首页> 外文期刊>Gene expression >Identification and characterization of DEDDL, a human-specific isoform of DEDD.
【24h】

Identification and characterization of DEDDL, a human-specific isoform of DEDD.

机译:鉴定和表征DEDDL,DEDD的人类特异性亚型。

获取原文
获取原文并翻译 | 示例
           

摘要

Death effector domain (DED) containing molecules are usually involved in the intracellular apoptosis cascade as executioners or regulators. One of these molecules, DEDD, was identified as a final target of the CD95 signaling pathway by which it would be transferred into the nucleolus to inhibit RNA polymerase I-dependent transcription. Here we describe a longer isoform of DEDD, DEDDL, produced by alternatively splicing, as an immune cell-specific DED-containing molecule. It is only expressed in human T lymphocytes and dendritic cells (DCs), and the mRNA expression in DCs was elevated upon inductive maturation. In cell lines MCF-7 and Jurkat, the overexpression of DEDDL could induce apoptosis more potently than that of DEDD. That DEDDL could bind FADD and cFLIP more potently than DEDD in vivo was revealed by cotransfection and immunoprecipitation. This may explain why DEDDL is a more potent apoptosis inducer, because DED-containing proteins usually induce apoptosis through DED binding. Finally, why DEDDand DEDDL are unstable in the overexpression and other studies may be explained by the finding that they are potential substrates of active caspases.
机译:包含死亡效应域(DED)的分子通常作为执行者或调节剂参与细胞内凋亡级联反应。这些分子之一DEDD被确定为CD95信号通路的最终靶标,通过该通路将其转移到核仁中以抑制RNA聚合酶I依赖性转录。在这里,我们描述了通过交替剪接而产生的DEDD,DEDDL的较长同工型,作为一种包含免疫细胞特异性DED的分子。它仅在人T淋巴细胞和树突状细胞(DC)中表达,并且诱导成熟后DC中的mRNA表达升高。在MCF-7和Jurkat细胞系中,DEDDL的过度表达比DEDD更有力地诱导细胞凋亡。共转染和免疫沉淀表明,DEDDL比DEDD在体内能更有效地结合FADD和cFLIP。这可以解释为什么DEDDL是更有效的凋亡诱导剂,因为含DED的蛋白质通常通过DED结合诱导凋亡。最后,可以通过发现DEDD和DEDDL是活性胱天蛋白酶的潜在底物来解释为什么它们在过表达和其他研究中不稳定。

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