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陶伟

邮  箱: weitao@pku.edu.cn

职  称:教授

办公室地址:北京市海淀区颐和园路5号,北京大学,金光生命科学大楼,100871

所属实验室:陶伟实验室

实验室地址:北京市海淀区颐和园路5号,北京大学,金光生命科学大楼,100871

  • 个人简介
  • 科研领域
  • 代表性论文

教育经历:

1996-1999,博士,东北师范大学生命科学学院
1993-1996,硕士,东北师范大学生命科学学院
1985-1989,学士,东北林业大学生命科学学院

工作经历:

2001 - 至今,北京大学生命科学学院讲师,副教授,教授
2006 - 2007,Visiting Scholar, DKFZ, 德国国家癌症中心
2002 - 2005,Postdoctoral fellow, University of Wisconsin at Madison,美国威斯康星大学麦迪逊分校生物化学系
1999 - 2001,博士后,北京大学生命科学学院细胞生物学专业  

荣誉奖励:

北京大学东宝奖教金 , 2015
北大第五届青年教师教学基本功演示竞赛三等奖 , 2009
教育部自然科学奖二等奖, 2007

学术任职:

科技部国家重点研发计划项目首席科学家
北京大学伦理委员会委员
中国老年医学学会基础与转化医学分会委员
中国生物物理学会衰老分会理事
中国生理学会衰老与健康专业委员会委员

执教课程:

细胞衰老与死亡(研究生)
生命科学原理与前沿(本科生)
衰老生物学(本科生)
细胞生物学(本科生)
         作为第二遗传密码,表观遗传通过一维的组蛋白和DNA的修饰以及三维的空间结构来调控基因的表达以及基因组的稳定等。表观遗传各种修饰酶活复合体导致多种多样的组蛋白和DNA的化学修饰,这些修饰以动态的和组合的方式来应答细胞各种信号从而影响基因组的稳定性以及基因转录的活跃、休克和沉默。而基因的转录活动和稳定性调控着细胞的各种重大生命活动,如癌化和和衰老。

   细胞癌化和衰老是一个多种信号激发的、由多层次信号应答网络协调的和受表观遗传调控的细胞重大生命活动。实验室目前主要研究基因表达与表观遗传互作对细胞癌化、衰老和相关疾病的调控作用和表观遗传的编程规律。
    
   关键科学问题:
      1.研究衰老过程中表观遗传编程性变化的作用机制,利用合成生物学鉴别个体衰老的关键信号通路;
      2.筛选干预细胞和个体衰老的化学小分子;利用表观遗传遗传编辑转换衰老细胞的命运抉择。
      3 研究衰老相关的神经退行性病变的发病机制和表观遗传的调控作用。
      3.解析癌化中的表观遗传组、空间转录组以及三维基因组的变化规律和潜在机制。
      
         本实验室招收生信专业或有相关背景的将毕业的本科和硕士生读博。
      


  
Min Yang,Jennie Ong,Fanju Meng,Feixiang Zhang,Hui Shen,Kerstin Kitt,Tengfei Liu,Wei Tao and Peng Du*. Spatiotemporal insight into early pregnancy governed by immune-featured stromal cells. Cell, 2023, in print

Zhou JT†, Zhang C†, Wei R†, Han M, Wang S, Yang K, Zhang L, Chen W, Wen MZ, Li C, Tao W* and Yuan YJ*. (2021). Exogenous artificial DNA forms chromatin structure with active transcription in yeast.Sci China Life Sci, 2022,65: 851–860

Xiaoke Huang†,Xuebin Zhang†,Le Zong,Qianqian Gao,Chao Zhang,Ran Wei,Yiting Guan,Li Huang,Lijun Zhang, Guoliang Lyv* and Wei Tao*.Gene body methylation safeguards ribosomal DNA transcription by preventing PHF6-mediated enrichment of repressive histone mark H4K20me3. Journal of Biological Chemistry, 2021,297(4) 101195

Bo He†, Chao Zhang†, Xiaoxue Zhang†, Yu Fan†, Hu Zeng, Jun`e Liu, Haowei Meng, Dongsheng Bai, Jinying Peng, Qian Zhang*, and Wei Tao* and Chengqi Yi*.Tissue-specific 5-hydroxymethylcytosine landscape of the human genome. Nature Communications,2021, 12: 0-4249

