p73: Friend or foe in tumorigenesis

被引：494

作者：

Melino, G ^{[1
]}

De Laurenzi, V

Vousden, KH

机构：

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

[2] NCI, Regulat Cell Growth Lab, Frederick, MD 21702 USA

来源：

NATURE REVIEWS CANCER | 2002年 / 2卷 / 08期

关键词：

D O I：

10.1038/nrc861

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

As p53 and its homologue p73 have significant sequence and functional similarities, p73 might also be expected to act as a tumour suppressor However, p73 is activated after DNA damage in a way that is distinct from that of p53. The existence of DeltaNp73 - an isoform of p73 that is encoded by a distinct promoter and that lacks the transactivation domain - further complicates matters. It seems to function as an oncogene by inhibiting both p73- and p53-induced apoptosis. So how can these opposing functions be reconciled in human tumours?.

引用

页码：605 / 615

页数：11

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