RIP1 kinase activity-dependent roles in embryonic development of Fadd-deficient mice
文献类型：期刊论文
| 作者 | Liu, Yongbo2; Fan, Cunxian2; Yu, Xianjun2; Wu, Xiaoxia2; Zhang, Xixi2; Zhao, Qun2; Zhang, Haiwei2; Xie, Qun2; Li, Ming2; Li, Xiaoming2 |
| 刊名 | CELL DEATH AND DIFFERENTIATION
 |
| 出版日期 | 2017 |
| 卷号 | 24期号:8页码:1459-1469 |
| ISSN号 | 1350-9047 |
| DOI | 10.1038/cdd.2017.78 |
| 文献子类 | Article |
| 英文摘要 | RIP1 is an essential regulator of TNF-induced signaling complexes mediating NF-kappa B activation, apoptosis and necroptosis. Loss of Rip1 rescues the embryonic lethality of Fadd or Caspase-8-deficient mice, even though the double knockout mice die shortly after birth like Rip1-deficient mice. Recent studies demonstrated that mice expressing RIP1 kinase-dead mutants developed normally and resisted necroptotic stimuli in vitro and in vivo. However, the impact of RIP1 kinase activity on Fadd-/-embryonic development remains unknown. Here, we engineered two RIP1 kinase inactive mutant mouse lines, a Rip1(K45A/K45A) mouse line as previously reported and a novel Rip1(Delta/Delta) mouse line with an altered P-loop in the kinase domain. While RIP1(K45A) could not rescue the embryonic lethality of Fadd-deficient mice at E11.5, RIP1(Delta). rescued lethality of Fadd(-/-) mice at E11.5 and Fadd(-/-)Rip1(Delta/Delta) mice eventually died at E16.5 due to excessive death of fetal liver cells and unregulated inflammation. Under necropotosis-inducing conditions, comparing to Rip1(K45A/K45A) cells, Rip1(Delta/Delta) cells displayed reduced phosphorylation and oligomerization of RIP3 and MLKL, which lead to increased cell viability. Thus, our study provides genetic evidence that different kinase inactive mutations have distinct impacts on the embryogenesis of Fadd-deficient mice, which might attribute to their extents of protection on necroptosis signaling. |
| 学科主题 | Biochemistry & Molecular Biology ; Cell Biology |
| WOS关键词 | NF-KAPPA-B ; TNF-INDUCED NECROPTOSIS ; PROGRAMMED NECROSIS ; INDUCED APOPTOSIS ; DEATH DOMAIN ; CELL-DEATH ; SIGNALING COMPLEX ; DISTINCT ROLES ; INFLAMMATION ; PROTEIN |
| 语种 | 英语 |
| WOS记录号 | WOS:000405106000016 |
| 出版者 | NATURE PUBLISHING GROUP |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/1094]  |
| 专题 | 中国科学院上海生命科学研究院营养科学研究所 |
| 作者单位 | 1.ECNU, Shanghai Key Lab Regulatory Biol, Inst Biomed Sci, Shanghai, Peoples R China; 2.Univ Chinese Acad Sci, Shanghai Inst Biol Sci, Chinese Acad Sci, Key Lab Nutr & Metab,Inst Nutr Sci, 320 Yueyang Rd, Shanghai 200031, Peoples R China; 3.Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Dept Plast & Reconstruct Surg, Shanghai 200011, Peoples R China; 4.Hubei Univ Med, Dept Biochem, Shiyan 442000, Peoples R China; 5.Second Mil Med Univ, Changhai Hosp, Dept Anesthesiol, Shanghai 200433, Peoples R China; 6.Univ Chinese Acad Sci, Shanghai Inst Biol Sci, Chinese Acad Sci, Key Lab food safety Res,Inst Nutr Sci, Shanghai 200031, Peoples R China; 7.ECNU, Sch Life Sci, Shanghai, Peoples R China, |
| 推荐引用方式 GB/T 7714 | Liu, Yongbo,Fan, Cunxian,Yu, Xianjun,et al. RIP1 kinase activity-dependent roles in embryonic development of Fadd-deficient mice[J]. CELL DEATH AND DIFFERENTIATION,2017,24(8):1459-1469. |
| APA | Liu, Yongbo.,Fan, Cunxian.,Yu, Xianjun.,Wu, Xiaoxia.,Zhang, Xixi.,...&,.(2017).RIP1 kinase activity-dependent roles in embryonic development of Fadd-deficient mice.CELL DEATH AND DIFFERENTIATION,24(8),1459-1469. |
| MLA | Liu, Yongbo,et al."RIP1 kinase activity-dependent roles in embryonic development of Fadd-deficient mice".CELL DEATH AND DIFFERENTIATION 24.8(2017):1459-1469. |
入库方式： OAI收割
来源：上海营养与健康研究所
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