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• W2515679818 abstract "The kinases RIPK1 and RIPK3 and the pseudo-kinase MLKL have been identified as key regulators of the necroptotic cell death pathway, although a role for MLKL within the whole animal has not yet been established. Here, we have shown that MLKL deficiency rescued the embryonic lethality caused by loss of Caspase-8 or FADD. Casp8(-/-)Mlkl(-/-) and Fadd(-/-)Mlkl(-/-) mice were viable and fertile but rapidly developed severe lymphadenopathy, systemic autoimmune disease, and thrombocytopenia. These morbidities occurred more rapidly and with increased severity in Casp8(-/-)Mlkl(-/-) and Fadd(-/-)Mlkl(-/-) mice compared to Casp8(-/-)Ripk3(-/-) or Fadd(-/-)Ripk3(-/-) mice, respectively. These results demonstrate that MLKL is an essential effector of aberrant necroptosis in embryos caused by loss of Caspase-8 or FADD. Furthermore, they suggest that RIPK3 and/or MLKL may exert functions independently of necroptosis. It appears that non-necroptotic functions of RIPK3 contribute to the lymphadenopathy, autoimmunity, and excess cytokine production that occur when FADD or Caspase-8-mediated apoptosis is abrogated." @default.
• W2515679818 created "2016-09-16" @default.
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• W2515679818 date "2016-09-01" @default.
• W2515679818 modified "2023-10-12" @default.
• W2515679818 title "The Pseudokinase MLKL and the Kinase RIPK3 Have Distinct Roles in Autoimmune Disease Caused by Loss of Death-Receptor-Induced Apoptosis" @default.
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• W2515679818 doi "https://doi.org/10.1016/j.immuni.2016.07.016" @default.
• W2515679818 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5040700" @default.
• W2515679818 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27523270" @default.
• W2515679818 hasPublicationYear "2016" @default.
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