Induction of a tumor-associated activating mutation in protein tyrosine phosphatase Ptpn11 (Shp2) enhances mitochondrial metabolism, leading to oxidative stress and senescence.
第一作者:
Hong,Zheng
第一单位:
From the Department of Medicine, Division of Hematology and Oncology, Case Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106.
作者:
医学主题词
氨基酸取代(Amino Acid Substitution);动物(Animals);细胞, 培养的(Cells, Cultured);人类(Humans);小鼠(Mice);小鼠, 基因敲除(Mice, Knockout);线粒体(Mitochondria);线粒体蛋白质类(Mitochondrial Proteins);突变, 误义(Mutation, Missense);肿瘤(Neoplasms);氧化性应激(Oxidative Stress);氧耗量(Oxygen Consumption);磷酰化(Phosphorylation);蛋白质酪氨酸磷酸酶, 非受体11型(Protein Tyrosine Phosphatase, Non-Receptor Type 11);STAT3转录因子(STAT3 Transcription Factor);肿瘤抑制蛋白质p53(Tumor Suppressor Protein p53)
DOI
10.1074/jbc.M113.462291
PMID
23884424
发布时间
2021-10-21
- 浏览42
The Journal of biological chemistry
25727-25738页
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