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W
Wei Gu
H指数:91
被引数:4.9万
个人简介
Over the past 20 years, the integrative approach of the Gu Laboratory, combining biochemical analyses and advanced genetically manipulated mouse models has been instrumental to dissect the precise roles of protein modifications in regulating p53-mediated tumor suppression. The Gu lab has made significant contributions to establishing the roles of acetylation-mediated regulation of non-histone proteins. They established that site-specific acetylation plays a critical role in promoter-specific regulation of p53 targets. They discovered that the acidic domain containing proteins act as a new "reader" for acetylated substrates critically involved in acetylation-mediated actions. These studies have laid the foundation for the view that reversible acetylation is a general mechanism for regulation of non-histone proteins. Through in-depth investigation, the Gu lab has revealed that "dynamic ubiquitination" (polyubiquitination, monoubiquitination and deubiquitination) is the major mechanism by which the stability and subcellular localization of p53 protein are determined. They found that the deubiquitinase USP7 (also called HAUSP) interacts with both p53 and Mdm2; and is an important therapeutic target for human cancers through activating p53 and downregulating oncoproteins such as N-Myc. By using p53 acetylation-deficient mutant mice, the Gu lab has demonstrated that acetylation is required for p53-mediated cell-cycle arrest, senescence and apoptosis in vivo. Subsequently, they found that p53 is able to induce its tumor suppression through its metabolic targets including promoting ferroptosis.
教育背景
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工作经历
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荣誉奖项
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PLA2G2F通过磷脂重塑抑制铁死亡
GPX1-OSBPL8轴介导非经典体内铁死亡及肿瘤生长抑制
Cell
IF42.5
LMO7通过降解LRP1抑制肿瘤相关巨噬细胞对肿瘤细胞的吞噬作用
Advanced Science
IF14.1
菌株Meyerozyma guilliermondii Wyslmt对百草枯的微生物降解：转化产物的鉴定和降解途径的阐明
PURB–HOTAIR复合物调控p53依赖性的启动子特异性转录激活
p53-regulated非凋亡细胞死亡途径及其在癌症和其他疾病中的相关性
GENES & DISEASES
IF9.4
利用TAF1乙酰转移酶靶向肿瘤抑制因子p53的乙酰化
ADVANCED SCIENCE
IF14.1
Ferroptosis作为通过脂质过氧化抑制肿瘤的新工具
内质网应激通过tgf-β/SMAD途径诱导高脂饮食小鼠肾脏纤维化
MOLECULAR CELL
IF16.6
SCIENCE ADVANCES
IF12.5
PHLDA2-mediated磷脂酸过氧化在肿瘤抑制过程中触发明显的铁化反应
CELL METABOLISM
IF30.9
