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首页> 外文期刊>Cellular Signalling >Bid is not required for Bax translocation during UV-induced apoptosis
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Bid is not required for Bax translocation during UV-induced apoptosis

机译：在紫外线诱导的细胞凋亡过程中，Bax转运不需要出价

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UV irradiation triggers apoptosis through both the membrane death receptor and the intrinsic apoptotic signaling pathways. Bax, a member of the Bcl-2 family of proteins, translocates from the cytosol to the mitochondrial membrane during UV-induced apoptosis, but the regulation of Bax translocation by UV irradiation remains elusive. In this study, we show that Bax translocation, caspase-3 activation and cell death by UV irradiation are not affected by Z-IETD-fmk (caspase-8 inhibitor), but delayed by Pifithrin-alpha (p53 inhibitor), although Bid cleavage could be completely abolished by Z-IETD-fmk. Co-transfecting YFP-Bax and Bid-CFP into human lung adenocarcinoma cells, we demonstrate that translocation of YFP-Bax precedes that of Bid-CFP, there is no significant FRET (fluorescence resonance energy transfer) between them. Similar results are obtained in COS-7 cells expressing YFP-Bax and Bid-CFP. Furthermore, using acceptor photobleaching technique, we observe that there is no interaction between YFP-Bax and Bid-CFP in both healthy and apoptotic cells. Additionally, during UV-induced apoptosis there is downregulation of Bcl-x(L), an anti-apoptotic protein. Overexpression of Bcl-x(L) in cells susceptible to UV-induced apoptosis prevents Bax translocation and cell death; repression of Bid protein with siRNA (small interfering RNA) do not inhibit cell death by UV irradiation. Taken together, these data strongly suggest that Bax translocation by UV irradiation is a Bid-independent event and inhibited by overexpression of Bcl-x(L). (C) 2007 Published by Elsevier Inc.
机译：紫外线辐射通过膜死亡受体和固有的凋亡信号通路触发细胞凋亡。 Bax是Bcl-2蛋白质家族的成员，在UV诱导的细胞凋亡过程中从胞质溶胶转移到线粒体膜，但是通过UV辐射对Bax易位的调节仍然难以捉摸。在这项研究中，我们显示Bax易位，caspase-3激活和紫外线照射引起的细胞死亡不受Z-IETD-fmk（caspase-8抑制剂）的影响，但受Pifithrin-alpha（p53抑制剂）的影响，尽管可以进行Bid切割。 Z-IETD-fmk可以完全取消它。将YFP-Bax和Bid-CFP共转染到人肺腺癌细胞中，我们证明YFP-Bax的易位先于Bid-CFP的易位，它们之间没有明显的FRET（荧光共振能量转移）。在表达YFP-Bax和Bid-CFP的COS-7细胞中获得了相似的结果。此外，使用受体光漂白技术，我们观察到在健康细胞和凋亡细胞中，YFP-Bax和Bid-CFP之间没有相互作用。此外，在紫外线诱导的细胞凋亡过程中，抗凋亡蛋白Bcl-x（L）的表达下调。 Bcl-x（L）在易受紫外线诱导的细胞凋亡的细胞中过表达可防止Bax易位和细胞死亡;用siRNA（小干扰RNA）抑制Bid蛋白不会抑制紫外线照射引起的细胞死亡。综上所述，这些数据强烈表明，紫外线照射引起的Bax易位是一个独立于Bid的事件，并受到Bcl-x（L）过表达的抑制。 （C）2007年由Elsevier Inc.出版

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