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J. Biol. Chem., Vol. 277, Issue 1, 502-508, January 4, 2002

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RGC-32 Increases p34^CDC2 Kinase Activity and Entry of Aortic Smooth Muscle Cells into S-phase^*

Tudor Badea, Florin Niculescu, Lucian Soane, Matthew Fosbrink, Hila Sorana, Violeta Rus^§, Moon L. Shin, and Horea Rus^¶

From the University of Maryland School of Medicine, the Department of Pathology, and ^§ Division of Rheumatology and Clinical Immunology, Baltimore, Maryland 21201

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 p34^CDC2 and increased the kinase activity in vivo and in vitro. In addition, RGC-32 was phosphorylated by p34^CDC2-cyclin B1 in vitro. Mutation of RGC-32 protein at Thr-91 prevented the p34^CDC2-mediated phosphorylation and resulted in loss of p34^CDC2 kinase enhancing activity. Overexpression of RGC-32 induced quiescent aortic smooth muscle cells to enter S-phase. These data indicate that cell cycle activation by C5b-9 may involve p34^CDC2 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 p34^CDC2.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBank^TM/EBI Data Bank with accession number(s) AF036549.

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