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介导抑癌蛋白泛素化的新分子 被引量:2

Novel Molecules that Mediate Ubiquitination of Anti-Cancer Proteins
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摘要 抑癌蛋白泛素化机制在肿瘤发生发展过程中扮演重要角色。其中,NEDD4-1介导的PTEN泛素化与Cowden综合征密切相关,Livin介导的Smac/DIABLO泛素化,以及癌性锚蛋白重复序列、转录因子E4F1等介导的P53泛素化均在肿瘤发生过程中扮演重要角色。近期研究表明,这些介导抑癌蛋白泛素化的新分子有望成为肿瘤治疗的靶点。 Ubiquitin is a 76 amino acid long protein that can be covalently linked to target proteins, a process referred to as ubiquitination. The role of this posttranslational modification is to mark target proteins either for degradation or transport toward other membrane compartments. The ubiquiti- nation pathway, a major pathway for protein degradation in cells, plays a critical role in the protein metabolism. So abnormality of the ubiquitination pathway is closely related to many diseases, espe- cially cancer. Emerging evidence indicated an essential role of anti-cancer protein ubiquitination in the pathogenesis of cancer. This article reviews novel molecules that mediate anti-cancer protein ubiquitination, especially the relationship between these pathways and tumorigenesis.
出处 《医学分子生物学杂志》 CAS CSCD 2007年第5期431-433,共3页 Journal of Medical Molecular Biology
基金 国家重点基础研究发展规划项目(973计划)(No.2005CB522400) 国家杰出青年科学基金(No.30625034)~~
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