Title : Cyclic AMP inducible early repressor mediates the termination of corticotropin releasing hormone transcription in hypothalamic neurons.

Pub. Date : 2009 Dec

PMID : 19543827






11 Functional Relationships(s)
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1 Cotransfection of 4B cells with CREM siRNA and a CRH promoter-driven luciferase reporter gene markedly reduced the induction of ICER by forskolin and potentiated the stimulatory effect of forskolin on CRH promoter activity, compared with cells cotransfected with a nonspecific oligonucleotide. Colforsin corticotropin releasing hormone Homo sapiens
2 Cotransfection of 4B cells with CREM siRNA and a CRH promoter-driven luciferase reporter gene markedly reduced the induction of ICER by forskolin and potentiated the stimulatory effect of forskolin on CRH promoter activity, compared with cells cotransfected with a nonspecific oligonucleotide. Colforsin corticotropin releasing hormone Homo sapiens
3 Cotransfection of 4B cells with CREM siRNA and a CRH promoter-driven luciferase reporter gene markedly reduced the induction of ICER by forskolin and potentiated the stimulatory effect of forskolin on CRH promoter activity, compared with cells cotransfected with a nonspecific oligonucleotide. Colforsin corticotropin releasing hormone Homo sapiens
4 As observed during stress in vivo, forskolin-stimulated CRH hnRNA was transient, increasing up to 60 min and declining to near basal values by 3 h. Transfection of CREM siRNA reduced forskolin-induced ICER by about 45% 48-h later and partially reversed the declining phase of CRH hnRNA production at 3 h. The data provide evidence that endogenous ICER formation is required for termination of CRH transcription and support the hypothesis that ICER is part of an intracellular feedback mechanism limiting the activation of CRH transcription during stress. Colforsin corticotropin releasing hormone Homo sapiens
5 As observed during stress in vivo, forskolin-stimulated CRH hnRNA was transient, increasing up to 60 min and declining to near basal values by 3 h. Transfection of CREM siRNA reduced forskolin-induced ICER by about 45% 48-h later and partially reversed the declining phase of CRH hnRNA production at 3 h. The data provide evidence that endogenous ICER formation is required for termination of CRH transcription and support the hypothesis that ICER is part of an intracellular feedback mechanism limiting the activation of CRH transcription during stress. Colforsin corticotropin releasing hormone Homo sapiens
6 As observed during stress in vivo, forskolin-stimulated CRH hnRNA was transient, increasing up to 60 min and declining to near basal values by 3 h. Transfection of CREM siRNA reduced forskolin-induced ICER by about 45% 48-h later and partially reversed the declining phase of CRH hnRNA production at 3 h. The data provide evidence that endogenous ICER formation is required for termination of CRH transcription and support the hypothesis that ICER is part of an intracellular feedback mechanism limiting the activation of CRH transcription during stress. Colforsin corticotropin releasing hormone Homo sapiens
7 As observed during stress in vivo, forskolin-stimulated CRH hnRNA was transient, increasing up to 60 min and declining to near basal values by 3 h. Transfection of CREM siRNA reduced forskolin-induced ICER by about 45% 48-h later and partially reversed the declining phase of CRH hnRNA production at 3 h. The data provide evidence that endogenous ICER formation is required for termination of CRH transcription and support the hypothesis that ICER is part of an intracellular feedback mechanism limiting the activation of CRH transcription during stress. Colforsin corticotropin releasing hormone Homo sapiens
8 As observed during stress in vivo, forskolin-stimulated CRH hnRNA was transient, increasing up to 60 min and declining to near basal values by 3 h. Transfection of CREM siRNA reduced forskolin-induced ICER by about 45% 48-h later and partially reversed the declining phase of CRH hnRNA production at 3 h. The data provide evidence that endogenous ICER formation is required for termination of CRH transcription and support the hypothesis that ICER is part of an intracellular feedback mechanism limiting the activation of CRH transcription during stress. Colforsin corticotropin releasing hormone Homo sapiens
9 As observed during stress in vivo, forskolin-stimulated CRH hnRNA was transient, increasing up to 60 min and declining to near basal values by 3 h. Transfection of CREM siRNA reduced forskolin-induced ICER by about 45% 48-h later and partially reversed the declining phase of CRH hnRNA production at 3 h. The data provide evidence that endogenous ICER formation is required for termination of CRH transcription and support the hypothesis that ICER is part of an intracellular feedback mechanism limiting the activation of CRH transcription during stress. Colforsin corticotropin releasing hormone Homo sapiens
10 As observed during stress in vivo, forskolin-stimulated CRH hnRNA was transient, increasing up to 60 min and declining to near basal values by 3 h. Transfection of CREM siRNA reduced forskolin-induced ICER by about 45% 48-h later and partially reversed the declining phase of CRH hnRNA production at 3 h. The data provide evidence that endogenous ICER formation is required for termination of CRH transcription and support the hypothesis that ICER is part of an intracellular feedback mechanism limiting the activation of CRH transcription during stress. Colforsin corticotropin releasing hormone Homo sapiens
11 As observed during stress in vivo, forskolin-stimulated CRH hnRNA was transient, increasing up to 60 min and declining to near basal values by 3 h. Transfection of CREM siRNA reduced forskolin-induced ICER by about 45% 48-h later and partially reversed the declining phase of CRH hnRNA production at 3 h. The data provide evidence that endogenous ICER formation is required for termination of CRH transcription and support the hypothesis that ICER is part of an intracellular feedback mechanism limiting the activation of CRH transcription during stress. Colforsin corticotropin releasing hormone Homo sapiens