E1AF degradation by a ubiquitin-proteasome pathway

E1AF degradation by a ubiquitin-proteasome pathway
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DOI:
10.1016/j.bbrc.2004.12.045
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发表时间:
2005-02-11
影响因子:
3.1
通讯作者:
Shindoh, M
Shindoh, M
中科院分区:
生物学4区
文献类型:
--
作者:
Takahashi, A;Higashino, F;Shindoh, M

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E1 AF是ETS转录因子家族的成员。在乳腺肿瘤中。E1 AF的过度表达与肿瘤的发生有关,但E1 AF蛋白几乎未被检测到,其降解机制尚不清楚。在这里,我们表明,E1 AF蛋白是稳定的26 S蛋白酶抑制剂MG 132治疗。我们发现E1 AF通过C-末端区域被泛素修饰,泛素化的E1 AF聚集在核点中,并且蛋白酶体激活的转录抑制作用靶向E1 AF启动子。这些结果表明,E1 AF通过泛素-蛋白酶体途径降解。对E1 AF功能有一定影响。(C)2004年爱思唯尔公司All rights reserved.
E1AF is a member of the ETS family of transcription factors. In mammary tumors. overexpression of E1AF is associated with tumorigenesis, but E1AF protein has hardly been detected and its degradation mechanism is not yet clear. Here we show that E1AF protein is stabilized by treatment with the 26S protease inhibitor MG132. We found that E1AF was modified by ubiquitin through the C-terminal region and ubiquitinated E1AF aggregated in nuclear dots, and that the inhibition of proteasome-activated transcription from E1AF target promoters. These results suggest that E1AF is degraded via the ubiquitin-proteasome pathway. which has some effect on E1AF function. (C) 2004 Elsevier Inc. All rights reserved.