkylase activities in the PB-induced hepatocyte microsomes (up to 90-fold increase).	Phenobarbital	108-110	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	22-38
2085792-6	1990	The level of Yb1 was equally induced by MC or PB with no synergistic effect.	Phenobarbital	46-48	Y box binding protein 1	Rattus norvegicus	13-16
2233686-7	1990	In a similar experiment using two phenobarbital-like inducers, (trans)nonachlor and clotrimazole, the relative inductions of P450b, P450e, P450p, and P450pcn2 mRNAs proved to be similar to those produced by phenobarbital (P450p/P450b potency ratios = 14- and 16-fold, respectively).	Phenobarbital	34-47	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	150-158
1981220-8	1990	Both phenobarbital and 3-methylcholanthrene augmented the GGTP activity of NPE cells but not of PE cells.	Phenobarbital	5-18	inactive glutathione hydrolase 2	Homo sapiens	58-62
2233686-0	1990	Differentiated induction of cytochrome P450b/e and P450p mRNAs by dose of phenobarbital in primary cultures of adult rat hepatocytes.	Phenobarbital	74-87	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	28-44
2233686-7	1990	In a similar experiment using two phenobarbital-like inducers, (trans)nonachlor and clotrimazole, the relative inductions of P450b, P450e, P450p, and P450pcn2 mRNAs proved to be similar to those produced by phenobarbital (P450p/P450b potency ratios = 14- and 16-fold, respectively).	Phenobarbital	207-220	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	150-158
2233686-1	1990	Phenobarbital induces cytochromes P450 (P450s) of not only the class IIB gene subfamily (i.e., P450b and P450e) but also the class IIIA gene subfamily (P450p and P450pcn2).	Phenobarbital	0-13	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	95-100
2233686-1	1990	Phenobarbital induces cytochromes P450 (P450s) of not only the class IIB gene subfamily (i.e., P450b and P450e) but also the class IIIA gene subfamily (P450p and P450pcn2).	Phenobarbital	0-13	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	162-170
2233688-0	1990	Developmental expression and in situ localization of the phenobarbital-inducible rat hepatic mRNAs for cytochromes CYP2B1, CYP2B2, CYP2C6, and CYP3A1.	Phenobarbital	57-70	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	115-121
2233686-3	1990	Two-day treatments of the cultures with phenobarbital produced marked dose-dependent increases in the levels of P450b, P450e, and P450p mRNAs, which reached maximal inductions ranging from 11- to greater than 193-fold.	Phenobarbital	40-53	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	112-117
2233686-4	1990	Although the dose-response relationships for the inductions of P450b and P450e mRNAs by phenobarbital were similar (ED50 = 1.5 x 10(-5) and 5.7 x 10(-6) M, respectively), the dose-response curve for the induction of P450p mRNA was positioned distinctly to the right (ED50 = 3.0 x 10(-4) M).	Phenobarbital	88-101	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	63-68
2233686-6	1990	Phenobarbital also produced a weak dose-dependent induction of P450pcn2 mRNA, with a potency (ED50 = 3.4 x 10(-5) M) intermediate between those for P450b/e and P450p.	Phenobarbital	0-13	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	63-71
2233688-0	1990	Developmental expression and in situ localization of the phenobarbital-inducible rat hepatic mRNAs for cytochromes CYP2B1, CYP2B2, CYP2C6, and CYP3A1.	Phenobarbital	57-70	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	123-129
2233688-0	1990	Developmental expression and in situ localization of the phenobarbital-inducible rat hepatic mRNAs for cytochromes CYP2B1, CYP2B2, CYP2C6, and CYP3A1.	Phenobarbital	57-70	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	131-137
2233688-0	1990	Developmental expression and in situ localization of the phenobarbital-inducible rat hepatic mRNAs for cytochromes CYP2B1, CYP2B2, CYP2C6, and CYP3A1.	Phenobarbital	57-70	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	143-149
2233688-1	1990	In this study we examined the differential hepatic expression of four phenobarbital (PB)-inducible rat cytochrome P450 genes, CYP2B1, CYP2B2, CYP2C6, and CYP3A1.	Phenobarbital	85-87	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	154-160
2233688-6	1990	An exception to this trend was observed for rats of gestational day 22, which exhibited transiently increased constitutive levels of CYP2B1, CYP2B2, and CYP3A1 mRNAs, such that PB-induced levels were not elevated over those observed in untreated animals.	Phenobarbital	177-179	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	133-139
2233688-6	1990	An exception to this trend was observed for rats of gestational day 22, which exhibited transiently increased constitutive levels of CYP2B1, CYP2B2, and CYP3A1 mRNAs, such that PB-induced levels were not elevated over those observed in untreated animals.	Phenobarbital	177-179	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	141-147
2233688-6	1990	An exception to this trend was observed for rats of gestational day 22, which exhibited transiently increased constitutive levels of CYP2B1, CYP2B2, and CYP3A1 mRNAs, such that PB-induced levels were not elevated over those observed in untreated animals.	Phenobarbital	177-179	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	153-159
2233688-8	1990	Whereas patterns of PB-induced expression of CYP2C6 mRNAs were relatively homogeneous across the hepatic lobule, CYP3A1 mRNAs in PB-treated livers demonstrated marked centrilobular localization.	Phenobarbital	20-22	cytochrome P450, family 2, subfamily C, polypeptide 6, variant 1	Rattus norvegicus	45-51
2233688-8	1990	Whereas patterns of PB-induced expression of CYP2C6 mRNAs were relatively homogeneous across the hepatic lobule, CYP3A1 mRNAs in PB-treated livers demonstrated marked centrilobular localization.	Phenobarbital	129-131	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	113-119
2233688-9	1990	These results were in contrast to data obtained previously for PB-inducible CYP2B1 and CYP2B2 mRNAs, which were distributed homogeneously across the hepatic lobule except for cells in the immediate vicinity of the periportal tract.	Phenobarbital	63-65	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	76-82
2233688-9	1990	These results were in contrast to data obtained previously for PB-inducible CYP2B1 and CYP2B2 mRNAs, which were distributed homogeneously across the hepatic lobule except for cells in the immediate vicinity of the periportal tract.	Phenobarbital	63-65	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	87-93
2222449-1	1990	The involvement of CCl4 biotransformation mechanism in decreasing the Protein Kinase C activity has been analyzed in hepatocytes isolated from phenobarbital-pretreated rats.	Phenobarbital	143-156	C-C motif chemokine ligand 4	Rattus norvegicus	19-23
2393297-11	1990	We conclude that the pathways for the induction of P450b/e and P450p by phenobarbital, and the pathways for the gender-specific basal expression of P450PCN1(IIIA1) and P450PCN2(IIIA2) are not the same and can be distinguished by their differential response to inhibition of ongoing protein synthesis.	Phenobarbital	72-85	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	51-56
2118332-0	1990	Phenobarbital inducible UDP-glucuronosyltransferase is responsible for glucuronidation of 3"-azido-3"-deoxythymidine: characterization of the enzyme in human and rat liver microsomes.	Phenobarbital	0-13	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	24-51
2118332-12	1990	Altogether, the results strongly indicate that UDP-glucuronosyltransferase (phenobarbital inducible forms) is responsible for AZT glucuronidation.	Phenobarbital	76-89	UDP glycosyltransferase 2 family, polypeptide B	Rattus norvegicus	47-74
1701644-6	1990	When more phospholipid is available to provide the structural framework for biogenesis of endoplasmic reticulum, all of the hepatic actions of phenobarbital, including induction of cytochrome P-450, are amplified.	Phenobarbital	143-156	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	181-197
2393297-11	1990	We conclude that the pathways for the induction of P450b/e and P450p by phenobarbital, and the pathways for the gender-specific basal expression of P450PCN1(IIIA1) and P450PCN2(IIIA2) are not the same and can be distinguished by their differential response to inhibition of ongoing protein synthesis.	Phenobarbital	72-85	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	168-176
1981732-6	1990	Following incubation of CDE with hepatic microsomes isolated from rats treated with cytochrome P-450 inducers, measurement of fluoride release showed that phenobarbital induced CDE metabolism to the greatest degree at high CDE levels, isoniazid was the most effective inducer at low CDE concentrations, and beta-naphthoflavone was ineffective as an inducer.	Phenobarbital	155-168	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	84-100
2242403-4	1990	Phenobarbital doses of 3 x 0.05 mg per mouse increased the concentration of cytochrome P-450 and ketone groups on PE, whereas the vaccine Propionibacterium acnes (0.5 mg) and its pyridine fraction (0.5 and 1 mg) had the opposite effect.	Phenobarbital	0-13	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	76-92
2276091-1	1990	The mechanism-based inactivation of hepatic cytochrome P-450 by the suicide inhibitor 1-aminobenzotriazole and two of its derivatives, N-benzyl-1-aminobenzotriazole and N-alpha-methylbenzyl-1-aminobenzotriazole, was investigated in microsomes from untreated, phenobarbital-induced, and beta-naphthoflavone-induced guinea pigs.	Phenobarbital	259-272	cytochrome P450 3A14	Cavia porcellus	44-60
2245078-2	1990	Patients taking phenobarbital (PB) had an increase in alpha 1 and a decrease in alpha 2 activity in comparison with drug-free epileptics.	Phenobarbital	16-29	adrenoceptor alpha 1D	Homo sapiens	54-61
2245078-2	1990	Patients taking phenobarbital (PB) had an increase in alpha 1 and a decrease in alpha 2 activity in comparison with drug-free epileptics.	Phenobarbital	31-33	adrenoceptor alpha 1D	Homo sapiens	54-61
2245078-3	1990	Patients taking PB for generalized seizures with tonic-clonic convulsion only (GTC) also had a significant increase in alpha 1 and a decrease in alpha 2, whereas those with partial seizures (PS) had an increase in theta and beta 1 and a decrease in alpha 2 activity.	Phenobarbital	16-18	adrenoceptor alpha 1D	Homo sapiens	119-126
2245078-3	1990	Patients taking PB for generalized seizures with tonic-clonic convulsion only (GTC) also had a significant increase in alpha 1 and a decrease in alpha 2, whereas those with partial seizures (PS) had an increase in theta and beta 1 and a decrease in alpha 2 activity.	Phenobarbital	16-18	potassium calcium-activated channel subfamily M regulatory beta subunit 1	Homo sapiens	224-230
2122606-3	1990	Likewise, addition of t-butylquinone (20-100 microM) strikingly inhibited electron transfer from the flavoprotein reductase to cytochrome P-450 of liver microsomes from phenobarbital-treated rats.	Phenobarbital	169-182	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	127-143
2122607-5	1990	With liver microsomes from both 3-methylcholanthrene (MC)- and phenobarbital (PB)-pretreated rats, reverse type I difference spectra were observed, indicative of a weak interaction between mitomycin c and the substrate binding site of cytochrome P-450.	Phenobarbital	63-76	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	235-251
2122607-5	1990	With liver microsomes from both 3-methylcholanthrene (MC)- and phenobarbital (PB)-pretreated rats, reverse type I difference spectra were observed, indicative of a weak interaction between mitomycin c and the substrate binding site of cytochrome P-450.	Phenobarbital	78-80	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	235-251
1696822-7	1990	CCl4 administration to mirex or PB pretreated rats resulted in a smaller decrease in ATP levels (18-24%) only at 24 hr, returning to normal levels by 36-48 hr, in accord with rapid recovery from limited liver injury.	Phenobarbital	32-34	C-C motif chemokine ligand 4	Rattus norvegicus	0-4
2383252-3	1990	Pretreatment with phenobarbital (PB) significantly increased (60-85%) the activity of ECOD in neuronal and glial cells, while a 140% increase was observed in neuronal AHH activity.	Phenobarbital	18-31	aryl hydrocarbon receptor repressor	Homo sapiens	167-170
2200675-5	1990	Phenobarbital and rifampicin increased P-450 IIC8/9/10 mRNA transcripts and the corresponding protein, while 3-methylcholanthrene was ineffective.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-54
2379175-3	1990	PB produced the following changes: (a) accelerated appearance of neoplastic nodules and hepatocellular carcinoma (from 28 weeks onwards); (b) phenotypic changes in altered foci such as a shift from clear to eosinophilic appearance, enhanced expression of gamma-glutamyltranspeptidase and other markers, and more distinct borders from surrounding liver; (c) an increase in foci number; and (d) accelerated foci enlargement.	Phenobarbital	0-2	gamma-glutamyltransferase 1	Rattus norvegicus	255-283
2390286-5	1990	NADH-catalyzed CCl4 metabolism occurred to a similar extent in control and PB microsomes, amounting to 9-10% and 5-6% of the NADPH rate in control and PB microsomes, respectively.	Phenobarbital	75-77	C-C motif chemokine ligand 4	Rattus norvegicus	15-19
2390286-5	1990	NADH-catalyzed CCl4 metabolism occurred to a similar extent in control and PB microsomes, amounting to 9-10% and 5-6% of the NADPH rate in control and PB microsomes, respectively.	Phenobarbital	151-153	C-C motif chemokine ligand 4	Rattus norvegicus	15-19
2387028-6	1990	All pesticides studied were shown to be potent inducers of the phenobarbital-inducible cytochrome P450b isoenzyme and to cause hepatomegaly.	Phenobarbital	63-76	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	87-103
2117068-4	1990	A monoclonal antibody (MAb 1-7-1), which recognizes isozymes of cytochrome P-450 induced by 3-methylcholanthrene (P1-450 and P3-450), selectively inhibited the metabolism of 8-MOP (-57%) and covalent binding of its metabolites (-40%) in microsomes from mice pretreated with BNF, but had no effect in microsomes of mice pretreated with phenobarbital or vehicle.	Phenobarbital	335-348	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	64-80
2117068-5	1990	Monoclonal antibody 2-66-3, which recognizes the major isozymes of rat cytochrome P-450 induced by phenobarbital and unknown isozymes in the mouse, enhanced the covalent binding of 8-MOP metabolites in microsomes of mice pretreated with vehicle (+74%), phenobarbital (+44%) or BNF (+31%) without affecting the disappearance of 8-MOP.	Phenobarbital	99-112	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	71-87
2117068-5	1990	Monoclonal antibody 2-66-3, which recognizes the major isozymes of rat cytochrome P-450 induced by phenobarbital and unknown isozymes in the mouse, enhanced the covalent binding of 8-MOP metabolites in microsomes of mice pretreated with vehicle (+74%), phenobarbital (+44%) or BNF (+31%) without affecting the disappearance of 8-MOP.	Phenobarbital	253-266	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	71-87
2383252-3	1990	Pretreatment with phenobarbital (PB) significantly increased (60-85%) the activity of ECOD in neuronal and glial cells, while a 140% increase was observed in neuronal AHH activity.	Phenobarbital	33-35	aryl hydrocarbon receptor repressor	Homo sapiens	167-170
2377462-1	1990	The rat cytochrome P450 CYP2B2 gene encodes one of the two major phenobarbital-inducible forms of hepatic microsomal cytochrome P-450.	Phenobarbital	65-78	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	24-30
2377462-1	1990	The rat cytochrome P450 CYP2B2 gene encodes one of the two major phenobarbital-inducible forms of hepatic microsomal cytochrome P-450.	Phenobarbital	65-78	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	117-133
2339415-4	1990	Pretreatment with phenobarbital slowed the time course of acetylcholinesterase and hepatic aliesterase inhibition following parathion exposure, suggesting the induction of a detoxication pathway(s) to a greater extent than the induction of activation.	Phenobarbital	18-31	acetylcholinesterase	Rattus norvegicus	58-78
15374492-1	1990	The effect of age on distribution of the phenobarbital-inducible forms of cytochrome P-450 IIBI and IIB2 in the hepatic lobule was investigated immunohistochemically by the avidin-biotin-peroxidase complex (ABC) method in male rats of various ages pretreated with phenobarbital.	Phenobarbital	41-54	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	74-90
15374492-1	1990	The effect of age on distribution of the phenobarbital-inducible forms of cytochrome P-450 IIBI and IIB2 in the hepatic lobule was investigated immunohistochemically by the avidin-biotin-peroxidase complex (ABC) method in male rats of various ages pretreated with phenobarbital.	Phenobarbital	264-277	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	74-90
15374492-2	1990	Exposure of liver sections to anti-cytochrome P-450 serum resulted in intense immunostaining in centrilobular hepatocytes but produced staining of weaker intensity in periportal cells in phenobarbital-treated rats, while in livers of nontreated animals, no significant immunoreactivity was detectable.	Phenobarbital	187-200	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	35-51
15374492-6	1990	The results show that the administration of phenobarbital causes an increase in the content of these cytochrome P-450 isozymes in greater amount in the centrilobular hepatocytes than in the periportal cells in the liver lobule and that the content of cytochrome P-450 isozymes induced by the phenobarbital administration decreases with age in male rats.	Phenobarbital	44-57	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	101-117
15374492-6	1990	The results show that the administration of phenobarbital causes an increase in the content of these cytochrome P-450 isozymes in greater amount in the centrilobular hepatocytes than in the periportal cells in the liver lobule and that the content of cytochrome P-450 isozymes induced by the phenobarbital administration decreases with age in male rats.	Phenobarbital	44-57	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	251-267
15374492-6	1990	The results show that the administration of phenobarbital causes an increase in the content of these cytochrome P-450 isozymes in greater amount in the centrilobular hepatocytes than in the periportal cells in the liver lobule and that the content of cytochrome P-450 isozymes induced by the phenobarbital administration decreases with age in male rats.	Phenobarbital	292-305	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	101-117
1978428-1	1990	The phenobarbital and ionol administration to rats and mice increases considerably the glutathione transferase, glutathione reductase and gamma-glutamyl transferase activities in the liver.	Phenobarbital	4-17	glutathione reductase	Mus musculus	112-133
1978428-3	1990	A correlation was established between the induction of glutathione transferase, glutathione reductase and gamma-glutamyl transferase, their changes in mice and rats, phenobarbital and ionol effects.	Phenobarbital	166-179	glutathione S-transferase alpha 4	Rattus norvegicus	55-78
1978428-3	1990	A correlation was established between the induction of glutathione transferase, glutathione reductase and gamma-glutamyl transferase, their changes in mice and rats, phenobarbital and ionol effects.	Phenobarbital	166-179	glutathione reductase	Mus musculus	80-101
2120856-7	1990	Phenobarbital, an inducer of the GT2 isoform of UDPGT, increased rat microsomal UDPGT activity towards the dithiol.	Phenobarbital	0-13	beta-1,3-glucuronyltransferase 2	Rattus norvegicus	48-53
2120856-7	1990	Phenobarbital, an inducer of the GT2 isoform of UDPGT, increased rat microsomal UDPGT activity towards the dithiol.	Phenobarbital	0-13	beta-1,3-glucuronyltransferase 2	Rattus norvegicus	80-85
2337348-0	1990	Selective detection of mRNA forms encoding the major phenobarbital inducible cytochromes P450 and other members of the P450IIB family by the RNAse A protection assay.	Phenobarbital	53-66	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	89-93
2337348-0	1990	Selective detection of mRNA forms encoding the major phenobarbital inducible cytochromes P450 and other members of the P450IIB family by the RNAse A protection assay.	Phenobarbital	53-66	ribonuclease A family member 1, pancreatic	Homo sapiens	141-148
2334442-0	1990	Effect of dietary fat on the induction of hepatic microsomal cytochrome P450 isozymes by phenobarbital.	Phenobarbital	89-102	hydroperoxide lyase 1	Zea mays	72-76
2334442-7	1990	Analysis of gels showed 32, 59 and 124% more P450 protein, respectively, in FF Pb, corn oil control or corn oil Pb groups than in FF controls.	Phenobarbital	79-81	hydroperoxide lyase 1	Zea mays	45-49
2191770-1	1990	The frequency and mutational profile of H-ras gene activation were determined in spontaneous liver tumors of male C57BL/6 x C3H/He mice and in tumors induced with the genotoxic hepatocarcinogen benzidine.2 HCl or the nongenotoxic hepatocarcinogens phenobarbital, chloroform, and ciprofibrate.	Phenobarbital	248-261	Harvey rat sarcoma virus oncogene	Mus musculus	40-45
2395824-0	1990	Effects induced by phenobarbital and phenytoin on the activity of pseudocholinesterase in serum and liver in the mouse.	Phenobarbital	19-32	butyrylcholinesterase	Mus musculus	66-86
1696756-0	1990	Lethal effects of CCl4 and its metabolism by Mongolian gerbils pretreated with chlordecone, phenobarbital, or mirex.	Phenobarbital	92-105	C-C motif chemokine ligand 4	Rattus norvegicus	18-22
1696756-13	1990	However, the enhanced metabolism of CCl4 found in CD-, PB-, or M-pretreated gerbils did not lead to amplified hepatotoxic and lethal effects of CCl4.	Phenobarbital	55-57	C-C motif chemokine ligand 4	Rattus norvegicus	36-40
1978428-1	1990	The phenobarbital and ionol administration to rats and mice increases considerably the glutathione transferase, glutathione reductase and gamma-glutamyl transferase activities in the liver.	Phenobarbital	4-17	glutathione S-transferase alpha 4	Rattus norvegicus	87-110
2168718-2	1990	In the present work we demonstrate that insulin decreases the phenobarbital-induced activities of delta-aminolevulinic acid synthase and ferrochelatase in isolated hepatocytes from normal and experimental-diabetic rats.	Phenobarbital	62-75	ferrochelatase	Rattus norvegicus	137-151
2359402-3	1990	We have previously shown that a P450 mRNA that is homologous to rat liver P450IIB1 (P450b) is expressed in rat small intestine and is inducible by phenobarbital, polyhalogenated biphenyls, and organochlorine pesticides.	Phenobarbital	147-160	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	84-89
2359402-6	1990	These studies demonstrated that the amplified segment of the phenobarbital-inducible P450 mRNA in intestine was identical to this same segment of the hepatic P450b mRNA; furthermore, this analysis showed that P450e was not expressed in intestine.	Phenobarbital	61-74	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	158-163
2359402-9	1990	An increment in intestinal P450b mRNA was detected as early as 1 hr following a single intraperitoneal injection of phenobarbital; this prompt rise in mRNA suggested that transcriptional activation may be the primary mechanism for induction.	Phenobarbital	116-129	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	27-32
2359402-12	1990	Therefore, the predominant mechanism for the induction of P450b mRNA in intestine in response to phenobarbital was an increase in gene transcription.	Phenobarbital	97-110	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	58-63
2112112-7	1990	Immunoblots showed the presence of cytochromes P-450 UT-A, UT-H, PB-B, ISF-G and PCN-E, the last three isoenzymes being inducible by, respectively, phenobarbital, 3-methylcholanthrene and dexamethasone.	Phenobarbital	148-161	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	47-57
2322313-1	1990	The activity of human cytochrome P450 monooxygenases, aryl hydrocarbon hydroxylase and 7-ethoxycoumarin O-deethylase can be increased by 3-methylcholanthrene, phenobarbital and ethanol in human hepatocytes maintained in primary culture.	Phenobarbital	159-172	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	54-82
2318828-1	1990	Dexamethasone has a potentiating effect on phenobarbitone mediated induction of cytochrome P-450b + e mRNAs in adult rat liver.	Phenobarbital	43-57	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	80-97
2318828-2	1990	However, the glucocorticoid inhibits phenobarbitone-activated transcription of cytochrome P-450b + e mRNAs by 60-70%.	Phenobarbital	37-51	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	79-96
2318828-6	1990	It is proposed that a negative element may mediate the action of dexamethasone at the level of nuclear transcription and stabilization of the nuclear transcript may account for the potentiating effect of the glucocorticoid on phenobarbitone-mediated increase in cytochrome P-450b + e mRNAs in the cytoplasm of the adult rat liver.	Phenobarbital	226-240	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	262-279
2318828-7	1990	However, the cytochrome P-450b protein levels are slightly lower in phenobarbitone + dexamethasone treatment than in phenobarbitone-treated liver microsomes.	Phenobarbital	68-82	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	13-30
2318828-7	1990	However, the cytochrome P-450b protein levels are slightly lower in phenobarbitone + dexamethasone treatment than in phenobarbitone-treated liver microsomes.	Phenobarbital	117-131	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	13-30
2321956-11	1990	P450 PB-4 (P450b) and P450 PB-5 (P450e) are strongly induced in rat liver by phenobarbital in coordinate fashion.	Phenobarbital	77-90	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	11-16
2362916-3	1990	The absolute configuration (C-5 position) of the major phenobarbital N-beta-D-glucoside excreted in the urine was the S form.	Phenobarbital	55-68	complement C5	Homo sapiens	28-31
1691731-6	1990	Northern blots hybridized with oligonucleotides specific for P-450b or P-450e showed that, as in liver, both P-450b and P-450e genes were induced in response to phenobarbital.	Phenobarbital	161-174	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	61-67
1691731-6	1990	Northern blots hybridized with oligonucleotides specific for P-450b or P-450e showed that, as in liver, both P-450b and P-450e genes were induced in response to phenobarbital.	Phenobarbital	161-174	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	109-115
1691731-7	1990	Quantitative slot-blot hybridizations performed at 15 days and 1, 6, and 15 mo after hepatocyte transplantation revealed that cytochrome P-450b and P-450e messenger RNAs were induced about 20- to 30-fold by a single dose of phenobarbital.	Phenobarbital	224-237	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	126-143
1691731-10	1990	Moreover, these studies suggest that neither the organization of liver into acini nor a specific zonal sinusoidal microenvironment is necessary for adult hepatocytes to respond to phenobarbital with induction of P-450b and P-450e genes.	Phenobarbital	180-193	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	212-218
2169533-11	1990	Western blot analysis with antibodies to P450 isozymes induced with either phenobarbital (Pb) or 3-methylcholanthrene (3-MC) confirmed that both IIB1 and IA2 were induced, but that IA1 was not induced.	Phenobarbital	75-88	protein tyrosine phosphatase, receptor type, N	Mus musculus	154-157
2169533-11	1990	Western blot analysis with antibodies to P450 isozymes induced with either phenobarbital (Pb) or 3-methylcholanthrene (3-MC) confirmed that both IIB1 and IA2 were induced, but that IA1 was not induced.	Phenobarbital	90-92	protein tyrosine phosphatase, receptor type, N	Mus musculus	154-157
2404574-9	1990	The induction of the lower-Mr isoform of the basolateral plasma membrane protein CE 9 was not observed following two-thirds hepatectomy or upon the feeding of the antioxidants or phenobarbital but was specific to the feeding of the peroxisome proliferators.	Phenobarbital	179-192	basigin (Ok blood group)	Rattus norvegicus	81-85
1971568-0	1990	Selective inactivation by chlorofluoroacetamides of the major phenobarbital-inducible form(s) of rat liver cytochrome P-450.	Phenobarbital	62-75	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	107-123
1971568-1	1990	Five N-monosubstituted chlorofluoroacetamides have been tested as potential specific irreversible inhibitors of the major phenobarbital-inducible form of rat liver cytochrome P-450 (P450IIB1).	Phenobarbital	122-135	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	164-180
2319474-5	1990	Inducers of cytochrome P-450 enhanced phenytoin covalent binding as follows: phenobarbital greater than 3-methylcholanthrene greater than saline-treated controls.	Phenobarbital	77-90	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	12-28
2106321-6	1990	This isozyme constitutes approximately 40% of the total cytochrome P-450 of the hepatic microsomes from 3-methylcholanthrene-treated Golden hamsters but only 1% in the microsomes of phenobarbital-treated hamsters.	Phenobarbital	182-195	cytochrome P450 2A3-like	Mesocricetus auratus	56-72
2345545-5	1990	Phenobarbital/hydrocortisone showed a consistent, but not always significant increase in the NADPH and NADH cyt c reduction and benzanthracene an increase in the NADH cyt c reducing activity and cyt b5 content.	Phenobarbital	0-13	cytochrome c, somatic	Homo sapiens	108-113
2345545-5	1990	Phenobarbital/hydrocortisone showed a consistent, but not always significant increase in the NADPH and NADH cyt c reduction and benzanthracene an increase in the NADH cyt c reducing activity and cyt b5 content.	Phenobarbital	0-13	cytochrome c, somatic	Homo sapiens	167-172
2345545-5	1990	Phenobarbital/hydrocortisone showed a consistent, but not always significant increase in the NADPH and NADH cyt c reduction and benzanthracene an increase in the NADH cyt c reducing activity and cyt b5 content.	Phenobarbital	0-13	cytochrome b5 type A	Rattus norvegicus	195-201
2315927-0	1990	Phenobarbital pretreatment alters the localization of CCl4-induced changes in rat liver microsomal fatty acids.	Phenobarbital	0-13	C-C motif chemokine ligand 4	Rattus norvegicus	54-58
2315927-1	1990	Phenobarbital treatment induces an isozyme(s) of liver microsomal cytochrome P450 susceptible to CCl4 and enhances the latter"s lethality.	Phenobarbital	0-13	C-C motif chemokine ligand 4	Rattus norvegicus	97-101
2315927-6	1990	Phenobarbital pretreatment accelerated the CCl4-induced formation of diene conjugates in the microsomal lipids.	Phenobarbital	0-13	C-C motif chemokine ligand 4	Rattus norvegicus	43-47
