Transcriptional and Translational Control of Glucose-Stimulated (Pro)insulin Biosynthesis
نویسندگان
چکیده
منابع مشابه
Insulin does not mediate glucose stimulation of proinsulin biosynthesis.
It has recently been suggested that insulin augments its own production by a physiologically important feed-forward autocrine loop. We studied the kinetics of glucose-regulated proinsulin gene expression and proinsulin biosynthesis in normal rat islets with emphasis on the potential role of insulin as a mediator of the glucose effect. There was a time-dependent increase in steady-state proinsul...
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Monensin, a specific sodium ionophore~ has been shown to reduce glucose-induced proinsulin biosynthesis by 30% and to completely inhibit ~he intracellular conversion of proinsul in to insulin. Autoradiography of monensint r e a t e d cells d e m o n s t r a t e d the p resence of large quantities of newly synthesized proteins in amorphous vesicles close to the Golgi complex of B ceils. The r e ...
متن کاملGlucose-induced translational control of proinsulin biosynthesis is proportional to preproinsulin mRNA levels in islet beta-cells but not regulated via a positive feedback of secreted insulin.
Proinsulin biosynthesis is regulated in response to nutrients, most notably glucose. In the short term (</=2h) this is due to increases in the translation of pre-existing mRNA. However, prolonging glucose stimulation (24 h) also increases preproinsulin mRNA levels. It has been proposed that secreted insulin from the pancreatic beta-cell regulates its own synthesis through a positive autocrine f...
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Mcl-1 is an antiapoptotic member of the Bcl-2 family whose protein and mRNA have a short half-life. In this report, we studied the changes in Mcl-1 protein and mRNA expression induced by staurosporine and aspirin. Both drugs induced apoptosis in Jurkat cells and reduced the levels of Mcl-1 protein. The caspase inhibitor Z-VAD.fmk and the proteasome inhibitor MG132 partially protected Mcl-1 from...
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ODC (ornithine decarboxylase) activity is induced following ras activation. However, the Ras effector pathways responsible are unknown. These experiments used NIH-3T3 cells expressing partial-loss-of-function Ras mutants to activate selectively pathways downstream of Ras and examined the contribution of each pathway to ODC induction. Overexpression of Ras12V, a constitutively active mutant, res...
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ژورنال
عنوان ژورنال: European Journal of Biochemistry
سال: 1980
ISSN: 0014-2956,1432-1033
DOI: 10.1111/j.1432-1033.1980.tb04892.x