PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 28218408-7 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 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 3, subfamily a, polypeptide 11 Mus musculus 294-299 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 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 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 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 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 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 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 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 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 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 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 3, subfamily a, polypeptide 11 Mus musculus 174-179 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 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 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 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 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 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