2315927-11	1990	These data demonstrate that phenobarbital pretreatment is associated with a shift in the predominant phospholipid locus from phosphatidylserine to phosphatidylethanolamine for the early CCl4-induced fatty acid changes in rat liver microsomes.	Phenobarbital	28-41	C-C motif chemokine ligand 4	Rattus norvegicus	186-190
2160252-4	1990	Such currents were reversibly suppressed by bicuculline (a GABAA antagonist) and enhanced by phenobarbitone.	Phenobarbital	93-107	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	59-64
2114621-0	1990	[Purification and characteristics of highly active NADPH-cytochrome P-450 reductase from liver microsomes of phenobarbital-induced rabbits].	Phenobarbital	109-122	NADPH--cytochrome P450 reductase	Oryctolagus cuniculus	51-83
2114621-1	1990	Liver microsomal NADPH-cytochrome P-450 reductase from phenobarbital-induced rabbits was purified by a simple and reproducible method employing combination of 2",5"-ADP-sepharose affinity chromatography and 1-amino-2-hydroxypropyl-sepharose (ADP-sepharose) ion exchange chromatography.	Phenobarbital	55-68	NADPH--cytochrome P450 reductase	Oryctolagus cuniculus	17-49
2323573-1	1990	Cytochrome P450e (P450IIB2) is a phenobarbital(PB)-inducible member of the rat liver P450IIB subfamily.	Phenobarbital	33-46	cytochrome P450, family 2, subfamily b, polypeptide 2	Rattus norvegicus	0-16
2306705-0	1990	Modulatory interaction between initial clofibrate treatment and subsequent administration of 2-acetylaminofluorene or sodium phenobarbital on glutathione S-transferase positive lesion development.	Phenobarbital	118-138	hematopoietic prostaglandin D synthase	Rattus norvegicus	142-167
2315263-0	1990	Inverse relationship between total glutathione S-transferase content and bile acid release in isolated hepatocytes from untreated, phenobarbital pretreated and hypothyroid rats.	Phenobarbital	131-144	hematopoietic prostaglandin D synthase	Rattus norvegicus	35-60
2315263-6	1990	The levels of total glutathione S-transferase content were significantly (P less than 0.001) increased in the hepatocytes from both hypothyroid and phenobarbital pretreated animals.	Phenobarbital	148-161	hematopoietic prostaglandin D synthase	Rattus norvegicus	20-45
2340279-0	1990	A phenobarbital-inducible hepatic mitochondrial cytochrome P-450 immunochemically related to microsomal P-450b.	Phenobarbital	2-15	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	48-64
2340279-0	1990	A phenobarbital-inducible hepatic mitochondrial cytochrome P-450 immunochemically related to microsomal P-450b.	Phenobarbital	2-15	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	104-110
2340279-1	1990	We have purified and characterized a phenobarbital (PB)-inducible hepatic mitochondrial cytochrome P-450 (P-450), termed P-450mt4, which is distinctly different from the previously characterized mitochondrial isoforms.	Phenobarbital	37-50	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	88-104
2340279-1	1990	We have purified and characterized a phenobarbital (PB)-inducible hepatic mitochondrial cytochrome P-450 (P-450), termed P-450mt4, which is distinctly different from the previously characterized mitochondrial isoforms.	Phenobarbital	52-54	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	88-104
2340279-3	1990	P-450mt4 shows a close resemblance to microsomal P-450b (the major PB-inducible form) with respect to electrophoretic migration (apparent molecular mass of 50 kDa) and immunological cross-reactivity, although it exhibits a distinct isoelectric pH (pI 6.9 vs 6.5 for P-450b), peptide fingerprint pattern, and amino acid composition.	Phenobarbital	67-69	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	49-55
2133064-1	1990	The homogeneity of different preparations of cytochrome P450(LM2), the major form of cytochrome P450 found in the liver microsomes of phenobarbital-treated rabbits, was checked by SDS polyacrylamide gel electrophoresis and N-terminal amino acid sequencing.	Phenobarbital	134-147	cytochrome P-450	Oryctolagus cuniculus	45-64
2105734-0	1990	Effect of phenobarbital induction, charcoal treatment and storage on the spectral binding characteristics and NADPH-cytochrome P-450 reductase activity of hepatic microsomes.	Phenobarbital	10-23	cytochrome p450 oxidoreductase	Homo sapiens	110-142
1688552-6	1990	Indeed, when cultures were treated with phenobarbital, there was a rise in mRNAs for the cytochromes P-450b/e and P-450p accompanied by a rise in mRNA for 5-aminolevulinate synthase, the rate-limiting enzyme in heme biosynthesis.	Phenobarbital	40-53	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	101-107
1688552-7	1990	Analysis of nuclei from the matrigel cultures established that phenobarbital treatment had activated transcription of the P-450b/e gene.	Phenobarbital	63-76	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	122-130
1688552-10	1990	The effect of GH was specific inasmuch as phenobarbital-inducible expression of P-450 reductase, glucocorticoid-inducible expression of tyrosine aminotransferase, and basal expression of albumin were unaffected by the presence or absence of growth hormone.	Phenobarbital	42-55	gonadotropin releasing hormone receptor	Rattus norvegicus	14-16
1688552-11	1990	Nuclear analysis revealed that growth hormone inhibited phenobarbital-induced P-450b/e gene transcription, whereas the hormone was without effect on transcription of the liver-specific gene, tyrosine aminotransferase.	Phenobarbital	56-69	gonadotropin releasing hormone receptor	Rattus norvegicus	31-45
1688552-11	1990	Nuclear analysis revealed that growth hormone inhibited phenobarbital-induced P-450b/e gene transcription, whereas the hormone was without effect on transcription of the liver-specific gene, tyrosine aminotransferase.	Phenobarbital	56-69	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	78-86
2241997-0	1990	Inhibition of arylhydrocarbon hydroxylase and cytochrome P-450 by 20-methylcholanthrene and phenobarbital in guinea pig on excessive doses of ascorbic acid.	Phenobarbital	92-105	cytochrome P450 3A14	Cavia porcellus	46-62
2171690-1	1990	Addition of phenobarbital, an inducer of the liver mixed function oxidase system, to sulphonylurea regimen improves insulin sensitivity and intracellular glucose handling in patients with non-insulin dependent diabetes mellitus.	Phenobarbital	12-25	insulin	Homo sapiens	116-123
2241997-1	1990	Treatment of guinea pigs on adequate ascorbic acid (AA) with 20-methylcholanthrene (MCA) and phenobarbital (PB) significantly increased hepatic arylhydrocarbon hydroxylase (AHH), cytochrome P-450 and cytochrome-b5 activities.	Phenobarbital	93-106	cytochrome P450 3A14	Cavia porcellus	179-195
2241997-1	1990	Treatment of guinea pigs on adequate ascorbic acid (AA) with 20-methylcholanthrene (MCA) and phenobarbital (PB) significantly increased hepatic arylhydrocarbon hydroxylase (AHH), cytochrome P-450 and cytochrome-b5 activities.	Phenobarbital	93-106	cytochrome b5	Cavia porcellus	200-213
2241997-1	1990	Treatment of guinea pigs on adequate ascorbic acid (AA) with 20-methylcholanthrene (MCA) and phenobarbital (PB) significantly increased hepatic arylhydrocarbon hydroxylase (AHH), cytochrome P-450 and cytochrome-b5 activities.	Phenobarbital	108-110	cytochrome P450 3A14	Cavia porcellus	179-195
2241997-1	1990	Treatment of guinea pigs on adequate ascorbic acid (AA) with 20-methylcholanthrene (MCA) and phenobarbital (PB) significantly increased hepatic arylhydrocarbon hydroxylase (AHH), cytochrome P-450 and cytochrome-b5 activities.	Phenobarbital	108-110	cytochrome b5	Cavia porcellus	200-213
2133064-1	1990	The homogeneity of different preparations of cytochrome P450(LM2), the major form of cytochrome P450 found in the liver microsomes of phenobarbital-treated rabbits, was checked by SDS polyacrylamide gel electrophoresis and N-terminal amino acid sequencing.	Phenobarbital	134-147	cytochrome P-450	Oryctolagus cuniculus	45-60
2400826-1	1990	The adaptive response of the liver to phenobarbital is characterized by a strong cell hypertrophy and coordinate induction of specific P450 forms (IIB1, 2; IIC7, IIIA1).	Phenobarbital	38-51	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	126-151
2295110-6	1990	Cytochrome P-450 content in control and BCNU-treated rats increased in a similar manner after phenobarbital or beta-naphthoflavone induction.	Phenobarbital	94-107	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	0-16
1973356-6	1990	The decrease of Cx32 in AHF was rapidly reversible after withdrawal of PB, and this change preceded a reduction in placental isozyme of glutathione-S-transferase (GST) expression in the same AHF.	Phenobarbital	71-73	gap junction protein, beta 1	Rattus norvegicus	16-20
1973356-8	1990	Chronic PB treatment also resulted in a reversible decrease in Cx32 specifically in mid- and centro-lobular hepatocytes.	Phenobarbital	8-10	gap junction protein, beta 1	Rattus norvegicus	63-67
2097280-6	1990	In all studied animals (with 28 months old rats) phenobarbital inhibited AHH activity.	Phenobarbital	49-62	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	73-76
1980873-0	1990	Purification and characterization of cytochrome P-450 isozymes from phenobarbital-induced adult hen liver.	Phenobarbital	68-81	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	37-53
1980873-2	1990	Two cytochrome P-450 isozymes (P-450 PB-A, PB-B) and cytochrome b5 were purified from livers of phenobarbital-treated adult hens.	Phenobarbital	96-109	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	4-20
1980873-2	1990	Two cytochrome P-450 isozymes (P-450 PB-A, PB-B) and cytochrome b5 were purified from livers of phenobarbital-treated adult hens.	Phenobarbital	96-109	cytochrome b5 type A	Gallus gallus	53-66
2369784-3	1990	Animals were either untreated or treated with the cytochrome P-450 inducers phenobarbitone, beta-napthoflavone or clofibrate.	Phenobarbital	76-90	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	50-66
2369784-8	1990	This data indicated that different amounts or forms of cytochrome P-450s were responsible for warfarin metabolism after phenobarbitone treatment in the two strains.	Phenobarbital	120-134	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	55-71
2373138-3	1990	Phenobarbital enhanced antipyrine elimination and increased the apolipoprotein A-I/A-II ratio.	Phenobarbital	0-13	apolipoprotein A1	Homo sapiens	64-82
2373138-3	1990	Phenobarbital enhanced antipyrine elimination and increased the apolipoprotein A-I/A-II ratio.	Phenobarbital	0-13	NLR family pyrin domain containing 3	Homo sapiens	83-87
2125940-16	1990	When sheep lung cytochrome P-450LgM2 and P-450LM2 purified from liver of phenobarbital (PB)-induced rabbit were subjected to Western Blotting and visualized immunochemically with anti-P-450LM2, they showed identical mobilities.	Phenobarbital	73-86	cytochrome P450 2B4	Oryctolagus cuniculus	41-49
2125940-16	1990	When sheep lung cytochrome P-450LgM2 and P-450LM2 purified from liver of phenobarbital (PB)-induced rabbit were subjected to Western Blotting and visualized immunochemically with anti-P-450LM2, they showed identical mobilities.	Phenobarbital	73-86	cytochrome P450 2B4	Oryctolagus cuniculus	184-192
1704318-0	1990	Phenobarbital-induced cytoprotective mechanisms in menadione metabolism: the role of glutathione reductase and DT-diaphorase.	Phenobarbital	0-13	glutathione-disulfide reductase	Rattus norvegicus	85-106
2125940-16	1990	When sheep lung cytochrome P-450LgM2 and P-450LM2 purified from liver of phenobarbital (PB)-induced rabbit were subjected to Western Blotting and visualized immunochemically with anti-P-450LM2, they showed identical mobilities.	Phenobarbital	88-90	cytochrome P450 2B4	Oryctolagus cuniculus	184-192
1704318-0	1990	Phenobarbital-induced cytoprotective mechanisms in menadione metabolism: the role of glutathione reductase and DT-diaphorase.	Phenobarbital	0-13	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	111-124
2121958-2	1990	Pretreatment of rats by phenobarbital or polychlorobiphenyl induced markedly the nuclei-dependent binding of AFB1 to DNA as well as the drug-metabolizing enzymes, such as aminopyrine-N-demethylase and epoxide hydratase.	Phenobarbital	24-37	epoxide hydrolase 2	Rattus norvegicus	201-218
1704318-8	1990	A greater proportion of menadione was metabolized by DT-diaphorase in the hepatocytes isolated from PB-pretreated rats.	Phenobarbital	100-102	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	53-66
2167416-3	1990	The addition of phenobarbital or 3-methylcholanthrene, which induce cytochrome P450, significantly enhanced the formation of Epo.	Phenobarbital	16-29	erythropoietin	Homo sapiens	125-128
2299585-9	1990	The most likely mechanisms for the effects observed are 1) inhibition of acetaminophen reactive metabolite formation in 3-methylcholanthrene-induced animals by each of the methylxanthines, and 2) activation of the phenobarbital-inducible forms of cytochrome(s) P-450 toward formation of acetaminophen reactive metabolites by caffeine and theophylline, but not theobromine.	Phenobarbital	214-227	VPS52 subunit of GARP complex	Rattus norvegicus	52-57
2122480-0	1990	Studies on the mechanism of monoclonal antibody inhibition of enzyme activity of phenobarbital-induced cytochrome P-450.	Phenobarbital	81-94	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	114-119
2122480-1	1990	Four monoclonal antibodies (MAbs) to phenobarbital-induced cytochrome P-450 (PB-P-450) show different patterns of inhibition of PB-P-450 catalyzed aryl hydrocarbon hydroxylase (AHH), 7-ethoxycoumarin deethylase, benzphetamine demethylase and ethylmorphine demethylase.	Phenobarbital	37-50	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	70-75
2122480-1	1990	Four monoclonal antibodies (MAbs) to phenobarbital-induced cytochrome P-450 (PB-P-450) show different patterns of inhibition of PB-P-450 catalyzed aryl hydrocarbon hydroxylase (AHH), 7-ethoxycoumarin deethylase, benzphetamine demethylase and ethylmorphine demethylase.	Phenobarbital	37-50	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	77-85
2122480-1	1990	Four monoclonal antibodies (MAbs) to phenobarbital-induced cytochrome P-450 (PB-P-450) show different patterns of inhibition of PB-P-450 catalyzed aryl hydrocarbon hydroxylase (AHH), 7-ethoxycoumarin deethylase, benzphetamine demethylase and ethylmorphine demethylase.	Phenobarbital	37-50	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	128-136
2122480-1	1990	Four monoclonal antibodies (MAbs) to phenobarbital-induced cytochrome P-450 (PB-P-450) show different patterns of inhibition of PB-P-450 catalyzed aryl hydrocarbon hydroxylase (AHH), 7-ethoxycoumarin deethylase, benzphetamine demethylase and ethylmorphine demethylase.	Phenobarbital	37-50	aryl hydrocarbon receptor repressor	Homo sapiens	177-180
1975953-4	1990	PB, in contrast, increased GGT activity in periportal hepatocytes.	Phenobarbital	0-2	gamma-glutamyltransferase 1	Rattus norvegicus	27-30
6860371-1	1983	In light of recent suggestions that hepatic microsomal aldrin expoxidation activity selectively reflects the phenobarbital (PB)-inducible form(s) of cytochrome P-450 (P-450PB), we tested the effect of pregnenolone-16 alpha-carbonitrile (PCN), a synthetic steroid that induces P-450PCN, a form of the cytochrome biochemically and immunochemically distinguishable from P-450PB.	Phenobarbital	109-122	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	149-165
20702214-3	1990	Phenobarbital and rifampicin were found to increase the levels of P-450 IIC8, 9, 10 mRNA and protein while troleandomycin and 3-methylcholanthrene were ineffective.	Phenobarbital	0-13	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	66-79
20702222-7	1990	The use of S-9 fractions from animals pretreated with phenobarbitone and beta-naphthoflavone resulted in greatly increased phorone toxicity, which indicates the involvement of cytochrome P-450 enzymes in its metabolism.	Phenobarbital	54-68	proteasome (prosome, macropain) 26S subunit, non-ATPase, 11	Mus musculus	11-14
20702222-7	1990	The use of S-9 fractions from animals pretreated with phenobarbitone and beta-naphthoflavone resulted in greatly increased phorone toxicity, which indicates the involvement of cytochrome P-450 enzymes in its metabolism.	Phenobarbital	54-68	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	176-192
1700861-3	1990	Altered liver phenotype was characterized by: (1) gamma-glutamyl-transpeptidase (GGT) and glutathione S-transferase (GST) activities; (2) the expression of two forms of cytochrome P-450; de novo PB-inducible P-450 II B 1,2 and P-450 II C 7 normally expressed in 45-day-old rats and PB-inducible, and (3) the expression of albumin and alpha-fetoprotein cDNAs.	Phenobarbital	195-197	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	169-185
1700861-3	1990	Altered liver phenotype was characterized by: (1) gamma-glutamyl-transpeptidase (GGT) and glutathione S-transferase (GST) activities; (2) the expression of two forms of cytochrome P-450; de novo PB-inducible P-450 II B 1,2 and P-450 II C 7 normally expressed in 45-day-old rats and PB-inducible, and (3) the expression of albumin and alpha-fetoprotein cDNAs.	Phenobarbital	282-284	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	169-185
6860371-1	1983	In light of recent suggestions that hepatic microsomal aldrin expoxidation activity selectively reflects the phenobarbital (PB)-inducible form(s) of cytochrome P-450 (P-450PB), we tested the effect of pregnenolone-16 alpha-carbonitrile (PCN), a synthetic steroid that induces P-450PCN, a form of the cytochrome biochemically and immunochemically distinguishable from P-450PB.	Phenobarbital	124-126	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	149-165
6860371-3	1983	Moreover, the aldrin epoxidation activity in microsomes prepared from PCN- or PB-pretreated rats was selectively inhibited by form-specific antibodies directed against P-450PCN or P-450PB, respectively, whereas anti-P-450MC antibodies gave no inhibition with microsomes prepared from induced or control animals.	Phenobarbital	78-80	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	216-223
33770100-2	2021	The death receptor ligand TRAIL can in combination with Smac mimetics induce apoptosis in some luminal-like ER-positive breast cancer cell lines, such as CAMA-1, but not in MCF-7 cells.	Phenobarbital	95-102	TNF superfamily member 10	Homo sapiens	26-31
33590845-8	2021	We showed that subfertility caused by loss of uterine Cripto is due to defects in uterine decidualization, remodeling and luminal closure and is accompanied by significant down-regulation of Bmp2, Wnt4 and several components of Notch signaling pathway which all are known to be important factors in uterine remodeling and decidualization.	Phenobarbital	122-129	teratocarcinoma-derived growth factor 1	Mus musculus	54-60
33811688-3	2021	The TRAP complex topologically has a small exposure on the cytosolic side of the ER via its TRAPgamma/SSR3 subunit, whereas TRAPbeta/SSR2 and TRAPdelta/SSR4 function along with TRAPalpha/SSR1 largely on the luminal side of the ER membrane.	Phenobarbital	207-214	signal sequence receptor subunit 1	Homo sapiens	124-132
33811688-3	2021	The TRAP complex topologically has a small exposure on the cytosolic side of the ER via its TRAPgamma/SSR3 subunit, whereas TRAPbeta/SSR2 and TRAPdelta/SSR4 function along with TRAPalpha/SSR1 largely on the luminal side of the ER membrane.	Phenobarbital	207-214	signal sequence receptor subunit 2	Homo sapiens	133-137
33811688-3	2021	The TRAP complex topologically has a small exposure on the cytosolic side of the ER via its TRAPgamma/SSR3 subunit, whereas TRAPbeta/SSR2 and TRAPdelta/SSR4 function along with TRAPalpha/SSR1 largely on the luminal side of the ER membrane.	Phenobarbital	207-214	signal sequence receptor subunit 4	Homo sapiens	142-151
33773601-12	2021	RESULTS: MAML1 was localized in the luminal epithelium, glandular epithelium and stroma of human endometrium and the increased expression identified in the mid-secretory phase was restricted only to the luminal epithelium (P < 0.05).	Phenobarbital	36-43	mastermind like transcriptional coactivator 1	Homo sapiens	9-14
33773601-12	2021	RESULTS: MAML1 was localized in the luminal epithelium, glandular epithelium and stroma of human endometrium and the increased expression identified in the mid-secretory phase was restricted only to the luminal epithelium (P < 0.05).	Phenobarbital	203-210	mastermind like transcriptional coactivator 1	Homo sapiens	9-14
33942062-0	2022	The intestinal luminal sources of alpha-synuclein: a gastroenterologist perspective.	Phenobarbital	15-22	synuclein alpha	Homo sapiens	34-49
33942735-6	2021	RESULTS: PRL was expressed diffusely and with a mild intensity in the cytoplasm of normal and tumor prostate luminal cells.	Phenobarbital	109-116	prolactin	Homo sapiens	9-12
33822049-2	2021	SUMMARY ANSWER: Podocalyxin (PCX), a transmembrane protein, was identified as a key negative regulator of endometrial epithelial receptivity; specific downregulation of PCX in the luminal epithelium in the mid-secretory phase, likely mediated by progesterone, may act as a critical step in converting endometrial surface from a non-receptive to an implantation-permitting state.	Phenobarbital	180-187	podocalyxin like	Homo sapiens	16-27
33822049-2	2021	SUMMARY ANSWER: Podocalyxin (PCX), a transmembrane protein, was identified as a key negative regulator of endometrial epithelial receptivity; specific downregulation of PCX in the luminal epithelium in the mid-secretory phase, likely mediated by progesterone, may act as a critical step in converting endometrial surface from a non-receptive to an implantation-permitting state.	Phenobarbital	180-187	podocalyxin like	Homo sapiens	29-32
33822049-2	2021	SUMMARY ANSWER: Podocalyxin (PCX), a transmembrane protein, was identified as a key negative regulator of endometrial epithelial receptivity; specific downregulation of PCX in the luminal epithelium in the mid-secretory phase, likely mediated by progesterone, may act as a critical step in converting endometrial surface from a non-receptive to an implantation-permitting state.	Phenobarbital	180-187	podocalyxin like	Homo sapiens	169-172
33822049-13	2021	MAIN RESULTS AND THE ROLE OF CHANCE: PCX was expressed on the apical surface of all epithelial and endothelial cells in the non-receptive endometrium, but selectively downregulated in the luminal epithelium from the mid-secretory phase coinciding with the establishment of receptivity.	Phenobarbital	188-195	podocalyxin like	Homo sapiens	37-40
33822049-14	2021	Progesterone was confirmed to be able to suppress PCX in primary HEECs, suggesting this hormone likely mediates the downregulation of luminal PCX in vivo for receptivity.	Phenobarbital	134-141	podocalyxin like	Homo sapiens	50-53
33822049-14	2021	Progesterone was confirmed to be able to suppress PCX in primary HEECs, suggesting this hormone likely mediates the downregulation of luminal PCX in vivo for receptivity.	Phenobarbital	134-141	podocalyxin like	Homo sapiens	142-145
33821427-3	2021	The percentage of p16-positive cells was determined in luminal, glandular and stromal endometrial cells.	Phenobarbital	55-62	cyclin dependent kinase inhibitor 2A	Homo sapiens	18-21
33821427-8	2021	The cut-off values with p16-positive luminal cells lower than 12.5% and p16-positive glandular cells lower than 3.2% could be predictive factors for miscarriage (AUC 0.80 and 0.79; sensitivity 71.3% and 74.5%; specificity 74.2% and 71.2%, respectively).	Phenobarbital	37-44	cyclin dependent kinase inhibitor 2A	Homo sapiens	24-27
33821427-11	2021	The percentage of p16-positive luminal epithelial cells may be clinically useful as a biomarker of miscarriage.	Phenobarbital	31-38	cyclin dependent kinase inhibitor 2A	Homo sapiens	18-21
33818537-2	2021	The finding of a potential correlation between high L1CAM expression and recurrent/metastatic disease in luminal A and B breast carcinomas may be helpful for risk stratification and open opportunities for targeted therapies.	Phenobarbital	105-112	L1 cell adhesion molecule	Homo sapiens	52-57
33770100-2	2021	The death receptor ligand TRAIL can in combination with Smac mimetics induce apoptosis in some luminal-like ER-positive breast cancer cell lines, such as CAMA-1, but not in MCF-7 cells.	Phenobarbital	95-102	diablo IAP-binding mitochondrial protein	Homo sapiens	56-60
33768386-8	2021	IQ9 upregulated protein expression of thioredoxin reductase in luminal but not in triple-negative breast cancer cells which may explain the observed differential radiosensitisation.	Phenobarbital	63-70	peroxiredoxin 5	Homo sapiens	38-59
33816261-9	2021	Further subgroup analyses showed the Luminal subtype (HR+/HER2-), triple-negative breast cancer (TNBC), and bone-only metastasis patients presented with the most promising survival in the radiotherapy group.	Phenobarbital	37-44	erb-b2 receptor tyrosine kinase 2	Homo sapiens	58-62
33763657-6	2021	Overexpression of luminal progenitor cluster-derived signatures in HER2+, but not in other subtypes, is associated with unfavorable outcome.	Phenobarbital	18-25	erb-b2 receptor tyrosine kinase 2	Homo sapiens	67-71
7988581-3	1994	Pentobarbitone, phenobarbitone and thiopentone dose-dependently decreased FMLP-induced chemiluminescence and cell-free chemiluminescence.	Phenobarbital	16-30	formyl peptide receptor 1	Homo sapiens	74-78
18803253-0	2009	Docosahexaenoic acid downregulates phenobarbital-induced cytochrome P450 2B1 gene expression in rat primary hepatocytes via the c-Jun NH2-terminal kinase mitogen-activated protein kinase pathway.	Phenobarbital	35-48	cytochrome P450 2B1	Rattus norvegicus	57-76
18803253-0	2009	Docosahexaenoic acid downregulates phenobarbital-induced cytochrome P450 2B1 gene expression in rat primary hepatocytes via the c-Jun NH2-terminal kinase mitogen-activated protein kinase pathway.	Phenobarbital	35-48	mitogen-activated protein kinase 8	Rattus norvegicus	128-153
18803253-3	2009	Cytochrome P450 2B1 (CYP 2B1) is a DME that is dramatically induced by phenobarbital-type inducers.	Phenobarbital	71-84	cytochrome P450 2B1	Rattus norvegicus	0-19
18803253-3	2009	Cytochrome P450 2B1 (CYP 2B1) is a DME that is dramatically induced by phenobarbital-type inducers.	Phenobarbital	71-84	cytochrome P450 2B1	Rattus norvegicus	21-28
18803253-5	2009	In the present study, we determined the effect of DHA on MAPK transactivation and its role in CYP 2B1 expression induced by phenobarbital.	Phenobarbital	124-137	mitogen activated protein kinase 3	Rattus norvegicus	57-61
18803253-5	2009	In the present study, we determined the effect of DHA on MAPK transactivation and its role in CYP 2B1 expression induced by phenobarbital.	Phenobarbital	124-137	cytochrome P450 2B1	Rattus norvegicus	94-101
18803253-6	2009	c-Jun NH2-terminal kinase (JNK) JNK1/2 and ERK1/2 were activated by phenobarbital in a dose-dependent manner.	Phenobarbital	68-81	mitogen-activated protein kinase 8	Rattus norvegicus	0-25
18803253-6	2009	c-Jun NH2-terminal kinase (JNK) JNK1/2 and ERK1/2 were activated by phenobarbital in a dose-dependent manner.	Phenobarbital	68-81	mitogen-activated protein kinase 8	Rattus norvegicus	27-30
18803253-6	2009	c-Jun NH2-terminal kinase (JNK) JNK1/2 and ERK1/2 were activated by phenobarbital in a dose-dependent manner.	Phenobarbital	68-81	mitogen activated protein kinase 3	Rattus norvegicus	43-49
18803253-7	2009	DHA (100 muM) inhibited JNK1/2 and ERK2 activation induced by phenobarbital in a time-dependent manner.	Phenobarbital	62-75	mitogen activated protein kinase 1	Rattus norvegicus	35-39
33777113-2	2021	A tri-allelic polymorphism in the NQO2 gene might be associated with the risk of luminal-like breast cancer.	Phenobarbital	81-88	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	34-38
33777113-10	2021	Conclusion: The tri-allelic polymorphism in the NQO2 gene is associated with breast cancer risk, especially for the luminal-like subtype.	Phenobarbital	116-123	N-ribosyldihydronicotinamide:quinone reductase 2	Homo sapiens	48-52
33235218-7	2020	Several pivotal lncRNAs showed a distinct molecular subtype attribution: e.g. MALAT1 showed a downregulation in the basal subtype (p = 0.009), TUG1 and CBR3AS1 showed an upregulation in the luminal subtype (p <= 0.001).	Phenobarbital	190-197	CBR3 antisense RNA 1	Homo sapiens	152-159
18803253-8	2009	Both SP600125 (a JNK inhibitor) and SB203580 (a p38 MAPK inhibitor) inhibited CYP 2B1 protein and mRNA expression induced by phenobarbital.	Phenobarbital	125-138	mitogen-activated protein kinase 8	Rattus norvegicus	17-20
18803253-8	2009	Both SP600125 (a JNK inhibitor) and SB203580 (a p38 MAPK inhibitor) inhibited CYP 2B1 protein and mRNA expression induced by phenobarbital.	Phenobarbital	125-138	cytochrome P450 2B1	Rattus norvegicus	78-85
18803253-10	2009	Our results suggest that inhibition of JNK activation by DHA is at least part of the mechanisms of DHA"s downregulation of CYP 2B1 expression induced by phenobarbital.	Phenobarbital	153-166	mitogen-activated protein kinase 8	Rattus norvegicus	39-42
18803253-10	2009	Our results suggest that inhibition of JNK activation by DHA is at least part of the mechanisms of DHA"s downregulation of CYP 2B1 expression induced by phenobarbital.	Phenobarbital	153-166	cytochrome P450 2B1	Rattus norvegicus	123-130
1289339-0	1992	Phenobarbital-responsive episodic dyscontrol (rage) in dogs.	Phenobarbital	0-13	MOK protein kinase	Canis lupus familiaris	25-51
1289339-1	1992	Episodic dyscontrol (rage) was diagnosed from the clinical history, electroencephalographic findings, and response to oral treatment with phenobarbital in 3 dogs.	Phenobarbital	138-151	MOK protein kinase	Canis lupus familiaris	0-20
1289339-1	1992	Episodic dyscontrol (rage) was diagnosed from the clinical history, electroencephalographic findings, and response to oral treatment with phenobarbital in 3 dogs.	Phenobarbital	138-151	MOK protein kinase	Canis lupus familiaris	21-25
34688712-10	2022	EEC activation by optogenetics and forces led to Piezo2-dependent alterations in colonic propagating contractions driven by intrinsic circuitry, with Piezo2+ EECs detecting small luminal forces and luminal contents" physical properties to regulate transit times in the small and large bowel.	Phenobarbital	179-186	piezo-type mechanosensitive ion channel component 2	Mus musculus	49-55
34920330-5	2022	Existing single-cell RNA sequencing data were used to evaluate the expression of the six COX/PG genes in luminal and basal epithelial cells from normal breast tissues.	Phenobarbital	105-112	cytochrome c oxidase subunit 8A	Homo sapiens	89-95
34920330-10	2022	PTGES3 is the most highly expressed enzymes within the COX/PG pathway in both luminal and basal epithelial cells in normal breast tissues.	Phenobarbital	78-85	prostaglandin E synthase 3	Homo sapiens	0-6
34920330-10	2022	PTGES3 is the most highly expressed enzymes within the COX/PG pathway in both luminal and basal epithelial cells in normal breast tissues.	Phenobarbital	78-85	cytochrome c oxidase subunit 8A	Homo sapiens	55-61
