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10.1007/s00125-016-4072-7 http://scihub22266oqcxt.onion/10.1007/s00125-016-4072-7 C5506098!5506098 !27514532     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27514532 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27514532 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Diabetologia 2016 ; 59 (11 ): 2280-2291 Nephropedia Template TP {{tp|p=27514532 |t=2016. IRS proteins and diabetic complications |pdf=|usr=}}{{27514532 }} gab.com Text IRS proteins and diabetic complications JO: Diabetologia http://www.kidney.de/pget.php?&tw=1&pmid=27514532 #FOAvip IRS proteins are cellular adaptor molecules that mediate many of the key metabolic actions of insulin. When tyrosine is phosphorylated by the activated insulin receptor, IRS proteins recruit downstream effectors, such as phosphoinositide 3-kinase and mitogen-activated protein kinase, in order to elicit cellular responses such as glucose uptake, lipid metabolism and cell proliferation. There are two main IRS proteins in humans (IRS1 and IRS2), both of which are widely expressed. Given their central role in the insulin signalling pathway, it is not surprising that male mice lacking Irs1 or Irs2 present with elevated blood glucose or type 2 diabetes, respectively. For reasons yet to be identified, female Irs2 (-/-) mice do not develop type 2 diabetes. A number of organs are affected by complications of diabetes; macrovascular complications include stroke and coronary artery disease, while nephropathy, neuropathy and retinopathy fall into the category of microvascular complications. Given the serious consequences of these complications on patient morbidity and mortality, it is essential to identify the molecular pathogenesis underlying diabetic complications, with a view to improving therapeutic intervention and patient outcomes. A number of recently published papers have converged on the hypothesis that the loss of insulin signalling and IRS proteins is instrumental to the development and/or progression of diabetic complications. This review will summarise some highlights from the published work in which this hypothesis is discussed. Twit Text FOAVip IRS proteins and diabetic complications ????Diabetologia http://www.kidney.de/pget.php?&tw=1&pmid=27514532 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27514532 #FOAvip English Wikipedia <ref>{{Cite pmid|27514532 }}</ref> IRS proteins and diabetic complications #MMPMID27514532 Lavin DP ; White MF ; Brazil DP Diabetologia 2016[Nov]; 59 (11 ): 2280-2291 PMID27514532 show ga IRS proteins are cellular adaptor molecules that mediate many of the key metabolic actions of insulin. When tyrosine is phosphorylated by the activated insulin receptor, IRS proteins recruit downstream effectors, such as phosphoinositide 3-kinase and mitogen-activated protein kinase, in order to elicit cellular responses such as glucose uptake, lipid metabolism and cell proliferation. There are two main IRS proteins in humans (IRS1 and IRS2), both of which are widely expressed. Given their central role in the insulin signalling pathway, it is not surprising that male mice lacking Irs1 or Irs2 present with elevated blood glucose or type 2 diabetes, respectively. For reasons yet to be identified, female Irs2 (-/-) mice do not develop type 2 diabetes. A number of organs are affected by complications of diabetes; macrovascular complications include stroke and coronary artery disease, while nephropathy, neuropathy and retinopathy fall into the category of microvascular complications. Given the serious consequences of these complications on patient morbidity and mortality, it is essential to identify the molecular pathogenesis underlying diabetic complications, with a view to improving therapeutic intervention and patient outcomes. A number of recently published papers have converged on the hypothesis that the loss of insulin signalling and IRS proteins is instrumental to the development and/or progression of diabetic complications. This review will summarise some highlights from the published work in which this hypothesis is discussed. |Animals [MESH] |Diabetes Complications/genetics/*metabolism [MESH] |Diabetes Mellitus, Type 2/genetics/metabolism [MESH] |Female [MESH] |Humans [MESH] |Insulin Receptor Substrate Proteins/genetics/*metabolism [MESH] |Male [MESH] |Mice [MESH]IRS proteins and diabetic complications (epmc).pdf DeepDyve Pubget Overpricing