• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Interleukin-1 beta induces posttranslational carboxymethylation and alterations in subnuclear distribution of lamin B in insulin-secreting RINm5F cells.
【24h】

Interleukin-1 beta induces posttranslational carboxymethylation and alterations in subnuclear distribution of lamin B in insulin-secreting RINm5F cells.

机译：白介素-1β诱导胰岛素分泌的RINm5F细胞中翻译后羧甲基化和层粘连蛋白B的亚核分布改变。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

We examined the effects of interleukin-1beta (IL-1beta) treatment on the distribution and degradation of lamin B in the nuclear fraction from insulin-secreting RINm5F cells. Western blot analysis indicated that IL-1beta treatment caused significant alterations in the redistribution of lamin B, specifically between the Triton X-100-soluble (membrane) and -insoluble (matrix) fractions of the nucleus. IL-1beta treatment also increased the lamin carboxymethyltransferase activity and the relative abundance of the carboxymethylated lamin in the nuclear fraction. A significant increase in the relative abundance of lamin B degradation products was also observed in the nuclear fraction from the IL-1beta-treated cells. These findings are compatible with a measurable increase in the lamin-degrading caspase-6 activity in IL-1beta-treated cells. Confocal microscopic observation of IL-1beta-treated cells suggested a significant dissociation of lamin B from the nuclear lamina and its subsequent association with the DNA-rich elements within the nucleus. N(G)-monomethyl-l-arginine, a known inhibitor of inducible nitric oxide synthetase (iNOS), markedly inhibited IL-1beta-induced iNOS gene expression, NO release, caspase-3 and caspase-6 activation, lamin B degradation, and loss of metabolic cell viability, indicating that the observed IL-1beta-induced effects on nuclear lamin B involve the intermediacy of NO. Together, our data support the hypothesis that IL-1beta treatment results in significant increase in the carboxymethylation of lamin B, which would place lamin B in a strategic location for its degradation mediated by caspases. This could possibly lead to dissolution of the nuclear envelope, culminating in the demise of the effete beta-cell.
机译：我们检查了白细胞介素-1β（IL-1β）处理对胰岛素分泌RINm5F细胞核级分中层粘连蛋白B的分布和降解的影响。蛋白质印迹分析表明，IL-1beta处理导致层粘连蛋白B的重新分布发生了显着变化，特别是在Triton X-100可溶（膜）部分和不可溶（矩阵）部分细胞核之间。 IL-1β处理还提高了核纤层蛋白的核纤层蛋白羧甲基转移酶活性和相对丰度。在IL-1β处理的细胞的核级分中也观察到了lamin B降解产物相对丰度的显着增加。这些发现与IL-1β处理的细胞中层粘连蛋白降解caspase-6活性的可测量增加相符。共聚焦显微镜观察IL-1β处理的细胞表明，lamin B从核层中显着解离，并随后与核内富含DNA的元素相关联。 N（G）-单甲基-1-精氨酸，一种已知的诱导型一氧化氮合成酶（iNOS）抑制剂，可显着抑制IL-1beta诱导的iNOS基因表达，NO释放，caspase-3和caspase-6活化，层粘连蛋白B降解，以及代谢细胞活力的丧失，表明观察到的IL-1β诱导的核纤层蛋白B的作用涉及NO的中介。总之，我们的数据支持以下假设：IL-1β处理会导致lamin B的羧甲基化显着增加，这将使lamin B处于由胱天蛋白酶介导的降解的关键位置。这可能导致核被膜的溶解，最终导致有效的β细胞死亡。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号