Mouse cytomegalovirus M36 and M45 death suppressors cooperate to prevent inflammation resulting from antiviral programmed cell death pathways.

@article{DaleyBauer2017MouseCM,
  title={Mouse cytomegalovirus M36 and M45 death suppressors cooperate to prevent inflammation resulting from antiviral programmed cell death pathways.},
  author={Lisa P. Daley-Bauer and Linda Roback and Lynsey N Crosby and A. Louise McCormick and Yanjun Feng and William J. Kaiser and Edward S. Mocarski},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={2017},
  volume={114 13},
  pages={
          E2786-E2795
        }
}
  • Lisa P. Daley-Bauer, Linda Roback, +4 authors Edward S. Mocarski
  • Published in
    Proceedings of the National…
    2017
  • Biology, Medicine
  • The complex interplay between caspase-8 and receptor-interacting protein (RIP) kinase RIP 3 (RIPK3) driving extrinsic apoptosis and necroptosis is not fully understood. Murine cytomegalovirus triggers both apoptosis and necroptosis in infected cells; however, encoded inhibitors of caspase-8 activity (M36) and RIP3 signaling (M45) suppress these antiviral responses. Here, we report that this virus activates caspase-8 in macrophages to trigger apoptosis that gives rise to secondary necroptosis… CONTINUE READING

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