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                发布日期:2019-05-14 浏览次数: 字号:[ ]

                  报告题目: The acetylation code of p53 in tumor suppression

                  报 告 人: Wei Gu, Ph.D.

                  Abraham and Mildred Goldstein Professor

                  Vice Chair, Department of Pathology and Cell Biology

                  Institute for Cancer Genetics, Columbia University

                  时    间: 2019 年 5 月 17 日(星期五)下午 2:30-3:30

                  地    点: 医学︻部国际合作处会议室

                  主 持 人: 罗建沅 教授


                  Dr. Wei Gu is recognized internationally for the pioneering contributions to the regulation of p53-mediated tumor suppressor function. The research of his laboratory has also made significant impacts in establishing two major basic concepts in biochemistry. The first one is that reversal acetylation of non-histone proteins is important for controlling its activities. The second concept is that ubiquitination is reversible and that deubiquitination is a critical step for modulating protein stability.

                  Representative Publications:

                  1. Luo, J, Su, F., Chen, D., Shiloh, A., and Gu, W. (2000) Deacetylation of p53 modulates its effect on cell growth and apoptosis. Nature 408, 377-381.

                  2. Luo, J., Nikolaev, A. Y., Imai, S., Chen, D., Su, F., Shiloh, A., Guarente, L., and Gu, W. (2001) Negative control of p53 by Sir2a promotes cell survival under stress. Cell. 107, 137-148.

                  3. Li, M., Chen, D., Shiloh, A., Luo, J., Nikolaev, A. Y., Qin, J., and Gu. W. (2002). Deubiquitination of p53 by HAUSP is an important pathway for p53 stabilization. Nature 416, 648-653.

                  4. Nikolaev, A. Y., Li, M., Puskas, N., Qin, J., and Gu, W. (2003). Parc: a cytoplasmic anchor for p53. Cell 112, 29-40.

                  5. Li, M., Brooks, C, Wu-Baer, F., Chen, D., Baer, R., and Gu, W. (2003). Mono- versus polyubiquitination: differential control of p53 fate by Mdm2. Science 302, 1972-5.

                  6. Chen, D., Kon, N., Li, M., Zhang, W., Qin, J., and Gu, W. (2005) ARF-BP1 is a critical mediator of the ARF tumor suppressor. Cell. 121,1071-83.

                  7. Zhao, W., Kruse, JP, Tang, Y., Jung, S., Qin, J., and Gu, W. (2008) Negative Regulation of the Sirt1 deacetylase by DBC1. Nature 451, 587-590.

                  8. Kruse, J.P. and Gu, W. (2008) Snapshot: p53 post-translational modifications. Cell 133, 930.

                  9. Tang, Y., Zhao, W., Chen, Y., Zhao, Y., and Gu, W. (2008) Acetylation is indispensible for p53 activation. Cell,133, 612-626.

                  10. Kruse JP, Gu W.  (2009) Modes of p53 regulation. Cell. 137, 609-622.

                  11. Chen, D., Shan, J., Zhu, W., Qin, J. and Gu, W. (2010) Transcription-independent ARF regulation in oncogenic stress-mediated p53 responses. Nature. 464, 624-627.

                  12. Li T., Kon N., Jiang L., Tan M., Ludwig T., Zhao Y., Baer R., and Gu W. (2012) Tumor suppression in the absence of p53-mediated cell cycle arrest, apoptosis, and senescence. Cell, 149, 1269-1283. PMID: 22682249.

                  13. Jiang L., Kon N., Li T., Wang S., Su T, Hibshoosh H., Baer R., and Gu W(2015). Ferroptosis as a p53-mediated activity during tumor suppression. Nature. 520, 57-62.

                  14. Wang D, Kon N, Lasso G, Jiang L, Leng W, Zhu WG, Qin J, Honig B, Gu W. (2016) Acetylation-regulated interaction between p53 and SET reveals a widespread regulatory mode. Nature. 6; 538(7623):118-122.

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