换一批p38<sup>MAPK</sup>/MK2-dependent phosphorylation controls cytotoxic RIPK1 signalling in inflammation and infection.
第一作者：
Manoj B,Menon
第一单位：
Institute of Cell Biochemistry, Hannover Medical School, Hannover 30625, Germany.
作者：
医学主题词
动物(Animals);细胞凋亡(Apoptosis);细菌蛋白质类(Bacterial Proteins);胞质溶胶(Cytosol);女(雌)性(Female);基因型(Genotype);HEK293细胞(HEK293 Cells);宿主与病原体相互作用(Host-Pathogen Interactions);人类(Humans);I-κB激酶(I-kappa B Kinase);炎症(Inflammation);细胞内信号肽和蛋白质类(Intracellular Signaling Peptides and Proteins);MAP激酶激酶激酶类(MAP Kinase Kinase Kinases);巨噬细胞(Macrophages);男(雄)性(Male);膜蛋白质类(Membrane Proteins);小鼠, 基因敲除(Mice, Knockout);坏死(Necrosis);表型(Phenotype);磷酰化(Phosphorylation);受体作用蛋白丝氨酸苏氨酸激酶类(Receptor-Interacting Protein Serine-Threonine Kinases);受体, 肿瘤坏死因子, Ⅰ型(Receptors, Tumor Necrosis Factor, Type I);丝氨酸(Serine);信号传导(Signal Transduction);时间因素(Time Factors);转染(Transfection);肿瘤坏死因子α(Tumor Necrosis Factor-alpha);耶尔森菌感染(Yersinia Infections);小肠结肠炎耶尔森菌(Yersinia enterocolitica);p38丝裂原活化蛋白激酶类(p38 Mitogen-Activated Protein Kinases)
DOI
10.1038/ncb3614
PMID
28920954
发布时间
2023-01-20
- 浏览10
Nature cell biology
1248-1259页
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