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- W4313350000 abstract "Abstract FADD is a common adaptor shared by several death-receptors (DRs) for signaling apoptosis through recruitment and activation of caspase 8. DRs are essential for immune homeostasis, but dispensable during embryogenesis. Surprisingly, FADD-/- mice die in utero and conditional deletion of FADD leads to impaired lymphocyte proliferation. How FADD regulates embryogenesis and lymphocyte responses has been a long standing enigma. FADD could directly bind to RIP1, a serine/threonine kinase which mediates both necrosis and NF-kB activation. Our data indicate that FADD plays a role in regulating RIP1 expression and necrosis in embryos. To investigate a potential in vivo functional interaction between RIP1 and FADD, we generated mice lacking both FADD and RIP1and performed analyses of the resulting double knockout mutant mouse embryos and lymphocytes. The data from these studies have revealed an unexpected cell type-specific interplay between FADD and RIP1, which is critical for the regulation of apoptosis, necrosis and NF-kB activation during embryogenesis and lymphocyte function." @default.
- W4313350000 created "2023-01-06" @default.
- W4313350000 creator A5026174803 @default.
- W4313350000 date "2011-04-01" @default.
- W4313350000 modified "2023-10-01" @default.
- W4313350000 title "Complementary functions of FADD and RIP1 critical for embryogenesis and T cell proliferation (50.8)" @default.
- W4313350000 doi "https://doi.org/10.4049/jimmunol.186.supp.50.8" @default.
- W4313350000 hasPublicationYear "2011" @default.
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