34856346-18	2022	Tyramide-amplified AQP3 antibody staining was observed in the basal membrane of the invaginated epithelial cell layer of secondary intestinal folds in luminal surface of either the side wall of the spiral valve intestine or in internal valve tissue "flaps".	Phenobarbital	151-158	aquaporin 3 (Gill blood group) S homeolog	Xenopus laevis	19-23
34688712-10	2022	EEC activation by optogenetics and forces led to Piezo2-dependent alterations in colonic propagating contractions driven by intrinsic circuitry, with Piezo2+ EECs detecting small luminal forces and luminal contents" physical properties to regulate transit times in the small and large bowel.	Phenobarbital	179-186	piezo-type mechanosensitive ion channel component 2	Mus musculus	150-156
34688712-11	2022	CONCLUSION: The GI tract has intrinsic tactile sensitivity that depends on Piezo2+ EECs and allows it to detect luminal forces and physical properties of luminal contents to modulate physiology.	Phenobarbital	112-119	piezo-type mechanosensitive ion channel component 2	Mus musculus	75-81
34688712-11	2022	CONCLUSION: The GI tract has intrinsic tactile sensitivity that depends on Piezo2+ EECs and allows it to detect luminal forces and physical properties of luminal contents to modulate physiology.	Phenobarbital	154-161	piezo-type mechanosensitive ion channel component 2	Mus musculus	75-81
34730282-2	2022	The study aimed to predict the potential dose regimens of quinine when coadministered with phenobarbital in adult patients with cerebral malaria and complications (e.g., lactic acidosis and acute renal failure) and concurrent with seizures and acute renal failure who carry wild-type and polymorphic CYP2C19.	Phenobarbital	91-104	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	300-307
34845001-3	2022	In contrast, luminal A tumors express ERalpha and can undergo endocrine therapy for treatment.	Phenobarbital	13-20	estrogen receptor 1	Homo sapiens	38-45
34845001-7	2022	Inhibition of BCL11A and HDAC1/2 effectively drove basal-like cells to transition to luminal A cells and increased ERalpha expression, leading to increased tamoxifen sensitivity.	Phenobarbital	85-92	BAF chromatin remodeling complex subunit BCL11A	Homo sapiens	14-20
34845001-7	2022	Inhibition of BCL11A and HDAC1/2 effectively drove basal-like cells to transition to luminal A cells and increased ERalpha expression, leading to increased tamoxifen sensitivity.	Phenobarbital	85-92	histone deacetylase 1	Homo sapiens	25-32
34845001-10	2022	SIGNIFICANCE: A network model enables investigation of mechanisms regulating the basal-to-luminal transition in breast cancer, identifying BCL11A and HDAC1/2 as optimal targets that can induce basal-like breast cancer reprogramming and endocrine therapy sensitivity.	Phenobarbital	90-97	BAF chromatin remodeling complex subunit BCL11A	Homo sapiens	139-145
34845001-10	2022	SIGNIFICANCE: A network model enables investigation of mechanisms regulating the basal-to-luminal transition in breast cancer, identifying BCL11A and HDAC1/2 as optimal targets that can induce basal-like breast cancer reprogramming and endocrine therapy sensitivity.	Phenobarbital	90-97	histone deacetylase 1	Homo sapiens	150-157
34710432-2	2022	Consequently, LPL is regulated by several proteins during synthesis, folding, secretion, and transport to its site of action at the luminal side of capillaries, as well as during the catalytic reaction.	Phenobarbital	132-139	lipoprotein lipase	Homo sapiens	14-17
34839023-7	2022	A microbiota-based vaccination promoted an immunoglobulin-G (IgG) response directed against bacterial extract antigens, where subcutaneous injection of mice with the luminal contents of the lower SI elicited a bacterial extract-specific IgG response that is compartmentalized to the lower SI of vaccinated mice.	Phenobarbital	166-173	immunoglobulin heavy variable V1-62	Mus musculus	43-59
34839023-7	2022	A microbiota-based vaccination promoted an immunoglobulin-G (IgG) response directed against bacterial extract antigens, where subcutaneous injection of mice with the luminal contents of the lower SI elicited a bacterial extract-specific IgG response that is compartmentalized to the lower SI of vaccinated mice.	Phenobarbital	166-173	immunoglobulin heavy variable V1-62	Mus musculus	237-240
34934057-3	2021	H19 regulates PCa lineage plasticity by driving a bidirectional cell identity of NE phenotype (H19 overexpression) or luminal phenotype (H19 knockdown).	Phenobarbital	118-125	H19 imprinted maternally expressed transcript	Homo sapiens	0-3
34782719-2	2022	Here, we report that mammary epithelial-specific disruption of beta1 integrin in a murine model of Luminal B human breast cancer drastically impairs tumour growth with proliferation block, apoptosis induction and cellular senescence.	Phenobarbital	99-106	integrin subunit beta 1	Homo sapiens	63-77
34875536-9	2022	Experiments in the presence of galectins revealed that abundant N-glycans bound to the peptide core of the luminal side of the cell surface membrane LAMP-2 mediated cell adhesion of choriocarcinoma cells by interacting with galectins in the extracellular matrix (ECM).	Phenobarbital	107-114	lysosomal associated membrane protein 2	Homo sapiens	149-155
34973338-5	2022	Interestingly, we found that TRIB2 downregulates the luminal markers AR (androgen receptor) and CK8 (cytokeratin 8) in prostate cancer cells but upregulates the neuronal transcription factor BRN2 (Brain-2) and the stemness factor SOX2 (SRY-box 2) to induce neuroendocrine characteristics.	Phenobarbital	53-60	tribbles pseudokinase 2	Homo sapiens	29-34
34973338-5	2022	Interestingly, we found that TRIB2 downregulates the luminal markers AR (androgen receptor) and CK8 (cytokeratin 8) in prostate cancer cells but upregulates the neuronal transcription factor BRN2 (Brain-2) and the stemness factor SOX2 (SRY-box 2) to induce neuroendocrine characteristics.	Phenobarbital	53-60	androgen receptor	Homo sapiens	69-71
34973338-5	2022	Interestingly, we found that TRIB2 downregulates the luminal markers AR (androgen receptor) and CK8 (cytokeratin 8) in prostate cancer cells but upregulates the neuronal transcription factor BRN2 (Brain-2) and the stemness factor SOX2 (SRY-box 2) to induce neuroendocrine characteristics.	Phenobarbital	53-60	androgen receptor	Homo sapiens	73-90
34939230-1	2022	The FoxQ1 is an oncogenic transcription factor that is overexpressed in basal-like and luminal-type human breast cancers when compared to the normal mammary tissue.	Phenobarbital	87-94	forkhead box Q1	Homo sapiens	4-9
34939230-6	2022	Consistent with these results, the basal and ATP-linked oxygen consumption rates were significantly increased by FoxQ1 overexpression in SUM159 and luminal-type MCF-7 cells.	Phenobarbital	148-155	forkhead box Q1	Homo sapiens	113-118
34936871-3	2021	Using single-cell RNA-sequencing to perform an unbiased assessment of the cellular landscape of human prostate, we identify a subset of tumor-enriched androgen receptor-negative luminal epithelial cells with increased expression of cancer-associated genes.	Phenobarbital	178-185	androgen receptor	Homo sapiens	151-168
34953615-2	2022	showed that the mechanoreceptor Piezo2 enables enteroendocrine cells in the intestinal epithelium to sense luminal contents.	Phenobarbital	107-114	piezo type mechanosensitive ion channel component 2	Homo sapiens	32-38
34952235-0	2021	Interruption of Klf5 acetylation in basal progenitor cells promotes luminal commitment by activating Notch signaling.	Phenobarbital	68-75	Kruppel like factor 5	Homo sapiens	16-20
34932179-5	2021	Here we show that Nfatc1 is expressed in a small subset of mammary basal epithelial cells and its epithelial-specific deletion results in mild defects in side branching and basal-luminal cell balance.	Phenobarbital	179-186	nuclear factor of activated T cells 1	Homo sapiens	18-24
34934057-3	2021	H19 regulates PCa lineage plasticity by driving a bidirectional cell identity of NE phenotype (H19 overexpression) or luminal phenotype (H19 knockdown).	Phenobarbital	118-125	H19 imprinted maternally expressed transcript	Homo sapiens	137-140
34943250-6	2021	The pharmacological inhibition of CaMKII with the compound KN93 increases the active form of the NCC (phospho-NCC) at the luminal membrane and also increases NCC activity in mDCT15 cells.	Phenobarbital	122-129	calcium/calmodulin dependent protein kinase II gamma	Homo sapiens	34-40
34608481-2	2021	Following elongation, pig conceptuses secrete interferon gamma (IFNG) during attachment to the endometrial luminal epithelium.	Phenobarbital	107-114	interferon gamma	Sus scrofa	46-62
34608481-2	2021	Following elongation, pig conceptuses secrete interferon gamma (IFNG) during attachment to the endometrial luminal epithelium.	Phenobarbital	107-114	interferon gamma	Sus scrofa	64-68
34927257-9	2022	Moreover, mdm2 can potentially be utilized as a therapeutic target in the Luminal subtype.	Phenobarbital	74-81	MDM2 proto-oncogene	Homo sapiens	10-14
34911496-3	2021	Cancer de-differentiation transforms luminal-like (differentiated) adenocarcinoma into less luminal-like and more stem-like (undifferentiated) small cell carcinoma through a sequential activation of stem cell transcription factors (scTF) POU5F1, LIN28A, SOX2 and NANOG.	Phenobarbital	37-44	POU class 5 homeobox 1	Homo sapiens	238-244
34911496-3	2021	Cancer de-differentiation transforms luminal-like (differentiated) adenocarcinoma into less luminal-like and more stem-like (undifferentiated) small cell carcinoma through a sequential activation of stem cell transcription factors (scTF) POU5F1, LIN28A, SOX2 and NANOG.	Phenobarbital	37-44	lin-28 homolog A	Homo sapiens	246-252
34911496-3	2021	Cancer de-differentiation transforms luminal-like (differentiated) adenocarcinoma into less luminal-like and more stem-like (undifferentiated) small cell carcinoma through a sequential activation of stem cell transcription factors (scTF) POU5F1, LIN28A, SOX2 and NANOG.	Phenobarbital	37-44	SRY-box transcription factor 2	Homo sapiens	254-258
34911496-3	2021	Cancer de-differentiation transforms luminal-like (differentiated) adenocarcinoma into less luminal-like and more stem-like (undifferentiated) small cell carcinoma through a sequential activation of stem cell transcription factors (scTF) POU5F1, LIN28A, SOX2 and NANOG.	Phenobarbital	37-44	Nanog homeobox	Homo sapiens	263-268
34911733-3	2022	We found that HER2 TKIs evoke DTPs with a luminal-like or a mesenchymal-like transcriptome.	Phenobarbital	42-49	erb-b2 receptor tyrosine kinase 2	Homo sapiens	14-18
34911733-7	2022	Finally, biochemical experiments indicate that luminal-like DTPs survive via estrogen receptor-dependent induction of SGK3, leading to rewiring of the PI3K/AKT/mTORC1 pathway to enable AKT-independent mTORC1 activation.	Phenobarbital	47-54	estrogen receptor 1	Homo sapiens	77-94
34911733-7	2022	Finally, biochemical experiments indicate that luminal-like DTPs survive via estrogen receptor-dependent induction of SGK3, leading to rewiring of the PI3K/AKT/mTORC1 pathway to enable AKT-independent mTORC1 activation.	Phenobarbital	47-54	serum/glucocorticoid regulated kinase family member 3	Homo sapiens	118-122
34911733-7	2022	Finally, biochemical experiments indicate that luminal-like DTPs survive via estrogen receptor-dependent induction of SGK3, leading to rewiring of the PI3K/AKT/mTORC1 pathway to enable AKT-independent mTORC1 activation.	Phenobarbital	47-54	AKT serine/threonine kinase 1	Homo sapiens	156-159
34911733-7	2022	Finally, biochemical experiments indicate that luminal-like DTPs survive via estrogen receptor-dependent induction of SGK3, leading to rewiring of the PI3K/AKT/mTORC1 pathway to enable AKT-independent mTORC1 activation.	Phenobarbital	47-54	CREB regulated transcription coactivator 1	Mus musculus	160-166
34911733-7	2022	Finally, biochemical experiments indicate that luminal-like DTPs survive via estrogen receptor-dependent induction of SGK3, leading to rewiring of the PI3K/AKT/mTORC1 pathway to enable AKT-independent mTORC1 activation.	Phenobarbital	47-54	AKT serine/threonine kinase 1	Homo sapiens	185-188
34911733-7	2022	Finally, biochemical experiments indicate that luminal-like DTPs survive via estrogen receptor-dependent induction of SGK3, leading to rewiring of the PI3K/AKT/mTORC1 pathway to enable AKT-independent mTORC1 activation.	Phenobarbital	47-54	CREB regulated transcription coactivator 1	Mus musculus	201-207
34907395-10	2022	Different from classical NTFs, CDNF can function both as an extracellular trophic factor and as an intracellular, endoplasmic reticulum (ER) luminal protein that protects neurons and other cell types against ER stress.	Phenobarbital	141-148	cerebral dopamine neurotrophic factor	Mus musculus	31-35
34645736-9	2021	The results revealed that MUC1 was expressed and localized to the apical surface of luminal epithelial cells in the bovine endometrium.	Phenobarbital	84-91	mucin 1, cell surface associated	Bos taurus	26-30
34915027-6	2022	The TRPML2 homo-tetramer structure at pH 7.4 in the apo state reveals an inactive conformation and some unique features of the extracytosolic/luminal domain and voltage sensor-like domain that have implications for the ion-conducting pathway.	Phenobarbital	142-149	mucolipin 2	Mus musculus	4-10
34880407-5	2021	Hormone receptor negative breast cancers are highly aggressive, and are thought to originate from a subtype of epithelial cells called the luminal progenitor.	Phenobarbital	139-146	nuclear receptor subfamily 4 group A member 1	Homo sapiens	0-16
34944881-8	2021	CONCLUSION: Our data supports the role of apoERalpha in maintaining the luminal phenotype of BC cells by extensively regulating gene expression at the alternative splicing level.	Phenobarbital	72-79	estrogen receptor 1	Homo sapiens	42-52
34517157-6	2021	Combined expression of FOXA1 and GATA3 was statistically higher in luminal subtypes in comparison to non-luminal subtypes.	Phenobarbital	67-74	forkhead box A1	Homo sapiens	23-28
34950044-6	2021	Under a range of conditions, the maximum apical GLUT2 flux is about half of the SGLT1 flux and is achieved at high luminal glucose (> 50 mM), high blood flow rates, and low inlet blood concentrations.	Phenobarbital	115-122	solute carrier family 2 member 2	Homo sapiens	48-53
34950044-10	2021	Recruitment of GLUT2 from a cytosolic pool elicits a 10-20% increase in absorption for luminal glucose levels in the a 20-100 mM range.	Phenobarbital	87-94	solute carrier family 2 member 2	Homo sapiens	15-20
34940599-10	2021	Our data demonstrate the existence of a cross-talk between luminal bacteria and human intestinal epithelium via metabolites, which might affect the numbers of physiologic processes including the composition of commensal flora via bactericidal effects.	Phenobarbital	59-66	bone morphogenetic protein receptor type 2	Homo sapiens	46-50
34517157-6	2021	Combined expression of FOXA1 and GATA3 was statistically higher in luminal subtypes in comparison to non-luminal subtypes.	Phenobarbital	67-74	GATA binding protein 3	Homo sapiens	33-38
34347212-6	2021	Current use of angiotensin-converting enzyme inhibitors was associated with increased risks of both recurrence and breast cancer-specific mortality among luminal patients (HR: 2.5; 95% CI: 1.5, 4.3 and HR: 1.9; 95% CI: 1.2, 3.0, respectively).	Phenobarbital	154-161	angiotensin I converting enzyme	Homo sapiens	15-44
34517157-7	2021	In Luminal A subtype; GRB7, EGFR, PTGS2, ID1, and KRT5 were significantly downregulated.	Phenobarbital	3-10	growth factor receptor bound protein 7	Homo sapiens	22-26
34517157-7	2021	In Luminal A subtype; GRB7, EGFR, PTGS2, ID1, and KRT5 were significantly downregulated.	Phenobarbital	3-10	epidermal growth factor receptor	Homo sapiens	28-32
34517157-7	2021	In Luminal A subtype; GRB7, EGFR, PTGS2, ID1, and KRT5 were significantly downregulated.	Phenobarbital	3-10	prostaglandin-endoperoxide synthase 2	Homo sapiens	34-39
34517157-7	2021	In Luminal A subtype; GRB7, EGFR, PTGS2, ID1, and KRT5 were significantly downregulated.	Phenobarbital	3-10	inhibitor of DNA binding 1, HLH protein	Homo sapiens	41-44
34517157-7	2021	In Luminal A subtype; GRB7, EGFR, PTGS2, ID1, and KRT5 were significantly downregulated.	Phenobarbital	3-10	keratin 5	Homo sapiens	50-54
34517157-8	2021	FOXA1 and GATA3 were significantly upregulated in luminal B subtype, where EGFR and PTGS2 were significantly downregulated.	Phenobarbital	50-57	forkhead box A1	Homo sapiens	0-5
34517157-8	2021	FOXA1 and GATA3 were significantly upregulated in luminal B subtype, where EGFR and PTGS2 were significantly downregulated.	Phenobarbital	50-57	GATA binding protein 3	Homo sapiens	10-15
34517157-8	2021	FOXA1 and GATA3 were significantly upregulated in luminal B subtype, where EGFR and PTGS2 were significantly downregulated.	Phenobarbital	50-57	epidermal growth factor receptor	Homo sapiens	75-79
34517157-8	2021	FOXA1 and GATA3 were significantly upregulated in luminal B subtype, where EGFR and PTGS2 were significantly downregulated.	Phenobarbital	50-57	prostaglandin-endoperoxide synthase 2	Homo sapiens	84-89
34517157-12	2021	Combined expression of ESR1, FOXA1 and GATA3 represents a molecular signature of luminal subtypes.	Phenobarbital	81-88	estrogen receptor 1	Homo sapiens	23-27
34517157-12	2021	Combined expression of ESR1, FOXA1 and GATA3 represents a molecular signature of luminal subtypes.	Phenobarbital	81-88	forkhead box A1	Homo sapiens	29-34
34517157-12	2021	Combined expression of ESR1, FOXA1 and GATA3 represents a molecular signature of luminal subtypes.	Phenobarbital	81-88	GATA binding protein 3	Homo sapiens	39-44
34561764-12	2021	Moreover, among the 294 ER-positive breast cancer samples, reduced menin expression was not only associated with larger tumors (P = 0.01) and higher SBR grades (P = 0.005) but also with the luminal B-like breast cancer subtype (P = 0.006).	Phenobarbital	190-197	menin 1	Homo sapiens	67-72
34561764-13	2021	Consistent with our clinical data, we demonstrated that GATA3 and FOXA1, co-factors in ESR1 regulation, interact physically with menin in MCF7 cells, and MEN1 knockdown led to altered protein expression of GATA3, the latter being a known marker of the luminal A subtype, in MCF7 cells.	Phenobarbital	252-259	menin 1	Homo sapiens	154-158
34561764-13	2021	Consistent with our clinical data, we demonstrated that GATA3 and FOXA1, co-factors in ESR1 regulation, interact physically with menin in MCF7 cells, and MEN1 knockdown led to altered protein expression of GATA3, the latter being a known marker of the luminal A subtype, in MCF7 cells.	Phenobarbital	252-259	GATA binding protein 3	Homo sapiens	206-211
34943889-1	2021	Phenobarbital (PB), a widely used antiepileptic drug, is known to upregulate the expression of numerous drug-metabolizing enzymes and transporters in the liver primarily via activation of the constitutive androstane receptor (CAR, NR1I3).	Phenobarbital	0-13	nuclear receptor subfamily 1 group I member 3	Homo sapiens	192-224
34943889-1	2021	Phenobarbital (PB), a widely used antiepileptic drug, is known to upregulate the expression of numerous drug-metabolizing enzymes and transporters in the liver primarily via activation of the constitutive androstane receptor (CAR, NR1I3).	Phenobarbital	0-13	nuclear receptor subfamily 1 group I member 3	Homo sapiens	226-229
34943889-0	2021	Phenobarbital Induces SLC13A5 Expression through Activation of PXR but Not CAR in Human Primary Hepatocytes.	Phenobarbital	0-13	solute carrier family 13 member 5	Homo sapiens	22-29
34943889-1	2021	Phenobarbital (PB), a widely used antiepileptic drug, is known to upregulate the expression of numerous drug-metabolizing enzymes and transporters in the liver primarily via activation of the constitutive androstane receptor (CAR, NR1I3).	Phenobarbital	0-13	nuclear receptor subfamily 1 group I member 3	Homo sapiens	231-236
34943889-0	2021	Phenobarbital Induces SLC13A5 Expression through Activation of PXR but Not CAR in Human Primary Hepatocytes.	Phenobarbital	0-13	nuclear receptor subfamily 1 group I member 2	Homo sapiens	63-66
34943889-1	2021	Phenobarbital (PB), a widely used antiepileptic drug, is known to upregulate the expression of numerous drug-metabolizing enzymes and transporters in the liver primarily via activation of the constitutive androstane receptor (CAR, NR1I3).	Phenobarbital	15-17	nuclear receptor subfamily 1 group I member 3	Homo sapiens	192-224
34943889-1	2021	Phenobarbital (PB), a widely used antiepileptic drug, is known to upregulate the expression of numerous drug-metabolizing enzymes and transporters in the liver primarily via activation of the constitutive androstane receptor (CAR, NR1I3).	Phenobarbital	15-17	nuclear receptor subfamily 1 group I member 3	Homo sapiens	226-229
34943889-1	2021	Phenobarbital (PB), a widely used antiepileptic drug, is known to upregulate the expression of numerous drug-metabolizing enzymes and transporters in the liver primarily via activation of the constitutive androstane receptor (CAR, NR1I3).	Phenobarbital	15-17	nuclear receptor subfamily 1 group I member 3	Homo sapiens	231-236
34943889-3	2021	Here, we show that PB markedly elevates the expression of SLC13A5 through a pregnane X receptor (PXR)-dependent but CAR-independent signaling pathway.	Phenobarbital	19-21	solute carrier family 13 member 5	Homo sapiens	58-65
34943889-3	2021	Here, we show that PB markedly elevates the expression of SLC13A5 through a pregnane X receptor (PXR)-dependent but CAR-independent signaling pathway.	Phenobarbital	19-21	nuclear receptor subfamily 1 group I member 2	Homo sapiens	76-95
34943889-3	2021	Here, we show that PB markedly elevates the expression of SLC13A5 through a pregnane X receptor (PXR)-dependent but CAR-independent signaling pathway.	Phenobarbital	19-21	nuclear receptor subfamily 1 group I member 2	Homo sapiens	97-100
34943889-3	2021	Here, we show that PB markedly elevates the expression of SLC13A5 through a pregnane X receptor (PXR)-dependent but CAR-independent signaling pathway.	Phenobarbital	19-21	nuclear receptor subfamily 1 group I member 3	Homo sapiens	116-119
34943889-4	2021	In human primary hepatocytes, the mRNA and protein expression of SLC13A5 was robustly induced by PB treatment, while genetic knockdown or pharmacological inhibition of PXR significantly attenuated this induction.	Phenobarbital	97-99	solute carrier family 13 member 5	Homo sapiens	65-72
34943889-5	2021	Utilizing genetically modified HepaRG cells, we found that PB induces SLC13A5 expression in both wild type and CAR-knockout HepaRG cells, whereas such induction was fully abolished in the PXR-knockout HepaRG cells.	Phenobarbital	59-61	solute carrier family 13 member 5	Homo sapiens	70-77
34943889-8	2021	Collectively, these data reveal PB as a potent inducer of SLC13A5 through the activation of PXR but not CAR in human primary hepatocytes.	Phenobarbital	32-34	solute carrier family 13 member 5	Homo sapiens	58-65
34943889-8	2021	Collectively, these data reveal PB as a potent inducer of SLC13A5 through the activation of PXR but not CAR in human primary hepatocytes.	Phenobarbital	32-34	nuclear receptor subfamily 1 group I member 2	Homo sapiens	92-95
34880650-3	2021	NHE3 inhibition in the small intestine results in luminal sodium and water retention, leading to a general decrease in paracellular water flux and diffusional driving force, reduced intestinal sodium absorption, and increased stool sodium excretion.	Phenobarbital	50-57	solute carrier family 9 member A3	Homo sapiens	0-4
34967537-10	2021	The highest levels of PKN1 were detected blood sera of the patients with luminal B and basal subtypes; its expression levels were just 10-100-fold higher in BC samples compared to healthy donors.	Phenobarbital	73-80	protein kinase N1	Homo sapiens	22-26
34117603-2	2021	In normal breast epithelium AP-2beta is expressed in a scattered subpopulation of luminal cells.	Phenobarbital	82-89	transcription factor AP-2 beta	Homo sapiens	28-36
34117603-8	2021	In summary, AP-2beta is a new luminal mammary epithelial differentiation marker, which is expressed in the GATA3-positive subpopulation of luminal epithelial cells.	Phenobarbital	30-37	transcription factor AP-2 beta	Homo sapiens	12-20
34117603-8	2021	In summary, AP-2beta is a new luminal mammary epithelial differentiation marker, which is expressed in the GATA3-positive subpopulation of luminal epithelial cells.	Phenobarbital	30-37	GATA binding protein 3	Homo sapiens	107-112
34419398-1	2021	OBJECTIVES: This study sought to investigate the impact of low tube voltage scanning heterogeneity of coronary luminal attenuation on plaque quantification and characterization with coronary computed tomography angiography (CCTA).	Phenobarbital	111-118	tubulin epsilon 1	Homo sapiens	63-67
34419398-8	2021	Higher tube voltage scanning (80, 100, and 120 kV) resulted in decreasing luminal attenuation (689 +- 135, 497 +- 89, and 391 +- 73 HU; P < 0.001) and calcified plaque volume (59%, 34%, and 23%; P < 0.001) and increased fibrofatty plaque (3%, 9%, and 18%; P < 0.001) and necrotic core (0.2%, 0.1%, and 0.6%; P < 0.001).	Phenobarbital	74-81	tubulin epsilon 1	Homo sapiens	7-11
34419398-10	2021	Tube voltage scanning of 80 kV maintained a direct effect on fibrofatty plaque and necrotic core in addition to an indirect effect through the luminal attenuation.	Phenobarbital	143-150	tubulin epsilon 1	Homo sapiens	0-4
34419398-11	2021	CONCLUSIONS: Low tube voltage usage affected plaque morphology, mainly through an increase in luminal HU with a resultant increase in calcified plaque and a reduction in fibrofatty and necrotic core.	Phenobarbital	94-101	tubulin epsilon 1	Homo sapiens	17-21
34743025-6	2021	In contrast, suppression of apoptosis by the CAR or PXR activators phenobarbital or dexamethasone were CAR- or PXR-specific.	Phenobarbital	67-80	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	45-48
34852011-10	2021	We observed similar ezrin and F-actin recruitment in exfoliated cervical epithelial cells but not in those that remained in the ectocervical epithelium, as the luminal layer of ectocervical epithelial cells expressed ten-fold lower levels of ezrin than those beneath.	Phenobarbital	160-167	ezrin	Homo sapiens	242-247
34710830-3	2021	In the present study, we investigated the expression of E-Cad and N-Cad in the mouse endometrial luminal epithelium and its modulation by estrogen, progesterone, and embryonic stimuli.	Phenobarbital	97-104	cadherin 1	Mus musculus	56-61
34710830-3	2021	In the present study, we investigated the expression of E-Cad and N-Cad in the mouse endometrial luminal epithelium and its modulation by estrogen, progesterone, and embryonic stimuli.	Phenobarbital	97-104	cadherin 2	Mus musculus	66-71
34710830-4	2021	We observed that E-Cad is diffusely expressed in the luminal epithelium of mouse endometrium during the estrus stage and upon estrogen treatment.	Phenobarbital	53-60	cadherin 1	Mus musculus	17-22
34710830-7	2021	at the time of embryo implantation, there is loss of E-Cad along with the gain of N-Cad and SNAIL expression suggestive of EMT in the luminal epithelium.	Phenobarbital	134-141	cadherin 2	Homo sapiens	82-87
34710830-7	2021	at the time of embryo implantation, there is loss of E-Cad along with the gain of N-Cad and SNAIL expression suggestive of EMT in the luminal epithelium.	Phenobarbital	134-141	snail family transcriptional repressor 1	Homo sapiens	92-97
34743025-6	2021	In contrast, suppression of apoptosis by the CAR or PXR activators phenobarbital or dexamethasone were CAR- or PXR-specific.	Phenobarbital	67-80	nuclear receptor subfamily 1, group I, member 2	Rattus norvegicus	52-55
34743025-6	2021	In contrast, suppression of apoptosis by the CAR or PXR activators phenobarbital or dexamethasone were CAR- or PXR-specific.	Phenobarbital	67-80	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	103-106
34743025-6	2021	In contrast, suppression of apoptosis by the CAR or PXR activators phenobarbital or dexamethasone were CAR- or PXR-specific.	Phenobarbital	67-80	nuclear receptor subfamily 1, group I, member 2	Rattus norvegicus	111-114
34944621-10	2021	Infiltration levels observed in specific types of immune cell, especially the cluster of differentiation found on macrophages and neutrophils, were positively linked with SLC35A2 expression in multiple BRCA subclasses (luminal A, luminal B, basal, and human epidermal growth factor receptor 2).	Phenobarbital	219-226	solute carrier family 35 member A2	Homo sapiens	171-178
34806938-3	2021	In vivo study, Sprague-Dawley male rats were treated with MTBH (25, 50 or 100 mg/kg for 28 consecutive days), phenobarbital (80 mg/kg for 12 consecutive days) or 0.5% CMC-Na solution (control group) by intragastric administration, then, the mRNA, protein levels and activities of liver P450s were analyzed by real-time PCR, western blotting and probe-drug incubation systems, respectively.The in vitro study indicated that MTBH inhibits the activities of CYP3A1/4 and CYP2E1 in rat and human liver microsomes.	Phenobarbital	110-123	cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1	Rattus norvegicus	455-463
34806938-3	2021	In vivo study, Sprague-Dawley male rats were treated with MTBH (25, 50 or 100 mg/kg for 28 consecutive days), phenobarbital (80 mg/kg for 12 consecutive days) or 0.5% CMC-Na solution (control group) by intragastric administration, then, the mRNA, protein levels and activities of liver P450s were analyzed by real-time PCR, western blotting and probe-drug incubation systems, respectively.The in vitro study indicated that MTBH inhibits the activities of CYP3A1/4 and CYP2E1 in rat and human liver microsomes.	Phenobarbital	110-123	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	468-474
34944621-10	2021	Infiltration levels observed in specific types of immune cell, especially the cluster of differentiation found on macrophages and neutrophils, were positively linked with SLC35A2 expression in multiple BRCA subclasses (luminal A, luminal B, basal, and human epidermal growth factor receptor 2).	Phenobarbital	230-237	solute carrier family 35 member A2	Homo sapiens	171-178
34869761-7	2021	Compared to other BRCA subtypes, the enrichment functions of upregulated genes in luminal A BRCA were related to hormone biological processes and receptor activity, and the downregulated genes were associated with the cell cycle and nuclear division.	Phenobarbital	82-89	BRCA1 DNA repair associated	Homo sapiens	18-22
34917597-8	2021	In addition, release of NO stimulated Sca-1+ vascular progenitor cells (VPCs) to differentiate and contribute to rapid luminal endothelialization.	Phenobarbital	119-126	ataxin 1	Rattus norvegicus	38-43
34848728-4	2021	Mechanistically, WFS1 directly binds to vesicular cargo proteins including proinsulin via its ER luminal C-terminal segment, whereas pathogenic mutations within this region disrupt the interaction.	Phenobarbital	97-104	wolframin ER transmembrane glycoprotein	Homo sapiens	17-21
