The HECT family of E3 ubiquitin ligases: Multiple players in cancer development

被引：438

作者：

Bernassola, Francesca ^{[5
]}

Karin, Michael ^{[1
]}

Ciechanover, Aaron ^{[2
,3
]}

Melino, Gerry ^{[4
,5
]}

机构：

[1] Univ Calif San Diego, Sch Med, Lab Gene Regulat & Signal Transduct, La Jolla, CA 92093 USA

[2] Technion Israel Inst Technol, Rappaport Fac Med, Canc & Vasc Biol Ctr, IL-31096 Haifa, Israel

[3] Technion Israel Inst Technol, Res Inst, IL-31096 Haifa, Israel

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

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

来源：

CANCER CELL | 2008年 / 14卷 / 01期

基金：

英国医学研究理事会;

关键词：

D O I：

10.1016/j.ccr.2008.06.001

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The involvement of the homologous to E6-AP carboxyl terminus (HECT)-type E3s in crucial signaling pathways implicated in tumorigenesis is presently an area of intense research and extensive scientific interest. This review highlights recent discoveries on the ubiquitin-mediated degradation of crucial tumor suppressor molecules catalyzed by the HECT-type E3s. By providing a portrait of their protein targets, we intend to link the substrate specificity of HECT-type E3s with their contribution to tumorigenesis. Moreover, we discuss the relevance of targeting the HECT E3s, through the development of small-molecule inhibitors, as an anticancer therapeutic strategy. © 2008 Elsevier Inc. All rights reserved.

引用

页码：10 / 21

页数：12

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