Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 277, Issue 1, Pages 502-508Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M109354200
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Funding
- NIAID NIH HHS [R0-1 AI19006] Funding Source: Medline
- NINDS NIH HHS [R0-1 NS 199006] Funding Source: Medline
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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).
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