34848728-4	2021	Mechanistically, WFS1 directly binds to vesicular cargo proteins including proinsulin via its ER luminal C-terminal segment, whereas pathogenic mutations within this region disrupt the interaction.	Phenobarbital	97-104	insulin	Homo sapiens	75-85
34845227-3	2021	A major barrier to the understanding of the ERalpha-pathway biology and therapeutic discoveries is the restricted repertoire of luminal ERalpha + breast cancer models.	Phenobarbital	128-135	estrogen receptor 1	Homo sapiens	44-51
34845227-3	2021	A major barrier to the understanding of the ERalpha-pathway biology and therapeutic discoveries is the restricted repertoire of luminal ERalpha + breast cancer models.	Phenobarbital	128-135	estrogen receptor 1	Homo sapiens	136-143
34868337-8	2021	Subtype analysis showed that MRPL13 was overexpressed in luminal, HER2-positive BRCA, and TNBC samples and was highest in TNBC samples.	Phenobarbital	57-64	mitochondrial ribosomal protein L13	Homo sapiens	29-35
34869761-7	2021	Compared to other BRCA subtypes, the enrichment functions of upregulated genes in luminal A BRCA were related to hormone biological processes and receptor activity, and the downregulated genes were associated with the cell cycle and nuclear division.	Phenobarbital	82-89	BRCA1 DNA repair associated	Homo sapiens	92-96
34808009-6	2022	SLFN11 expression correlated significantly with the expression of luminal subtype marker GATA3.	Phenobarbital	66-73	schlafen family member 11	Homo sapiens	0-6
34808009-6	2022	SLFN11 expression correlated significantly with the expression of luminal subtype marker GATA3.	Phenobarbital	66-73	GATA binding protein 3	Homo sapiens	89-94
34554931-3	2021	RAF1-amplified tumors had activation of the RAF/MEK/ERK signaling pathway and exhibited a luminal gene expression pattern.	Phenobarbital	90-97	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	0-4
34880749-6	2021	Moreover, treatment of mice with phenobarbital, a known inducer of both CAR and Cyp2a5, increases expression of Cyp2a5 suggesting a potential relationship between CAR and Cyp2a5 expression.	Phenobarbital	33-46	nuclear receptor subfamily 1, group I, member 3	Mus musculus	72-75
34880749-6	2021	Moreover, treatment of mice with phenobarbital, a known inducer of both CAR and Cyp2a5, increases expression of Cyp2a5 suggesting a potential relationship between CAR and Cyp2a5 expression.	Phenobarbital	33-46	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	80-86
34880749-6	2021	Moreover, treatment of mice with phenobarbital, a known inducer of both CAR and Cyp2a5, increases expression of Cyp2a5 suggesting a potential relationship between CAR and Cyp2a5 expression.	Phenobarbital	33-46	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	112-118
34880749-6	2021	Moreover, treatment of mice with phenobarbital, a known inducer of both CAR and Cyp2a5, increases expression of Cyp2a5 suggesting a potential relationship between CAR and Cyp2a5 expression.	Phenobarbital	33-46	nuclear receptor subfamily 1, group I, member 3	Mus musculus	163-166
34880749-6	2021	Moreover, treatment of mice with phenobarbital, a known inducer of both CAR and Cyp2a5, increases expression of Cyp2a5 suggesting a potential relationship between CAR and Cyp2a5 expression.	Phenobarbital	33-46	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	171-177
34795307-6	2021	PD-L1 expression was also associated with the non-luminal-HER2+ and triple negative immunohistochemical profiles of BC.	Phenobarbital	50-57	CD274 molecule	Homo sapiens	0-5
34344022-4	2021	We have previously shown that conditional deletion of uterine EZH2 results in increased proliferation of luminal and glandular epithelial cells, and RNAseq analyses reveal several uterine transcriptomic changes in Ezh2 conditional (c) knockout (KO) mice that can affect estrogen signaling pathways.	Phenobarbital	105-112	enhancer of zeste 2 polycomb repressive complex 2 subunit	Mus musculus	62-66
34715014-4	2021	ATP13A2 autophosphorylation opens a lysosome luminal gate to reveal a narrow lumen access channel that holds a spermine ion in its entrance.	Phenobarbital	45-52	ATPase cation transporting 13A2	Homo sapiens	0-7
34831231-5	2021	Based on control and FGFR1 overexpressing luminal A cell line models, we demonstrated that FGFR1 overexpression rendered the cells resistant to palbociclib.	Phenobarbital	42-49	fibroblast growth factor receptor 1	Homo sapiens	21-26
34741235-11	2022	Altogether, data suggest that the regulation of NT5E by miRNAs in MCF7 lineage may direct the molecular profile of luminal BC.	Phenobarbital	115-122	5'-nucleotidase ecto	Homo sapiens	48-52
34648034-0	2021	STAG2 loss-of-function affects short-range genomic contacts and modulates the basal-luminal transcriptional program of bladder cancer cells.	Phenobarbital	84-91	stromal antigen 2	Homo sapiens	0-5
34648034-6	2021	STAG2 knockdown results in down-regulation of the luminal urothelial signature and up-regulation of the basal transcriptional program, mirroring differences between STAG2-high and STAG2-low human bladder tumors.	Phenobarbital	50-57	stromal antigen 2	Homo sapiens	0-5
34648034-9	2021	Our findings indicate that STAG2 participates in the DNA looping that keeps the basal transcriptional program silent and thus sustains the luminal program.	Phenobarbital	139-146	stromal antigen 2	Homo sapiens	27-32
34121071-1	2021	BACKGROUND: Androgen receptor (AR) expression is a potential therapeutic target in breast cancer (BC) as it is frequently expressed in the luminal A and B subtypes and in approximately one third of basal-like cancers.	Phenobarbital	139-146	androgen receptor	Homo sapiens	12-29
34804958-4	2021	The low expression of ARID1A is associated with poor disease-free survival and overall survival of patients with luminal A or HER2-rich breast cancer.	Phenobarbital	113-120	AT-rich interaction domain 1A	Homo sapiens	22-28
34804958-5	2021	In addition, ARID1A plays a prominent role in maintaining luminal characteristics and has an advantage for identifying responses to treatment, including endocrine therapies, HDAC inhibitors and CDK4/6 inhibitors.	Phenobarbital	58-65	AT-rich interaction domain 1A	Homo sapiens	13-19
34725332-5	2021	Furthermore, we found a set of hormone-responsive lineage-specific transcription factors, FOXA1, GATA3, ERalpha, directly drove high expression of ARSD through chromatin looping in luminal subtype BC cells.	Phenobarbital	181-188	forkhead box A1	Homo sapiens	90-95
34725332-5	2021	Furthermore, we found a set of hormone-responsive lineage-specific transcription factors, FOXA1, GATA3, ERalpha, directly drove high expression of ARSD through chromatin looping in luminal subtype BC cells.	Phenobarbital	181-188	GATA binding protein 3	Homo sapiens	97-102
34725332-5	2021	Furthermore, we found a set of hormone-responsive lineage-specific transcription factors, FOXA1, GATA3, ERalpha, directly drove high expression of ARSD through chromatin looping in luminal subtype BC cells.	Phenobarbital	181-188	estrogen receptor 1	Homo sapiens	104-111
34725332-5	2021	Furthermore, we found a set of hormone-responsive lineage-specific transcription factors, FOXA1, GATA3, ERalpha, directly drove high expression of ARSD through chromatin looping in luminal subtype BC cells.	Phenobarbital	181-188	arylsulfatase D	Homo sapiens	147-151
34121071-1	2021	BACKGROUND: Androgen receptor (AR) expression is a potential therapeutic target in breast cancer (BC) as it is frequently expressed in the luminal A and B subtypes and in approximately one third of basal-like cancers.	Phenobarbital	139-146	androgen receptor	Homo sapiens	31-33
34121071-11	2021	CONCLUSION: AR is expressed in more than one third of BC BM with the highest rates among the luminal/HER2-negative BC subtype and may therefore be a potential prognostic and predictive biomarker in this particular BC population.	Phenobarbital	93-100	androgen receptor	Homo sapiens	12-14
34400221-8	2021	Intriguingly, the Rnf144a KO tumors also express GATA3, a marker for the luminal subtype, suggesting that RNF144A loss of function promotes features of cellular differentiation.	Phenobarbital	73-80	ring finger protein 144A	Mus musculus	18-25
34183353-6	2021	Luminal A/B to HER2-Enriched switching was associated with TP53 and/or PIK3CA mutations.	Phenobarbital	0-7	erb-b2 receptor tyrosine kinase 2	Homo sapiens	15-19
34183353-6	2021	Luminal A/B to HER2-Enriched switching was associated with TP53 and/or PIK3CA mutations.	Phenobarbital	0-7	tumor protein p53	Homo sapiens	59-63
34183353-6	2021	Luminal A/B to HER2-Enriched switching was associated with TP53 and/or PIK3CA mutations.	Phenobarbital	0-7	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	71-77
34400221-8	2021	Intriguingly, the Rnf144a KO tumors also express GATA3, a marker for the luminal subtype, suggesting that RNF144A loss of function promotes features of cellular differentiation.	Phenobarbital	73-80	GATA binding protein 3	Mus musculus	49-54
34400221-8	2021	Intriguingly, the Rnf144a KO tumors also express GATA3, a marker for the luminal subtype, suggesting that RNF144A loss of function promotes features of cellular differentiation.	Phenobarbital	73-80	ring finger protein 144A	Mus musculus	106-113
34537302-3	2021	METHODS AND RESULTS: In the present study, we performed in silico analysis of microarray data from luminal, Her2+, and TNBC cell lines and identified 15 relatively unexplored EMT-related differentially expressed genes (DEGs) along with the markedly high expression of EMT-transcription factor (EMT-TF), SNAI1.	Phenobarbital	99-106	snail family transcriptional repressor 1	Homo sapiens	303-308
34516042-5	2021	According to a 10-transmembrane segment model supported by topology analysis of PSS1, all the eight amino acid residues crucial for the enzyme activity were localized to the luminal side of the lipid bilayer or the lumen of the ER, whereas all the nine amino acid residues involved in the enzyme regulation were localized to the cytosol or the cytoplasmic side of the lipid bilayer of the ER.	Phenobarbital	174-181	phosphatidylserine synthase 1	Homo sapiens	80-84
34529751-7	2021	The macrophage-TNF-IEC axis avoids responses to luminal microbiota LPS but enables crypt- or tissue-scale epithelial NF-kappaB responses in proportion to the microbial threat.	Phenobarbital	48-55	tumor necrosis factor	Mus musculus	15-18
34368974-1	2021	INTRODUCTION/AIMS: Stromal Interaction Molecule 1 (STIM1) is a reticular Ca2+ sensor composed of a luminal and a cytosolic domain.	Phenobarbital	99-106	stromal interaction molecule 1	Homo sapiens	19-49
34368974-1	2021	INTRODUCTION/AIMS: Stromal Interaction Molecule 1 (STIM1) is a reticular Ca2+ sensor composed of a luminal and a cytosolic domain.	Phenobarbital	99-106	stromal interaction molecule 1	Homo sapiens	51-56
34758082-4	2021	ROBO1 is expressed in both luminal and basal cells, but loss of Robo1 in basal cells results in the luminal differentiation defect.	Phenobarbital	100-107	roundabout guidance receptor 1	Mus musculus	64-69
34758082-6	2021	Together, our studies reveal how ROBO1/CTTNB1/JAG1 signaling in the basal compartment exerts paracrine control of Notch signaling in the luminal compartment to regulate alveolar differentiation during pregnancy.	Phenobarbital	137-144	roundabout guidance receptor 1	Mus musculus	33-38
34584219-7	2021	SOX4-knockout organoids are characterized by the presence of more differentiated cells that exhibit luminal or basal gene expression patterns, but lower expression of cell cycle genes.	Phenobarbital	100-107	SRY (sex determining region Y)-box 4	Mus musculus	0-4
34516042-6	2021	This localization of the functional amino acid residues suggests that PSS1 is regulated by inhibition with PS in the cytoplasmic leaflet of the ER membrane and synthesizes PS at the luminal leaflet.	Phenobarbital	182-189	phosphatidylserine synthase 1	Homo sapiens	70-74
34706362-3	2021	In this study, we aimed to correlate FOXA1, a marker for differentiation of the basal and luminal subtypes, with tumor immune cell infiltration and the effect of chemotherapy in bladder cancer.	Phenobarbital	90-97	forkhead box A1	Homo sapiens	37-42
34831189-3	2021	ERalpha is expressed in a subset of luminal cells corresponding to less than 10% of normal mammary epithelial cells and in over 70% of breast tumors (ER+ tumors), but the basis for its selective expression in normal or cancer tissues remains incompletely understood.	Phenobarbital	36-43	estrogen receptor 1	Homo sapiens	0-7
34831189-7	2021	In particular, we discuss the impact of genetic alterations, chromatin modifications, and enhanced expression of other luminal transcription regulators on ESR1 expression in tumor cells.	Phenobarbital	119-126	estrogen receptor 1	Homo sapiens	155-159
34707238-0	2021	Author Correction: Single-cell profiling defines the prognostic benefit of CD39high tissue resident memory CD8+ T cells in luminal-like breast cancer.	Phenobarbital	123-130	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	75-79
34707238-0	2021	Author Correction: Single-cell profiling defines the prognostic benefit of CD39high tissue resident memory CD8+ T cells in luminal-like breast cancer.	Phenobarbital	123-130	CD8a molecule	Homo sapiens	107-110
34323996-9	2021	However, glycosylation and secretion assays revealed that-unlike APOL2-APOL1 membrane insertion or association occurs in different orientations at the ER, with the disease-associated mutants facing either the luminal (cis) or cytoplasmic (trans) side of the ER.	Phenobarbital	209-216	apolipoprotein L1	Homo sapiens	71-76
34707101-0	2021	NRIP1 is activated by C-JUN/C-FOS and activates the expression of PGR, ESR1 and CCND1 in luminal A breast cancer.	Phenobarbital	89-96	nuclear receptor interacting protein 1	Homo sapiens	0-5
34707101-0	2021	NRIP1 is activated by C-JUN/C-FOS and activates the expression of PGR, ESR1 and CCND1 in luminal A breast cancer.	Phenobarbital	89-96	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	22-27
34707101-0	2021	NRIP1 is activated by C-JUN/C-FOS and activates the expression of PGR, ESR1 and CCND1 in luminal A breast cancer.	Phenobarbital	89-96	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	28-33
34707101-0	2021	NRIP1 is activated by C-JUN/C-FOS and activates the expression of PGR, ESR1 and CCND1 in luminal A breast cancer.	Phenobarbital	89-96	progesterone receptor	Homo sapiens	66-69
34707101-0	2021	NRIP1 is activated by C-JUN/C-FOS and activates the expression of PGR, ESR1 and CCND1 in luminal A breast cancer.	Phenobarbital	89-96	cyclin D1	Homo sapiens	80-85
34707101-2	2021	In silico analysis confirmed by western blot and immunohistochemistry revealed that C-JUN and C-FOS transcription factors are activated in luminal A patients as potential upstream regulators of these differentially expressed genes.	Phenobarbital	139-146	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	84-89
34707101-2	2021	In silico analysis confirmed by western blot and immunohistochemistry revealed that C-JUN and C-FOS transcription factors are activated in luminal A patients as potential upstream regulators of these differentially expressed genes.	Phenobarbital	139-146	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	94-99
34707101-6	2021	NRIP1 is not only upregulated in luminal A patients and cell lines but also regulates breast cancer-related genes, including PR, ESR1 and CCND1.	Phenobarbital	33-40	nuclear receptor interacting protein 1	Homo sapiens	0-5
34707101-6	2021	NRIP1 is not only upregulated in luminal A patients and cell lines but also regulates breast cancer-related genes, including PR, ESR1 and CCND1.	Phenobarbital	33-40	transmembrane protein 37	Homo sapiens	125-127
34707101-6	2021	NRIP1 is not only upregulated in luminal A patients and cell lines but also regulates breast cancer-related genes, including PR, ESR1 and CCND1.	Phenobarbital	33-40	estrogen receptor 1	Homo sapiens	129-133
34707101-6	2021	NRIP1 is not only upregulated in luminal A patients and cell lines but also regulates breast cancer-related genes, including PR, ESR1 and CCND1.	Phenobarbital	33-40	cyclin D1	Homo sapiens	138-143
34771489-0	2021	A DOCK1 Gene-Derived Circular RNA Is Highly Expressed in Luminal Mammary Tumours and Is Involved in the Epithelial Differentiation, Growth, and Motility of Breast Cancer Cells.	Phenobarbital	57-64	dedicator of cytokinesis 1	Homo sapiens	2-7
34695137-15	2021	Significant associations were found between p53 overexpression and histological grade (p = 0.034), triple negative (p = 0.0333) and luminal B (p<0.01) tumors.	Phenobarbital	132-139	transformation related protein 53, pseudogene	Mus musculus	44-47
34828271-3	2021	H2A.J showed cell-type specific expression with a striking enrichment in luminal epithelial cells of multiple glands including those of breast, prostate, pancreas, thyroid, stomach, and salivary glands.	Phenobarbital	73-80	H2J.A histone	Mus musculus	0-5
34695904-6	2021	The ORRs of Luminal, human epidermal growth factor receptor 2 (HER2) overexpression and triple-negative breast cancer patients underwent albumin-bound paclitaxel treatment were 37.3%, 45.5% and 31.0%, respectively, the DCRs were 85.5%, 68.2% and 78.9%, respectively.	Phenobarbital	12-19	albumin	Homo sapiens	137-144
34675248-1	2021	We developed a transgenic mouse line that expresses the codon-optimized Flp recombinase under the control of the MMTV promoter in luminal epithelial cells of the mammary gland.	Phenobarbital	130-137	4-hydroxyphenylpyruvic acid dioxygenase	Mus musculus	72-75
34675248-2	2021	In this report, we demonstrate the versatile applicability of the new MMTV-Flp strain to manipulate genes in a temporally and spatially controlled manner in the normal mammary gland, in luminal-type mammary tumors that overexpress ERBB2, and in a new KRAS-associated mammary cancer model.	Phenobarbital	186-193	4-hydroxyphenylpyruvic acid dioxygenase	Mus musculus	75-78
34675248-2	2021	In this report, we demonstrate the versatile applicability of the new MMTV-Flp strain to manipulate genes in a temporally and spatially controlled manner in the normal mammary gland, in luminal-type mammary tumors that overexpress ERBB2, and in a new KRAS-associated mammary cancer model.	Phenobarbital	186-193	erb-b2 receptor tyrosine kinase 2	Homo sapiens	231-236
34675248-3	2021	Although the MMTV-Flp is expressed in a mosaic pattern in the luminal epithelium, the Flp-mediated activation of a mutant KrasG12D allele resulted in basal-like mammary tumors that progressively acquired mesenchymal features.	Phenobarbital	62-69	4-hydroxyphenylpyruvic acid dioxygenase	Mus musculus	18-21
34829293-6	2021	High PXR expression was positively associated with nuclear grade (p = 0.0112) and histological grade of differentiation (p = 0.0305), as well as with tumor cells" proliferative capacity (p = 0.0051), and negatively with luminal A subtype (p = 0.0295).	Phenobarbital	220-227	nuclear receptor subfamily 1 group I member 2	Homo sapiens	5-8
34760039-7	2021	SI and CD10 were expressed on the luminal surfaces of the columnar cells.	Phenobarbital	34-41	sucrase-isomaltase	Homo sapiens	0-2
34760039-7	2021	SI and CD10 were expressed on the luminal surfaces of the columnar cells.	Phenobarbital	34-41	membrane metalloendopeptidase	Homo sapiens	7-11
34645803-4	2021	Via its luminal domain, PGRMC1 captures misfolded prohormones, targeting them for RTN3-dependent ER-phagy.	Phenobarbital	8-15	progesterone receptor membrane component 1	Homo sapiens	24-30
34663908-4	2022	MS4A15 localizes to the endoplasmic reticulum, where it blocks ferroptosis by depleting luminal Ca2+ stores and reprogramming membrane phospholipids to ferroptosis-resistant species.	Phenobarbital	88-95	membrane spanning 4-domains A15	Homo sapiens	0-6
34654813-6	2021	Luminal localization is mediated by augmin, which is linked to the centriole inner scaffold through POC5.	Phenobarbital	0-7	POC5 centriolar protein	Homo sapiens	100-104
34754406-15	2021	Severity of mucosal inflammatory changes is proportional to luminal (NO), which might be tied to IL-8 production.	Phenobarbital	60-67	C-X-C motif chemokine ligand 8	Homo sapiens	97-101
34645803-4	2021	Via its luminal domain, PGRMC1 captures misfolded prohormones, targeting them for RTN3-dependent ER-phagy.	Phenobarbital	8-15	reticulon 3	Homo sapiens	82-86
34229086-4	2021	We analyzed MIF mRNA expression levels in tumors from breast cancer patients from different subtypes and found that Luminal B, HER2 and Basal subtypes, which are associated to high proliferation, displayed high MIF levels.	Phenobarbital	116-123	macrophage migration inhibitory factor	Homo sapiens	12-15
34515738-0	2021	Rab35 controls formation of luminal projections required for bile canalicular morphogenesis.	Phenobarbital	28-35	RAB35, member RAS oncogene family	Homo sapiens	0-5
34665234-1	2021	Purpose: The purpose of this study was to investigate the choroidal luminal and interstitial stromal alterations using choroidal vascularity index (CVI) among different cohorts of dry age-related macular degeneration (dAMD) compared to healthy subjects.	Phenobarbital	68-75	renin binding protein	Homo sapiens	184-187
34639136-5	2021	Furthermore, oral alpha-CD administration disrupts lipid micelle formation through its inclusion of lecithin in the gut luminal fluid.	Phenobarbital	120-127	adrenocortical dysplasia	Mus musculus	18-26
34229086-4	2021	We analyzed MIF mRNA expression levels in tumors from breast cancer patients from different subtypes and found that Luminal B, HER2 and Basal subtypes, which are associated to high proliferation, displayed high MIF levels.	Phenobarbital	116-123	macrophage migration inhibitory factor	Homo sapiens	211-214
34312179-4	2021	mRNA and protein levels, and metabolic activity, of CYP2B10 were significantly higher in D mice treated with the CAR activator phenobarbital (PB), but not with 1,4-bis((3,5-dichloropyridin-2-yl)oxy)benzene, compared with WT mice.	Phenobarbital	127-140	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	52-59
34269478-7	2021	In a multivariate analysis, low FFR at the LCx was associated with post-stenting minimal luminal area (MLA) of LCx (odds ratio (OR): 0.032, p < .001), post-stenting LCx plaque burden (OR: 1.166, p < .001), poststenting LM MLA (OR: 0.821, p = .038), and prestenting LCx MLA (OR: 0.371, p = .044).	Phenobarbital	89-96	tet methylcytosine dioxygenase 1	Homo sapiens	43-46
34358678-8	2021	The statistical model based on Luminal B-like patients adjusted by menopausal status and phenotype (OR= 37.49; 95% CI= 6.74-208.42 P= 0.001), GATA3-AS1 was established as an independent predictor of response.	Phenobarbital	31-38	GATA binding protein 3	Homo sapiens	142-147
34358678-8	2021	The statistical model based on Luminal B-like patients adjusted by menopausal status and phenotype (OR= 37.49; 95% CI= 6.74-208.42 P= 0.001), GATA3-AS1 was established as an independent predictor of response.	Phenobarbital	31-38	prostaglandin D2 receptor	Homo sapiens	148-151
34312179-4	2021	mRNA and protein levels, and metabolic activity, of CYP2B10 were significantly higher in D mice treated with the CAR activator phenobarbital (PB), but not with 1,4-bis((3,5-dichloropyridin-2-yl)oxy)benzene, compared with WT mice.	Phenobarbital	127-140	nuclear receptor subfamily 1, group I, member 3	Mus musculus	113-116
34312179-4	2021	mRNA and protein levels, and metabolic activity, of CYP2B10 were significantly higher in D mice treated with the CAR activator phenobarbital (PB), but not with 1,4-bis((3,5-dichloropyridin-2-yl)oxy)benzene, compared with WT mice.	Phenobarbital	142-144	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	52-59
34312179-4	2021	mRNA and protein levels, and metabolic activity, of CYP2B10 were significantly higher in D mice treated with the CAR activator phenobarbital (PB), but not with 1,4-bis((3,5-dichloropyridin-2-yl)oxy)benzene, compared with WT mice.	Phenobarbital	142-144	nuclear receptor subfamily 1, group I, member 3	Mus musculus	113-116
34629731-1	2021	The constitutive androstane receptor (CAR)-mediated mode of action (MOA) for phenobarbital (PB)-induced rodent liver tumor formation has been established, with increased hepatocyte proliferation, which is a key event in tumor formation.	Phenobarbital	77-90	nuclear receptor subfamily 1, group I, member 3	Mus musculus	4-36
34312179-6	2021	The mRNA levels of Cyp2b10 in primary hepatocytes from WT and D mice treated with PB alone or in combination with SKI-1 (a Src inhibitor), or U0126 (a MEK inhibitor), were evaluated.	Phenobarbital	82-84	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	19-26
34629731-1	2021	The constitutive androstane receptor (CAR)-mediated mode of action (MOA) for phenobarbital (PB)-induced rodent liver tumor formation has been established, with increased hepatocyte proliferation, which is a key event in tumor formation.	Phenobarbital	77-90	nuclear receptor subfamily 1, group I, member 3	Mus musculus	38-41
34312179-7	2021	Treatment of hepatocytes from D mice with the combination of PB with U0126, but not SKI-1, significantly increased the mRNA levels of Cyp2b10 compared with those from the corresponding WT mice.	Phenobarbital	61-63	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	134-141
34629731-1	2021	The constitutive androstane receptor (CAR)-mediated mode of action (MOA) for phenobarbital (PB)-induced rodent liver tumor formation has been established, with increased hepatocyte proliferation, which is a key event in tumor formation.	Phenobarbital	92-94	nuclear receptor subfamily 1, group I, member 3	Mus musculus	4-36
34629731-1	2021	The constitutive androstane receptor (CAR)-mediated mode of action (MOA) for phenobarbital (PB)-induced rodent liver tumor formation has been established, with increased hepatocyte proliferation, which is a key event in tumor formation.	Phenobarbital	92-94	nuclear receptor subfamily 1, group I, member 3	Mus musculus	38-41
34131071-8	2021	d16HER2 incited homogenous and proliferative luminal-like lesions which infrequently progressed to invasive phenotypes whereas p95HER2 lesions were heterogenous and invasive at the smallest detectable stage.	Phenobarbital	45-52	erb-b2 receptor tyrosine kinase 2	Mus musculus	3-7
34158394-6	2021	Moreover, we found that the expression levels of the PARP-1- and estrogen-coregulated gene set are enriched in the luminal subtype of breast cancers, and high PARP-1 expression in ER+ cases correlates with poor survival.	Phenobarbital	115-122	poly(ADP-ribose) polymerase 1	Homo sapiens	53-59
34399386-8	2021	GCR was expressed in the cytoplasm and the nucleus in the luminal and glandular epithelium as well as in the stroma.	Phenobarbital	58-65	nuclear receptor subfamily 3 group C member 1	Equus caballus	0-3
34586414-9	2021	V1aR are expressed in the luminal side of the collecting duct and in inner medullary interstitial cells, and their activation induces the production of prostaglandins, mostly PGE2.	Phenobarbital	26-33	arginine vasopressin receptor 1A	Homo sapiens	0-4
34586062-0	2021	Phosphorylation of luminal region of the SUN-domain protein Mps3 promotes nuclear envelope localization during meiosis.	Phenobarbital	19-26	Mps3p	Saccharomyces cerevisiae S288C	60-64
34586062-4	2021	We also found that the luminal region of Mps3 juxtaposed to the inner nuclear membrane is required for meiosis-specific localisation of Mps3 on NE.	Phenobarbital	23-30	Mps3p	Saccharomyces cerevisiae S288C	41-45
34586062-4	2021	We also found that the luminal region of Mps3 juxtaposed to the inner nuclear membrane is required for meiosis-specific localisation of Mps3 on NE.	Phenobarbital	23-30	Mps3p	Saccharomyces cerevisiae S288C	136-140
34586062-5	2021	Negative charges introduced by meiosis-specific phosphorylation in the luminal region of Mps3 alter its interaction with negatively charged lipids by electric repulsion in reconstituted liposomes.	Phenobarbital	71-78	Mps3p	Saccharomyces cerevisiae S288C	89-93
34586062-6	2021	Phospho-mimetic substitution in the luminal region suppresses the localisation of Mps3 via the inactivation of CDK or DDK.	Phenobarbital	36-43	Mps3p	Saccharomyces cerevisiae S288C	82-86
34524460-6	2021	This led to the temporal misexpression of several epithelial genes (Cftr (Cystic fibrosis transmembrane conductance regulator), Aqp5 (aquaporin 5), Aqp8 (aquaporin 8) and Cldn7 (claudin 7)) that mediate luminal fluid secretion and luminal opening.	Phenobarbital	203-210	cystic fibrosis transmembrane conductance regulator	Mus musculus	68-72
34524460-6	2021	This led to the temporal misexpression of several epithelial genes (Cftr (Cystic fibrosis transmembrane conductance regulator), Aqp5 (aquaporin 5), Aqp8 (aquaporin 8) and Cldn7 (claudin 7)) that mediate luminal fluid secretion and luminal opening.	Phenobarbital	203-210	cystic fibrosis transmembrane conductance regulator	Mus musculus	74-125
34524460-6	2021	This led to the temporal misexpression of several epithelial genes (Cftr (Cystic fibrosis transmembrane conductance regulator), Aqp5 (aquaporin 5), Aqp8 (aquaporin 8) and Cldn7 (claudin 7)) that mediate luminal fluid secretion and luminal opening.	Phenobarbital	203-210	aquaporin 5	Mus musculus	128-132
34524460-6	2021	This led to the temporal misexpression of several epithelial genes (Cftr (Cystic fibrosis transmembrane conductance regulator), Aqp5 (aquaporin 5), Aqp8 (aquaporin 8) and Cldn7 (claudin 7)) that mediate luminal fluid secretion and luminal opening.	Phenobarbital	203-210	claudin 7	Mus musculus	171-176
34531680-10	2021	Detailed, survival difference between CLMN high and low expression groups was observed in patients with stage 1 (P=0.0250), positive ER status (P=0.0042), negative HER status (P=0.0433), luminal A (P=0.0065), luminal B (P=0.0123) and positive lymph node status (P=0.0069).	Phenobarbital	187-194	calmin	Homo sapiens	38-42
34524460-6	2021	This led to the temporal misexpression of several epithelial genes (Cftr (Cystic fibrosis transmembrane conductance regulator), Aqp5 (aquaporin 5), Aqp8 (aquaporin 8) and Cldn7 (claudin 7)) that mediate luminal fluid secretion and luminal opening.	Phenobarbital	203-210	claudin 7	Mus musculus	178-187
34638686-6	2021	Using the crystal structure of AtTPC1, protein modeling, molecular dynamics (MD) simulations, and free energy calculations, we identified a free energy minimum for Ca2+, but not for K+, at the luminal side next to the selectivity filter.	Phenobarbital	193-200	two-pore channel 1	Arabidopsis thaliana	31-37
34125599-10	2021	Trem1,3-/- mice also had reduced erosion of the luminal epithelium.	Phenobarbital	48-55	triggering receptor expressed on myeloid cells 1	Mus musculus	0-5
34108177-8	2021	Results: NECTIN4 expression is heterogenous across molecular subtypes of bladder cancer and significantly enriched in luminal subtypes.	Phenobarbital	118-125	nectin cell adhesion molecule 4	Homo sapiens	9-16
34108177-9	2021	NECTIN4 expression is positively correlated with luminal markers GATA3, FOXA1, and PPARG across all cohorts.	Phenobarbital	49-56	nectin cell adhesion molecule 4	Homo sapiens	0-7
34108177-9	2021	NECTIN4 expression is positively correlated with luminal markers GATA3, FOXA1, and PPARG across all cohorts.	Phenobarbital	49-56	GATA binding protein 3	Homo sapiens	65-70
