| Membrane attack by complement: the assembly and biology of terminal complement complexes. | |
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MedLine Citation:
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PMID: 21850539 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Complement system activation plays an important role in both innate and acquired immunity. Activation of the complement and the subsequent formation of C5b-9 channels (the membrane attack complex) on the cell membranes lead to cell death. However, when the number of channels assembled on the surface of nucleated cells is limited, sublytic C5b-9 can induce cell cycle progression by activating signal transduction pathways and transcription factors and inhibiting apoptosis. This induction by C5b-9 is dependent upon the activation of the phosphatidylinositol 3-kinase/Akt/FOXO1 and ERK1 pathways in a Gi protein-dependent manner. C5b-9 induces sequential activation of CDK4 and CDK2, enabling the G1/S-phase transition and cellular proliferation. In addition, it induces RGC-32, a novel gene that plays a role in cell cycle activation by interacting with Akt and the cyclin B1-CDC2 complex. C5b-9 also inhibits apoptosis by inducing the phosphorylation of Bad and blocking the activation of FLIP, caspase-8, and Bid cleavage. Thus, sublytic C5b-9 plays an important role in cell activation, proliferation, and differentiation, thereby contributing to the maintenance of cell and tissue homeostasis. |
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Authors:
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Cosmin A Tegla; Cornelia Cudrici; Snehal Patel; Richard Trippe; Violeta Rus; Florin Niculescu; Horea Rus |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-8-18 |
Journal Detail:
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Title: Immunologic research Volume: - ISSN: 1559-0755 ISO Abbreviation: - Publication Date: 2011 Aug |
Date Detail:
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Created Date: 2011-8-18 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8611087 Medline TA: Immunol Res Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Department of Neurology, School of Medicine, University of Maryland, 655 W. Baltimore Street, BRB 12-033, Baltimore, MD, 21201, USA. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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