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GLP—1受体基因表达cAMP-PKA途径调控的研究 被引量:1

Regulation of Expression of GLP—1 Receptor by cAMP—PKA Pathway
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摘要 本文利用蛋白激酶A(PKA)的激活剂Forsolin对大白鼠胰岛素瘤细胞(RINm5F)上GLP一1受体的基因表达进行了研究。在forskolin的作用下,使类胰高血糖素肽I(GLP—1)受体的转水平明显下降,即GLP一1受体mRNA的量明显减少,出现了GLP一1受体基因表达的负调控,但forskoln可以使GLP—1受体的mRNA的稳定性增加结果表明,GLP—1受体的转录是通过cAMP—蛋白激酶A途径进行调控的,因此,影响此途径的物质对类胰高血糖素肽—1的生理功能以及在临床应用方面起着重要作用。 Glucagon—like peptide(GLP—1)is a potent incretin hormone and mediatesits actions via specific receptors at pancreatic B—cells.The GLP—1 receptor belongsto the seven—transmem- brane receptors coupled to G—proteins.We have presently analyzed the regulation of GLP—1 re- ceptor expression in rat insulinoma—derived B—cells(RINm5F)with forskolin that is activator of protein kinase A(PKA).The GLP—1 receptor mRNA levels were down—regulated during incu- bation of cells with forskolin.But forskolin stabilized the GLP—1 receptor mRNA.The results show that the GLP—1 receptor expression is regulated by cAMP—PKA pathway,thereforthe ma- teries,that influence the pathway,are very important for the functions of GLP—1 and the treat- ment of NIDDM.
出处 《佳木斯医学院学报》 1996年第3期1-4,共4页
关键词 GLP-1 基因表达 FORSKOLIN 蛋白激酶A Giucagon—like peptide—1(GLP—1)receptor gene expression forskolin cAMP Protein kinase A(PKA)
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  • 1M. A. Nauck,M. Büsing,C. ?rskov,E. G. Siegel,J. Talartschik,A. Baartz,T. Baartz,U. T. Hopt,H. -D. Becker,W. Creutzfeldt. Preserved incretin effect in type 1 diabetic patients with end-stage nephropathy treated by combined heterotopic pancreas and kidney transplantation[J] 1993,Acta Diabetologica(1):39~45

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