Degadration of mismatch repair hMutSα heterodimer by the ubiquitin-proteasome pathway
Degadration of mismatch repair hMutSα heterodimer by the ubiquitin-proteasome pathway
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DOI：
10.1016/s0014-5793(04)00181-4
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发表时间：
2004-03-26
期刊：
影响因子：
3.5
通讯作者：
Lautier, D
中科院分区：
文献类型：
--
作者：
Hernandez-Pigeon, H;Laurent, G;Lautier, D
错配修复在基因组稳定性中起着至关重要的作用。这个过程需要包括hMSH2/hMSH6(HMutSalpha)异二聚体在内的几种蛋白质参与这个过程的第一阶段，即错对识别。我们先前报道，在U937和HL-60细胞系中，hMSH2和hMSH6蛋白的表达明显低于HeLa和KG1a细胞。在这里，我们证明了hMutSalpha表达的降低是由于泛素-蛋白酶体途径导致两种蛋白质降解速度的差异。我们的数据表明，在人类细胞系中，泛素-蛋白酶体可能在hMutSalpha蛋白表达的调节中发挥重要作用，从而调节错配修复活性。(C)2004年欧洲生化学会联合会。爱思唯尔出版，版权所有。
Mismatch repair plays a critical role in genome stability. This process requires several proteins including hMSH2/hMSH6 (hMutSalpha) heterodimer involved in the first stage of the process, the mispair recognition. We previously reported that in U937 and HL-60 cell lines, hMSH2 and hMSH6 protein expression was much lower than that in HeLa and KG1a cells. Here, we showed that the decreased expression of hMutSalpha results from differences in the degradation rate of both proteins by the ubiquitin-proteasome pathway. Our data suggest that in human cell lines, ubiquitin-proteasome could play an important role in the regulation of hMutSalpha protein expression, thereby regulating mismatch repair activity. (C) 2004 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.