期刊
IMMUNOLOGICAL REVIEWS
卷 180, 期 -, 页码 49-55出版社
MUNKSGAARD INT PUBL LTD
DOI: 10.1034/j.1600-065X.2001.1800104.x
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资金
- NINDS NIH HHS [NS15662, NS36231] Funding Source: Medline
Assembly of C5b-9 on cell membranes results in transmembrane channels and causes cell death. When the number of C5b-9 molecules is limited, nucleated cells are able to escape cell death by endocytosis and by shedding of membranes bearing C5b-9. Sublytic C5b-9 induces proto-oncogenes, activates the cell cycle, and enhances cell survival. In addition, C5b-9 reverses the differentiated phenotype of postmitotic cells, such as oligodendrocytes and skeletal muscle cells. The signal transduction pathways responsible for cell cycle activation by C5b-9 include Gi-mediated activation of extracellular signal-regulated kinase 1 and phosphatidylinositol 3-kinase (PI3-K). Cell survival enhanced by C5b-9 is mediated by the PI3-K/Akt pathway, which inhibits apoptosis through regulation of BAD. These findings indicate that complement activation and membrane assembly of syblytic C5b-9 play an important role in inflammation by promoting cell proliferation and by rescuing apoptotic cells.
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