Family friction as ΔNp73 antagonises p73 and p53

被引：20

作者：

Bailey, Sarah G. ^{[1
]}

Cragg, Mark S. ^{[2
]}

Townsend, Paul A. ^{[1
]}

机构：

[1] Univ Southampton, Sch Med, Div Human Genet, Southampton SO16 6YD, Hants, England

[2] Univ Southampton, Sch Med, Canc Sci Div, Southampton SO16 6YD, Hants, England

来源：

INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY | 2011年 / 43卷 / 04期

关键词：

Delta Np73; p53; p73; DNA-DAMAGE; TUMOR-SUPPRESSOR; IN-VIVO; GROWTH SUPPRESSION; PROTEIN STABILITY; GENOTOXIC STRESS; FEEDBACK LOOP; CROSS-TALK; EXPRESSION; APOPTOSIS;

D O I：

10.1016/j.biocel.2010.12.022

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

p53 and its homolog p73 are responsible for guarding the genome and regulating cellular responses to genotoxic damage. However, life is never simple and in fact multiple isoforms of each gene exist which may have opposing functions. Delta Np73 is a truncated isoform of p73 which lacks the N-terminal transactivation domain and is up-regulated in a number of diverse primary tumour types. Although its exact cellular function is unclear, upregulation of Delta Np73 has been linked to various pro-tumour activities. Here we review the current literature surrounding this mysterious protein and reveal its potentially important functions in tumourigenesis and treatment resistance. (C) 2011 Elsevier Ltd. All rights reserved.

引用

页码：482 / 486

页数：5

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