期刊
JOURNAL OF VIROLOGY
卷 74, 期 17, 页码 8135-8139出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.74.17.8135-8139.2000
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资金
- NIA NIH HHS [1RO1AG14071] Funding Source: Medline
- NIGMS NIH HHS [GM30324, R37 GM030324, R01 GM030324] Funding Source: Medline
Members of the tumor necrosis factor (TNF) receptor superfamily and their activating ligands transmit apoptotic signals in a variety of systems. We now show that the binding of TNF-related, apoptosis-inducing ligand (TRAIL) to its cellular receptors DR5 (TRAILR2) and DR4 (TRAILR1) mediates reovirus-induced apoptosis. Anti-TRAIL antibody and soluble TRAIL receptors block reovirus-induced apoptosis by preventing TRAIL-receptor binding. In addition, reovirus induces both TRAIL release and an increase in the expression of DR5 and DR4 in infected cells. Reovirus-induced apoptosis is also blocked following inhibition of the death receptor-associated, apoptosis-inducing molecules FADD (for LAS-associated death domain) and caspase 8. We propose that reovirus infection promotes apoptosis via the expression of DR5 and the release of TRAIL from infected cells. Virus-induced regulation of the TRAIL apoptotic pathway defines a novel mechanism for virus-induced apoptosis.
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