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CD47 augments Fas/CD95-mediated apoptosis.
Umeå University, Faculty of Medicine, Integrative Medical Biology, Histology and Cell Biology.
2005 (English)In: Journal of Biological Chemistry, ISSN 0021-9258, Vol. 280, no 33, 29637-44 p.Article in journal (Refereed) Published
Abstract [en]

Fas (CD95) mediates apoptosis of many cell types, but the susceptibility of cells to killing by Fas ligand and anti-Fas antibodies is highly variable. Jurkat T cells lacking CD47 (integrin-associated protein) are relatively resistant to Fas-mediated death but are efficiently killed by Fas ligand or anti-Fas IgM (CH11) upon expression of CD47. Lack of CD47 impairs events downstream of Fas activation including caspase activation, poly-(ADP-ribose) polymerase cleavage, cytochrome c release from mitochondria, loss of mitochondrial membrane potential, and DNA cleavage. Neither CD47 signaling nor raft association of CD47 is required to enable Fas apoptosis. CH11 induces association of Fas and CD47. Primary T cells from CD47-null mice are also protected from Fas-mediated killing relative to wild type T cells. Thus CD47 associates with Fas upon its activation and augments Fas-mediated apoptosis.

Place, publisher, year, edition, pages
2005. Vol. 280, no 33, 29637-44 p.
Keyword [en]
Animals, Antigens; CD/*physiology, Antigens; CD47, Antigens; CD95/*physiology, Apoptosis, Humans, Jurkat Cells, Mice, Mice; Inbred C57BL
Identifiers
URN: urn:nbn:se:umu:diva-12282DOI: doi:10.1074/jbc.M500922200PubMedID: 15917238OAI: oai:DiVA.org:umu-12282DiVA: diva2:151953
Available from: 2008-01-10 Created: 2008-01-10 Last updated: 2011-01-12Bibliographically approved

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