Chao Zhang†,Xuebin Zhang†,Li Huang,Yiting Guan,Xiaoke Huang,XiaoLi Tian,Lijun Zhang and Wei Tao*. ATF3 drives senescence by reconstructing accessible chromatin profiles. Aging Cell, 2021, 20(3): e13315

Yiting Guan†, Chao Zhang†, Guoliang Lyu, Xiaoke Huang, Xuebin Zhang, Tenghan Zhuang, Lumeng Jia, Lijun Zhang, Chen Zhang*, Cheng Li* and Wei Tao*. Senescence-activated enhancer landscape orchestrates the senescence-associated secretory phenotype in murine fibroblasts. Nucleic Acids Research, 2020, 48:10909–10923

Chao Zhang†, Zihan Xu†, shangda Yang†, Guohua Sun, Lumeng Jia, Lumeng Jia, Zhaofeng Zheng, Quan Gu, Wei Tao*, Hui Cheng*, Cheng Li* and Tao Cheng*. Chromatin architecture landscape in hematopoietic stem and progenitor cell populations. Cell Reports, 2020, 32:108206

Guoliang Lyu#, Yuting Guan# , Chao Zahng, Le Zong, Sun Lei, Xiaoke Huang. Li Huang, Lijun Zhang,Xiaoli Tian,Zhongjun Zhou and Wei Tao*.TGF-β signaling alters H4K20me3 status via miR-29 and contributes to cellular senescence and cardiac aging. Nature Communications, 2018,Jul 2;9(1):2560

Meng Chen#, Guoliang Lyu#, Miao Han#, Hongbo Nie#, Ting Shen, Wei Chen, Yichi Niu, Yifan Song, Xueping Li, Huan Li, Xinyu Chen, Ziyue Wang, Zheng Xia, Wei Li, Xiao-Li Tian, Chen Ding, Jun Gu, Yufang Zheng, Xinhua Liu, Jinfeng Hu, Gang Wei*, Wei Tao*, Ting Ni.* 3′ UTR lengthening as a novel mechanism in regulating cellular senescence. Genome Research, 2018, 28: 285-294

Guoliang Lyu, Chao Zhang, Te Ling, Rui Liu, Le Zong, Yiting Guan, Xiaoke Huang, Lei Sun, Lijun Zhang, Cheng Li*, Yu Nie* and Wei Tao*. Genome and epigenome analysis of monozygotic twins discordant for congenital heart disease. BMC Genomics, 2018 19:428

Kai Liu, Lianggong Ding, Yuhong Li, Hui Yang, Chunyue Zhao, Ye Lei , Shuting Han, Wei Tao, Dengshun Miao, Hermann Steller, Michael Welsh* and Lei Liu*.Neuronal necrosis is regulated by a conserved chromatin-modifying cascade. PNAS. 2014,111:13960-65

Min Luo#, Te Ling#, WenbingXie#, He Sun, Yonggang Zhou, Qiaoyun Zhu, Meili Shen, Le Zong, Yun Zhao, Tao Ye, Jun Gu, Wei Tao*, Zhigang Lu*, Ingrid Grummt*. NuRD blocks reprogramming of mouse somatic cells into pluripotent stem cells. Stem Cells, 2013, 31:1278-86

Guoliang Lyu, Le Zong, Chao Zhang, Xiaoke Huang, Wenbing Xie, Junnan Fang, Yiting Guan, Lijun Zhang, Ting Ni#, Jun Gu#, Wei Tao# . Metastasis-related methyltransferase Merm1 represses the methyltransferase activity of Dnmt3a and facilitates RNA polymerase I transcriptional elongation. Journal of Molecular Cell Biology, 2019, 11(1), 78–90

Ling T, Xie W, Luo M, Shen M, Zhu Q, Zong L, Zhou T, Gu J, Lu Z, Zhang F, Tao W* , CHD4 maintains demethylation state of rDNA promoters through inhibiting the expression of the rDNA methyltransferase recruiter TIP5 , Biochem Biophys Res Commun, 2013, 19:101-107

Xie W, Ling T, Zhou Y, Feng W, Zhu Q, Stunnenberg HG, Grummt I*, Tao W* , The chromatin remodeling complex NuRD establishes the poised state of rRNA genes characterized by bivalent histone modifications and altered nucleosome positions, PNAS, 2012, 109:8161-8166

Guanghliang LV, Tan Tan, Zong L, Yuting Guan, Lei Sun, Liang QJ* and Tao W*, Changes in the position and volume of inctive X Chromosomes during G0/G1 trnasition, Chromosome Research, 2018, 26:179-189

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