CD47 Augments Fas/CD95-mediated Apoptosis

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...

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Published inThe Journal of biological chemistry Vol. 280; no. 33; pp. 29637 - 29644
Main Authors Manna, Partha P, Dimitry, Julie, Oldenborg, Per-Arne, Frazier, William A
Format Journal Article
LanguageEnglish
Published United States American Society for Biochemistry and Molecular Biology 19.08.2005
Subjects
Animals
Antigens, CD - physiology
Apoptosis
CD47 Antigen
fas Receptor - physiology
Humans
Jurkat Cells
Mice
Mice, Inbred C57BL
Antigens
Mice
CD95/physiology
CD47
Inbred C57BL
CD/physiology
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Summary: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.
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ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.M500922200