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介导抑癌蛋白泛素化的新分子
引用本文:张燕捷,房静远. 介导抑癌蛋白泛素化的新分子[J]. 医学分子生物学杂志, 2007, 4(5): 431-433
作者姓名:张燕捷  房静远
作者单位:1. 上海交通大学医学院附属仁济医院,上海市,200001
2. 上海市消化疾病研究所,上海市,200001
基金项目: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)~~
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。

关 键 词:NEDD4-1  凋亡蛋白抑制因子Livin  癌性锚蛋白重复序列  转录因子E4F1

Novel Molecules that Mediate Ubiquitination of Anti-Cancer Proteins
ZHANG Yanjie,FANG Jingyuan. Novel Molecules that Mediate Ubiquitination of Anti-Cancer Proteins[J]. Journal of Medical Molecular Biology, 2007, 4(5): 431-433
Authors:ZHANG Yanjie  FANG Jingyuan
Abstract: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 ubiquitination 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,especially 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.
Keywords:NEDD4-1  Livin  Gankyrin  E4F1
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