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Repression of glucocorticoid receptor gene transcription by c-Jun.
Cabral, A L; Hays, A N; Housley, P R; Brentani, M M; Martins, V R.
Afiliação
  • Cabral AL; Ludwig Institute for Cancer Research, 01509-900, São Paulo, Brazil.
Mol Cell Endocrinol ; 175(1-2): 67-79, 2001 Apr 25.
Article em En | MEDLINE | ID: mdl-11325517
The regulation of glucocorticoid receptor gene expression by members of the AP-1 family was examined in glucocorticoid-free NIH3T3 cells transfected with the human glucocorticoid receptor gene promoter driving expression of a CAT reporter gene. c-Jun inhibited the promoter activity by 80% and JunB by 30%, whereas c-Fos and JunD had no inhibitory effect. Electrophoretic mobility shift assays showed that c-Jun is unable to efficiently interact with the AP-1-like site present in the human glucocorticoid receptor promoter. Moreover, c-Jun was still able to repress promoter mutants in which the region containing the AP-1-like site was deleted. NIH3T3 cell clones overexpressing c-Jun exhibited lower glucocorticoid receptor mRNA levels, which suggests that the murine glucocorticoid receptor gene can also be regulated by AP-1. These results provide a new mechanism for cross-talk between the glucocorticoid receptor and the AP-1 family of transcription factors in the absence of glucocorticoid ligands.
Assuntos
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Transcrição Gênica / Receptores de Glucocorticoides / Proteínas Proto-Oncogênicas c-jun Limite: Animals / Humans Idioma: En Revista: Mol Cell Endocrinol Ano de publicação: 2001 Tipo de documento: Article País de afiliação: Brasil País de publicação: Irlanda
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Transcrição Gênica / Receptores de Glucocorticoides / Proteínas Proto-Oncogênicas c-jun Limite: Animals / Humans Idioma: En Revista: Mol Cell Endocrinol Ano de publicação: 2001 Tipo de documento: Article País de afiliação: Brasil País de publicação: Irlanda