Background and activities


  • 2016-now:  PhD Candidate, NTNU, Trondheim, Norway

  • 2012-2015:  M.S., Biochemistry and Molecular Biology, Peking University, China

  • 2008-2012:  B.S., Biological Science, Peking University, China

Research interests

DNA double-strand breaks (DSBs) are highly deleterious lesions caused by cell-extrinsic factors, such as ionizing radiation (IR), and cell-intrinsic factors, for instance, aberrant replication. Non-homologous end joining (NHEJ) is a major pathway for detection and repair of DSBs in mammalian cells. For canonical NHEJ (C-NHEJ), when DSBs occur in cells, the lesions are first recognized by Ku70/Ku80 (Ku) complex, which will recruit downstream NHEJ factor DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and an XRCC4-like factor (XLF). Then DNA Ligase 4/XRCC4 ligates the ends.

We identified a novel XRCC4-like protein named paralogue of XRCC4 and XLF (PAXX) through systematic analysis of the human NHEJ factor interactome, and found that PAXX is a direct interactor of Ku (Nature communations, 2015).

Besides C-NHEJ, homologous recombination (HR) is the other key DSB repair pathway. DSB repair pathway choice is governed by the opposing activities of 53BP1 and BRCA1 controlled by the RNF8 and RNF168 E3 ubiquitin ligases. We identified that RIF1 is recruited to the DSB sites by interacting with ATM-phosphorylated 53BP1, restricting BRCA1 accumulation at DSB sites to the S/G2 phases of the cell cycle, during which RIF1 accumulation at DSB sites is strongly antagonized by BRCA1 and its interacting partner CtIP. Thus we identified 53BP1-RIF1 and BRCA1-CtIP as a cell cycle-dependent regulatory circuit controls DSB repair pathway choice (Molecular cell, 2013). 


  • Role of NHEJ factors XLF and PAXX in DNA repair (Project leader: Valentyn Oksenych)

  • Role of DSB repair factors in V(D)J recombination and B lymphocyte development (Project leader: Valentyn Oksenych)


  • Xing, M., Yang, M., Huo, W., Feng, F., Wei, L., Jiang, W., ... & Xu, D. (2015). Interactome analysis identifies a new paralogue of XRCC4 in non-homologous end joining DNA repair pathway. Nature communications, 6.

  • Escribano-Díaz, C., Orthwein, A., Fradet-Turcotte, A., Xing, M., Young, J. T., Tkáč, J., ... & Durocher, D. (2013). A cell cycle-dependent regulatory circuit composed of 53BP1-RIF1 and BRCA1-CtIP controls DNA repair pathway choice. Molecular cell, 49(5), 872-883.


Scientific, academic and artistic work

A selection of recent journal publications, artistic productions, books, including book and report excerpts. See all publications in the database

Journal publications