34108177-10	2021	NECTIN4 expression is both necessary and sufficient for EV sensitivity in luminal and basal subtypes of urothelial bladder cancer cells.	Phenobarbital	74-81	nectin cell adhesion molecule 4	Homo sapiens	0-7
34108177-12	2021	Conclusions: Sensitivity to EV is mediated by expression of NECTIN4, which is enriched in luminal subtypes of bladder cancer.	Phenobarbital	90-97	nectin cell adhesion molecule 4	Homo sapiens	60-67
34754452-7	2021	Functional depletion of MLPH in prostate organoids, by CRISPR/Cas9 mutation, impacted lineage commitment of progenitor cells promoting luminal versus basal cell differentiation and on resistance to androgen deprivation.	Phenobarbital	135-142	melanophilin	Homo sapiens	24-28
34508103-7	2021	Finally, relapse-free survival (RFS) analysis showed that low expression levels of PER3 were linked to a significant lower RSF in luminal A (p = 3 x 10-12) but not in the rest of breast cancer subtypes.	Phenobarbital	130-137	period circadian regulator 3	Homo sapiens	83-87
34548395-4	2021	Here, we show that E-NTPD8 is highly expressed in large-intestinal epithelial cells and hydrolyzes microbiota-derived luminal ATP.	Phenobarbital	118-125	ectonucleoside triphosphate diphosphohydrolase 8	Mus musculus	19-26
34561423-3	2021	Our results reveal that SEMA7A is expressed on live mammary epithelial cells during involution, that SEMA7A expression is primarily observed in alpha6-integrin expressing cells, and that luminal progenitor cells, specifically, are decreased in mammary glands of SEMA7A-/- mice during involution.	Phenobarbital	187-194	sema domain, immunoglobulin domain (Ig), and GPI membrane anchor, (semaphorin) 7A	Mus musculus	262-268
34552178-3	2021	By using high-dimensional single-cell technologies, we identify heterogeneous behavior within the tissue-resident memory CD8+ T (Trm) cells infiltrating luminal-like tumors.	Phenobarbital	153-160	CD8a molecule	Homo sapiens	121-124
34545139-7	2021	In addition, our data reveal that downregulation of c-FLIP promotes luminal filling in mammary acini and that c-FLIP overexpression in cancer cells inhibits colony formation in cells exposed to ECM-detachment.	Phenobarbital	68-75	CASP8 and FADD like apoptosis regulator	Homo sapiens	52-58
34531680-10	2021	Detailed, survival difference between CLMN high and low expression groups was observed in patients with stage 1 (P=0.0250), positive ER status (P=0.0042), negative HER status (P=0.0433), luminal A (P=0.0065), luminal B (P=0.0123) and positive lymph node status (P=0.0069).	Phenobarbital	209-216	calmin	Homo sapiens	38-42
34493329-8	2021	Moreover, in patients suffering from ulcerative colitis (UC), we find diminished P-gp expression coupled to the reduction of epithelial-derived anti-inflammatory endocannabinoids and luminal content (e.g., microbes or their metabolites) with a reduced capability to induce P-gp expression.	Phenobarbital	183-190	ATP binding cassette subfamily B member 1	Homo sapiens	81-85
34575183-17	2021	The decreased expression of MiR-379/656 was found to be associated with poorer clinical outcome in Basal and Luminal B subtypes, increasing tumor stage and tumor size/extent, and overall patient survival.	Phenobarbital	109-116	microRNA 379	Homo sapiens	28-35
34578649-6	2021	In vitro co-culture of mouse PAECs and their corresponding smooth muscle cells (SMCs) showed that the luminal endothelialization governs the biophysical integrity of the newly formed extracellular matrix (e.g., collagen and elastin fibers) and structural remodeling of SMCs.	Phenobarbital	102-109	elastin	Mus musculus	224-231
34329471-6	2021	In 157 paired breast cancer and adjacent normal samples, tumour suppressor gene GPER1 and miR-339 are both downregulated in Luminal A/B and Triple Negative Breast Cancer subtypes.	Phenobarbital	124-131	G protein-coupled estrogen receptor 1	Homo sapiens	80-85
34329471-6	2021	In 157 paired breast cancer and adjacent normal samples, tumour suppressor gene GPER1 and miR-339 are both downregulated in Luminal A/B and Triple Negative Breast Cancer subtypes.	Phenobarbital	124-131	microRNA 339	Homo sapiens	90-97
34144121-6	2021	RESULTS: In subAKI, PT albumin overload induced TII development, measured by: (1) increase in urinary lactate dehydrogenase and gamma-glutamyltranspeptidase activity; (2) proteinuria associated with impairment in megalin-mediated albumin reabsorption; (3) increase in luminal and interstitial space in tubular cortical segments.	Phenobarbital	268-275	albumin	Sus scrofa	23-30
34513997-5	2021	IFNT acts mainly in the endometrium of the luminal epithelium.	Phenobarbital	43-50	interferon tau-2	Bos taurus	0-4
34308669-2	2021	Thick ascending limb (THAL) NO synthase 3 (NOS3) is a major source of renal NO, and luminal flow enhances its activity.	Phenobarbital	84-91	nitric oxide synthase 3	Rattus norvegicus	28-41
34308669-2	2021	Thick ascending limb (THAL) NO synthase 3 (NOS3) is a major source of renal NO, and luminal flow enhances its activity.	Phenobarbital	84-91	nitric oxide synthase 3	Rattus norvegicus	43-47
34288721-3	2021	We addressed the role of NHE8 (SLC9A8) and its interplay with NHE2 (SLC9A2) in luminal proton extrusion during acute and chronic enterocyte acidosis, and studied the differential effects of NHE8 and NHE2 on enterocyte proliferation.	Phenobarbital	79-86	solute carrier family 9 member A2	Homo sapiens	68-74
34240392-10	2021	IA rats injected with ex-miR-144-5p mimic showed significant luminal dilation, declined smooth muscle layers, and thinned vascular wall.	Phenobarbital	61-68	microRNA 144	Rattus norvegicus	25-32
34412014-6	2021	Protein secretion was modulated with a two-fold increase in luminal mucin-2 secretion and a significant reduction in basal interleukin-8 secretion.	Phenobarbital	60-67	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	68-75
34244869-8	2021	Importantly, the proportion of stage I and "luminal" BC (HR + /HER2 -) were significantly higher in SDBC vs. non-SDBC.	Phenobarbital	44-51	erb-b2 receptor tyrosine kinase 2	Homo sapiens	63-67
34076969-10	2021	Finally, in the luminal A subgroup, high levels of CD3+ and FOXP3+ TILs were associated with shorter recurrence-free survival, and high counts of FOXP3+ were linked to reduced breast cancer-specific survival.	Phenobarbital	16-23	forkhead box P3	Homo sapiens	60-65
34076969-10	2021	Finally, in the luminal A subgroup, high levels of CD3+ and FOXP3+ TILs were associated with shorter recurrence-free survival, and high counts of FOXP3+ were linked to reduced breast cancer-specific survival.	Phenobarbital	16-23	forkhead box P3	Homo sapiens	146-151
34076969-13	2021	Notably, presence of TIL subsets showed prognostic value within the luminal A category.	Phenobarbital	68-75	toll like receptor 1	Homo sapiens	21-24
34288015-20	2021	By immunohistochemistry, COX1 was predominantly observed in the prostatic stroma while COX2 was present in scattered luminal cells of isolated prostatic glands in S-BPH.	Phenobarbital	117-124	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	87-91
34527198-6	2021	S-II is luminal/metabolism-active and responsive to androgen deprivation therapy with frequent TMPRSS2-ERG fusion and a good prognosis.	Phenobarbital	8-15	transcription elongation factor A1	Homo sapiens	0-4
34502262-8	2021	Atoh8 null mice showed an increase in transcytosis capacity of luminal antigens.	Phenobarbital	63-70	atonal bHLH transcription factor 8	Mus musculus	0-5
34446052-0	2021	Expression profiles and functional prediction of long non-coding RNAs LINC01133, ZEB1-AS1 and ABHD11-AS1 in the luminal subtype of breast cancer.	Phenobarbital	112-119	abhydrolase domain containing 11	Homo sapiens	94-100
34153681-8	2021	In lactation, GLUT8 is expressed mainly in luminal epithelial cells, at the compartments of the endomembrane system.	Phenobarbital	43-50	solute carrier family 2 member 8	Homo sapiens	14-19
34446052-0	2021	Expression profiles and functional prediction of long non-coding RNAs LINC01133, ZEB1-AS1 and ABHD11-AS1 in the luminal subtype of breast cancer.	Phenobarbital	112-119	prostaglandin D2 receptor	Homo sapiens	101-104
34446052-11	2021	Moreover, several datasets were used to discover the potential roles and functions of LINC01133, ZEB1-AS1 and ABHD11-AS1 in luminal subtype of BC.	Phenobarbital	124-131	abhydrolase domain containing 11	Homo sapiens	110-116
34446052-11	2021	Moreover, several datasets were used to discover the potential roles and functions of LINC01133, ZEB1-AS1 and ABHD11-AS1 in luminal subtype of BC.	Phenobarbital	124-131	prostaglandin D2 receptor	Homo sapiens	117-120
34446052-12	2021	RESULTS: According to the qRT-PCR assay, the expression levels of LINC01133 and ZEB1-AS1 were decreased in luminal BC tissues and cell lines.	Phenobarbital	107-114	long intergenic non-protein coding RNA 1133	Homo sapiens	66-75
34446052-12	2021	RESULTS: According to the qRT-PCR assay, the expression levels of LINC01133 and ZEB1-AS1 were decreased in luminal BC tissues and cell lines.	Phenobarbital	107-114	ZEB1 antisense RNA 1	Homo sapiens	80-88
34446052-17	2021	CONCLUSIONS: Taken together, our findings disclosed the dysregulation of LINC01133, ZEB1-AS1, and ABHD11-AS1 in luminal BC.	Phenobarbital	112-119	long intergenic non-protein coding RNA 1133	Homo sapiens	73-82
34446052-17	2021	CONCLUSIONS: Taken together, our findings disclosed the dysregulation of LINC01133, ZEB1-AS1, and ABHD11-AS1 in luminal BC.	Phenobarbital	112-119	zinc finger E-box binding homeobox 1	Homo sapiens	84-88
34446052-17	2021	CONCLUSIONS: Taken together, our findings disclosed the dysregulation of LINC01133, ZEB1-AS1, and ABHD11-AS1 in luminal BC.	Phenobarbital	112-119	prostaglandin D2 receptor	Homo sapiens	89-92
34446052-17	2021	CONCLUSIONS: Taken together, our findings disclosed the dysregulation of LINC01133, ZEB1-AS1, and ABHD11-AS1 in luminal BC.	Phenobarbital	112-119	abhydrolase domain containing 11	Homo sapiens	98-104
34446052-17	2021	CONCLUSIONS: Taken together, our findings disclosed the dysregulation of LINC01133, ZEB1-AS1, and ABHD11-AS1 in luminal BC.	Phenobarbital	112-119	prostaglandin D2 receptor	Homo sapiens	105-108
34446052-18	2021	It was revealed that LINC01133 and ZEB1-AS1 expression was significantly downregulated in luminal BC tissues and cell lines, while ABHD11-AS1 was upregulated considerably in the mentioned tissues and cell lines.	Phenobarbital	90-97	long intergenic non-protein coding RNA 1133	Homo sapiens	21-30
34446052-18	2021	It was revealed that LINC01133 and ZEB1-AS1 expression was significantly downregulated in luminal BC tissues and cell lines, while ABHD11-AS1 was upregulated considerably in the mentioned tissues and cell lines.	Phenobarbital	90-97	ZEB1 antisense RNA 1	Homo sapiens	35-43
34446052-18	2021	It was revealed that LINC01133 and ZEB1-AS1 expression was significantly downregulated in luminal BC tissues and cell lines, while ABHD11-AS1 was upregulated considerably in the mentioned tissues and cell lines.	Phenobarbital	90-97	prostaglandin D2 receptor	Homo sapiens	138-141
34445706-1	2021	Here, we present the main features of human acid sphingomyelinase (ASM), its biosynthesis, processing and intracellular trafficking, its structure, its broad substrate specificity, and the proposed mode of action at the surface of the phospholipid substrate carrying intraendolysosomal luminal vesicles.	Phenobarbital	286-293	sphingomyelin phosphodiesterase 1	Homo sapiens	44-65
34522866-5	2021	Upregulation of basal markers in luminal cells, including KRT14 and AXL, were a prominent consequence of aging.	Phenobarbital	33-40	keratin 14	Homo sapiens	58-63
34522866-5	2021	Upregulation of basal markers in luminal cells, including KRT14 and AXL, were a prominent consequence of aging.	Phenobarbital	33-40	AXL receptor tyrosine kinase	Homo sapiens	68-71
34522866-6	2021	PEAK1 was identified as an age-dependent signaling kinase in luminal cells, which revealed a potential age-dependent vulnerability for targeted ablation.	Phenobarbital	61-68	pseudopodium enriched atypical kinase 1	Homo sapiens	0-5
34522866-6	2021	PEAK1 was identified as an age-dependent signaling kinase in luminal cells, which revealed a potential age-dependent vulnerability for targeted ablation.	Phenobarbital	61-68	renin binding protein	Homo sapiens	27-30
34522866-6	2021	PEAK1 was identified as an age-dependent signaling kinase in luminal cells, which revealed a potential age-dependent vulnerability for targeted ablation.	Phenobarbital	61-68	renin binding protein	Homo sapiens	103-106
34413267-7	2021	ACE2 expression level in the luminal subtype was positively correlated with CD8A and CD8B markers in CD8+ T cells, and CEACAM3, S100A12 in neutrophils.	Phenobarbital	29-36	angiotensin converting enzyme 2	Homo sapiens	0-4
34413267-7	2021	ACE2 expression level in the luminal subtype was positively correlated with CD8A and CD8B markers in CD8+ T cells, and CEACAM3, S100A12 in neutrophils.	Phenobarbital	29-36	CD8a molecule	Homo sapiens	76-80
34413267-7	2021	ACE2 expression level in the luminal subtype was positively correlated with CD8A and CD8B markers in CD8+ T cells, and CEACAM3, S100A12 in neutrophils.	Phenobarbital	29-36	CD8b molecule	Homo sapiens	85-89
34413267-7	2021	ACE2 expression level in the luminal subtype was positively correlated with CD8A and CD8B markers in CD8+ T cells, and CEACAM3, S100A12 in neutrophils.	Phenobarbital	29-36	CD8a molecule	Homo sapiens	101-104
34445706-1	2021	Here, we present the main features of human acid sphingomyelinase (ASM), its biosynthesis, processing and intracellular trafficking, its structure, its broad substrate specificity, and the proposed mode of action at the surface of the phospholipid substrate carrying intraendolysosomal luminal vesicles.	Phenobarbital	286-293	sphingomyelin phosphodiesterase 1	Homo sapiens	67-70
34413267-7	2021	ACE2 expression level in the luminal subtype was positively correlated with CD8A and CD8B markers in CD8+ T cells, and CEACAM3, S100A12 in neutrophils.	Phenobarbital	29-36	CEA cell adhesion molecule 3	Homo sapiens	119-126
34389665-4	2021	We further demonstrate that the TGN calcium/manganese pump, SPCA1, which regulates the calcium concentration within the Golgi, and Cab45, a calcium-binding luminal Golgi resident protein, are essential for the formation of GPI-AP homoclusters in the Golgi and for their subsequent apical sorting.	Phenobarbital	156-163	stromal cell derived factor 4	Homo sapiens	131-136
34413267-7	2021	ACE2 expression level in the luminal subtype was positively correlated with CD8A and CD8B markers in CD8+ T cells, and CEACAM3, S100A12 in neutrophils.	Phenobarbital	29-36	S100 calcium binding protein A12	Homo sapiens	128-135
34445530-9	2021	The decreased IL-33 expression in the sufficient and supplemented microswine could be a potential mechanism for controlling the inflammatory process and neointima formation leading to attenuated luminal narrowing of the coronary artery.	Phenobarbital	195-202	interleukin 33	Homo sapiens	14-19
34439314-7	2021	EFHB expression is upregulated in luminal and triple negative breast cancer (TNBC) cells and is essential for full SOCE in these cells.	Phenobarbital	34-41	EF-hand domain family member B	Homo sapiens	0-4
34422318-5	2021	Material and methods: We retrospectively reviewed clinical, pathological, and radiological findings of six patients with luminal-like breast cancers treated with neoadjuvant CDK4/6I + E treatment.	Phenobarbital	121-128	cyclin dependent kinase 4	Homo sapiens	174-181
34111473-10	2021	The luminal epithelial cells from human endometrial biopsies had higher PDIA1 protein expression in the proliferative phase than in the secretory phase.	Phenobarbital	4-11	prolyl 4-hydroxylase subunit beta	Homo sapiens	72-77
34483846-10	2021	The latter was a consequence of the activated NF-kappaB pathway, stimulating MMP-9 and ABCB1 transporter activity on the luminal side of the endothelium.	Phenobarbital	121-128	matrix metallopeptidase 9	Mus musculus	77-82
34483846-10	2021	The latter was a consequence of the activated NF-kappaB pathway, stimulating MMP-9 and ABCB1 transporter activity on the luminal side of the endothelium.	Phenobarbital	121-128	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	87-92
34439272-7	2021	In the Luminal subtype, amplifications of LSM1, CLNS1A, and ILF2 showed a strong significant association with prognosis.	Phenobarbital	7-14	LSM1 homolog, mRNA degradation associated	Homo sapiens	42-46
34439272-7	2021	In the Luminal subtype, amplifications of LSM1, CLNS1A, and ILF2 showed a strong significant association with prognosis.	Phenobarbital	7-14	chloride nucleotide-sensitive channel 1A	Homo sapiens	48-54
34439272-7	2021	In the Luminal subtype, amplifications of LSM1, CLNS1A, and ILF2 showed a strong significant association with prognosis.	Phenobarbital	7-14	interleukin enhancer binding factor 2	Homo sapiens	60-64
34429650-8	2021	YBX1 expression was positively correlated with the M2 macrophage infiltration and expression of T cell exhaustion markers such as indoleamine 2,3-dioxygenase 1 (IDO1) (rs = 0.388, P = 4.93e-37) and cytotoxic T-lymphocyte-associated protein 4 (CTLA4) (rs = 0.321, P = 2.54e-25) in luminal BRCA.	Phenobarbital	280-287	Y-box binding protein 1	Homo sapiens	0-4
34429650-10	2021	Co-culture with macrophages or T cells enhanced the decrease in luminal BRCA cell viability induced by YBX1 knockdown.	Phenobarbital	64-71	Y-box binding protein 1	Homo sapiens	103-107
34429650-11	2021	Conclusion: High YBX1 mRNA levels predict a poor prognosis in luminal BRCA, which is correlated with M2 macrophage infiltration and T cell exhaustion in the tumor microenvironment.	Phenobarbital	62-69	Y-box binding protein 1	Homo sapiens	17-21
34429650-12	2021	Combining classic therapeutics with immune checkpoint inhibitors and M1 polarization agents may be an effective treatment strategy for luminal BRCA with YBX1 overexpression.	Phenobarbital	135-142	Y-box binding protein 1	Homo sapiens	153-157
34445283-5	2021	The assay is composed of two chimeric proteins: a receptor-simulating protein, consisting of the fourth luminal loop of synaptic vesicle protein 2C fused to glutathione-S-transferase, and a toxin-simulating protein, consisting of the receptor-binding domain of BoNT/A fused to beta-galactosidase.	Phenobarbital	104-111	synaptic vesicle glycoprotein 2c	Mus musculus	120-147
34375386-3	2021	IRE1 is an ER-resident type I transmembrane protein exhibiting an ER luminal domain that senses the protein folding status and a catalytic kinase and RNase cytosolic domain.	Phenobarbital	69-76	endoplasmic reticulum (ER) to nucleus signalling 2	Mus musculus	0-4
34384367-4	2021	Two segments of Ii, the luminal C-terminal region (TRIM) and the transmembrane domain (TM), have been shown to participate in the trimerization process but their relative importance and impact on the assembly with MHCII molecules remains debated.	Phenobarbital	24-31	T cell receptor associated transmembrane adaptor 1	Homo sapiens	51-55
34344433-11	2021	High FGFR4 phosphorylation characterized a luminal B PDX model and treatment with BLU9931 significantly decreased tumor growth.	Phenobarbital	43-50	fibroblast growth factor receptor 4	Homo sapiens	5-10
34436456-9	2021	Here, we detail the formative hours of the insulin SG from the luminal perspective.	Phenobarbital	63-70	insulin	Homo sapiens	43-50
34342774-5	2021	Within the 15 mammalian FKBPs known, FKBP1 is merely the only one proven to form complexes with rapamycin and FK506 in the cytosol and facilitate their T cells immunosuppressive effects, FKBP2 is a luminal protein of the endoplasmic reticulum (ER) and is reported to take part in protein folding in the ER.	Phenobarbital	198-205	FKBP prolyl isomerase 2	Homo sapiens	187-192
34344433-14	2021	Characterization of a PDO panel identified a luminal A PDO with high FGFR4 expression that was sensitive to BLU9931 treatment, further highlighting FGFR4 as a potential therapeutic target.	Phenobarbital	45-52	fibroblast growth factor receptor 4	Homo sapiens	69-74
34344433-14	2021	Characterization of a PDO panel identified a luminal A PDO with high FGFR4 expression that was sensitive to BLU9931 treatment, further highlighting FGFR4 as a potential therapeutic target.	Phenobarbital	45-52	fibroblast growth factor receptor 4	Homo sapiens	148-153
34083096-10	2021	RESULTS: CA9 expression was higher in cancer tissue compared to benign urothelium and was particularly highly expressed in luminal papillary and basal squamous tumors.	Phenobarbital	123-130	carbonic anhydrase 9	Homo sapiens	9-12
34156490-4	2021	We describe the cellular and molecular features of the luminal cell lineage expressing ERalpha and provide an overview of the transgenic mouse models impacting ERalpha signaling, highlighting the pivotal role of ERalpha in mammary gland morphogenesis and function and its implication in the tumorigenic processes.	Phenobarbital	55-62	estrogen receptor 1 (alpha)	Mus musculus	87-94
34156490-4	2021	We describe the cellular and molecular features of the luminal cell lineage expressing ERalpha and provide an overview of the transgenic mouse models impacting ERalpha signaling, highlighting the pivotal role of ERalpha in mammary gland morphogenesis and function and its implication in the tumorigenic processes.	Phenobarbital	55-62	estrogen receptor 1 (alpha)	Mus musculus	212-219
34231878-5	2021	However, CA1 cell numbers of KD-treated hippocampi were not significantly different from those seen in wild-type (WT) mice, whereas CA1 cell counts in standard diet and PB-treated Kcna1-null mice were 23% and 31% lower than WT animals, respectively.	Phenobarbital	169-171	potassium voltage-gated channel, shaker-related subfamily, member 1	Mus musculus	180-185
34140348-2	2021	We show that expression of ELF5, a transcription factor critical for normal mammary development, is downregulated in mammary luminal epithelia with age.	Phenobarbital	125-132	E74 like ETS transcription factor 5	Homo sapiens	27-31
34140348-8	2021	We propose that the changes in ELF5 expression or ELF5-proximal DNA methylation in luminal epithelia are emergent properties of at-risk breast tissue and constitute breast-specific biological clocks.	Phenobarbital	83-90	E74 like ETS transcription factor 5	Homo sapiens	31-35
34140348-8	2021	We propose that the changes in ELF5 expression or ELF5-proximal DNA methylation in luminal epithelia are emergent properties of at-risk breast tissue and constitute breast-specific biological clocks.	Phenobarbital	83-90	E74 like ETS transcription factor 5	Homo sapiens	50-54
34273808-12	2021	Among patients with de novo metastatic luminal A/B-like HER2-negative BC (n = 295), 17.3% (n = 51) received upfront chemotherapy.	Phenobarbital	39-46	erb-b2 receptor tyrosine kinase 2	Homo sapiens	56-60
34326344-8	2021	However, constitutive EPO expression resulted in macrophage infiltration and luminal obstruction of the TVC, thus limiting longer-term efficacy.	Phenobarbital	77-84	erythropoietin	Rattus norvegicus	22-25
34360932-3	2021	Expression and localization of wild type N36- and/or N52-mutated CD24 were analyzed using immunofluorescence in luminal (MCF-7) and basal B (MDA-MB-231 and Hs578T) breast cancer cells lines, as well as HEK293T cells.	Phenobarbital	112-119	CD24 molecule	Homo sapiens	65-69
34451819-0	2021	Quercetin and/or Ascorbic Acid Modulatory Effect on Phenobarbital-Induced Sleeping Mice Possibly through GABAA and GABAB Receptor Interaction Pathway.	Phenobarbital	52-65	gamma-aminobutyric acid (GABA) A receptor, subunit gamma 1	Mus musculus	105-110
34367377-9	2021	Results: The luminal obliteration rates of IL-18 of the siRNA-IL-18 group were significantly lower than those of the negative control group (p < 0.0001) and the blank control group (p = 0.0002).	Phenobarbital	13-20	interleukin 18	Mus musculus	43-48
34367377-9	2021	Results: The luminal obliteration rates of IL-18 of the siRNA-IL-18 group were significantly lower than those of the negative control group (p < 0.0001) and the blank control group (p = 0.0002).	Phenobarbital	13-20	interleukin 18	Mus musculus	56-67
34360867-7	2021	We also found that higher EphB2 expression could be a prognostic factor for distant metastasis, specifically in the luminal subtypes of breast cancer.	Phenobarbital	116-123	EPH receptor B2	Homo sapiens	26-31
34360867-10	2021	Increased EFNB1 expression is correlated with longer OS in lymph node (LN)-negative patients and the luminal B subtype.	Phenobarbital	101-108	ephrin B1	Homo sapiens	10-15
34314419-2	2021	ERG expression promotes prostate tumor formation and luminal epithelial cell fates when combined with PI3K/AKT pathway activation, however the mechanism of synergy is not known.	Phenobarbital	53-60	ETS transcription factor ERG	Homo sapiens	0-3
34314419-8	2021	In contrast, AKT activation altered the ERG cistrome and promoted expression of luminal cell fate genes.	Phenobarbital	80-87	AKT serine/threonine kinase 1	Homo sapiens	13-16
34314419-9	2021	These data suggest that, depending on AKT status, ERG can promote either luminal or EMT transcription programs, but ERG can promote tumorigenesis independent of these cell fates and tumorigenesis requires only the transcriptional activation function.	Phenobarbital	73-80	ETS transcription factor ERG	Homo sapiens	50-53
34336839-7	2021	Furthermore, we observed that loss of BMPR1a in myoepithelium results in the upregulation of a secreted protein Spp1 that could account for the precocious alveolar differentiation in luminal layer, suggesting a defective basal-to-luminal paracrine signaling mechanism.	Phenobarbital	183-190	bone morphogenetic protein receptor, type 1A	Mus musculus	38-44
34336839-7	2021	Furthermore, we observed that loss of BMPR1a in myoepithelium results in the upregulation of a secreted protein Spp1 that could account for the precocious alveolar differentiation in luminal layer, suggesting a defective basal-to-luminal paracrine signaling mechanism.	Phenobarbital	183-190	secreted phosphoprotein 1	Mus musculus	112-116
34101624-7	2021	FOXA1 overexpression could be a prognostic factor to predict therapy resistance and a viable target to sensitize luminal prostate, breast and bladder cancer to immuno- and chemotherapy.	Phenobarbital	113-120	forkhead box A1	Homo sapiens	0-5
34336839-7	2021	Furthermore, we observed that loss of BMPR1a in myoepithelium results in the upregulation of a secreted protein Spp1 that could account for the precocious alveolar differentiation in luminal layer, suggesting a defective basal-to-luminal paracrine signaling mechanism.	Phenobarbital	230-237	bone morphogenetic protein receptor, type 1A	Mus musculus	38-44
34336839-7	2021	Furthermore, we observed that loss of BMPR1a in myoepithelium results in the upregulation of a secreted protein Spp1 that could account for the precocious alveolar differentiation in luminal layer, suggesting a defective basal-to-luminal paracrine signaling mechanism.	Phenobarbital	230-237	secreted phosphoprotein 1	Mus musculus	112-116
34345195-2	2021	CF is caused by mutations in the cystic fibrosis transmembrane conductance regulator gene (CFTR), which leads to aberrant luminal fluid secretions in organs such as the lungs and pancreas.	Phenobarbital	122-129	CF transmembrane conductance regulator	Homo sapiens	33-84
34345195-2	2021	CF is caused by mutations in the cystic fibrosis transmembrane conductance regulator gene (CFTR), which leads to aberrant luminal fluid secretions in organs such as the lungs and pancreas.	Phenobarbital	122-129	CF transmembrane conductance regulator	Homo sapiens	91-95
34242292-7	2021	Using nasal inhalation of the sensor and spectral unmixing to generate images, E149C/A213R GBP-IANBD fluorescence was detected in luminal regions of cryosections of the murine distal lung that was greater in db/db than wildtype mice.	Phenobarbital	130-137	lectin, galactose binding, soluble 3	Mus musculus	91-94
34356640-4	2021	In the heart, the majority of LPL is produced in cardiomyocytes and subsequently is translocated to the apical luminal surface.	Phenobarbital	111-118	lipoprotein lipase	Homo sapiens	30-33
34242313-8	2021	Our results suggest that the MTHFR C677T polymorphism is significantly associated with susceptibility to luminal B breast cancer and TNBC.	Phenobarbital	105-112	methylenetetrahydrofolate reductase	Homo sapiens	29-34
34192549-2	2021	Despite structural determination of the Scap and Insig-2 complex bound to 25-hydroxycholesterol, the luminal domains of Scap remain unresolved.	Phenobarbital	101-108	SREBF chaperone	Homo sapiens	120-124
34139175-0	2021	Scap structures highlight key role for rotation of intertwined luminal loops in cholesterol sensing.	Phenobarbital	63-70	SREBF chaperone	Gallus gallus	0-4
34139175-2	2021	Transport requires interaction between Scap"s two ER luminal loops (L1 and L7), which flank an intramembrane sterol-sensing domain (SSD).	Phenobarbital	53-60	SREBF chaperone	Gallus gallus	39-43
34219652-7	2021	Accordingly, we observe reduced survival for patients suffering from Luminal A or Basal-like/triple-negative breast cancer with high SLC4A7 and/or low SLC9A1 mRNA expression.	Phenobarbital	69-76	solute carrier family 4 member 7	Homo sapiens	133-139
34209776-9	2021	KCNQ1OT1, LOC100270804, and FLJ10038 median levels were found to be significantly higher in the luminal subtype.	Phenobarbital	96-103	KCNQ1 opposite strand/antisense transcript 1	Homo sapiens	0-8
34139175-5	2021	Strikingly, L1 and L7 intertwine tightly to form a globular domain that acts as a luminal platform connecting the SSD to the rest of Scap.	Phenobarbital	82-89	SREBF chaperone	Gallus gallus	133-137
34277402-4	2021	A pilot retrospective analysis revealed that, in the Luminal subclass, the combination of the two ZNF217 variants (the ZNF217-DeltaE4-WT gene-expression signature) provided more information than the mRNA expression levels of each isoform alone.	Phenobarbital	53-60	zinc finger protein 217	Homo sapiens	98-104
34187874-5	2021	The post-luminal migration of T cells occurred in a PNAd-dependent manner.	Phenobarbital	9-16	N-terminal asparagine amidase	Homo sapiens	52-56
34209776-9	2021	KCNQ1OT1, LOC100270804, and FLJ10038 median levels were found to be significantly higher in the luminal subtype.	Phenobarbital	96-103	GABPB1 intronic transcript	Homo sapiens	28-36
34192549-4	2021	The luminal domain loop 1 and a co-folded segment in loop 7 of Scap resemble those of the luminal/extracellular domain in NPC1 and related proteins, providing clues to the cholesterol-regulated interaction of loop 1 and loop 7.	Phenobarbital	4-11	SREBF chaperone	Homo sapiens	63-67
34192549-4	2021	The luminal domain loop 1 and a co-folded segment in loop 7 of Scap resemble those of the luminal/extracellular domain in NPC1 and related proteins, providing clues to the cholesterol-regulated interaction of loop 1 and loop 7.	Phenobarbital	4-11	NPC intracellular cholesterol transporter 1	Homo sapiens	122-126
34192549-4	2021	The luminal domain loop 1 and a co-folded segment in loop 7 of Scap resemble those of the luminal/extracellular domain in NPC1 and related proteins, providing clues to the cholesterol-regulated interaction of loop 1 and loop 7.	Phenobarbital	90-97	SREBF chaperone	Homo sapiens	63-67
