机译:胰岛淀粉样多肽诱导的UCH-L1缺乏症介导的2型糖尿病中β细胞功能异常的ERAD /泛素/蛋白酶体系统。
Safia Costes,1 Chang-jiang Huang,1 Tatyana Gurlo,1 Marie Daval,1 Aleksey V. Matveyenko,1 Robert A. Rizza,2 Alexandra E. Butler,1 and Peter C. Butler1From the 1 Larry Hillblom Islet Research Center, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, and the 2 Endocrine Research Unit, Mayo Clinic and Medical College, Rochester, Minnesota.Corresponding author Safia Costes, scostes@mednet.ucla.edu.Received 12 April 2010 and accepted 14 October 2010. Published ahead of print at http://diabetes.diabetesjournals.org on 27 October 2010. DOl: 10.2337/dbl0-0522.© 2011 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativeeonunons.org/licenses/by-nc-nd/3.0/ for details.The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.,;
机译:胰岛淀粉样多肽诱导的UCH-L1缺乏症介导的2型糖尿病的β细胞功能失调的ERAD /泛素/蛋白酶体系统
机译:UCHL1缺乏症加剧了人类胰岛淀粉样多肽在β细胞中的毒性作用泛素/蛋白酶体系统与自噬之间相互作用的证据
机译:分离的人类胰岛转录组在2型糖尿病中的微阵列分析以及泛素-蛋白酶体系统在胰腺β细胞功能异常中的作用
机译:通过刺激人类肉瘤细胞中的ER应激和泛素 - 蛋白酶体系的ER应激和抑制来诱导细胞凋亡和自噬
机译:昼夜节律的破坏损害胰岛胰岛功能,并增加对β细胞衰竭的敏感性,而2型糖尿病的病理并发症对昼夜节律体系具有很少的影响
机译:胰岛淀粉样多肽介导的UCH-L1缺乏症介导的2型糖尿病的β细胞功能异常的ERAD /泛素/蛋白酶体系统
机译:胰岛淀粉样多肽介导的UCH-L1缺乏症介导的2型糖尿病的β细胞功能异常的ERAD /泛素/蛋白酶体系统