Research Center for Translational Medicine
East Hospital
Tongji University
Shanghai 200092

MAO Zhiyong, Ph.D


School of Life Sciences and Technology

Tongji University

Shanghai, 200092 China


BRIEF HISTORY….  Defects in DNA repair, such as those arising from mutations in BRCA1, can initiate tumor development.  Mao’s laboratory uses easy-to-quantify and real-time reporter cassettes to measure the efficiency of two pathways of DNA double strand break repair: nonhomologous end joining (NHEJ) and homologous recombination (HR).  Through its studies, the group aims to understand the regulatory mechanisms of NHEJ and HR during tumorigenesis, and to eventually develop novel ways to diagnose and treat cancer.


Selected publications:

  1.  Chen S, Wang C, Sun L, Wang DL, Chen L, Huang Z, Yang Q, Gao J, Yang XB, Chang JF, Chen P, Lan L, Mao Z#, Sun FL#. RAD6 promotes homologous recombination repair by activating the autophagy-mediated degradation of heterochromatin protein HP1. Mol Cell Biol. 35:406-16 (2015).
  2.  Xu Z, Zhang L, Zhang W, Meng D, Zhang H, Jiang Y, Xu X, Van Meter M, Seluanov A, Gorbunova V, Mao Z. SIRT6 rescues the age related decline in base excision repair in a PARP1-dependent manner. Cell Cycle 14:269-76 (2015).
  3.  Cao Y, Xu Y, Zhang L, Li Z, Jiang Y, Tian X, Seluanov A, Gorbunova V#, Mao Z#. Utilization of Rad51C promoter for transcriptional targeting of cancer cells. Oncotarget 5:1805-11 (2014).
  4.  Mao Z, Tian X, Van Meter M, Ke Z, Gorbunova V, Seluanov A. Sirtuin 6 (SIRT6) rescues the decline of homologous recombination repair during replicative senescence. Proc. Natl. Acad. Sci. USA 109:11800-5 (2012).
  5.  Mao Z, Hine C, Tian X, Van Meter M, Au M, Vaidya A, Seluanov A, Gorbunova V. SIRT6 promotes DNA repair under stress by activating PARP1. Science 332:1443-1446 (2011).

# co-corresponding author

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