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论文题目: RIPK3 Mediates Necroptosis during Embryonic Development and Postnatal Inflammation in Fadd-Deficient Mice
英文论文题目: RIPK3 Mediates Necroptosis during Embryonic Development and Postnatal Inflammation in Fadd-Deficient Mice
第一作者: Zhao, Q; Yu, XJ; Zhang, HW; Liu, YB; Zhang, XX; Wu, XX; Xie, Q; Li, M; Ying, H; Zhang, HB
英文第一作者: Zhao, Q; Yu, XJ; Zhang, HW; Liu, YB; Zhang, XX; Wu, XX; Xie, Q; Li, M; Ying, H; Zhang, HB
联系作者: Zhang, HB (reprint author), Univ Chinese Acad Sci, Shanghai Inst Biol Sci, Chinese Acad Sci, Key Lab Nutr & Metab,Inst Nutr Sci, Shanghai 200031, Peoples R China.
英文联系作者: Zhang, HB (reprint author), Univ Chinese Acad Sci, Shanghai Inst Biol Sci, Chinese Acad Sci, Key Lab Nutr & Metab,Inst Nutr Sci, Shanghai 200031, Peoples R China.
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发表年度: 2017
卷: 19
期: 4
页码: 798-808
摘要: 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 (Ripk3(Delta/Delta) mice), thus abolishing its kinase activity. Ripk3(Delta/Delta) cells were resistant to necroptosis stimulation in vitro, and Ripk3(Delta/Delta) mice were protected from necroptotic diseases. Although the Ripk3(Delta/Delta) mutation rescued embryonic lethality in Fadd(-/-) embryos, Fadd(-/)-Ripk3(Delta/Delta) 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.
英文摘要: 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 (Ripk3(Delta/Delta) mice), thus abolishing its kinase activity. Ripk3(Delta/Delta) cells were resistant to necroptosis stimulation in vitro, and Ripk3(Delta/Delta) mice were protected from necroptotic diseases. Although the Ripk3(Delta/Delta) mutation rescued embryonic lethality in Fadd(-/-) embryos, Fadd(-/)-Ripk3(Delta/Delta) 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.
刊物名称: CELL REPORTS
英文刊物名称: CELL REPORTS
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学科: Cell Biology
英文学科: Cell Biology
影响因子: 8.282
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论文类别: Article
英文论文类别: Article
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