PKCdelta blues for the beta-cell.
作者信息
Schmitz-Peiffer Carsten, Biden Trevor J
机构信息
Garvan Institute of Medical Research, Sydney, Australia.
出版信息
Diabetes. 2010 Jan;59(1):1-3. doi: 10.2337/db09-1439.
Abstract
摘要
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本文引用的文献
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Overexpression of kinase-negative protein kinase Cdelta in pancreatic beta-cells protects mice from diet-induced glucose intolerance and beta-cell dysfunction.蛋白激酶 C 激酶阴性结构域在胰岛β细胞中的过表达可保护小鼠免于饮食诱导的葡萄糖不耐受和β细胞功能障碍。
Diabetes. 2010 Jan;59(1):119-27. doi: 10.2337/db09-0512. Epub 2009 Oct 13.
2
Diverse roles for protein kinase C delta and protein kinase C epsilon in the generation of high-fat-diet-induced glucose intolerance in mice: regulation of lipogenesis by protein kinase C delta.蛋白激酶 C 三角洲和蛋白激酶 C epsilon 在高脂饮食诱导的小鼠葡萄糖不耐受中的多种作用：蛋白激酶 C 三角洲对脂肪生成的调节。
Diabetologia. 2009 Dec;52(12):2616-20. doi: 10.1007/s00125-009-1543-0. Epub 2009 Oct 7.
3
Deletion of PKCepsilon selectively enhances the amplifying pathways of glucose-stimulated insulin secretion via increased lipolysis in mouse beta-cells.删除蛋白激酶Cε可通过增加小鼠β细胞中的脂肪分解，选择性增强葡萄糖刺激的胰岛素分泌的放大途径。
Diabetes. 2009 Aug;58(8):1826-34. doi: 10.2337/db09-0132. Epub 2009 Apr 28.
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Cytokine-induced beta-cell death is independent of endoplasmic reticulum stress signaling.细胞因子诱导的β细胞死亡与内质网应激信号无关。
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Protein kinase C function in muscle, liver, and beta-cells and its therapeutic implications for type 2 diabetes.蛋白激酶C在肌肉、肝脏和β细胞中的功能及其对2型糖尿病的治疗意义。
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The PKCdelta -Abl complex communicates ER stress to the mitochondria - an essential step in subsequent apoptosis.蛋白激酶Cδ-阿卜林复合物将内质网应激传递至线粒体，这是随后细胞凋亡过程中的关键一步。
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