Shan Zha, MD, PhD

  • James A Wolff Professor of Pediatrics, Pathology and Cell Biology and of Microbiology and Immunology (in the Institute for Cancer Genetics and in the Herbert Irving Comprehensive Cancer Center)
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Overview

Academic Appointments

  • James A Wolff Professor of Pediatrics, Pathology and Cell Biology and of Microbiology and Immunology (in the Institute for Cancer Genetics and in the Herbert Irving Comprehensive Cancer Center)

Research

The Zha lab investigates how defects in DNA repair and DNA damage responses impact normal immune system development, lymphomagenesis, and treatment responses. The lab has developed cutting-edge technologies, including high-throughput translocation sequencing, sing cell-seq, multi-color flow-cytometry, CRISPR-based depletion and activation screens, high-content live-cell imaging, and a collection of over sixty-five unique mouse models, including the serial of mouse models expressing catalytically inactive ATM, ATR, DNA-PKcs, and now PARP1 and PARP2, which revealed unexpected structural function of DNA damage response factors. More details can be found at zhalab.org. We invite committed young scientists to join us in the adventures.

Selected Publications

  • Milanovic M, Houghton LM, Menolfi D, Lee JH, Yamamoto K, Li Y, Lee BJ, Xu J, Estes VM, Wang D, McKinnon PJ, Paull TT, Zha S. The cancer-associated ATM R3008H mutation reveals the link between ATM activation and its exchange. Cancer Res. 2020. PMID: 33239428, DOI: 10.1158/0008-5472.CAN-20-2447
  • Shao Z, Lee BJ, Rouleau-Turcotte É, Langelier MF, Lin X, Estes VM, Pascal JM, Zha S. Clinical PARP inhibitors do not abrogate PARP1 exchange at DNA damage sites in vivo. Nucleic Acids Res. 2020. PMID: 32890402, DOI: 10.1093/nar/gkaa718
  • Dual-Color Plasmonic Nanosensor for Radiation Dosimetry. Tao Y, Li M, Liu X, Leong KW, Gautier J, Zha S. ACS Appl Mater Interfaces. 2020. PMID: 32337977, DOI: 10.1021/acsami.0c03001
  • DNA-PKcs has KU-dependent function in rRNA processing and haematopoiesis. Shao Z, Flynn RA, Crowe JL, Zhu Y, Liang J, Jiang W, Aryan F, Aoude P, Bertozzi CR, Estes VM, Lee BJ, Bhagat G, Zha S, Calo E. Nature. 2020. PMID: 32103174, DOI: 10.1038/s41586-020-2041-2
  • Liu X, Wang XS, Lee BJ, Wu-Baer FK, Lin X, Shao Z, Estes VM, Gautier J, Baer R, Zha S. CtIP is essential for early B cell proliferation and development in mice. J Exp Med. 2019. PMID: 31097467, DOI: 10.1084/jem.20181139
  • Menolfi D, Jiang W, Lee BJ, Moiseeva T, Shao Z, Estes V, Frattini MG, Bakkenist CJ, Zha S. Kinase-dead ATR differs from ATR loss by limiting the dynamic exchange of ATR and RPA. Nat Commun. 2018. PMID: 30559436, DOI: 10.1038/s41467-018-07798-3
  • Crowe JL, Shao Z, Wang XS, Wei PC, Jiang W, Lee BJ, Estes VM, Alt FW, Zha S. Kinase-dependent structural role of DNA-PKcs during immunoglobulin class switch recombination. Proc Natl Acad Sci USA. 2018. PMID: 30072430, DOI: 10.1073/pnas.1808490115
  • Liu X, Shao Z, Jiang W, Lee BJ, Zha S. PAXX promotes KU accumulation at DNA breaks and is essential for end-joining in XLF-deficient mice. Nat Commun. 2017. PMID: 28051062, DOI: 10.1038/ncomms13816
  • Yamamoto K, Wang J, Sprinzen L, Xu J, Haddock CJ, Li C, Lee BJ, Loredan DG, Jiang W, Vindigni A, Wang D, Rabadan R, Zha S. Kinase-dead ATM protein is highly oncogenic and can be preferentially targeted by Topo-isomerase I inhibitors. Elife. 2016. PMID: 27304073, DOI: 10.7554/eLife.14709
  • Jiang W, Crowe JL, Liu X, Nakajima S, Wang Y, Li C, Lee BJ, Dubois RL, Liu C, Yu X, Lan L, Zha S. Differential phosphorylation of DNA-PKcs regulates the interplay between end-processing and end-ligation during nonhomologous end-joining. Mol Cell. 2015. PMID: 25818648, DOI: 10.1016/j.molcel.2015.02.024
  • Yamamoto K, Wang Y, Jiang W, Liu X, Dubois RL, Lin CS, Ludwig T, Bakkenist CJ, Zha S. Kinase-dead ATM protein causes genomic instability and early embryonic lethality in mice. J Cell Biol. 2012. PMID: 22869596, DOI: 10.1083/jcb.201204098
  • Zha S, Guo C, Boboila C, Oksenych V, Cheng HL, Zhang Y, Wesemann DR, Yuen G, Patel H, Goff PH, Dubois RL, Alt FW. ATM damage response and XLF repair factor are functionally redundant in joining DNA breaks. Nature. 2011. PMID: 21160472, DOI: 10.1038/nature09604
  • Li G, Alt FW, Cheng HL, Brush JW, Goff PH, Murphy MM, Franco S, Zhang Y, Zha S. Lymphocyte-specific compensation for XLF/cernunnos end-joining functions in V(D)J recombination. Mol Cell. 2008. PMID: 18775323, DOI: 10.1016/j.molcel.2008.07.017

For a complete list of publications, please visit PubMed.gov