演讲嘉宾--冯新华

冯新华
xhfeng@zju.edu.cn
http://lsi.zju.edu.cn/redir.php?catalog_id=277
浙江大学教授、校长特别助理、生命科学研究院院长 国家特聘专家
研究学习经历:

1983年于武汉大学获得学士学位,其后在中科院遗传学研究所获得硕士学位 (1986), 美国University of Maryland-College Park获得博士学位 (1992)。在University of California-San Francisco (UCSF)接受博士后训练 (1993-1997),并担任UCSF研究助理教授 (1997-1999)。1999年底担任Baylor College of Medicine助理教授,后晋升为副教授 (2003)和教授 (2007)。2009年10月回到浙江大学任职。

冯新华教授长期从事细胞信号网络在干细胞、器官发育以及癌症中的作用与机理,尤其在TGF-信号领域的研究处于国际领先地位。研究成果包括在Nature、Cell、PNAS等发表论文100多篇以及百余次国内外学术报告和大会报告,并多次组织与主持重大国际会议。先后获得过美国Keck Young Scholar (2001)、Leukemia & Lymphoma Society Scholar (2003)、American Cancer Society Research Scholar (2003)、国家杰青(B) (2004)、长江学者讲座教授 (2008)、“千人计划”国家特聘专家(2009)和美国AAAS Fellow (2012)等荣誉。回国后,担任国家重大研究计划项目首席科学家、国家自然科学基金重大项目负责人。现任美国细胞学学会(ASCB)国际事务委员会委员、中国细胞生物学学会理事与细胞信号转导分会会长、中国蛋白质科学专业委员会委员、中国科协生命科学学会联合体学术咨询顾问委员会委员、Cell Research与Open Biology等杂志编委,曾任JBC编委、美洲华人生物科学学会(SCBA)财务长、华人生物科学家协会(CBIS)理事等学术兼职。

近期发表论文:
  1. Xiang W, Zhang Q, Lin X, Wu S, Zhou Y, Meng F, Fan Y, Shen T, Xiao M, Xia Z, Zou J, Feng X-H*, Xu P*. (2016). PPM1A silences cytosolic RNA sensing and antiviral defense through direct dephosphorylation of MAVS and TBK1.  Sci Adv. 2016 Jul 1;2(7):e1501889. doi: 10.1126/sciadv.1501889.
  2. Liu T, Zhao M, Liu J, He Z, Zhang Y, You H, Huang J, Lin X, Feng X-H. (2016). Tumor suppressor bromodomain-containing protein 7 cooperates with Smads to promote transforming growth factor-b responses. Oncogene. 2016 Jun 6. doi: 10.1038/onc.2016.204. [Epub ahead of print]
  3. Wang G, Yu Y, Sun C, Liu T, Liang T, Zhan L, Lin X, Feng X-H (2015). STAT3 selectively interacts with Smad3 to antagonize TGF-b signaling. Oncogene, 30 November 2015. doi: 10.1038/onc.2015.446.
  4. Chen FF, Lin X, Xu P, Zhang ZM, Chen YZ, Wang C, Han JH, Zhao B, Xiao M, Feng X-H. (2015). Nuclear export of Smads by RanBP3L regulates BMP signaling and mesenchymal stem cell differentiation. Mol Cell Biol. 35:1700-1711.
  5. Jia S, Dai F, Wu D, Lin X, Xing C, Xue Y, Wang Y, Xiao M, Wu W, Feng X-H*, and Meng AM*. (2012). Protein phosphatase 4 cooperates with Smads to promote BMP signaling in dorsoventral patterning of zebrafish embryos. Dev. Cell, 22:1065-1078. (*co-corresponding author)
  6. Dai F, Shen T, Li Z-Y, Lin X, and Feng X-H. (2011). PPM1A dephosphorylates RanBP3 to enable efficient nuclear export of Smad2 and Smad3. EMBO Rep, 12:1175-1181.
  7. Dai F, Lin X, Chang C, and Feng X-H. (2009). Nuclear export of Smad2 and Smad3 by RanBP3 facilitates termination of TGFb signaling. Dev. Cell, 16:345-357.
  8. Wrighton K, Lin X, Feng X-H. (2008). Critical regulation of TGF-b signaling by HSP90. Proc Natl Acad Sci USA, 105: 9244-9249.
  9. Lin X, Duan X, Liang Y-Y, Su Y, Wrighton K, Hu M, Long J, Davis C, Wang J, Brunicardi FC, Shi Y, Chen Y-G, Meng A, Feng X-H. (2006). PPM1A functions a Smad phosphatase to terminate TGF-b signaling. Cell, 125: 915-928.
  10. Lin X, Liang M, Liang Y-Y Brunicardi FC, Melchior F, Feng X-H. (2003). Activation of TGF-b signaling by SUMO modification of tumor suppressor Smad4/DPC4. J Biol Chem 278: 18714-18719.  

  11. Feng X-H, Liang Y-Y, Liang M, Zhai W, Lin X. (2002). Direct interaction of c-Myc with Smad2 and Smad3 to inhibit TGF-b-mediated induction of the CDK inhibitor p15Ink4B.  Mol Cell 9: 133-143.
  12. Lin X, Liang M, Feng X-H. (2000) Smurf2 as a ubiquitin E3 ligase for proteasome-dependent degradation of Smad2 in TGF-b signaling.  J Biol Chem 275: 36818-36822.
会议报告摘要:
Oncogenic Activation Disables TGF-Signaling(4月22日,15:50-16:20 pm)

Loss of the TGF-beta antiproliferative response is a hallmark in human cancers. Tumor cells have developed a number of strategies to escape from TGF-control. One major mechanism to resist the cytostatic effect of TGF-beta is through inactivating mutations/deletions in the TGF- beta signaling pathway, which frequently occur in gastrointestinal and pancreatic cancer. For example, tumor suppressor Smad4/DPC4, the central transducer of TGF-beta signaling, is deleted in more than half of pancreatic cancer patients. However, deletion or mutations in the Smad4 gene are rare in other types of cancers. We have taken functional genomic, proteomic and cell biological approaches to study how the TGF-tumor suppressor function is regulated in normal and cancer cells. We found that activation of many oncoproteins can cause TGF- beta resistance. Our novel studies gain conceptual insights into the oncoprotein-tumor suppressor interplay in tumorigenesis and provide guidance to logical therapeutic designs in cancer prevention, diagnostics and treatment.

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第四届肿瘤基础和转化医学前沿国际研讨会