Activation and induction of Nur77/Nurr1 in corticotrophs by CRH/cAMP: Involvement of calcium, protein kinase a, and MAPK pathways

Molecular Endocrinology

Volumn 16, Issue 7, 2002, Pages 1638-1651

  Kovalovsky, Damián ^a   Refojo, Damián ^b   Liberman, Ana Clara ^a   Hochbaum, Daniel ^a,b   Pereda, Marcelo Paez ^a,b   Coso, Omar A ^a   Stalla, Günter K ^a   Holsboer, Florian ^a   Arzt, Eduardo ^a  

^a INSTITUTO DE FISIOLOGÍA   (Argentina)

^b MAX PLANCK INSTITUTE OF PSYCHIATRY   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

CORTICOSTEROID RECEPTOR; CYCLIC AMP DEPENDENT PROTEIN KINASE; MITOGEN ACTIVATED PROTEIN KINASE; PROOPIOMELANOCORTIN; PROTEIN KINASE (CALCIUM,CALMODULIN); CALCIUM; CALCIUM CHANNEL BLOCKING AGENT; CELL RECEPTOR; CORTICOTROPIN RELEASING FACTOR; CYCLIC AMP; DNA BINDING PROTEIN; ELK1 PROTEIN, MOUSE; NIFEDIPINE; NUCLEAR RECEPTOR NUR77; NURR1 NUCLEAR RECEPTOR; ONCOPROTEIN; STEROID RECEPTOR; TRANSCRIPTION FACTOR; TRANSCRIPTION FACTOR ELK 1;

ANIMAL CELL; ARTICLE; CELL TYPE; CORTICOTROPIN RELEASE; ENZYME ACTIVATION; ENZYME INDUCTION; GENE OVEREXPRESSION; HYPOTHALAMUS HYPOPHYSIS ADRENAL SYSTEM; NONHUMAN; POINT MUTATION; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; STIMULUS RESPONSE; STRESS; TRANSCRIPTION REGULATION; ANIMAL; CELL CULTURE; CYTOLOGY; DNA RESPONSIVE ELEMENT; DRUG EFFECT; GENETIC TRANSCRIPTION; GENETICS; HYPOPHYSIS; METABOLISM; MOUSE; MUTATION; PHOSPHORYLATION; PROMOTER REGION; SIGNAL TRANSDUCTION;

ANIMALIA;

ANIMALS; CALCIUM; CALCIUM CHANNEL BLOCKERS; CELLS, CULTURED; CORTICOTROPIN-RELEASING HORMONE; CYCLIC AMP; CYCLIC AMP-DEPENDENT PROTEIN KINASES; DNA-BINDING PROTEINS; ETS-DOMAIN PROTEIN ELK-1; MAP KINASE SIGNALING SYSTEM; MICE; MUTATION; NIFEDIPINE; PHOSPHORYLATION; PITUITARY GLAND; PRO-OPIOMELANOCORTIN; PROMOTER REGIONS (GENETICS); PROTO-ONCOGENE PROTEINS; RECEPTORS, CYTOPLASMIC AND NUCLEAR; RECEPTORS, STEROID; RESPONSE ELEMENTS; SIGNAL TRANSDUCTION; TRANSCRIPTION FACTORS; TRANSCRIPTION, GENETIC;

EID: 85047684179     PISSN: 08888809     EISSN: None     Source Type: Journal    
DOI: 10.1210/mend.16.7.0863     Document Type: Article

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