acute ablation of perk results in er dysfunctions followed by reduced insulin secretion and cell proliferation急性消融的活跃导致er障碍减少胰岛素分泌和细胞增殖.pdfVIP

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acute ablation of perk results in er dysfunctions followed by reduced insulin secretion and cell proliferation急性消融的活跃导致er障碍减少胰岛素分泌和细胞增殖.pdf

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BMC Cell Biology BioMed Central Research article Open Access Acute ablation of PERK results in ER dysfunctions followed by reduced insulin secretion and cell proliferation Daorong Feng, Jianwen Wei, Sounak Gupta, Barbara C McGrath and Douglas R Cavener* Address: Department of Biology, Pennsylvania State University, University Park, PA 16802, USA Email: Daorong Feng - dfeng@; Jianwen Wei - jw2707@; Sounak Gupta - sug149@; Barbara C McGrath - bcm5@; Douglas R Cavener* - drc9@ * Corresponding author Published: 4 September 2009 Received: 5 August 2008 Accepted: 4 September 2009 BMC Cell Biology 2009, 10:61 doi:10.1186/1471-2121-10-61 This article is available from: /1471-2121/10/61 © 2009 Feng et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: A deficiency in Perk (EIF2AK3) causes multiple neonatal defects in humans known as the Wolcott Rallison syndrome. Perk KO mice exhibit the same array of defects including permanent neonatal diabetes (PND). PND in mice was previously shown by us to be due to a decrease in beta cell proliferation and insulin secretion. The aim of this study was to determine if acute ablation of PERK in the 832/13 beta cells recapitulates these defects and to identify the primary molecular bas