Physiological Functions of Nedd4-2: Lessons from Knockout Mouse Models

被引：60

作者：

Manning, Jantina A. ^{[1
,2
]}

Kumar, Sharad ^{[1
,2
]}

机构：

[1] Univ South Australia, Ctr Canc Biol, GPO Box 2471, Adelaide, SA 5001, Australia

[2] SA Pathol, GPO Box 2471, Adelaide, SA 5001, Australia

来源：

TRENDS IN BIOCHEMICAL SCIENCES | 2018年 / 43卷 / 08期

基金：

英国医学研究理事会;

关键词：

EPITHELIAL NA+ CHANNEL; UBIQUITIN LIGASE NEDD4-2; TIGHT JUNCTION FORMATION; CELL-SURFACE EXPRESSION; GATED SODIUM-CHANNELS; HECT DOMAIN; LIDDLE SYNDROME; WW DOMAIN; PY MOTIF; PROTEIN;

D O I：

10.1016/j.tibs.2018.06.004

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：

Protein modification by ubiquitination plays a key evolutionarily conserved role in regulating membrane proteins. Nedd4-2, a ubiquitin ligase, targets membrane proteins such as ion channels and transporters for ubiquitination. This Nedd4-2-mediated ubiquitination provides a crucial step in controlling the membrane availability of these proteins, thus affecting their signaling and physiological outcomes. In one well-studied example, Nedd4-2 fine-tunes the physiological function of the epithelial sodium channel (ENaC), thus modulating Na+ reabsorption by epithelia to maintain whole-body Na+ homeostasis. This review summarizes the key signaling pathways regulated by Nedd4-2 and the possible implications of such regulation in various pathologies.

引用

页码：635 / 647

页数：13

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