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首页> 外文期刊>Diabetologia >Growth arrest- and DNA-damage-inducible 45β gene inhibits c-Jun N-terminal kinase and extracellular signal-regulated kinase and decreases IL-1β-induced apoptosis in insulin-producing INS-1E cells
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Growth arrest- and DNA-damage-inducible 45β gene inhibits c-Jun N-terminal kinase and extracellular signal-regulated kinase and decreases IL-1β-induced apoptosis in insulin-producing INS-1E cells

机译:生长停滞和DNA损伤诱导型45β基因抑制c-Jun N末端激酶和细胞外信号调节激酶并减少IL-1β诱导的胰岛素产生的INS-1E细胞凋亡

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摘要

IL-1β is a candidate mediator of apoptotic beta cell destruction, a process that leads to type 1 diabetes and progression of type 2 diabetes. IL-1β activates beta cell c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) and p38, all of which are members of the mitogen-activated protein kinase (MAPK) family. Inhibition of JNK prevents IL-1β-mediated beta cell destruction. In mouse embryo fibroblasts and 3DO T cells, overexpression of the gene encoding growth arrest and DNA-damage-inducible 45β (Gadd45b) downregulates pro-apoptotic JNK signalling. The aim of this study was to investigate if Gadd45b prevents IL-1β-induced beta cell MAPK signalling and apoptosis.
机译:IL-1β是凋亡性β细胞破坏的候选介质,该过程导致1型糖尿病和2型糖尿病的发展。 IL-1β激活β细胞c-Jun N末端激酶(JNK),细胞外信号调节激酶(ERK)和p38,它们都是促分裂原活化蛋白激酶(MAPK)家族的成员。抑制JNK可防止IL-1β介导的β细胞破坏。在小鼠胚胎成纤维细胞和3DO T细胞中,编码生长停滞和DNA损伤诱导型45β(Gadd45b)的基因的过表达下调了促凋亡JNK信号。这项研究的目的是研究Gadd45b是否能阻止IL-1β诱导的β细胞MAPK信号传导和凋亡。

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