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Papers In Press, published online ahead of print October 30, 2001
J. Biol. Chem, 10.1074/jbc.M109354200
Submitted on September 27, 2001
Revised on October 30, 2001
Accepted on October 29, 2001
Department of Pathology, University of Maryland, School of Medicine, Baltimore, MD 21201
Corresponding Author: hrus{at}umaryland.edu
Proliferation of aortic smooth muscle cells contributes to atherogenesis and neointima formation. Sublytic activation of complement, particularly C5b-9, induces cell cycle progression in aortic smooth muscle cells. RGC-32 is a novel protein that may promote cell cycle progression in response to complement activation. We cloned human RGC-32 cDNA from a human fetal brain cDNA library. The human RGC-32 cDNA encodes a 117-amino acid protein with 92% similarity to the rat and mouse protein. Human RGC-32 maps to chromosome 13 and is expressed in most tissues. Sublytic complement activation enhanced RGC-32 mRNA expression in human aortic smooth muscle cells and induced nuclear translocation of the protein. RGC-32 was physically associated with cyclin dependent kinase p34cdc2 and increased the kinase activity in vivo and in vitro. In addition, RGC-32 was phosphorylated by p34cdc2/cyclin B1 in vitro. Mutation of RGC-32 protein at Thr91 prevented the p34cdc2-mediated phosphorylation and resulted in loss of p34cdc2 kinase enhancing activity. Overexpression of RGC-32 induced quiescent aortic smooth muscle cells to enter S-phase and proliferate. These data indicate that cell cycle activation by C5b-9 may involve p34cdc2 activity through RGC-32. RGC-32 appears to be a cell cycle regulatory factor that mediates cell proliferation, both as an activator and substrate of p34cdc2.
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