Itch: a HECT-type E3 ligase regulating immunity, skin and cancer

被引：144
作者：
Melino, G. [1 ,2 ]
Gallagher, E. [3 ]
Aqeilan, R. I. [4 ]
Knight, R. [2 ]
Peschiaroli, A. [1 ]
Rossi, M. [2 ]
Scialpi, F. [1 ]
Malatesta, M. [1 ]
Zocchi, L. [1 ]
Browne, G. [2 ]
Ciechanover, A. [5 ]
Bernassola, F. [1 ]
机构：
[1] Univ Roma Tor Vergata, Dept Expt Med & Biochem Sci, IDI IRCCS Biochem Lab, I-00133 Rome, Italy
[2] Univ Leicester, MRC, Toxicol Unit, Leicester LE1 9HN, Leics, England
[3] UCL Royal Free & Univ Coll Med Sch, London W1T 4JF, England
[4] Ohio State Univ, Columbus, OH 43210 USA
[5] Technion Israel Inst Technol, Canc & Vasc Biol Ctr, Rappaport Fac Med & Res Inst, IL-31096 Haifa, Israel
来源：
CELL DEATH AND DIFFERENTIATION | 2008年 / 15卷 / 07期
基金：
英国医学研究理事会;
关键词：
ubiquitin E3 ligase; apoptosis; JunB; p53 family members; Notch;
D O I：
10.1038/cdd.2008.60
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：
The HECT-type E3 ubiquitin ligase (E3) Itch is absent in the non-agouti-lethal 18H or Itchy mice, which develop a severe immunological disease, including lung and stomach inflammation and hyperplasia of lymphoid and hematopoietic cells. The involvement of Itch in multiple signaling pathways and pathological conditions is presently an area of extensive scientific interest. This review aims to bring together a growing body of work exploring Itch-regulated biological processes, and to highlight recent discoveries on the regulatory mechanisms modulating its catalytic activity and substrate recognition capability. Our contribution is also an endeavor to correlate Itch substrate specificity with the pathological defects manifested by the mutant Itchy mice.
引用
收藏
页码：1103 / 1112
页数：10
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