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IGF‐1 enhances a store‐operated Ca 2+ channel in skeletal muscle myoblasts: Involvement of a CD20‐like protein
Author(s) -
Ju YueKun,
Wu MingJie,
Chaulet Herve,
Marciniec Tadeusz,
Graham Robert M.,
Allen David G.
Publication year - 2003
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.10347
Subject(s) - myocyte , c2c12 , myogenesis , microbiology and biotechnology , cd20 , biology , chemistry , antibody , immunology
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 Ca 2+ channel (SOCC) whose activity is enhanced with IGF‐1 overexpression. A membrane protein, CD20, can cause Ca 2+ 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 Ca 2+ 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. J. Cell. Physiol. 197: 53–60, 2003© 2003 Wiley‐Liss, Inc.