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Mehanizem Transporta Glukoze V Osmotskem Šoku V Inzulindko Rezistentnih 3T3-L1 Adipocitih

出版	A. Janež, 2000
URL	http://books.google.com.hk/books?id=xvleNAAACAAJ&hl=&source=gbs_api

註釋Osmotic shock treatment of 3T3-L1 adipocytes causes an increase in glucose transport activity and translocation of GLUT-4 protein similar to that elicited by insulin treatment. Insulin stimulation of GLUT-4 translocation andglucose transport activity was completely inhibited by wortmannin, however, activation by osmotic shock was only partialy blocked. Additionally, we have found that the newly identified insulin rcceptor substrate (IRS) Gab-1(Grb2-associated binder-1) is tyrosine phosphorylated following sorbitol stimulation. Treatment of cells with the tyrosine kinase inhibitor genestin inhibited osmotic shockstimulated Gab-1 phosphorylation, as well as shock-induced glucose transport. rurthennore, pretreatment with the selective Src family kinase inhibitor PP2 completely inhibited the ability of sorbitol treatment to cause tyrosine phosphorylation of Gab-1. We have also shown that microinjection of anti-Gab-1 antibody inhibits osmotic shock-induced GLUT-4 translocation. Furthermore, phosphorylated Gab-1 binds and activates phosphatidylinositol 3-kinase (PI 3-kinase) in response to osmotic shock. The PI 3-kinase activity associated with Gab-1 was 82% of that associated with antiphosphotyrosine, indicating that Gab-I is the major site for PI 3-kinase recruitment following osmotic shock stimulation. (Abstract truncated at 2000 characters).