A dominant interfering mutant of FADD/MORT1 enhances deletion of autoreactive thymocytes and inhibits proliferation of mature T lymphocytes - PubMed (original) (raw)
A dominant interfering mutant of FADD/MORT1 enhances deletion of autoreactive thymocytes and inhibits proliferation of mature T lymphocytes
K Newton et al. EMBO J. 1998.
Abstract
Members of the tumour necrosis factor receptor family that contain a death domain have pleiotropic activities. They induce apoptosis via interaction with intracellular FADD/MORT1 and trigger cell growth or differentiation via TRADD and TRAF molecules. The impact of FADD/MORT1-transduced signals on T lymphocyte development was investigated in transgenic mice expressing a dominant negative mutant protein, FADD-DN. Unexpectedly, FADD-DN enhanced negative selection of self-reactive thymic lymphocytes and inhibited T cell activation by increasing apoptosis. Thus signalling through FADD/MORT1 does not lead exclusively to cell death, but under certain circumstances can promote cell survival and proliferation.
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References
- EMBO J. 1995 Dec 15;14(24):6136-47 - PubMed
- Cell. 1996 Jan 26;84(2):299-308 - PubMed
- Cell. 1996 Feb 23;84(4):551-62 - PubMed
- Immunity. 1996 Apr;4(4):387-96 - PubMed
- J Biol Chem. 1997 Mar 21;272(12):7797-800 - PubMed
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