Title : Inhibition of cAMP-responsive element-mediated gene transcription by cyclosporin A and FK506 after membrane depolarization.

Pub. Date : 1993 Nov 5

PMID : 7693684






4 Functional Relationships(s)
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1 CsA and FK506 inhibited depolarization-induced glucagon gene transcription, FK506 being more potent than CsA. Tacrolimus ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens
2 CsA/FK506 responsiveness was mediated by the glucagon CRE and also by well characterized CREs of the choriogonadotropin and somatostatin genes. Tacrolimus ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens
3 Rapamycin antagonized the inhibitory effect of FK506 but not CsA, suggesting that FK506 and CsA may act through complex formation with distinct intracellular immunophilins. Tacrolimus ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens
4 The interference with CRE-mediated gene transcription represents a novel mechanism of CsA/FK506 action, which may underlie pharmacological effects and toxic manifestations of these potent immunosuppressive drugs. Tacrolimus ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens