p63 and p73, the Ancestors of p53

被引：250

作者：

Doetsch, V. ^{[2
]}

Bernassola, F. ^{[1
]}

Coutandin, D. ^{[2
]}

Candi, E. ^{[1
]}

Melino, G. ^{[1
,3
]}

机构：

[1] Univ Roma Tor Vergata, IDI IRCCS Biochem Lab, Dept Expt Med & Biochem Sci, I-00133 Rome, Italy

[2] Goethe Univ Frankfurt, Inst Biophys Chem, Frankfurt, Germany

[3] Univ Leicester, MRC, Toxicol Unit, Leicester LE1 9HN, Leics, England

来源：

COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY | 2010年 / 2卷 / 09期

基金：

英国医学研究理事会;

关键词：

TUMOR-SUPPRESSOR; CAENORHABDITIS-ELEGANS; P53-RELATED PROTEIN; DNA-BINDING; EXPRESSION; HOMOLOG; DELTA-NP73; ISOFORMS; SURVIVAL; NEUROBLASTOMA;

D O I：

10.1101/cshperspect.a004887

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：

p73 and p63 are two homologs of the tumor suppressive transcription factor p53. Given the high degree of structural similarity shared by the p53 family members, p73 and p63 can bind and activate transcription from the majority of the p53-responsive promoters. Besides overlapping functions shared with p53 (i.e., induction of apoptosis in response to cellular stress), the existence of extensive structural variability within the family determines unique roles for p63 and p73. Their crucial and specific functions in controlling development and differentiation are well exemplified by the p63 and p73 knockout mouse phenotypes. Here, we describe the contribution of p63 and p73 to human pathology with emphasis on their roles in tumorigenesis and development.

引用

页数：14

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