Abstract:
: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.
journal_name
J Cell Physioljournal_title
Journal of cellular physiologyauthors
Ju YK,Wu MJ,Chaulet H,Marciniec T,Graham RM,Allen DGdoi
10.1002/jcp.10347keywords:
subject
Has Abstractpub_date
2003-10-01 00:00:00pages
53-60issue
1eissn
0021-9541issn
1097-4652journal_volume
197pub_type
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