Ubiquitin and Ubiquitin-Like Modifications of the p53 Family

IF 7.7 2区医学 Q1 Biochemistry, Genetics and Molecular Biology

Neoplasia Pub Date : 2006-08-01 DOI:10.1593/neo.06439

Ian R. Watson , Meredith S. Irwin

引用次数: 79

Abstract

Regulation of p53 by the ubiquitin-proteasomal pathway has been studied considerably. Studies have also demonstrated that the ubiquitin-like proteins SUMO-1 and NEDD8 modify p53. Similarly, p63 and p73 are subject to regulation by ubiquitin and ubiquitin-like modifications, and perturbations of these pathways in the regulation of the p53 family have been implicated in tumorigenesis and developmental abnormalities. Here, we provide an overview of the current understanding of the regulation of the p53 family by covalent modification by ubiquitin, SUMO-1, and NEDD8.

查看原文本刊更多论文

p53家族的泛素和泛素样修饰

泛素-蛋白酶体途径对p53的调控已被大量研究。研究还表明泛素样蛋白SUMO-1和NEDD8可以修饰p53。同样，p63和p73也受到泛素和泛素样修饰的调控，而p53家族调控中这些通路的扰动与肿瘤发生和发育异常有关。在这里，我们概述了目前对泛素、SUMO-1和NEDD8共价修饰p53家族调控的理解。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Neoplasia 医学-肿瘤学

CiteScore

9.20

自引率

2.10%

发文量

审稿时长

26 days

期刊介绍： Neoplasia publishes the results of novel investigations in all areas of oncology research. The title Neoplasia was chosen to convey the journal’s breadth, which encompasses the traditional disciplines of cancer research as well as emerging fields and interdisciplinary investigations. Neoplasia is interested in studies describing new molecular and genetic findings relating to the neoplastic phenotype and in laboratory and clinical studies demonstrating creative applications of advances in the basic sciences to risk assessment, prognostic indications, detection, diagnosis, and treatment. In addition to regular Research Reports, Neoplasia also publishes Reviews and Meeting Reports. Neoplasia is committed to ensuring a thorough, fair, and rapid review and publication schedule to further its mission of serving both the scientific and clinical communities by disseminating important data and ideas in cancer research.