34192549-4	2021	The luminal domain loop 1 and a co-folded segment in loop 7 of Scap resemble those of the luminal/extracellular domain in NPC1 and related proteins, providing clues to the cholesterol-regulated interaction of loop 1 and loop 7.	Phenobarbital	90-97	NPC intracellular cholesterol transporter 1	Homo sapiens	122-126
34192549-5	2021	An additional luminal interface is observed between Scap and Insig.	Phenobarbital	14-21	SREBF chaperone	Homo sapiens	52-56
34161412-6	2021	Moreover, the immunoreactivity of CD44 was particularly evident in the non-luminal cells of these lesions.	Phenobarbital	75-82	CD44 molecule (Indian blood group)	Homo sapiens	34-38
34201429-18	2021	Collectively, our findings show that obese-ADS induction of LAT1 supports mTOR hyperactivity in luminal BC cells.	Phenobarbital	96-103	solute carrier family 7 member 5	Homo sapiens	60-64
34201429-18	2021	Collectively, our findings show that obese-ADS induction of LAT1 supports mTOR hyperactivity in luminal BC cells.	Phenobarbital	96-103	mechanistic target of rapamycin kinase	Homo sapiens	74-78
34202968-9	2021	Functional analysis of D3291V channels revealed a normal response to cytosolic Ca2+, a markedly reduced luminal Ca2+ sensitivity and, more importantly, an absence of normal response to 8-bromo-cAMP and forskolin stimulation in both transfected HEK293 and HL-1 cells.	Phenobarbital	104-111	carbonic anhydrase 2	Homo sapiens	112-115
34220957-2	2021	The aim of the current study was to explore the association between CD39 expression and clinic pathological characteristics and the prognosis in luminal BC patients.	Phenobarbital	145-152	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	68-72
34158497-6	2021	The N-retinylidene-phosphatidylethanolamine (NRPE), the physiological lipid substrate of ABCA4, is sandwiched between the two TMDs in the luminal leaflet and is further stabilized by an extended loop from extracellular domain 1.	Phenobarbital	138-145	ATP binding cassette subfamily A member 4	Homo sapiens	89-94
34128985-2	2021	Here, we show that Laminin alpha5 (Lama5) expression specifically in the luminal epithelial cells is necessary for normal mammary gland growth during puberty, and for alveologenesis during pregnancy.	Phenobarbital	73-80	laminin subunit alpha 5	Homo sapiens	35-40
34249460-0	2021	Deletion of Foxa1 in the mouse mammary gland results in abnormal accumulation of luminal progenitor cells: a link between reproductive factors and ER-/TNBC breast cancer?	Phenobarbital	81-88	forkhead box A1	Mus musculus	12-17
34249460-2	2021	We postulate that pregnancy-associated repression of FOXA1 results in the accumulation of aberrant, differentiation-arrested luminal progenitor cells which, following additional genetic and epigenetic insults, may give rise to ER- tumors.	Phenobarbital	125-132	forkhead box A1	Homo sapiens	53-58
34249460-2	2021	We postulate that pregnancy-associated repression of FOXA1 results in the accumulation of aberrant, differentiation-arrested luminal progenitor cells which, following additional genetic and epigenetic insults, may give rise to ER- tumors.	Phenobarbital	125-132	epiregulin	Homo sapiens	227-229
34128985-3	2021	Lama5 loss in the keratin 8-expressing cells results in reduced frequency and differentiation of hormone receptor expressing (HR+) luminal cells.	Phenobarbital	131-138	laminin subunit alpha 5	Homo sapiens	0-5
34249460-3	2021	Consistent with this hypothesis, we show that deletion of Foxa1 in the mouse mammary gland results in a two-fold increase in the proportion of luminal progenitor cells and a reduction in mammary gland epithelial cells that stain positive for ER.	Phenobarbital	143-150	forkhead box A1	Mus musculus	58-63
34128985-3	2021	Lama5 loss in the keratin 8-expressing cells results in reduced frequency and differentiation of hormone receptor expressing (HR+) luminal cells.	Phenobarbital	131-138	keratin 8	Homo sapiens	18-27
34128985-3	2021	Lama5 loss in the keratin 8-expressing cells results in reduced frequency and differentiation of hormone receptor expressing (HR+) luminal cells.	Phenobarbital	131-138	nuclear receptor subfamily 4 group A member 1	Homo sapiens	97-113
34128985-4	2021	Consequently, Wnt4-mediated crosstalk between HR+ luminal cells and basal epithelial cells is compromised during gland remodeling, and results in defective epithelial growth.	Phenobarbital	50-57	Wnt family member 4	Homo sapiens	14-18
34100381-1	2021	SLC26A6 (also known as putative anion transporter 1 (PAT1)) is a Cl-/HCO3- exchanger expressed at the luminal membrane of enterocytes where it facilitates intestinal Cl- and fluid absorption.	Phenobarbital	102-109	solute carrier family 26, member 6	Mus musculus	0-7
34109737-6	2022	In luminal A MCF-7 cells, the selection of a drug-resistant subline from parental cells with deregulation of p53 pathways occurred.	Phenobarbital	3-10	tumor protein p53	Homo sapiens	109-112
34100381-1	2021	SLC26A6 (also known as putative anion transporter 1 (PAT1)) is a Cl-/HCO3- exchanger expressed at the luminal membrane of enterocytes where it facilitates intestinal Cl- and fluid absorption.	Phenobarbital	102-109	solute carrier family 26, member 6	Mus musculus	23-51
34100381-1	2021	SLC26A6 (also known as putative anion transporter 1 (PAT1)) is a Cl-/HCO3- exchanger expressed at the luminal membrane of enterocytes where it facilitates intestinal Cl- and fluid absorption.	Phenobarbital	102-109	solute carrier family 26, member 6	Mus musculus	53-57
34193566-8	2021	In particular, we found transglutaminase 4 (Tgm4) to be highly expressed in prostate tumors that originate from luminal epithelial cells and only expressed at low levels in most extraprostatic tissues evaluated.	Phenobarbital	112-119	transglutaminase 4	Homo sapiens	24-42
34205013-6	2021	Our modeling shows that the very high plasma concentration of Tf leads to only 5% of the endothelial TfR expressed on the luminal endothelial membrane.	Phenobarbital	122-129	transferrin receptor	Homo sapiens	101-104
34076847-13	2022	Immunohistologically, the luminal cells were positive for gross cystic disease fluid protein-15.	Phenobarbital	26-33	prolactin induced protein	Homo sapiens	58-95
34181349-7	2021	RESULTS: TIMAP protein was strongly expressed in 46 (93.9%) HER2-only, 32 (97%) luminal A, 37 (94.9%) luminal B, and 29 (76.3%) triple negative.	Phenobarbital	80-87	protein phosphatase 1 regulatory subunit 16B	Homo sapiens	9-14
34181349-7	2021	RESULTS: TIMAP protein was strongly expressed in 46 (93.9%) HER2-only, 32 (97%) luminal A, 37 (94.9%) luminal B, and 29 (76.3%) triple negative.	Phenobarbital	102-109	protein phosphatase 1 regulatory subunit 16B	Homo sapiens	9-14
34193566-8	2021	In particular, we found transglutaminase 4 (Tgm4) to be highly expressed in prostate tumors that originate from luminal epithelial cells and only expressed at low levels in most extraprostatic tissues evaluated.	Phenobarbital	112-119	transglutaminase 4	Homo sapiens	44-48
34086481-1	2021	PURPOSE: Luminal, human epidermal growth factor receptor 2-negative breast cancer represents the most common subtype of breast malignancies.	Phenobarbital	9-16	erb-b2 receptor tyrosine kinase 2	Homo sapiens	24-58
34188682-13	2021	bcl-2 (protein) and p53 significantly correlated with Luminal B and TNBC (p < 0.01).	Phenobarbital	54-61	BCL2 apoptosis regulator	Homo sapiens	0-5
34188682-13	2021	bcl-2 (protein) and p53 significantly correlated with Luminal B and TNBC (p < 0.01).	Phenobarbital	54-61	tumor protein p53	Homo sapiens	20-23
34072329-6	2021	These simulations suggest that SGLT2 inhibition may attenuate glomerular hyperfiltration by limiting Na+-glucose transport, raising luminal (Cl-) at the macula densa, restoring the tubuloglomerular feedback signal, thereby reducing single-nephron glomerular filtration rate.	Phenobarbital	132-139	solute carrier family 5 member 2	Homo sapiens	31-36
34070901-0	2021	Syndecan-1 Depletion Has a Differential Impact on Hyaluronic Acid Metabolism and Tumor Cell Behavior in Luminal and Triple-Negative Breast Cancer Cells.	Phenobarbital	104-111	syndecan 1	Homo sapiens	0-10
34075163-2	2021	We utilized the established non-malignant HPr1-AR prostate epithelial cell model that upon androgen exposure commits to a luminal cell differentiation trajectory from that of a basal-like state.	Phenobarbital	122-129	THO complex 1	Homo sapiens	42-46
34070901-9	2021	We conclude that Sdc-1 knockdown differentially affects HA metabolism in luminal and triple-negative breast cancer model cell lines and impacts the stem phenotype, cell survival, and angiogenic factors.	Phenobarbital	73-80	syndecan 1	Homo sapiens	17-22
34073233-9	2021	Tumours with an elevated expression of markers associated with luminal differentiation (KRT20, ERBB2, ESR1) were associated with a higher chance of pCR (55% vs. 15.8%, p = 0.009).	Phenobarbital	63-70	keratin 20	Homo sapiens	88-93
34073233-9	2021	Tumours with an elevated expression of markers associated with luminal differentiation (KRT20, ERBB2, ESR1) were associated with a higher chance of pCR (55% vs. 15.8%, p = 0.009).	Phenobarbital	63-70	erb-b2 receptor tyrosine kinase 2	Homo sapiens	95-100
34073233-9	2021	Tumours with an elevated expression of markers associated with luminal differentiation (KRT20, ERBB2, ESR1) were associated with a higher chance of pCR (55% vs. 15.8%, p = 0.009).	Phenobarbital	63-70	estrogen receptor 1	Homo sapiens	102-106
34094675-9	2021	Overexpression of miR-22 impaired the DEN/PB-induced primary HCC formation and the growth of Hepa1-6 subcutaneous tumors by promoting Th17 differentiation.	Phenobarbital	42-44	microRNA 22	Homo sapiens	18-24
34073233-10	2021	Elevated ERBB2 expression was positively correlated with luminal expression features such as KRT20, and negatively with basal characteristics such as KRT5.	Phenobarbital	57-64	erb-b2 receptor tyrosine kinase 2	Homo sapiens	9-14
34073233-10	2021	Elevated ERBB2 expression was positively correlated with luminal expression features such as KRT20, and negatively with basal characteristics such as KRT5.	Phenobarbital	57-64	keratin 20	Homo sapiens	93-98
34264181-2	2021	Studies with phenobarbital (PB) and other compounds have identified the key events for this MOA: CAR activation; increased hepatocellular proliferation; altered foci formation; and ultimately the development of adenomas/carcinomas.	Phenobarbital	13-26	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	97-100
34150026-10	2021	Moreover, there was an increase in the expression levels of Perilipin 1 (PLIN1), PLIN3, Perilipin 4 (PLIN4) and Perilipin 5 (PLIN5) in the luminal A and luminal B subgroups.	Phenobarbital	139-146	perilipin 1	Homo sapiens	60-71
34150026-10	2021	Moreover, there was an increase in the expression levels of Perilipin 1 (PLIN1), PLIN3, Perilipin 4 (PLIN4) and Perilipin 5 (PLIN5) in the luminal A and luminal B subgroups.	Phenobarbital	139-146	perilipin 1	Homo sapiens	73-78
34150026-10	2021	Moreover, there was an increase in the expression levels of Perilipin 1 (PLIN1), PLIN3, Perilipin 4 (PLIN4) and Perilipin 5 (PLIN5) in the luminal A and luminal B subgroups.	Phenobarbital	139-146	perilipin 3	Homo sapiens	81-86
34150026-10	2021	Moreover, there was an increase in the expression levels of Perilipin 1 (PLIN1), PLIN3, Perilipin 4 (PLIN4) and Perilipin 5 (PLIN5) in the luminal A and luminal B subgroups.	Phenobarbital	139-146	perilipin 4	Homo sapiens	88-99
34150026-10	2021	Moreover, there was an increase in the expression levels of Perilipin 1 (PLIN1), PLIN3, Perilipin 4 (PLIN4) and Perilipin 5 (PLIN5) in the luminal A and luminal B subgroups.	Phenobarbital	139-146	perilipin 4	Homo sapiens	101-106
34150026-10	2021	Moreover, there was an increase in the expression levels of Perilipin 1 (PLIN1), PLIN3, Perilipin 4 (PLIN4) and Perilipin 5 (PLIN5) in the luminal A and luminal B subgroups.	Phenobarbital	139-146	perilipin 5	Homo sapiens	112-123
34150026-10	2021	Moreover, there was an increase in the expression levels of Perilipin 1 (PLIN1), PLIN3, Perilipin 4 (PLIN4) and Perilipin 5 (PLIN5) in the luminal A and luminal B subgroups.	Phenobarbital	139-146	perilipin 5	Homo sapiens	125-130
34150026-10	2021	Moreover, there was an increase in the expression levels of Perilipin 1 (PLIN1), PLIN3, Perilipin 4 (PLIN4) and Perilipin 5 (PLIN5) in the luminal A and luminal B subgroups.	Phenobarbital	153-160	perilipin 1	Homo sapiens	60-71
34150026-10	2021	Moreover, there was an increase in the expression levels of Perilipin 1 (PLIN1), PLIN3, Perilipin 4 (PLIN4) and Perilipin 5 (PLIN5) in the luminal A and luminal B subgroups.	Phenobarbital	153-160	perilipin 1	Homo sapiens	73-78
34150026-10	2021	Moreover, there was an increase in the expression levels of Perilipin 1 (PLIN1), PLIN3, Perilipin 4 (PLIN4) and Perilipin 5 (PLIN5) in the luminal A and luminal B subgroups.	Phenobarbital	153-160	perilipin 3	Homo sapiens	81-86
34150026-10	2021	Moreover, there was an increase in the expression levels of Perilipin 1 (PLIN1), PLIN3, Perilipin 4 (PLIN4) and Perilipin 5 (PLIN5) in the luminal A and luminal B subgroups.	Phenobarbital	153-160	perilipin 4	Homo sapiens	88-99
34150026-10	2021	Moreover, there was an increase in the expression levels of Perilipin 1 (PLIN1), PLIN3, Perilipin 4 (PLIN4) and Perilipin 5 (PLIN5) in the luminal A and luminal B subgroups.	Phenobarbital	153-160	perilipin 4	Homo sapiens	101-106
34150026-10	2021	Moreover, there was an increase in the expression levels of Perilipin 1 (PLIN1), PLIN3, Perilipin 4 (PLIN4) and Perilipin 5 (PLIN5) in the luminal A and luminal B subgroups.	Phenobarbital	153-160	perilipin 5	Homo sapiens	112-123
34150026-10	2021	Moreover, there was an increase in the expression levels of Perilipin 1 (PLIN1), PLIN3, Perilipin 4 (PLIN4) and Perilipin 5 (PLIN5) in the luminal A and luminal B subgroups.	Phenobarbital	153-160	perilipin 5	Homo sapiens	125-130
34064473-8	2021	In METABRIC and SCAN-B cohorts, high levels of BIRC5 mRNA were associated with the basal-like and luminal B molecular BC subtypes and with increasing histologic grade.	Phenobarbital	98-105	baculoviral IAP repeat containing 5	Homo sapiens	47-52
34164526-5	2021	We analyzed the alterations of different malignancies of luminal cells by up-regulation of SLC7A5 in human luminal cell lines MCF-7.	Phenobarbital	57-64	solute carrier family 7 (cationic amino acid transporter, y+ system), member 5	Mus musculus	91-97
34164526-5	2021	We analyzed the alterations of different malignancies of luminal cells by up-regulation of SLC7A5 in human luminal cell lines MCF-7.	Phenobarbital	107-114	solute carrier family 7 (cationic amino acid transporter, y+ system), member 5	Mus musculus	91-97
34164526-6	2021	SLC7A5 was overexpressed in luminal cells, and then the AKT, mTOR, and p70-S6K phosphorylation and expression were analyzed by western blot analysis and real-time quantitative polymerase chain reaction (qPCR).	Phenobarbital	28-35	solute carrier family 7 (cationic amino acid transporter, y+ system), member 5	Mus musculus	0-6
34164526-8	2021	Elevated SLC7A5 messenger RNA (mRNA) and SLC7A5 protein expression was correlated to a worse clinical prognosis (P<0.001) in luminal subtypes of BC.	Phenobarbital	125-132	solute carrier family 7 member 5	Homo sapiens	9-15
34068438-7	2021	Therefore, treatment of CDDP with HDIs could be used to optimize a combined therapy based on CDDP against Notch1-altered luminal BC.	Phenobarbital	121-128	notch receptor 1	Homo sapiens	106-112
34093815-17	2021	Additionally, we found that the GPL+CUMS rats with tumors not only had strong expression of GKN2 on the luminal side and the lamina propria of the gastric mucosa and tumor, but also had expression of Ghrelin on the luminal side of the gastric mucosa.	Phenobarbital	104-111	gastrokine 2	Rattus norvegicus	92-96
34063062-9	2021	It is hypothesized that luminal food peptides that share cross-reactive epitopes with human alpha-synuclein and have molecular similarity with brain antigens are involved in the synucleinopathy.	Phenobarbital	24-31	synuclein alpha	Homo sapiens	92-107
34264181-2	2021	Studies with phenobarbital (PB) and other compounds have identified the key events for this MOA: CAR activation; increased hepatocellular proliferation; altered foci formation; and ultimately the development of adenomas/carcinomas.	Phenobarbital	28-30	nuclear receptor subfamily 1, group I, member 3	Rattus norvegicus	97-100
34937822-1	2021	Dipeptidyl peptidase 4 (DPP4), a serine protease expressed on luminal and apical cell membrane, is identical to the lymphocyte cell surface protein CD26.	Phenobarbital	62-69	dipeptidyl peptidase 4	Homo sapiens	0-22
34221828-7	2021	The molecular subtypes of her right and left primary BC were HER2-enriched type and luminal-HER2 type, respectively.	Phenobarbital	84-91	erb-b2 receptor tyrosine kinase 2	Homo sapiens	92-96
34345857-9	2021	For the CYP2B/C/D"s, phenobarbital and rifampicin caused increases in expression.	Phenobarbital	21-34	cytochrome P450 family 2 subfamily B member 7, pseudogene	Homo sapiens	8-13
34345857-11	2021	Both phenobarbital, rifampicin and omeprazole increased CYP3A expression in PHH and PPH.	Phenobarbital	5-18	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	56-61
34937822-1	2021	Dipeptidyl peptidase 4 (DPP4), a serine protease expressed on luminal and apical cell membrane, is identical to the lymphocyte cell surface protein CD26.	Phenobarbital	62-69	dipeptidyl peptidase 4	Homo sapiens	24-28
34937822-1	2021	Dipeptidyl peptidase 4 (DPP4), a serine protease expressed on luminal and apical cell membrane, is identical to the lymphocyte cell surface protein CD26.	Phenobarbital	62-69	coagulation factor II, thrombin	Homo sapiens	33-48
34238461-2	2021	In the renal collecting duct, vasopressin binds to the V2 receptor, increasing water permeability through activation of aquaporin-2 redistribution to the luminal membrane.	Phenobarbital	154-161	arginine vasopressin	Homo sapiens	30-41
34238461-2	2021	In the renal collecting duct, vasopressin binds to the V2 receptor, increasing water permeability through activation of aquaporin-2 redistribution to the luminal membrane.	Phenobarbital	154-161	aquaporin 2	Homo sapiens	120-131
35367370-11	2022	CYP7A1, the enzyme involved in production of 7alpha-HC, was significantly more abundant in TNBC than other subtypes (vs Luminal A; P = 0.0321, vs Luminal B; P = 0.0048, vs HER2; P = 0.0103).	Phenobarbital	120-127	cytochrome P450 family 7 subfamily A member 1	Homo sapiens	0-6
34609431-6	2021	According to chi-squared analysis of molecular cancer subtypes correlation to receptors and Ki67 index, we found significant associations between both luminal A and luminal B HER2-negative subtypes and hormone receptors (ER, PR).	Phenobarbital	151-158	estrogen receptor 1	Homo sapiens	221-223
34609431-6	2021	According to chi-squared analysis of molecular cancer subtypes correlation to receptors and Ki67 index, we found significant associations between both luminal A and luminal B HER2-negative subtypes and hormone receptors (ER, PR).	Phenobarbital	151-158	progesterone receptor	Homo sapiens	225-227
34609431-6	2021	According to chi-squared analysis of molecular cancer subtypes correlation to receptors and Ki67 index, we found significant associations between both luminal A and luminal B HER2-negative subtypes and hormone receptors (ER, PR).	Phenobarbital	165-172	erb-b2 receptor tyrosine kinase 2	Homo sapiens	175-179
34609431-6	2021	According to chi-squared analysis of molecular cancer subtypes correlation to receptors and Ki67 index, we found significant associations between both luminal A and luminal B HER2-negative subtypes and hormone receptors (ER, PR).	Phenobarbital	165-172	estrogen receptor 1	Homo sapiens	221-223
34609431-6	2021	According to chi-squared analysis of molecular cancer subtypes correlation to receptors and Ki67 index, we found significant associations between both luminal A and luminal B HER2-negative subtypes and hormone receptors (ER, PR).	Phenobarbital	165-172	progesterone receptor	Homo sapiens	225-227
35543228-9	2022	In addition, XBP1 mRNA and protein levels were higher in the luminal subtype than in normal tissues and basal-like subtype, which might be attributed to membrane transport-related processes.	Phenobarbital	61-68	X-box binding protein 1	Homo sapiens	13-17
35134122-9	2022	In Sirt1d/d Group #1, nuclear FOXO1 expression in luminal epithelial cells was significantly decreased.	Phenobarbital	50-57	forkhead box O1	Mus musculus	30-35
35471456-6	2022	Furthermore, downregulation of NR2F1 promoted a hybrid luminal/basal phenotype.	Phenobarbital	55-62	nuclear receptor subfamily 2 group F member 1	Homo sapiens	31-36
35181405-4	2022	Here, the distinction between these direct and indirect effects of MT PTMs are exemplified by acetylation of the luminal alpha-tubulin K40 resulting in decreased rigidity of MTs, and by MT detyrosination which decreases interaction with depolymerizing proteins, thus causing more stable MTs.	Phenobarbital	113-120	parathymosin	Homo sapiens	70-74
35348632-7	2022	IL10 protein was localized to luminal epithelial (LE), stromal cells, and macrophages; IL10RA protein to LE, endothelial, stromal, and T cells; and IL10RB mRNA to LE cells in the endometrium.	Phenobarbital	30-37	IL10	Sus scrofa	0-4
35181405-4	2022	Here, the distinction between these direct and indirect effects of MT PTMs are exemplified by acetylation of the luminal alpha-tubulin K40 resulting in decreased rigidity of MTs, and by MT detyrosination which decreases interaction with depolymerizing proteins, thus causing more stable MTs.	Phenobarbital	113-120	keratin 40	Homo sapiens	135-138
35217253-8	2022	Biotin-C3 peptide characterized luminal BC according to p53 status and to HER2 expression, being the biosensor a better strategy when compared to ELISA test.	Phenobarbital	32-39	tumor protein p53	Homo sapiens	56-59
35217253-8	2022	Biotin-C3 peptide characterized luminal BC according to p53 status and to HER2 expression, being the biosensor a better strategy when compared to ELISA test.	Phenobarbital	32-39	erb-b2 receptor tyrosine kinase 2	Homo sapiens	74-78
35633393-0	2022	Newly identified breast luminal progenitor and gestational stem cell populations likely give rise to HER2-overexpressing and basal-like breast cancers.	Phenobarbital	24-31	erb-b2 receptor tyrosine kinase 2	Homo sapiens	101-105
35577558-4	2022	RESULTS: After ischemia-reperfusion injury with contralateral nephrectomy, Arg1-expressing macrophages were almost exclusively located in the outer stripe of the medulla adjacent to injured S3 tubule segments containing luminal debris or casts.	Phenobarbital	220-227	arginase, liver	Mus musculus	75-79
35182544-1	2022	Podocalyxin (PODXL) is a highly sialylated transmembrane protein that is expressed on the luminal membrane of brain microvascular endothelial cells.	Phenobarbital	90-97	podocalyxin like	Homo sapiens	0-11
35182544-1	2022	Podocalyxin (PODXL) is a highly sialylated transmembrane protein that is expressed on the luminal membrane of brain microvascular endothelial cells.	Phenobarbital	90-97	podocalyxin like	Homo sapiens	13-18
35633393-11	2022	A novel luminal progenitor cell population and HER2-overexpressing BrCs are marked by S100A7, S100A8, and S100A9 expression.	Phenobarbital	8-15	S100 calcium binding protein A7	Homo sapiens	86-92
35633393-11	2022	A novel luminal progenitor cell population and HER2-overexpressing BrCs are marked by S100A7, S100A8, and S100A9 expression.	Phenobarbital	8-15	S100 calcium binding protein A8	Homo sapiens	94-100
35633393-11	2022	A novel luminal progenitor cell population and HER2-overexpressing BrCs are marked by S100A7, S100A8, and S100A9 expression.	Phenobarbital	8-15	S100 calcium binding protein A9	Homo sapiens	106-112
35633393-14	2022	In summary, normal SC and the novel luminal progenitor cell population likely give rise to basal-like and HER2-overexpressing BrCs, respectively.	Phenobarbital	36-43	erb-b2 receptor tyrosine kinase 2	Mus musculus	106-110
35048960-2	2022	Here, we report that Vascular Endothelial Growth Factor (VEGF) signaling at the luminal side of the brain microvasculature plays an integral role in the capillary stalling phenomenon of the APP/PS1 mouse model.	Phenobarbital	80-87	vascular endothelial growth factor A	Mus musculus	21-55
35048960-2	2022	Here, we report that Vascular Endothelial Growth Factor (VEGF) signaling at the luminal side of the brain microvasculature plays an integral role in the capillary stalling phenomenon of the APP/PS1 mouse model.	Phenobarbital	80-87	vascular endothelial growth factor A	Mus musculus	57-61
35612672-0	2022	Uroplakin II as a single marker for luminal versus basal molecular subtypes in muscle invasive urothelial carcinoma.	Phenobarbital	36-43	uroplakin 2	Homo sapiens	0-12
35048960-2	2022	Here, we report that Vascular Endothelial Growth Factor (VEGF) signaling at the luminal side of the brain microvasculature plays an integral role in the capillary stalling phenomenon of the APP/PS1 mouse model.	Phenobarbital	80-87	presenilin 1	Mus musculus	194-197
35612672-4	2022	The 1% cutoff of the UPII stain predicts the luminal subtype with the sensitivity and specificity of 95% and 56%, respectively.	Phenobarbital	45-52	uroplakin 2	Homo sapiens	21-25
35048960-7	2022	Reducing leucocyte adhesion by inhibiting luminal VEGF signaling may provide a novel and well-tolerated strategy for improving brain microvascular blood flow in Alzheimer"s disease.	Phenobarbital	42-49	vascular endothelial growth factor A	Homo sapiens	50-54
35612672-8	2022	The current study shows that evaluating the staining proportion score of UPII can accurately predict basal and luminal subtypes of muscle-invasive bladder cancer.	Phenobarbital	111-118	uroplakin 2	Homo sapiens	73-77
35605014-4	2022	Solute carrier family 20 member 1 (SLC20A1) is a sodium/inorganic phosphate symporter that has been proposed to be a viable prognostic marker for the luminal A and luminal B types of ER+ breast cancer.	Phenobarbital	150-157	solute carrier family 20 member 1	Homo sapiens	0-33
35608730-9	2022	Compared to luminal tumors, triple-negative tumors had relative under-expression of TSC1 (log2 fold-change = - 0.42, 95% CI - 0.22, - 0.01).	Phenobarbital	12-19	TSC complex subunit 1	Homo sapiens	84-88
35613593-5	2022	Furthermore, single-cell analyses of the tumor samples reveal that secretory luminal cells are the cell population particularly affected by stromal AR deletion, as they transition to a cellular state of potentiated PI3K-mTORC1 activities.	Phenobarbital	77-84	androgen receptor	Mus musculus	148-150
35613593-6	2022	Our results suggest that stromal AR normally inhibits prostate cancer progression by restraining secretory luminal cells and imply possible unintended negative effects of androgen deprivation therapy.	Phenobarbital	107-114	androgen receptor	Mus musculus	33-35
35605014-4	2022	Solute carrier family 20 member 1 (SLC20A1) is a sodium/inorganic phosphate symporter that has been proposed to be a viable prognostic marker for the luminal A and luminal B types of ER+ breast cancer.	Phenobarbital	150-157	solute carrier family 20 member 1	Homo sapiens	35-42
35605014-4	2022	Solute carrier family 20 member 1 (SLC20A1) is a sodium/inorganic phosphate symporter that has been proposed to be a viable prognostic marker for the luminal A and luminal B types of ER+ breast cancer.	Phenobarbital	164-171	solute carrier family 20 member 1	Homo sapiens	0-33
35605014-4	2022	Solute carrier family 20 member 1 (SLC20A1) is a sodium/inorganic phosphate symporter that has been proposed to be a viable prognostic marker for the luminal A and luminal B types of ER+ breast cancer.	Phenobarbital	164-171	solute carrier family 20 member 1	Homo sapiens	35-42
35605014-4	2022	Solute carrier family 20 member 1 (SLC20A1) is a sodium/inorganic phosphate symporter that has been proposed to be a viable prognostic marker for the luminal A and luminal B types of ER+ breast cancer.	Phenobarbital	164-171	epiregulin	Homo sapiens	183-185
35605014-8	2022	In addition, this SLC20A1high subgroup of patients exhibited less responses to endocrine therapy, specifically in those with the luminal A and luminal B subtypes of breast cancer.	Phenobarbital	129-136	solute carrier family 20 member 1	Homo sapiens	18-25
35605014-8	2022	In addition, this SLC20A1high subgroup of patients exhibited less responses to endocrine therapy, specifically in those with the luminal A and luminal B subtypes of breast cancer.	Phenobarbital	143-150	solute carrier family 20 member 1	Homo sapiens	18-25
35502723-6	2022	Additionally, we found that only cells with luminal features were able to acquire transformed characteristics after an oncogenic HER2 mutant was introduced in their genomes.	Phenobarbital	44-51	erb-b2 receptor tyrosine kinase 2	Mus musculus	129-133
35590106-7	2022	ASOR activation requires Na+-mediated depolarization and luminal acidification by redundant transporters including H+-ATPases and CLC 2Cl-/H+ exchangers.	Phenobarbital	57-64	proton activated chloride channel 1	Homo sapiens	0-4
35628286-4	2022	Transcriptomic mapping of CDKs in breast cancer demonstrated that the expression of CDK9 predicted a detrimental outcome in basal-like tumors (HR = 1.51, CI = 1.08-2.11, p = 0.015) and, particularly, in the luminal B subtype with HER2+ expression (HR = 1.82, CI = 1.17-2.82, p = 0.0069).	Phenobarbital	207-214	cyclin dependent kinase 9	Homo sapiens	26-30
35577139-8	2022	The proliferation index of the luminal B group was significantly (p < 0.001) higher in the low HR (hormone receptor) group than in the HR group.	Phenobarbital	31-38	nuclear receptor subfamily 4 group A member 1	Homo sapiens	99-115
35562350-3	2022	We demonstrate that MYC overexpression significantly diminishes the androgen receptor (AR) transcriptional program (the set of genes directly targeted by the AR protein) in luminal prostate cells without altering AR expression.	Phenobarbital	173-180	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	20-23
35562350-3	2022	We demonstrate that MYC overexpression significantly diminishes the androgen receptor (AR) transcriptional program (the set of genes directly targeted by the AR protein) in luminal prostate cells without altering AR expression.	Phenobarbital	173-180	androgen receptor	Homo sapiens	68-85
35628294-4	2022	Both ectopic expression and platelet MV-mediated delivery of miR-126-3p downregulated AKT2 expression, thus suppressing proliferating and invading properties, in either triple negative (BT549 cells) or less aggressive Luminal A (MCF-7 cells) BC subtypes.	Phenobarbital	218-225	microRNA 1263	Homo sapiens	61-71
35628294-4	2022	Both ectopic expression and platelet MV-mediated delivery of miR-126-3p downregulated AKT2 expression, thus suppressing proliferating and invading properties, in either triple negative (BT549 cells) or less aggressive Luminal A (MCF-7 cells) BC subtypes.	Phenobarbital	218-225	AKT serine/threonine kinase 2	Homo sapiens	86-90
