Glucocorticoid-mediated induction of CYP3A4 is decreased by disruption of a protein: DNA interaction distinct from the pregnane X receptor response element

Drug Metabolism and Disposition

Volumn 30, Issue 9, 2002, Pages 1029-1034

  El Sankary, Wafaa ^a   Bombail, Vincent ^a   Gibson, G Gordon ^a   Plant, Nick ^a  

^a UNIVERSITY OF SURREY   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

ANDROSTANE RECEPTOR; CCAAT ENHANCER BINDING PROTEIN ALPHA; CELL NUCLEUS RECEPTOR; CYTOCHROME P450 3A4; DEXAMETHASONE; DNA; GLUCOCORTICOID; GLUCOCORTICOID RECEPTOR; HEPATOCYTE NUCLEAR FACTOR 3; HYDROCORTISONE; PREGNANE X RECEPTOR; PROTEIN; RIFAMPICIN; STEROID RECEPTOR; UNCLASSIFIED DRUG; VITAMIN D RECEPTOR; CELL RECEPTOR; CYP3A PROTEIN, HUMAN; CYP3A4 PROTEIN, HUMAN; CYTOCHROME P450; DEOXYRIBONUCLEASE I; DNA BINDING PROTEIN; FOXA1 PROTEIN, HUMAN; HEPATOCYTE NUCLEAR FACTOR 3ALPHA; LIGAND; NUCLEAR PROTEIN; TRANSCRIPTION FACTOR;

ANIMAL CELL; ARTICLE; BINDING SITE; CONTROLLED STUDY; CYP3A4 GENE; DNA RESPONSIVE ELEMENT; DRUG POTENCY; ENZYME INDUCTION; GENE CONSTRUCT; GENE DISRUPTION; GENE EXPRESSION REGULATION; GENE ISOLATION; GENE MUTATION; LIGAND BINDING; NONHUMAN; PRIORITY JOURNAL; PROMOTER REGION; PROTEIN CONTENT; PROTEIN DNA BINDING; RAT; REPORTER GENE; STEROID THERAPY; TRANSCRIPTION REGULATION; BIOSYNTHESIS; CELL CULTURE; DNA FOOTPRINTING; GEL MOBILITY SHIFT ASSAY; GENETICS; HUMAN; METABOLISM; MUTATION;

BINDING SITES; CCAAT-ENHANCER-BINDING PROTEIN-ALPHA; CYTOCHROME P-450 ENZYME SYSTEM; DEOXYRIBONUCLEASE I; DEXAMETHASONE; DNA; DNA FOOTPRINTING; DNA-BINDING PROTEINS; ELECTROPHORETIC MOBILITY SHIFT ASSAY; ENZYME INDUCTION; GLUCOCORTICOIDS; HUMAN; HYDROCORTISONE; LIGANDS; MUTATION; NUCLEAR PROTEINS; RECEPTORS, CYTOPLASMIC AND NUCLEAR; RECEPTORS, STEROID; RESPONSE ELEMENTS; RIFAMPIN; TUMOR CELLS, CULTURED; HEPATOCYTE NUCLEAR FACTOR 3-ALPHA; HUMANS; TRANSCRIPTION FACTORS;

ANIMALIA;

EID: 0036707623     PISSN: 00909556     EISSN: None     Source Type: Journal    
DOI: 10.1124/dmd.30.9.1029     Document Type: Article

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