IGF-1 enhances a store-operated Ca2+ channel in skeletal muscle myoblasts:: Involvement of a CD20-like protein

被引:15
作者
Ju, YK
Wu, MJ
Chaulet, H
Marciniec, T
Graham, RM
Allen, DG [1 ]
机构
[1] Univ Sydney, Dept Physiol, Sydney, NSW 2006, Australia
[2] Victor Chang Cardiac Res Inst, Mol Cardiol Unit, Darlinghurst, NSW, Australia
关键词
D O I
10.1002/jcp.10347
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Overexpression of IGF-1 in C2C12 myoblasts causes hypertrophy when myoblasts fuse to form myotubes, a response that requires elevated intracellular calcium. We show that myoblasts contain a store-operated Ca2+ channel (SOCC) whose activity is enhanced with IGF-1 overexpression. A membrane protein, CD20, can cause Ca2+ entry, which is increased by IGF-1. We therefore tested whether CD20 mediates the SOCC activity in myoblasts. An antibody to the extracellular loop of CD20 detected a protein in myoblasts and this antibody also inhibited Ca2+ entry through SOCC. Overexpression of CD20 in myoblasts increased SOCC activity. However, we Could not detect mRNA for CD20 in myoblasts and an antibody to the intracellular C-terminus of CD20 was unable to detect CD20 in these cells. These studies demonstrate that CD20 is a novel SOCC or modulates SOCC activity. However, the SOCC activity observed in C2C12 myoblasts is mediated not by CD20, but by a CD20-like protein. Activation of this SOCC may contribute to IGF-1-induced hypertrophy in these cells. (C) 2003Wiley-Liss, Inc.
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收藏
页码:53 / 60
页数:8
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