p53 mutations in cancer

被引：1335

作者：

Muller, Patricia A. J. ^{[1
]}

Vousden, Karen H. ^{[1
]}

机构：

[1] Beatson Inst Canc Res, Glasgow G61 1BD, Lanark, Scotland

来源：

NATURE CELL BIOLOGY | 2013年 / 15卷 / 01期

关键词：

TUMOR-SUPPRESSOR FUNCTIONS; KNOCKOUT MICE REVEAL; LI-FRAUMENI-SYNDROME; C-TERMINAL PEPTIDE; MUTANT P53; DNA-BINDING; CORE DOMAIN; WILD-TYPE; GENETIC INSTABILITY; GENOMIC INSTABILITY;

D O I：

10.1038/ncb2641

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

In the past fifteen years, it has become apparent that tumour-associated p53 mutations can provoke activities that are different to those resulting from simply loss of wild-type tumour-suppressing p53 function. Many of these mutant p53 proteins acquire oncogenic properties that enable them to promote invasion, metastasis, proliferation and cell survival. Here we highlight some of the emerging molecular mechanisms through which mutant p53 proteins can exert these oncogenic functions.

引用

页码：2 / 8

页数：7

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