35562350-3	2022	We demonstrate that MYC overexpression significantly diminishes the androgen receptor (AR) transcriptional program (the set of genes directly targeted by the AR protein) in luminal prostate cells without altering AR expression.	Phenobarbital	173-180	androgen receptor	Homo sapiens	87-89
35628286-4	2022	Transcriptomic mapping of CDKs in breast cancer demonstrated that the expression of CDK9 predicted a detrimental outcome in basal-like tumors (HR = 1.51, CI = 1.08-2.11, p = 0.015) and, particularly, in the luminal B subtype with HER2+ expression (HR = 1.82, CI = 1.17-2.82, p = 0.0069).	Phenobarbital	207-214	cyclin dependent kinase 9	Homo sapiens	84-88
35562350-3	2022	We demonstrate that MYC overexpression significantly diminishes the androgen receptor (AR) transcriptional program (the set of genes directly targeted by the AR protein) in luminal prostate cells without altering AR expression.	Phenobarbital	173-180	androgen receptor	Homo sapiens	158-160
35527554-13	2022	CONCLUSION: These findings reveal the importance of pathological changes within the gut-vagus-brain signaling in response to luminal bacterial amyloid that might play a vital role in central Abeta pathogenesis seen in the AD brain.	Phenobarbital	125-132	amyloid beta precursor protein	Homo sapiens	191-196
35561288-8	2022	Strong progesterone receptor expression was observed in at least 90% of glandular cells in the middle and luminal portions, whereas weak staining and significant decrease in positivity were detected in the basal portions of the glands.	Phenobarbital	106-113	progesterone receptor	Bos taurus	7-28
35551511-6	2022	We identified three main roles for NSP6: to act as a filter in RO-ER communication allowing lipid flow but restricting access of ER luminal proteins to the DMVs, to position and organize DMV clusters, and to mediate contact with lipid droplets (LDs) via the LD-tethering complex DFCP1-Rab18.	Phenobarbital	132-139	ORF1a polyprotein;ORF1ab polyprotein	Severe acute respiratory syndrome coronavirus 2	35-39
35626649-6	2022	Here, we employed the prime editing tool to revert a TP53 missense C > T mutation (L194F) in a T47D luminal A breast cancer cell line.	Phenobarbital	100-107	tumor protein p53	Homo sapiens	53-57
35446032-4	2022	Luminal targeting of seed particles occurs through covalently linked Fab fragments of an antibody recognizing the acetylated lysine 40 on the luminal side of alpha-tubulin.	Phenobarbital	0-7	FA complementation group B	Homo sapiens	69-72
35446032-4	2022	Luminal targeting of seed particles occurs through covalently linked Fab fragments of an antibody recognizing the acetylated lysine 40 on the luminal side of alpha-tubulin.	Phenobarbital	0-7	tubulin alpha 1b	Homo sapiens	158-171
35446032-4	2022	Luminal targeting of seed particles occurs through covalently linked Fab fragments of an antibody recognizing the acetylated lysine 40 on the luminal side of alpha-tubulin.	Phenobarbital	142-149	FA complementation group B	Homo sapiens	69-72
35446032-4	2022	Luminal targeting of seed particles occurs through covalently linked Fab fragments of an antibody recognizing the acetylated lysine 40 on the luminal side of alpha-tubulin.	Phenobarbital	142-149	tubulin alpha 1b	Homo sapiens	158-171
35501337-4	2022	Nuclear SOX10 was detected in normal mammary luminal progenitor cells, the histogenic origin of most TNBCs.	Phenobarbital	45-52	SRY-box transcription factor 10	Homo sapiens	8-13
35181505-9	2022	Luminal A specific were enriched in the translational elongation process in mitochondria, and the enhanced process in luminal B subtypes was interferon-alpha/beta signaling.	Phenobarbital	0-7	interferon alpha 2	Homo sapiens	141-162
35181505-9	2022	Luminal A specific were enriched in the translational elongation process in mitochondria, and the enhanced process in luminal B subtypes was interferon-alpha/beta signaling.	Phenobarbital	118-125	interferon alpha 2	Homo sapiens	141-162
35512572-4	2022	Western blot analysis confirmed increased expression of MCT1 protein in SUM159 (basal-like) and MCF-7 cells (luminal-type) stably transfected to overexpress FoxQ1.	Phenobarbital	109-116	solute carrier family 16 member 1	Homo sapiens	56-60
35512572-4	2022	Western blot analysis confirmed increased expression of MCT1 protein in SUM159 (basal-like) and MCF-7 cells (luminal-type) stably transfected to overexpress FoxQ1.	Phenobarbital	109-116	forkhead box Q1	Homo sapiens	157-162
35504668-4	2022	In this present case report, we describe the presence of cluster of differentiation (CD) 163-positive macrophages in close proximity to the stent struts at the luminal site 72 hours after drug-eluting stent implantation in the culprit coronary lesion for ST elevation myocardial infarction by postmortem examination.	Phenobarbital	160-167	CD163 molecule	Homo sapiens	84-92
35288975-6	2022	Immunoreactivity for leptin and obestatin was present in the cytoplasms of luminal and glandular cells, while smooth muscle cells were immunoreactant for ghrelin, in both bull and ram abomasums.	Phenobarbital	75-82	leptin	Homo sapiens	21-27
35288975-7	2022	Immunoreactivity for OB-R was present in luminal and glandular cell, parietal cell cytoplasms, and blood vessels.	Phenobarbital	41-48	leptin receptor	Homo sapiens	21-25
35227076-1	2022	Purpose: The authors aimed to evaluate the prognostic and predictive value of androgen receptor (AR) expression in patients with luminal/human EGFR2 negative (HER2-) T1N0 breast cancer.	Phenobarbital	129-136	androgen receptor	Homo sapiens	78-95
35344382-9	2022	Maximal luminal diameters of the abdominal aorta were determined by ultrasound before and after Ang II infusion, which indicated a significant increase in aortic luminal diameters in wild type and TKO-TGfat mice but not in TKO mice.	Phenobarbital	162-169	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	96-102
35401805-0	2022	BTG2 as a tumor target for the treatment of luminal A breast cancer.	Phenobarbital	44-51	BTG anti-proliferation factor 2	Homo sapiens	0-4
35489754-0	2022	The MDM2 and CDKN2A Copy-number-variation Influence the TP53-signature-score in Wild-type TP53 Luminal Type Breast Cancer.	Phenobarbital	95-102	MDM2 proto-oncogene	Homo sapiens	4-8
35489754-0	2022	The MDM2 and CDKN2A Copy-number-variation Influence the TP53-signature-score in Wild-type TP53 Luminal Type Breast Cancer.	Phenobarbital	95-102	cyclin dependent kinase inhibitor 2A	Homo sapiens	13-19
35489754-0	2022	The MDM2 and CDKN2A Copy-number-variation Influence the TP53-signature-score in Wild-type TP53 Luminal Type Breast Cancer.	Phenobarbital	95-102	tumor protein p53	Homo sapiens	56-60
35489754-0	2022	The MDM2 and CDKN2A Copy-number-variation Influence the TP53-signature-score in Wild-type TP53 Luminal Type Breast Cancer.	Phenobarbital	95-102	tumor protein p53	Homo sapiens	90-94
35489754-8	2022	Moreover, samples with MDM2 CN amplification or those with CDKN2A CN deep deletion had more characteristics of the luminal B type.	Phenobarbital	115-122	cyclin dependent kinase inhibitor 2A	Homo sapiens	59-65
35218811-8	2022	HER2+ tumors also had lower stromal content, particularly among RNA-based HER2-enriched (35.2% vs. 44.0% in Luminal A; RFD (95% CI): -8.8%, (-13.8, -3.8)).	Phenobarbital	108-115	erb-b2 receptor tyrosine kinase 2	Homo sapiens	0-4
35218811-8	2022	HER2+ tumors also had lower stromal content, particularly among RNA-based HER2-enriched (35.2% vs. 44.0% in Luminal A; RFD (95% CI): -8.8%, (-13.8, -3.8)).	Phenobarbital	108-115	erb-b2 receptor tyrosine kinase 2	Homo sapiens	74-78
35227076-1	2022	Purpose: The authors aimed to evaluate the prognostic and predictive value of androgen receptor (AR) expression in patients with luminal/human EGFR2 negative (HER2-) T1N0 breast cancer.	Phenobarbital	129-136	androgen receptor	Homo sapiens	97-99
35227076-1	2022	Purpose: The authors aimed to evaluate the prognostic and predictive value of androgen receptor (AR) expression in patients with luminal/human EGFR2 negative (HER2-) T1N0 breast cancer.	Phenobarbital	129-136	erb-b2 receptor tyrosine kinase 2	Homo sapiens	159-163
35367211-2	2022	CAR activation has been established as the mode of action by which phenobarbital-like non-genotoxic carcinogens promote liver tumor formation in rodents.	Phenobarbital	67-80	nuclear receptor subfamily 1 group I member 3	Homo sapiens	0-3
35151947-6	2022	C3 with highest level of Siglec15 expression was correlated with early tumor stage, hormone receptor-positive tumors, luminal A molecular subtype, lowest tumor mutational burden (TMB) score, lowest programmed cell death protein 1 (PD-1) and programmed death-ligand 1 (PD-L1) expression, upregulated PI3K-Akt pathway and advantage of prognosis.	Phenobarbital	118-125	sialic acid binding Ig like lectin 15	Homo sapiens	25-33
35151947-9	2022	Siglec15 related immunotherapy may be an important candidate for breast cancer patients especially for luminal subtype, independently of blockade of PD-1/PD-L1 immunotherapy.	Phenobarbital	103-110	sialic acid binding Ig like lectin 15	Homo sapiens	0-8
35563193-3	2022	In the hormone-receptor-positive Luminal A and Luminal B molecular subtypes of clinical breast cancer, conventional endocrine therapy predominantly targets estrogen receptor function and estrogen biosynthesis and/or growth factor receptors.	Phenobarbital	33-40	estrogen receptor 1	Homo sapiens	156-173
35437049-5	2022	We demonstrated that a published algorithm using routine assays (GATA3, KRT5, p16) classified basal/luminal subtypes and basal/Uro/GU subtypes with 86%-95% and 67%-86% accuracies, respectively.	Phenobarbital	100-107	cyclin dependent kinase inhibitor 2A	Homo sapiens	78-81
35437049-6	2022	KRT14 and RB1 are less frequently used in pathology practice but achieved the simplest, most accurate models for basal/luminal and basal/Uro/GU discrimination, with 93%-96% and 85%-86% accuracies, respectively.	Phenobarbital	119-126	keratin 14	Homo sapiens	0-5
35437049-6	2022	KRT14 and RB1 are less frequently used in pathology practice but achieved the simplest, most accurate models for basal/luminal and basal/Uro/GU discrimination, with 93%-96% and 85%-86% accuracies, respectively.	Phenobarbital	119-126	RB transcriptional corepressor 1	Homo sapiens	10-13
35563280-8	2022	We found that the endothelial cells treated with Lacidipine showed enhanced activity of caspase-3 in the luminal space.	Phenobarbital	105-112	caspase 3	Homo sapiens	88-97
35452617-3	2022	One such process is ER-phagy, a selective degradation of ER fragments (including membranes and luminal content), which serves to preserve the size of ER while adapting its morphology under basal and stress conditions.	Phenobarbital	95-102	epiregulin	Homo sapiens	20-22
35477723-5	2022	Targeting ASCL1 switches the neuroendocrine lineage back to the luminal epithelial state.	Phenobarbital	64-71	achaete-scute family bHLH transcription factor 1	Homo sapiens	10-15
35474355-15	2022	Compared with normal, luminal, and Her-2 positive tissues, CCNA2, MSH2, and CDK6 were significantly upregulated in TNBC.	Phenobarbital	22-29	cyclin A2	Homo sapiens	59-64
35421371-7	2022	Imaging experiments revealed that VAP-A promotes luminal filling of multivesicular bodies (MVBs), CERT localizes to MVBs, and the ceramide-generating enzyme neutral sphingomyelinase 2 colocalizes with VAP-A-positive ER.	Phenobarbital	49-56	VAMP associated protein A	Homo sapiens	34-39
35459234-1	2022	Preneoplastic mammary tissues from human female BRCA1 mutation carriers, or Brca1-mutant mice, display unexplained abnormalities in luminal differentiation.	Phenobarbital	132-139	BRCA1 DNA repair associated	Homo sapiens	48-53
35459234-1	2022	Preneoplastic mammary tissues from human female BRCA1 mutation carriers, or Brca1-mutant mice, display unexplained abnormalities in luminal differentiation.	Phenobarbital	132-139	BRCA1 DNA repair associated	Homo sapiens	76-81
35459234-4	2022	We also analyse 15 genetically-edited BRCA1 mutant/+ human mammary cell-lines and find that cells carrying pathogenic BRCA1 mutations acquire an analogous defect in their division axis accompanied by deficient expression of features of mature luminal cells.	Phenobarbital	243-250	BRCA1 DNA repair associated	Homo sapiens	38-43
35459234-4	2022	We also analyse 15 genetically-edited BRCA1 mutant/+ human mammary cell-lines and find that cells carrying pathogenic BRCA1 mutations acquire an analogous defect in their division axis accompanied by deficient expression of features of mature luminal cells.	Phenobarbital	243-250	BRCA1 DNA repair associated	Homo sapiens	118-123
35449374-2	2022	Defective CFTR leads to accumulation of dehydrated viscous mucus within the small intestine, luminal acidification and altered intestinal motility, resulting in blockage.	Phenobarbital	93-100	CF transmembrane conductance regulator	Homo sapiens	10-14
35452617-3	2022	One such process is ER-phagy, a selective degradation of ER fragments (including membranes and luminal content), which serves to preserve the size of ER while adapting its morphology under basal and stress conditions.	Phenobarbital	95-102	epiregulin	Homo sapiens	57-59
35452617-3	2022	One such process is ER-phagy, a selective degradation of ER fragments (including membranes and luminal content), which serves to preserve the size of ER while adapting its morphology under basal and stress conditions.	Phenobarbital	95-102	epiregulin	Homo sapiens	150-152
35514347-3	2022	Localized primarily on the apical membranes in small intestines and proximal tubules, the key action of NHE3 is to facilitate the entry of luminal Na+ and the extrusion of intracellular H+ from intestinal and proximal tubule tubular epithelial cells.	Phenobarbital	139-146	solute carrier family 9 (sodium/hydrogen exchanger), member 3	Mus musculus	104-108
35440032-5	2022	RESULTS: Overexpression of PTHrP in luminal epithelial cells caused alveolar hyperplasia and secretory differentiation of the mammary epithelium with milk production.	Phenobarbital	36-43	parathyroid hormone like hormone	Homo sapiens	27-32
35530281-9	2022	JTB protein itself is involved in mitotic spindle pathway by its role in cell division/cytokinesis, and within estrogen response early and late pathways, contributing to discrimination between luminal and mesenchymal breast cancer.	Phenobarbital	193-200	jumping translocation breakpoint	Homo sapiens	0-3
35444456-9	2022	The results of immunohistochemical staining from clinical samples further confirmed that high expression of CCND1 and FADD was frequently detected in luminal B and high-grade breast cancer with shorter metastasis-free survival times (P < 0.05).	Phenobarbital	150-157	cyclin D1	Homo sapiens	108-113
35559406-12	2022	CONCLUSION: In conclusion, LGALS2 has potential as a valuable biomarker for envisaging a satisfactory prognosis in patients with breast tumours, particularly those with luminal and basal B types, all stages and grade III tumours.	Phenobarbital	169-176	galectin 2	Homo sapiens	27-33
35411503-9	2022	The 3D-cultured hiPS-BMECs showed asymmetric transport of substrates of BCRP, CAT1 and LAT1 between the luminal (blood) and abluminal (brain) sides.	Phenobarbital	104-111	BCR pseudogene 1	Homo sapiens	72-76
35418303-11	2022	CONCLUSIONS: CHK1 could be considered as an appealing novel pharmacological target for the treatment of luminal primary and MBCs.	Phenobarbital	104-111	checkpoint kinase 1	Homo sapiens	13-17
35411503-9	2022	The 3D-cultured hiPS-BMECs showed asymmetric transport of substrates of BCRP, CAT1 and LAT1 between the luminal (blood) and abluminal (brain) sides.	Phenobarbital	104-111	transient receptor potential cation channel subfamily V member 6	Homo sapiens	78-82
35411503-9	2022	The 3D-cultured hiPS-BMECs showed asymmetric transport of substrates of BCRP, CAT1 and LAT1 between the luminal (blood) and abluminal (brain) sides.	Phenobarbital	104-111	solute carrier family 7 member 5	Homo sapiens	87-91
35418303-0	2022	Clinically relevant CHK1 inhibitors abrogate wild-type and Y537S mutant ERalpha expression and proliferation in luminal primary and metastatic breast cancer cells.	Phenobarbital	112-119	checkpoint kinase 1	Homo sapiens	20-24
35418303-8	2022	Accordingly, CHK1 and ERalpha activations are correlated in ERalpha-positive BC cell lines, and the ATR:CHK1 pathway controls ERalpha stability and cell proliferation in luminal A BC cells.	Phenobarbital	170-177	ATR serine/threonine kinase	Homo sapiens	100-103
35418303-8	2022	Accordingly, CHK1 and ERalpha activations are correlated in ERalpha-positive BC cell lines, and the ATR:CHK1 pathway controls ERalpha stability and cell proliferation in luminal A BC cells.	Phenobarbital	170-177	checkpoint kinase 1	Homo sapiens	104-108
35418303-8	2022	Accordingly, CHK1 and ERalpha activations are correlated in ERalpha-positive BC cell lines, and the ATR:CHK1 pathway controls ERalpha stability and cell proliferation in luminal A BC cells.	Phenobarbital	170-177	estrogen receptor 1	Homo sapiens	126-133
35393570-4	2022	Oncogenic KRAS and TMPRSS2-ERG synergized to promote tumorigenesis and metastasis of primary luminal cells.	Phenobarbital	93-100	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	10-14
35393570-4	2022	Oncogenic KRAS and TMPRSS2-ERG synergized to promote tumorigenesis and metastasis of primary luminal cells.	Phenobarbital	93-100	transmembrane protease, serine 2	Mus musculus	19-26
35393570-4	2022	Oncogenic KRAS and TMPRSS2-ERG synergized to promote tumorigenesis and metastasis of primary luminal cells.	Phenobarbital	93-100	ETS transcription factor	Mus musculus	27-30
35422983-9	2022	Intriguingly, SGSCspheroid-implanted mice exhibited greater amelioration of tissue damage and preservation of KRT7+ terminally differentiated luminal ductal cells than SGSCmonolayer-implanted mice.	Phenobarbital	142-149	keratin 7	Mus musculus	110-114
35373395-8	2022	PPARalpha, PPARdelta and PPARgamma were detected in the luminal epithelium, glandular epithelium, and stromal cells.	Phenobarbital	56-63	peroxisome proliferator activated receptor alpha	Canis lupus familiaris	0-9
35373395-8	2022	PPARalpha, PPARdelta and PPARgamma were detected in the luminal epithelium, glandular epithelium, and stromal cells.	Phenobarbital	56-63	peroxisome proliferator activated receptor delta	Canis lupus familiaris	11-20
35373395-8	2022	PPARalpha, PPARdelta and PPARgamma were detected in the luminal epithelium, glandular epithelium, and stromal cells.	Phenobarbital	56-63	peroxisome proliferator activated receptor gamma	Canis lupus familiaris	25-34
35365723-4	2022	ATX-LPA signaling showed a dose-dependent stimulatory effect especially on cellular functions of triple-negative and luminal A breast cancer cell lines.	Phenobarbital	117-124	ectonucleotide pyrophosphatase/phosphodiesterase 2	Homo sapiens	0-3
35485672-6	2022	RESULTS: High intra-tumoral VDR expression was found in carcinomas with luminal molecular subtypes (p=0.039) and low histological degrees (p=0.035).	Phenobarbital	72-79	vitamin D receptor	Homo sapiens	28-31
35485672-8	2022	CONCLUSIONS: High intra-tumoral VDR expression is found in breast carcinomas with luminal subtypes and low histological grade (I/II).	Phenobarbital	82-89	vitamin D receptor	Homo sapiens	32-35
35084573-10	2022	The number of ChAT-immunoreactive cells was increased in the luminal epithelium in the caudal compartment compared to the cranial region of the uterine horn, and at the LUT compared to PB and FOL stages.	Phenobarbital	61-68	choline O-acetyltransferase	Homo sapiens	14-18
35435364-6	2022	Results: PD-L1 expression was detected in 4 (21%) cases, 3 (75%) of them were in luminal B and 1 (25%) were in the luminal A group.	Phenobarbital	81-88	CD274 molecule	Homo sapiens	9-14
35409257-4	2022	According to the obtained results, hVKORC1 is a modular protein composed of the stable transmembrane domain (TMD) and intrinsically disordered luminal (L) loop, possessing the great plasticity/adaptability required to perform various steps of the activation process.	Phenobarbital	143-150	vitamin K epoxide reductase complex subunit 1	Homo sapiens	35-42
35433725-17	2022	The ratio of the inner/outer luminal diameter of arterioles correlated with the intensity of C3d deposition (r = -0.174, p = 0.001).	Phenobarbital	29-36	endogenous retrovirus group K member 13	Homo sapiens	93-96
35406395-6	2022	The KRT7 staining is lost in luminal cells from localized tumors and found as an aberrant sporadic staining (2.2%) in advanced PC.	Phenobarbital	29-36	keratin 7	Homo sapiens	4-8
35356986-5	2022	Here we show that MaSCs from both wild-type (WT) and Tg mice expressed IGF-1R and that overexpression of Tg IGF-1 increased numbers of MaSCs by undergoing symmetric division, resulting in an expansion of the MaSC and luminal progenitor (LP) compartments in pre-pubertal female mice.	Phenobarbital	217-224	insulin-like growth factor 1	Mus musculus	108-113
35433513-3	2022	C5aR1-deficient mice had reduced bladder bacterial load and attenuated bladder tissue injury, which is associated with reduced expression of terminal alpha-mannosyl residues (Man) (a potential ligand for type 1 fimbriae of E. coli) at the luminal surface of the bladder epithelium and reduced early bacterial colonization of the bladder.	Phenobarbital	239-246	complement component 5a receptor 1	Mus musculus	0-5
35347798-2	2022	Endoplasmic reticulum oxidoreductase 1alpha (ERO1alpha) is an oxidase that exists in the luminal side of the ER membrane, participating in protein folding and secretion and inhibiting apoptosis, but the underlying mechanism on liver injury induced by homocysteine (Hcy) remains obscure.	Phenobarbital	89-96	endoplasmic reticulum oxidoreductase 1 alpha	Mus musculus	45-54
35409055-10	2022	Progesterone upregulates Caveolin-1 expression in luminal epithelium.	Phenobarbital	50-57	caveolin 1	Homo sapiens	25-35
35408925-4	2022	As expected, PB increased the total cytochrome P450 (CYP) content and the extent of metyrapone binding; moreover, an augmentation of protein amounts and related enzyme activities was observed for known PB targets such as CYP2B, 2C, and 3A, but also CYP2E1.	Phenobarbital	13-15	cytochrome P450 subfamily 2B	Bos taurus	221-230
35408925-4	2022	As expected, PB increased the total cytochrome P450 (CYP) content and the extent of metyrapone binding; moreover, an augmentation of protein amounts and related enzyme activities was observed for known PB targets such as CYP2B, 2C, and 3A, but also CYP2E1.	Phenobarbital	13-15	cytochrome P450 2E1	Bos taurus	249-255
35430163-11	2022	CONCLUSIONS: HER2-targeted therapies dramatically altered the natural history of HER2-positive breast cancer, with overall survival approaching those of luminal subtype.	Phenobarbital	153-160	erb-b2 receptor tyrosine kinase 2	Homo sapiens	81-85
35406503-7	2022	PARP-1 expression was higher in luminal (61%) and early BC (54%), compared to TNBC (41%) and metastatic (33%) patients.	Phenobarbital	32-39	poly(ADP-ribose) polymerase 1	Homo sapiens	0-6
35406503-8	2022	In addition, PARP-1 distribution was mostly cytoplasmic in luminal patients (p = 0.024), whereas it was mostly nuclear in TNBC patients.	Phenobarbital	59-66	poly(ADP-ribose) polymerase 1	Homo sapiens	13-19
35351192-11	2022	qPCR results revealed significantly increased mRNA expression of CK5, CK18 and CEA in iSGCs, as well as activation of the duct marker CK10 and luminal functional marker AQP5.	Phenobarbital	143-150	aquaporin 5	Mus musculus	169-173
35456533-8	2022	Luminal fluids obtained from the tiny-TIM system showed a higher solubilization capacity for venetoclax, and a better read-out for the drug permeability, as compared to FaSSIF or FeSSIF media.	Phenobarbital	0-7	Rho guanine nucleotide exchange factor 5	Homo sapiens	38-41
35304514-9	2022	MiR-206 is reported to be down-regulated in Luminal-A type of breast cancer.	Phenobarbital	44-51	microRNA 206	Homo sapiens	0-7
35322139-1	2022	Recombinant peptides were designed using the C-terminal domain (receptor binding domain, RBD) and its subdomain (peptide A2) of a heavy chain of botulinum neurotoxin A-type 1 (BoNT/A1), which can bind to the luminal domain of synaptic vesicle glycoprotein 2C (SV2C-LD).	Phenobarbital	208-215	calcium voltage-gated channel subunit alpha1 D	Rattus norvegicus	89-92
35322139-1	2022	Recombinant peptides were designed using the C-terminal domain (receptor binding domain, RBD) and its subdomain (peptide A2) of a heavy chain of botulinum neurotoxin A-type 1 (BoNT/A1), which can bind to the luminal domain of synaptic vesicle glycoprotein 2C (SV2C-LD).	Phenobarbital	208-215	synaptic vesicle glycoprotein 2c	Rattus norvegicus	226-258
35322139-1	2022	Recombinant peptides were designed using the C-terminal domain (receptor binding domain, RBD) and its subdomain (peptide A2) of a heavy chain of botulinum neurotoxin A-type 1 (BoNT/A1), which can bind to the luminal domain of synaptic vesicle glycoprotein 2C (SV2C-LD).	Phenobarbital	208-215	synaptic vesicle glycoprotein 2c	Rattus norvegicus	260-264
35453827-3	2022	Preferential expression of both proteins was observed in the glandular and luminal epithelial cells of the eutopic endometrium of patients with and without endometriosis with a ~2.5-fold stronger expression of MT3-MMP compared to MT2-MMP.	Phenobarbital	75-82	matrix metallopeptidase 16	Homo sapiens	210-217
35328104-7	2022	HK2 and PKM2 were found to be upregulated in luminal B, whereas PFKM was overexpressed in the luminal A subtype of breast cancer.	Phenobarbital	45-52	hexokinase 2	Homo sapiens	0-3
35328104-7	2022	HK2 and PKM2 were found to be upregulated in luminal B, whereas PFKM was overexpressed in the luminal A subtype of breast cancer.	Phenobarbital	45-52	pyruvate kinase M1/2	Homo sapiens	8-12
35328104-7	2022	HK2 and PKM2 were found to be upregulated in luminal B, whereas PFKM was overexpressed in the luminal A subtype of breast cancer.	Phenobarbital	94-101	phosphofructokinase, muscle	Homo sapiens	64-68
35273332-8	2022	Upon transplantation, CD200low MEP progenitors distinguish from CD200high by the formation of multilayered structures with a hyperplastic inner layer of luminal epithelial cells.	Phenobarbital	153-160	CD200 molecule	Homo sapiens	22-27
35290409-11	2022	Kaplan-Meier analysis showed that in patients with Luminal A and Normal like breast cancers and Stage1 and stage2 breast cancers, patients with high expression of RRM2 had worse overall survival and DMFS.	Phenobarbital	51-58	ribonucleotide reductase regulatory subunit M2	Homo sapiens	163-167
35191758-6	2022	ST- and LT-mediated luminal fluid accumulation in vivo correlates with significant increases in IL-33 and IL-1Ra in small intestinal mucosal scrapings.	Phenobarbital	20-27	interleukin 33	Homo sapiens	96-101
35191758-6	2022	ST- and LT-mediated luminal fluid accumulation in vivo correlates with significant increases in IL-33 and IL-1Ra in small intestinal mucosal scrapings.	Phenobarbital	20-27	interleukin 1 receptor antagonist	Homo sapiens	106-112
34998874-5	2022	We show that CD320 is expressed on the luminal surface in the small intestine and in proximal tubules in the kidney, suggesting that, in addition to its role in vitamin B12 uptake in peripheral tissues, CD320 may participate in vitamin B12 absorption in the small intestine and reabsorption in the kidney.	Phenobarbital	39-46	CD320 antigen	Mus musculus	13-18
34998874-5	2022	We show that CD320 is expressed on the luminal surface in the small intestine and in proximal tubules in the kidney, suggesting that, in addition to its role in vitamin B12 uptake in peripheral tissues, CD320 may participate in vitamin B12 absorption in the small intestine and reabsorption in the kidney.	Phenobarbital	39-46	CD320 antigen	Mus musculus	203-208
35273332-8	2022	Upon transplantation, CD200low MEP progenitors distinguish from CD200high by the formation of multilayered structures with a hyperplastic inner layer of luminal epithelial cells.	Phenobarbital	153-160	CD200 molecule	Homo sapiens	64-69
35372533-8	2022	The level of pro-inflammatory cytokines accumulated in the CA endometrium, and high abundance of integrin-beta and THBS1 were localized in the luminal epithelium of the NCA endometrium, but not in the CA endometrium.	Phenobarbital	143-150	thrombospondin 1	Homo sapiens	115-120
35245335-4	2022	Specially, as the bronchial branches extended, the pIgR expression level in ciliated cells significantly declined (p<0.05), and the corresponding bronchial luminal areas obviously decreased (p<0.05).	Phenobarbital	156-163	polymeric immunoglobulin receptor	Camelus bactrianus	51-55
35271636-6	2022	ALAS1, HEPHL1, and PITX3 were expressed in the apical cells of the luminal epithelium and lamina propria cells of the uterine mucosa of the wild-type quail, while their expression levels were downregulated in the cells of the mutant quail.	Phenobarbital	67-74	LOW QUALITY PROTEIN: hephaestin-like protein 1	Coturnix japonica	7-13
35271636-6	2022	ALAS1, HEPHL1, and PITX3 were expressed in the apical cells of the luminal epithelium and lamina propria cells of the uterine mucosa of the wild-type quail, while their expression levels were downregulated in the cells of the mutant quail.	Phenobarbital	67-74	pituitary homeobox 3	Coturnix japonica	19-24
35020452-4	2022	GP2 is also secreted by the pancreas and various mucous glands, interacting with luminal type 1 fimbriae-positive E. coli.	Phenobarbital	81-88	glycoprotein 2	Bos taurus	0-3
35248133-4	2022	METHODS: We performed siRNA knockdown screens of genes differentially expressed between lapatinib-responsive and -resistant HER2+ breast cancer cells, which corresponded largely to luminal versus basal subtypes.	Phenobarbital	181-188	erb-b2 receptor tyrosine kinase 2	Homo sapiens	124-128
35311103-10	2022	Upon classification according to the molecular subtypes, the luminal subtype showed the highest GPR68 expression followed by triple-negative and Her2-enriched cells.	Phenobarbital	61-68	G protein-coupled receptor 68	Homo sapiens	96-101
35245335-7	2022	Moreover, the pIgR expression level in ciliated cells was positively correlated with the bronchial luminal areas; but negatively correlated with the cleanliness of airflow through the bronchial cross-sections, showing that the pIgR expression level in the bronchial epithelium was inhomogeneous.	Phenobarbital	99-106	polymeric immunoglobulin receptor	Camelus bactrianus	14-18
35121857-2	2022	Cholesterol can bind and covalently conjugate to the luminal cysteine-rich domain (CRD) of human SMO at the D95 residue (D99 in mouse).	Phenobarbital	53-60	smoothened, frizzled class receptor	Homo sapiens	97-100
35511868-0	2022	A Runx1-enhancer Element eR1 Identified Lineage Restricted Mammary Luminal Stem Cells.	Phenobarbital	67-74	runt related transcription factor 1	Mus musculus	2-7
35511868-0	2022	A Runx1-enhancer Element eR1 Identified Lineage Restricted Mammary Luminal Stem Cells.	Phenobarbital	67-74	MEIR1 treanscription regulator	Mus musculus	25-28
35511868-5	2022	Here, we identified eR1 activity in a rare subpopulation of the ERalpha-negative luminal epithelium in mouse mammary glands.	Phenobarbital	81-88	MEIR1 treanscription regulator	Mus musculus	20-23
35511868-5	2022	Here, we identified eR1 activity in a rare subpopulation of the ERalpha-negative luminal epithelium in mouse mammary glands.	Phenobarbital	81-88	estrogen receptor 1 (alpha)	Mus musculus	64-71
35511868-6	2022	Lineage-tracing using an eR1-CreERT2 mouse model revealed that eR1+ luminal cells generated the entire luminal lineage and milk-secreting alveoli-eR1 therefore specifically marks lineage-restricted luminal stem cells.	Phenobarbital	103-110	MEIR1 treanscription regulator	Mus musculus	63-66
35511868-6	2022	Lineage-tracing using an eR1-CreERT2 mouse model revealed that eR1+ luminal cells generated the entire luminal lineage and milk-secreting alveoli-eR1 therefore specifically marks lineage-restricted luminal stem cells.	Phenobarbital	198-205	MEIR1 treanscription regulator	Mus musculus	25-28
35511868-6	2022	Lineage-tracing using an eR1-CreERT2 mouse model revealed that eR1+ luminal cells generated the entire luminal lineage and milk-secreting alveoli-eR1 therefore specifically marks lineage-restricted luminal stem cells.	Phenobarbital	198-205	MEIR1 treanscription regulator	Mus musculus	63-66
35511868-6	2022	Lineage-tracing using an eR1-CreERT2 mouse model revealed that eR1+ luminal cells generated the entire luminal lineage and milk-secreting alveoli-eR1 therefore specifically marks lineage-restricted luminal stem cells.	Phenobarbital	198-205	MEIR1 treanscription regulator	Mus musculus	146-149
35511868-7	2022	eR1-targeted-conditional knockout of Runx1 led to the expansion of luminal epithelial cells, accompanied by elevated ERalpha expression.	Phenobarbital	67-74	MEIR1 treanscription regulator	Mus musculus	0-3
35511868-7	2022	eR1-targeted-conditional knockout of Runx1 led to the expansion of luminal epithelial cells, accompanied by elevated ERalpha expression.	Phenobarbital	67-74	runt related transcription factor 1	Mus musculus	37-42
35511868-7	2022	eR1-targeted-conditional knockout of Runx1 led to the expansion of luminal epithelial cells, accompanied by elevated ERalpha expression.	Phenobarbital	67-74	estrogen receptor 1 (alpha)	Mus musculus	117-124
35511868-8	2022	Our findings demonstrate a definitive role for Runx1 in the regulation of the eR1-positive luminal stem cell proliferation during mammary homeostasis.	Phenobarbital	91-98	runt related transcription factor 1	Mus musculus	47-52
35511868-8	2022	Our findings demonstrate a definitive role for Runx1 in the regulation of the eR1-positive luminal stem cell proliferation during mammary homeostasis.	Phenobarbital	91-98	MEIR1 treanscription regulator	Mus musculus	78-81
35511868-10	2022	Runx1 inactivation is therefore likely to be an early hit in the cell-of-origin of ERalpha+ luminal type breast cancer.	Phenobarbital	92-99	runt related transcription factor 1	Mus musculus	0-5
35511868-10	2022	Runx1 inactivation is therefore likely to be an early hit in the cell-of-origin of ERalpha+ luminal type breast cancer.	Phenobarbital	92-99	estrogen receptor 1 (alpha)	Mus musculus	83-90
34998785-5	2022	Here we show that in the mouse trachea which contain epithelial cell types similar to human airway, epithelium-specific inactivation of Fbxw7, which encodes an E3 ubiquitin ligase, led to reduced club and ciliated cells, increased goblet cells, and ectopic P63-negative, Keratin5-positive transitory basal cells in the luminal layer.	Phenobarbital	319-326	F-box and WD repeat domain containing 7	Homo sapiens	136-141
35147994-1	2022	We demonstrated that serpinA3c/k relocates from the cytoplasm to the apical tubular membrane (ATM) in chronic kidney disease (CKD), suggesting its secretion in luminal space in pathophysiological contexts.	Phenobarbital	160-167	serine (or cysteine) proteinase inhibitor, clade A, member 3C	Rattus norvegicus	21-30
35182852-0	2022	Claudin-3 regulates luminal fluid accumulation in the developing chick lung.	Phenobarbital	20-27	claudin 3	Gallus gallus	0-9
35104505-0	2022	N-Acetylglucosaminyltransferase-V requires a specific non-catalytic luminal domain for its activity toward glycoprotein substrates.	Phenobarbital	68-75	alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase	Homo sapiens	0-33
35104505-4	2022	In this study, we focused on an uncharacterized domain at the N-terminal side of the luminal region (N domain) of GnT-V, which was previously identified in a crystal structure, and aimed to reveal its role in GnT-V action.	Phenobarbital	85-92	alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase	Homo sapiens	114-119
35124009-5	2022	We showed using a microperfusion technique that azPC rapidly stimulated Na+/HCO3- cotransporter 1 (NBCe1) and luminal Na+/H+ exchanger (NHE) activities in a dose-dependent manner at submicromolar concentrations in isolated PTs from rats and humans.	Phenobarbital	110-117	solute carrier family 9 member C1	Homo sapiens	136-139
35104569-6	2022	Capillary luminal accumulation of fluorescent substrates of P-glycoprotein and Bcrp was decreased in the presence of transporter inhibitors.	Phenobarbital	10-17	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	60-74
34990407-3	2022	SVAS is caused by heterozygous loss-of-function, hypomorphic or deletion mutations in the elastin gene ELN, and SVAS patients and elastin mutant mice display increased arterial wall cellularity and luminal obstructions.	Phenobarbital	198-205	elastin	Homo sapiens	90-97
35104569-7	2022	Moreover, luminal accumulation of the Oat3 and Mrp4 substrate, 8-(2-(fluoresceinyl)aminoethylthio) adenosine-3",5"-cyclic monophosphate (8-(fluo)-cAMP), was reduced by substrates/inhibitors of Oat3 and Mrp4.	Phenobarbital	10-17	solute carrier family 22 member 8	Rattus norvegicus	38-42
34990407-3	2022	SVAS is caused by heterozygous loss-of-function, hypomorphic or deletion mutations in the elastin gene ELN, and SVAS patients and elastin mutant mice display increased arterial wall cellularity and luminal obstructions.	Phenobarbital	198-205	elastin	Homo sapiens	130-137
35104569-7	2022	Moreover, luminal accumulation of the Oat3 and Mrp4 substrate, 8-(2-(fluoresceinyl)aminoethylthio) adenosine-3",5"-cyclic monophosphate (8-(fluo)-cAMP), was reduced by substrates/inhibitors of Oat3 and Mrp4.	Phenobarbital	10-17	ATP binding cassette subfamily C member 4	Rattus norvegicus	47-51
35104569-7	2022	Moreover, luminal accumulation of the Oat3 and Mrp4 substrate, 8-(2-(fluoresceinyl)aminoethylthio) adenosine-3",5"-cyclic monophosphate (8-(fluo)-cAMP), was reduced by substrates/inhibitors of Oat3 and Mrp4.	Phenobarbital	10-17	solute carrier family 22 member 8	Rattus norvegicus	193-197
35104569-7	2022	Moreover, luminal accumulation of the Oat3 and Mrp4 substrate, 8-(2-(fluoresceinyl)aminoethylthio) adenosine-3",5"-cyclic monophosphate (8-(fluo)-cAMP), was reduced by substrates/inhibitors of Oat3 and Mrp4.	Phenobarbital	10-17	ATP binding cassette subfamily C member 4	Rattus norvegicus	202-206
35459982-2	2022	Increased CCND1 copy number (CN) in breast cancer (BC) is associated with high histopathological grade, high proliferation, and Luminal B subtype.	Phenobarbital	128-135	cyclin D1	Homo sapiens	10-15
35459982-8	2022	CCND1 CN (>= 6) was seen in all molecular subtypes, most frequently in Luminal B (HER2-) (20/126; 16%).	Phenobarbital	71-78	cyclin D1	Homo sapiens	0-5
35459982-8	2022	CCND1 CN (>= 6) was seen in all molecular subtypes, most frequently in Luminal B (HER2-) (20/126; 16%).	Phenobarbital	71-78	erb-b2 receptor tyrosine kinase 2	Homo sapiens	82-86
35459982-12	2022	High CCND1 CN was most frequent in Luminal B (HER2-) tumours.	Phenobarbital	35-42	erb-b2 receptor tyrosine kinase 2	Homo sapiens	46-50
34993725-9	2022	Further, increased miR-548b-5p levels have been partially associated with higher grades, multifocality, Ki-67 positivity, and luminal B rather than luminal A samples.	Phenobarbital	126-133	microRNA 548b	Homo sapiens	19-27
35205789-2	2022	Here, we over-expressed WT-PD-L1 in human TNBC cells (express endogenous PD-L1) and in luminal-A breast cancer cells (no endogenous PD-L1 expression) and demonstrated that cell-autonomous PD-L1 activities lead to increased tumor cell growth, invasion and release of pro-metastatic factors (CXCL8, sICAM-1, GM-CSF).	Phenobarbital	87-94	CD274 molecule	Homo sapiens	27-32
35195579-3	2022	We assessed 300 endometrial carcinomas/carcinosarcomas to ascertain the specificity of TTF-1/GATA3/luminal CD10 expression with or without ER staining for this diagnosis.	Phenobarbital	99-106	membrane metalloendopeptidase	Homo sapiens	107-111
35216942-3	2022	Using gene expression data from four clinical cohorts with >1400 patient samples of muscle-invasive BC and a BC tissue microarray, we found that TROP2 mRNA and protein are highly expressed across basal, luminal, and stroma-rich subtypes, but depleted in the neuroendocrine subtype.	Phenobarbital	203-210	tumor associated calcium signal transducer 2	Homo sapiens	145-150
35154423-6	2022	Expression level of peroxisome proliferator-activated receptor (PPAR)gamma, a marker of luminal type, increased 3.0-4.4 fold in SCaBER cells altered with 9q compared with parental SCaBER cells.	Phenobarbital	88-95	peroxisome proliferator activated receptor gamma	Homo sapiens	20-74
35328144-4	2022	The analysis of the KCTD15 levels indicates a significant overexpression of the protein in Luminal A and Luminal B breast cancer patients as well as in the related cell lines.	Phenobarbital	91-98	potassium channel tetramerization domain containing 15	Homo sapiens	20-26
35280304-6	2022	Results: Significant differences were identified in the expression levels of interferon-gamma (IFN-gamma) (P < 0.001), interleukin (IL)-6 (P = 0.008) and tumor necrosis factor-alpha (TNF-alpha) (P = 0.036) in the luminal fluid of the ES comparing between the MD and AN groups.	Phenobarbital	213-220	interferon gamma	Homo sapiens	77-93
35280304-6	2022	Results: Significant differences were identified in the expression levels of interferon-gamma (IFN-gamma) (P < 0.001), interleukin (IL)-6 (P = 0.008) and tumor necrosis factor-alpha (TNF-alpha) (P = 0.036) in the luminal fluid of the ES comparing between the MD and AN groups.	Phenobarbital	213-220	interferon gamma	Homo sapiens	95-104
35280304-6	2022	Results: Significant differences were identified in the expression levels of interferon-gamma (IFN-gamma) (P < 0.001), interleukin (IL)-6 (P = 0.008) and tumor necrosis factor-alpha (TNF-alpha) (P = 0.036) in the luminal fluid of the ES comparing between the MD and AN groups.	Phenobarbital	213-220	interleukin 6	Homo sapiens	119-137
35280304-6	2022	Results: Significant differences were identified in the expression levels of interferon-gamma (IFN-gamma) (P < 0.001), interleukin (IL)-6 (P = 0.008) and tumor necrosis factor-alpha (TNF-alpha) (P = 0.036) in the luminal fluid of the ES comparing between the MD and AN groups.	Phenobarbital	213-220	tumor necrosis factor	Homo sapiens	154-181
35280304-6	2022	Results: Significant differences were identified in the expression levels of interferon-gamma (IFN-gamma) (P < 0.001), interleukin (IL)-6 (P = 0.008) and tumor necrosis factor-alpha (TNF-alpha) (P = 0.036) in the luminal fluid of the ES comparing between the MD and AN groups.	Phenobarbital	213-220	tumor necrosis factor	Homo sapiens	183-192
35183222-2	2022	The extracellular/luminal moiety of SorLA has a unique mosaic domain composition and interacts with a large number of different and partially unrelated ligands, including the amyloid precursor protein as well as amyloid-beta.	Phenobarbital	18-25	sortilin related receptor 1	Homo sapiens	36-41
35183222-2	2022	The extracellular/luminal moiety of SorLA has a unique mosaic domain composition and interacts with a large number of different and partially unrelated ligands, including the amyloid precursor protein as well as amyloid-beta.	Phenobarbital	18-25	amyloid beta precursor protein	Homo sapiens	175-200
35183222-7	2022	Most of these adaptors and several ligands of the extracellular/luminal moiety are shared with the Vps10p-D receptor Sortilin.	Phenobarbital	64-71	sortilin 1	Homo sapiens	117-125
35184041-3	2022	Phenobarbital, an enzyme inducer and liver tumor promoter, activates both rodent and human CAR but causes liver tumors only in rodents.	Phenobarbital	0-13	nuclear receptor subfamily 1 group I member 3	Homo sapiens	91-94
35184041-4	2022	Although the precise mechanism for phenobarbital/CAR-mediated liver tumor formation remains to be established, intracellular pathways, including the Hippo pathway/YAP-TEAD system and beta-catenin signaling, seem to be involved.	Phenobarbital	35-48	nuclear receptor subfamily 1 group I member 3	Homo sapiens	49-52
35184041-4	2022	Although the precise mechanism for phenobarbital/CAR-mediated liver tumor formation remains to be established, intracellular pathways, including the Hippo pathway/YAP-TEAD system and beta-catenin signaling, seem to be involved.	Phenobarbital	35-48	Yes1 associated transcriptional regulator	Homo sapiens	163-166
35184041-4	2022	Although the precise mechanism for phenobarbital/CAR-mediated liver tumor formation remains to be established, intracellular pathways, including the Hippo pathway/YAP-TEAD system and beta-catenin signaling, seem to be involved.	Phenobarbital	35-48	catenin beta 1	Homo sapiens	183-195
35205789-2	2022	Here, we over-expressed WT-PD-L1 in human TNBC cells (express endogenous PD-L1) and in luminal-A breast cancer cells (no endogenous PD-L1 expression) and demonstrated that cell-autonomous PD-L1 activities lead to increased tumor cell growth, invasion and release of pro-metastatic factors (CXCL8, sICAM-1, GM-CSF).	Phenobarbital	87-94	CD274 molecule	Homo sapiens	188-193
35252216-7	2021	Furthermore, we found that HPS6 interacted with ATP6V0D1, suggesting that HPS6 transports ATP6V0D1 to the WPB limiting membrane for the assembly of the v-ATPase complex to maintain its acidic luminal pH, which is critical for the formation of vWF tubules during WPB maturation.	Phenobarbital	192-199	HPS6, biogenesis of lysosomal organelles complex 2 subunit 3	Mus musculus	27-31
35203681-3	2022	We have investigated if GATA2 exogenous expression in prostate epithelial basal-like cells could induce AR transcription or luminal differentiation.	Phenobarbital	124-131	GATA binding protein 2	Homo sapiens	24-29
35203681-11	2022	The appearance of AR mRNA and additional luminal marker gene expression changes following proteasome inhibition suggests control of essential cofactor(s) of AR mRNA expression and luminal differentiation at this proteolytic level.	Phenobarbital	41-48	androgen receptor	Homo sapiens	157-159
35371692-16	2022	In the HER2-low subgroup, 70% of tumors were luminal-like and 64.5% of HER2-0 patients had triple-negative BC (p = 0.03).	Phenobarbital	45-52	erb-b2 receptor tyrosine kinase 2	Homo sapiens	7-11
35252216-7	2021	Furthermore, we found that HPS6 interacted with ATP6V0D1, suggesting that HPS6 transports ATP6V0D1 to the WPB limiting membrane for the assembly of the v-ATPase complex to maintain its acidic luminal pH, which is critical for the formation of vWF tubules during WPB maturation.	Phenobarbital	192-199	ATPase H+ transporting V0 subunit d1	Homo sapiens	48-56
35252216-7	2021	Furthermore, we found that HPS6 interacted with ATP6V0D1, suggesting that HPS6 transports ATP6V0D1 to the WPB limiting membrane for the assembly of the v-ATPase complex to maintain its acidic luminal pH, which is critical for the formation of vWF tubules during WPB maturation.	Phenobarbital	192-199	HPS6, biogenesis of lysosomal organelles complex 2 subunit 3	Mus musculus	74-78
35252216-7	2021	Furthermore, we found that HPS6 interacted with ATP6V0D1, suggesting that HPS6 transports ATP6V0D1 to the WPB limiting membrane for the assembly of the v-ATPase complex to maintain its acidic luminal pH, which is critical for the formation of vWF tubules during WPB maturation.	Phenobarbital	192-199	ATPase H+ transporting V0 subunit d1	Homo sapiens	90-98
35143573-6	2022	This method can be extended to address other transient ternary interactions between cytosolic proteins and luminal or extracellular proteins through a transmembrane receptor within the endomembrane system.	Phenobarbital	107-114	neuropilin 1	Homo sapiens	151-173
35173185-7	2022	In the ER+/PR+/HER2-negative subset (n = 356) of The Cancer Genome Atlas, the non-luminal A intrinsic subtype was more prevalent in the group with mutant TP53.	Phenobarbital	82-89	erb-b2 receptor tyrosine kinase 2	Homo sapiens	15-19
35173185-7	2022	In the ER+/PR+/HER2-negative subset (n = 356) of The Cancer Genome Atlas, the non-luminal A intrinsic subtype was more prevalent in the group with mutant TP53.	Phenobarbital	82-89	tumor protein p53	Homo sapiens	154-158
35177712-10	2022	Moreover, high LAT1 expression was an independent poor prognostic factor in luminal B-like breast cancer with aggressive features (HR = 3.39; 95% CI 1.35-8.52; p = 0.0094).	Phenobarbital	76-83	solute carrier family 7 member 5	Homo sapiens	15-19
35143593-4	2022	We found that intestinal transit, intestinal permeability, and luminal pH regulation are all aberrant in sox10 mutants, independent of microbially induced inflammation.	Phenobarbital	63-70	SRY-box transcription factor 10	Danio rerio	105-110
35143593-5	2022	Treatment with the proton pump inhibitor, omeprazole, corrected the more acidic luminal pH of sox10 mutants to wild type levels.	Phenobarbital	80-87	SRY-box transcription factor 10	Danio rerio	94-99
35125121-12	2022	CONCLUSION: MCM6 can differentiate luminal A and luminal B subtypes and is correlated with mitotic counts.	Phenobarbital	35-42	minichromosome maintenance complex component 6	Homo sapiens	12-16
35208951-2	2022	In this study, mass spectrometry analysis identified the leucine richness and found a luminal binding protein (LBP).	Phenobarbital	86-93	lipopolysaccharide binding protein	Rattus norvegicus	111-114
35125121-12	2022	CONCLUSION: MCM6 can differentiate luminal A and luminal B subtypes and is correlated with mitotic counts.	Phenobarbital	49-56	minichromosome maintenance complex component 6	Homo sapiens	12-16
35419102-6	2022	T47D and MCF7 belonged to the luminal subtype of breast cancer (BC) that CK19 expression regulated with an ER marker.	Phenobarbital	30-37	keratin 19	Homo sapiens	73-77
35178392-4	2022	Luminal lipid droplets that emerge into the nucleoplasm do so at regions of the inner nuclear membrane that become enriched in promyelocytic leukemia (PML) protein.	Phenobarbital	0-7	PML nuclear body scaffold	Homo sapiens	127-163
35019140-5	2022	The formation of Stac-positive luminal EVs depends on the tracheal tip-cell-specific GTPase Arl3, which is also required for the formation of Stac-positive multivesicular bodies, suggesting that Stac-EVs derive from fusion of Stac-MVBs with the luminal membrane in tip cells during anastomosis formation.	Phenobarbital	31-38	dead end	Drosophila melanogaster	92-96
35019140-5	2022	The formation of Stac-positive luminal EVs depends on the tracheal tip-cell-specific GTPase Arl3, which is also required for the formation of Stac-positive multivesicular bodies, suggesting that Stac-EVs derive from fusion of Stac-MVBs with the luminal membrane in tip cells during anastomosis formation.	Phenobarbital	245-252	dead end	Drosophila melanogaster	92-96
35121782-4	2022	Neuropeptide Y Receptor Y1 (NPY1R) gene and protein expression were significantly higher in Luminal A tumors versus other BC subtypes.	Phenobarbital	92-99	neuropeptide Y receptor Y1	Homo sapiens	28-33
35121782-5	2022	The trend of NPY1R gene, protein, and phosphosite (NPY1R-S368s) expression was decreasing in the order of Luminal A, Luminal B, Basal, and human epidermal growth factor receptor 2 (HER2) subtypes.	Phenobarbital	106-113	neuropeptide Y receptor Y1	Homo sapiens	13-18
35121782-5	2022	The trend of NPY1R gene, protein, and phosphosite (NPY1R-S368s) expression was decreasing in the order of Luminal A, Luminal B, Basal, and human epidermal growth factor receptor 2 (HER2) subtypes.	Phenobarbital	106-113	neuropeptide Y receptor Y1	Homo sapiens	51-56
35121782-5	2022	The trend of NPY1R gene, protein, and phosphosite (NPY1R-S368s) expression was decreasing in the order of Luminal A, Luminal B, Basal, and human epidermal growth factor receptor 2 (HER2) subtypes.	Phenobarbital	117-124	neuropeptide Y receptor Y1	Homo sapiens	13-18
35121782-5	2022	The trend of NPY1R gene, protein, and phosphosite (NPY1R-S368s) expression was decreasing in the order of Luminal A, Luminal B, Basal, and human epidermal growth factor receptor 2 (HER2) subtypes.	Phenobarbital	117-124	neuropeptide Y receptor Y1	Homo sapiens	51-56
35118379-6	2022	Furthermore, the epigenomic changes in basal cells due to BRCA1 mutation appear to facilitate their transformation into luminal progenitor cells.	Phenobarbital	120-127	BRCA1 DNA repair associated	Homo sapiens	58-63
35195972-2	2022	For example, estrogen receptor (ER) positive breast cancer is composed of two different subtypes (luminal A and luminal B) with different biologic processes and distinct prognosis.	Phenobarbital	98-105	estrogen receptor 1	Homo sapiens	13-30
35195972-2	2022	For example, estrogen receptor (ER) positive breast cancer is composed of two different subtypes (luminal A and luminal B) with different biologic processes and distinct prognosis.	Phenobarbital	98-105	estrogen receptor 1	Homo sapiens	32-34
35195972-2	2022	For example, estrogen receptor (ER) positive breast cancer is composed of two different subtypes (luminal A and luminal B) with different biologic processes and distinct prognosis.	Phenobarbital	112-119	estrogen receptor 1	Homo sapiens	13-30
35195972-2	2022	For example, estrogen receptor (ER) positive breast cancer is composed of two different subtypes (luminal A and luminal B) with different biologic processes and distinct prognosis.	Phenobarbital	112-119	estrogen receptor 1	Homo sapiens	32-34
35079116-6	2022	RESULTS: The Luminal subtype of mCRPCs has higher Androgen Receptor (AR) expression and copy number alterations as compared with the other subtypes.	Phenobarbital	13-20	androgen receptor	Homo sapiens	50-67
35173328-8	2022	We demonstrate that RHBDL4 can shed luminal fragments of endoplasmic reticulum-resident type I transmembrane proteins to the extracellular space, as well as promoting non-canonical secretion of endogenous soluble endoplasmic reticulum-resident chaperones.	Phenobarbital	36-43	rhomboid like 3	Homo sapiens	20-26
35079116-6	2022	RESULTS: The Luminal subtype of mCRPCs has higher Androgen Receptor (AR) expression and copy number alterations as compared with the other subtypes.	Phenobarbital	13-20	androgen receptor	Homo sapiens	69-71
35159020-7	2022	Basal and luminal TRAMP cells exhibited distinct molecular signatures and gave rise to organoids with distinct phenotypes.	Phenobarbital	10-17	tumor necrosis factor receptor superfamily, member 25	Mus musculus	18-23
35174209-4	2021	Degradation of intra-luminal or ER membrane proteins occurs through distinct mechanisms that include ER-associated Degradation (ERAD) and ER-to-lysosome-associated degradation (ERLAD), which includes macro-ER-phagy, micro-ER-phagy, and Atg8/LC-3-dependent vesicular delivery.	Phenobarbital	21-28	GABA type A receptor associated protein like 1	Homo sapiens	236-245
35082296-4	2022	The gluten-sensitive small intestine enteropathy that develops in CD19-/- mice is associated with alterations to luminal bile acid composition in the SI, marked by significant reductions in the abundance of conjugated bile acids.	Phenobarbital	113-120	CD19 antigen	Mus musculus	66-70
35153824-9	2022	Model simulations also suggest that SGLT2 inhibition raises luminal (Cl-) at the macula densa, twice as much in males as in females, and could indicate activation of the tubuloglomerular feedback signal.	Phenobarbital	60-67	solute carrier family 5 member 2	Homo sapiens	36-41
35085258-3	2022	We found that PD-L1 and PD-L2 mRNA expressions were highly expressed in TNBC-type cell lines (HCC1937, MDA-MB-231), moderately expressed in HER2-type cell line (SK-BR-3), and poorly expressed in luminal-type cell lines (MDA-MB-361, MCF7).	Phenobarbital	195-202	CD274 molecule	Homo sapiens	14-19
35085258-3	2022	We found that PD-L1 and PD-L2 mRNA expressions were highly expressed in TNBC-type cell lines (HCC1937, MDA-MB-231), moderately expressed in HER2-type cell line (SK-BR-3), and poorly expressed in luminal-type cell lines (MDA-MB-361, MCF7).	Phenobarbital	195-202	programmed cell death 1 ligand 2	Homo sapiens	24-29
35163087-7	2022	We identified AR/P-gp double immunofluorescence co-expression of both proteins in normal luminal cells.	Phenobarbital	89-96	androgen receptor	Canis lupus familiaris	14-16
35163087-7	2022	We identified AR/P-gp double immunofluorescence co-expression of both proteins in normal luminal cells.	Phenobarbital	89-96	PGP	Canis lupus familiaris	17-21
35052843-7	2022	The luminal BC HER2 + AR+ was associated with lower histological grade, lower tumor size, higher PR expression and lower HER2 intensity of expression (2+).	Phenobarbital	4-11	progesterone receptor	Homo sapiens	97-99
35045283-5	2022	This PSAT1 expression disparity preexists in the putative cells of origin of basal and luminal tumors and is due to luminal-specific hypermethylation of the PSAT1 gene.	Phenobarbital	116-123	phosphoserine aminotransferase 1	Homo sapiens	5-10
35045283-5	2022	This PSAT1 expression disparity preexists in the putative cells of origin of basal and luminal tumors and is due to luminal-specific hypermethylation of the PSAT1 gene.	Phenobarbital	116-123	phosphoserine aminotransferase 1	Homo sapiens	157-162
35053617-8	2022	To further support our data, we also characterized CD24-/CD44+ BCSCs from human luminal MCF-7 breast cancer cells.	Phenobarbital	80-87	CD24 molecule	Homo sapiens	51-55
35052843-7	2022	The luminal BC HER2 + AR+ was associated with lower histological grade, lower tumor size, higher PR expression and lower HER2 intensity of expression (2+).	Phenobarbital	4-11	erb-b2 receptor tyrosine kinase 2	Homo sapiens	121-125
35052843-7	2022	The luminal BC HER2 + AR+ was associated with lower histological grade, lower tumor size, higher PR expression and lower HER2 intensity of expression (2+).	Phenobarbital	4-11	erb-b2 receptor tyrosine kinase 2	Homo sapiens	15-19
34636707-5	2022	Transient overexpression of myc-tagged Prss53 in COS-7 cells showed that Prss53 was strongly associated with the luminal surfaces of organellar membranes and that it underwent signal peptide cleavage and N-glycosylation.	Phenobarbital	113-120	protease, serine 53	Mus musculus	73-79
35021081-5	2022	2HG induces loss of motif accessibility to the luminal-defining transcriptional factors FOXA1, FOXP1, and GATA3 and a shift from luminal to basal-like gene expression.	Phenobarbital	47-54	forkhead box A1	Homo sapiens	88-93
35021081-5	2022	2HG induces loss of motif accessibility to the luminal-defining transcriptional factors FOXA1, FOXP1, and GATA3 and a shift from luminal to basal-like gene expression.	Phenobarbital	47-54	forkhead box P1	Homo sapiens	95-100
35021081-5	2022	2HG induces loss of motif accessibility to the luminal-defining transcriptional factors FOXA1, FOXP1, and GATA3 and a shift from luminal to basal-like gene expression.	Phenobarbital	47-54	GATA binding protein 3	Homo sapiens	106-111
35013146-4	2022	ERG-negative tumor cells, compared to ERG-positive cells, demonstrate shared heterogeneity with surrounding luminal epithelial cells and appear to give rise to common tumor microenvironment responses.	Phenobarbital	108-115	ETS transcription factor ERG	Homo sapiens	38-41
34636707-5	2022	Transient overexpression of myc-tagged Prss53 in COS-7 cells showed that Prss53 was strongly associated with the luminal surfaces of organellar membranes and that it underwent signal peptide cleavage and N-glycosylation.	Phenobarbital	113-120	protease, serine 53	Mus musculus	39-45
35366286-5	2022	The highest frequency of positive ANGPTL4 and IGF-1 expression was observed in the luminal A subtype, whereas the HER2-overexpression subtype exhibited the lowest expression frequency for both proteins.	Phenobarbital	83-90	angiopoietin like 4	Homo sapiens	34-41
35366286-5	2022	The highest frequency of positive ANGPTL4 and IGF-1 expression was observed in the luminal A subtype, whereas the HER2-overexpression subtype exhibited the lowest expression frequency for both proteins.	Phenobarbital	83-90	insulin like growth factor 1	Homo sapiens	46-51
34990895-3	2022	METHODS: HER2DX is a supervised learning algorithm incorporating tumour size, nodal staging, and 4 gene expression signatures tracking immune infiltration, tumour cell proliferation, luminal differentiation, and the expression of the HER2 amplicon, into a single score.	Phenobarbital	183-190	erb-b2 receptor tyrosine kinase 2	Homo sapiens	9-13
35600655-5	2022	Using the New Zealand male rabbit urethral injury model, the scaffold composed of tubular HA-SF nanofibers could recruit lumen and myoepithelial cells from the adjacent area of the host, rapidly reconstructing the urothelial barrier in the wound area in order to keep the urinary tract unobstructed, thereby promoting luminal epithelialization, smooth muscle bundle structural remodeling, and capillary formation.	Phenobarbital	318-325	divergent protein kinase domain 2A	Homo sapiens	90-95
35119658-5	2022	In this chapter, we describe several practical experimental procedures confirming that mouse ERalpha is phosphorylated at serine 216 in livers upon phenobarbital (PB) treatment.	Phenobarbital	148-161	estrogen receptor 1 (alpha)	Mus musculus	93-100
35119658-5	2022	In this chapter, we describe several practical experimental procedures confirming that mouse ERalpha is phosphorylated at serine 216 in livers upon phenobarbital (PB) treatment.	Phenobarbital	163-165	estrogen receptor 1 (alpha)	Mus musculus	93-100
35119658-7	2022	In response to PB, the conserved motif within the DBD activates the Sult1e1 gene.	Phenobarbital	15-17	sulfotransferase family 1E, member 1	Mus musculus	68-75
34976209-7	2022	Results: Haploid loss of Gata3 reduced mammary epithelial cell proliferation with induction of p18, impaired luminal differentiation, and promoted basal differentiation in mammary glands.	Phenobarbital	109-116	GATA binding protein 3	Mus musculus	25-30
34976209-9	2022	Haploid loss of Gata3 accelerated p18 deficient mammary tumor development and changed the properties of these tumors, resulting in their malignant and luminal-to-basal transformation.	Phenobarbital	151-158	GATA binding protein 3	Mus musculus	16-21
34976209-9	2022	Haploid loss of Gata3 accelerated p18 deficient mammary tumor development and changed the properties of these tumors, resulting in their malignant and luminal-to-basal transformation.	Phenobarbital	151-158	cyclin dependent kinase inhibitor 2C	Mus musculus	34-37
35158329-4	2021	cGMP/PKGII activates cystic fibrosis transmembrane conductance regulator for anion transport to the intestinal lumen, inhibits Na+/H+ exchanger that restricts H+ secretion and Na+ absorption, resulting in the retention of luminal fluid.	Phenobarbital	222-229	CF transmembrane conductance regulator	Homo sapiens	21-72