Posttranscriptional regulation of glucocorticoid-regulated functions.

摘要: Relying heavily on studies of TAT regulation in cultured rat hepatoma cell lines, we have attempted this brief review to discuss possible mechanisms for posttranscriptional glucocorticoid-sensitive enzymes and chronicle the evidence against specific enzyme induction by glucocorticoids. Initially, were considered that would reconcile results showing sensitivity both deinduction inhibitors RNA synthesis with demonstrating first glucocorticoids regulate rates and, then, levels enzyme-specific mRNA. Such reconciliation proved unnecessary when it was demonstrated such as actinomycin D not synthesis, but also had effects mRNA turnover protein metabolism. The bulk date establishes promote production proteins whose is regulated thses steroids. Nevertheless, there still very little direct steroids can modulate gene transcription. glucocorticoid stimulation mouse mammary tumor virus lines only example where a mechanism supported RNA-DNA hybridization studies. Posttranscriptional actions turnover, processing, or extranuclear transport precursors remain potential steps at which might function. rapid some glucocorticoid-regulated their mRNAs ensures response steroid addition withdrawal, subjects these relatively large fluctuations upon alterations overall Thus many inductions repressions hepatic TO mediators other than may be attributable entirely nonspecific mechanisms.