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10.18632/oncotarget.17969 http://scihub22266oqcxt.onion/10.18632/oncotarget.17969 C5609893/?report=reader!5609893!28968961     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28968961&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 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2017 ; 8 (38): 62939-52 Nephropedia Template TP {{tp|p=28968961|t=2017. Critical role of ?1 integrin in postnatal beta-cell function and expansion |pdf=|usr=}}{{28968961}} gab.com Text Critical role of 1 integrin in postnatal beta-cell function and expansion JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28968961 #FOAvip ?1 integrin is essential for pancreatic beta-cell development and maintenance in rodents and humans. However, the effects of a temporal beta-cell specific ?1 integrin knockout on adult islet function are unknown. We utilized a mouse insulin 1 promoter driven tamoxifen-inducible Cre-recombinase ?1 integrin knockout mouse model (MIP?1KO) to investigate ?1 integrin function in adult pancreatic beta-cells. Adult male MIP?1KO mice were significantly glucose intolerant due to impaired glucose-stimulated insulin secretion in vivo and ex vivo at 8 weeks post-tamoxifen. The expression of Insulin and Pancreatic and duodenal homeobox-1 mRNA was significantly reduced in MIP?1KO islets, along with reductions in insulin exocytotic proteins. Morphological analyses demonstrated that beta-cell mass, islet density, and the number of large-sized islets was significantly reduced in male MIP?1KO mice. Significant reductions in the phosphorylation of signaling molecules focal adhesion kinase, extracellular signal-regulated kinases 1 and 2, and v-Akt murine thymoma viral oncogene were observed in male MIP?1KO islets when compared to controls. MIP?1KO islets displayed a significant increase in protein levels of the apoptotic marker cleaved-Poly (ADP-ribose) polymerase and a reduction of the cell cycle marker cyclin D1. Female MIP?1KO mice did not develop glucose intolerance or reduced beta-cell mass until 16 weeks post-tamoxifen. Glucose intolerance remained in both genders of aged MIP?1KO mice. This data demonstrates that ?1 integrin is required for the maintenance of glucose homeostasis through postnatal beta-cell function and expansion. Twit Text FOAVip Critical role of 1 integrin in postnatal beta-cell function and expansion ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28968961 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28968961 #FOAvip English Wikipedia <ref>{{Cite pmid|28968961}}</ref> Critical role of ?1 integrin in postnatal beta-cell function and expansion #MMPMID28968961 Peart J; Li J; Lee H; Riopel M; Feng ZC; Wang R Oncotarget 2017[Sep]; 8 (38): 62939-52 PMID28968961show ga ?1 integrin is essential for pancreatic beta-cell development and maintenance in rodents and humans. However, the effects of a temporal beta-cell specific ?1 integrin knockout on adult islet function are unknown. We utilized a mouse insulin 1 promoter driven tamoxifen-inducible Cre-recombinase ?1 integrin knockout mouse model (MIP?1KO) to investigate ?1 integrin function in adult pancreatic beta-cells. Adult male MIP?1KO mice were significantly glucose intolerant due to impaired glucose-stimulated insulin secretion in vivo and ex vivo at 8 weeks post-tamoxifen. The expression of Insulin and Pancreatic and duodenal homeobox-1 mRNA was significantly reduced in MIP?1KO islets, along with reductions in insulin exocytotic proteins. Morphological analyses demonstrated that beta-cell mass, islet density, and the number of large-sized islets was significantly reduced in male MIP?1KO mice. Significant reductions in the phosphorylation of signaling molecules focal adhesion kinase, extracellular signal-regulated kinases 1 and 2, and v-Akt murine thymoma viral oncogene were observed in male MIP?1KO islets when compared to controls. MIP?1KO islets displayed a significant increase in protein levels of the apoptotic marker cleaved-Poly (ADP-ribose) polymerase and a reduction of the cell cycle marker cyclin D1. Female MIP?1KO mice did not develop glucose intolerance or reduced beta-cell mass until 16 weeks post-tamoxifen. Glucose intolerance remained in both genders of aged MIP?1KO mice. This data demonstrates that ?1 integrin is required for the maintenance of glucose homeostasis through postnatal beta-cell function and expansion. äCritical role of ?1 integrin in postnatal beta-cell function and expan(epmc).pdf DeepDyve Pubget Overpricing