Abstract：
:RIPK3 mediates cell death and regulates inflammatory responses. Although genetic studies have suggested that RIPK3-MLKL-mediated necroptosis leads to embryonic lethality in Fadd or Caspase-8-deficient mice, the exact mechanisms are not fully understood. Here, we generated Ripk3 mutant mice by altering the RIPK3 kinase domain (Ripk3Δ/Δ mice), thus abolishing its kinase activity. Ripk3Δ/Δ cells were resistant to necroptosis stimulation in vitro, and Ripk3Δ/Δ mice were protected from necroptotic diseases. Although the Ripk3Δ/Δ mutation rescued embryonic lethality in Fadd-/- embryos, Fadd-/-Ripk3Δ/Δ mice died within 1 day after birth due to massive inflammation. These results indicate that Ripk3 ablation rescues embryonic lethality in Fadd-deficient mice by suppressing two RIPK3-mediating processes: necroptosis during embryogenesis and inflammation during postnatal development in Fadd-/- mice.
journal_name
Cell Repjournal_title
Cell reportsauthors
Zhao Q,Yu X,Zhang H,Liu Y,Zhang X,Wu X,Xie Q,Li M,Ying H,Zhang Hdoi
10.1016/j.celrep.2017.04.011subject
Has Abstractpub_date
2017-04-25 00:00:00pages
798-808issue
4issn
2211-1247pii
S2211-1247(17)30486-2journal_volume
19pub_type
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