Immunologic Research

, Volume 31, Issue 1, pp 37–46

The role of C5b-9 terminal complement complex in activation of the cell cycle and transcription


  • Matthew Fosbrink
    • Toxicology ProgramUniversity of Maryland
    • Department of PathologyUniversity of Maryland School of Medicine
  • Florin Niculescu
    • Department of PathologyUniversity of Maryland School of Medicine
  • Horea Rus
    • Department of PathologyUniversity of Maryland School of Medicine
    • Department of NeurologyUniversity of Maryland School of Medicine and Veterans Administration Maryland Health Care System, Multiple Sclerosis Center of Excellence

DOI: 10.1385/IR:31:1:37

Cite this article as:
Fosbrink, M., Niculescu, F. & Rus, H. Immunol Res (2005) 31: 37. doi:10.1385/IR:31:1:37


Activation of the complement system plays an important role in innate and acquired immunity. Activation of complement and subsequent formation of C5b-9 channels on the surface of cellular membranes leads to cell lysis. When the number of channels assembled on the surface of nucleated cells is limited, C5b-9 doses not cause lysis, but instead can induce cell-cycle progression by activating signal transduction pathways, transcription factors, and key components of the cell-cycle machinery. Cell-cycle induction by C5b-9 is dependent on the activation of phosphatidylinositol 3-kinase and the ERK1 pathway in a Gi protein-dependent manner. Cell-cycle activation is regulated, in part, by activation of proto-oncogene c-jun and AP1 DNA binding activity. C5b-9 induces sequential activation of CDK4 and CDK2, leading to G1/S-phase transition and cellular proliferation. RGC-32 is a novel gene whose expression is induced by C5b-9. RGC-32 may play a key role in cell-cycle activation by increasing cyclin B1-CDC2 activity. C5b-9-mediated cell-cycle activation plays an important role in cellular proliferation and proctection from apoptosis.

Key Words

C5b-9 terminal complement complexCell cycleProto-oncogenesSignal transductionTranscriptional regulationRGC-32

Copyright information

© Human Press Inc 2005