The negative feedback regulation of TRPV4 Ca2+ ion channel function by its C-terminal cytoplasmic domain

被引：2
|
作者：
Chun, Jaesun [2 ]
Shin, Sung Hwa [1 ]
Kang, Sang Sun [1 ]
机构：
[1] Chungbuk Natl Univ, Dept Biol Educ, Cheongju 361763, Chungbuk, South Korea
[2] Korea Natl Univ Educ, Dept Biol Educ, Cheongwon 363791, Chungbuk, South Korea
来源：
CELLULAR SIGNALLING | 2012年 / 24卷 / 10期
关键词：
TRPV4; SGK1; Protein interaction; Phosphorylation; Calcium transport; PROTEIN-KINASE-C; POTENTIAL VANILLOID 4; INDUCED NEUROPATHIC PAIN; CALMODULIN-BINDING SITE; HEAT-EVOKED ACTIVATION; CELL-VOLUME REGULATION; ENDOTHELIAL-CELLS; AIRWAY EPITHELIA; S-NITROSYLATION; CATION CHANNEL;
D O I：
10.1016/j.cellsig.2012.06.008
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
The transient receptor potential vanilloid 4 (TRPV4) cation channel, a member of the TRP vanilloid subfamily, is expressed in a broad range of tissues where it participates in the generation of a Ca2+ signal and/or depolarization of the membrane potential. Regulation of the abundance of TRPV4 at the cell surface is critical in osmo- and mechanotransduction. In this review, we discussed that the potential effect of Ca2+ occurs via its action at an intracellular site in the C-terminus of the channel protein by the effect of the modulation on TRPV4 (such as 824 Ser residue phosphorylation), and its regulation for TRPV4 functions related with cell surface spread, wound healing or its polarity reorientation through its differential affinity with actin or tubulin. (c) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码：1918 / 1922
页数：5
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