Three mechanisms are involved in glucocorticoid receptor autoregulation in a human T-lymphoblast cell line

Biochemistry

Volumn 43, Issue 34, 2004, Pages 10851-10858

  Pedersen, Kim Brint ^a   Geng, Chuan Dong ^a   Vedeckis, Wayne V ^a  

^a LOUISIANA STATE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ACTIVATION ANALYSIS; BIOCHEMICAL ENGINEERING; GENETIC ENGINEERING; PROTEINS; RNA;

GLUCOCORTICOID RECEPTOR (GR); ISOFORMS; LYMPHOBLAST CELLS; RNA STABILIZATION;

CELLS;

GLUCOCORTICOID; GLUCOCORTICOID RECEPTOR; GLUCOCORTICOID RECEPTOR A; GLUCOCORTICOID RECEPTOR B; MESSENGER RNA; UNCLASSIFIED DRUG; DEXAMETHASONE; GLUCOCORTICOID RECEPTOR ALPHA; GLUCOCORTICOID RECEPTOR BETA; ISOPROTEIN; TRANSACTIVATOR PROTEIN;

ANIMAL CELL; ARTICLE; AUTOREGULATION; CONCENTRATION (PARAMETERS); EXON; GENETIC TRANSFECTION; HUMAN; HUMAN CELL; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROMOTER REGION; PROTEIN EXPRESSION; PROTEIN STABILITY; RECEPTOR UPREGULATION; RNA STABILITY; RNA TRANSLATION; T LYMPHOBLAST; TRANSACTIVATION; ANIMAL; CELL LINE; DRUG EFFECT; GENETIC TRANSCRIPTION; GENETICS; LYMPHOCYTE ACTIVATION; METABOLISM; PROTEIN SYNTHESIS; T LYMPHOCYTE; UPREGULATION;

ANIMALIA;

ANIMALS; CELL LINE, TRANSFORMED; DEXAMETHASONE; EXONS; HUMANS; LYMPHOCYTE ACTIVATION; MICE; PROMOTER REGIONS (GENETICS); PROTEIN BIOSYNTHESIS; PROTEIN ISOFORMS; RECEPTORS, GLUCOCORTICOID; RNA STABILITY; T-LYMPHOCYTES; TRANS-ACTIVATORS; TRANSCRIPTION, GENETIC; TRANSFECTION; UP-REGULATION;

EID: 4644226289     PISSN: 00062960     EISSN: None     Source Type: Journal    
DOI: 10.1021/bi049458u     Document Type: Article

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