Yuliang Wu, Assistant Professor

Ph.D. 2002, International Centre for Genetic Engineering and Biotechnology (ICGEB), New Delhi, India
M.Sc. 1995, Faculty of Agriculture, Life and Environ ment, Zhejiang University, Hangzhou, China
B.Sc. 1992, Faculty of Agriculture, Life and Environment, Zhejiang University, Hangzhou, China

  • Four Top Researcher Awards were given in four different categories. at the Saskatchewan Health Research Foundation’s annual Santé! Awards evening in Saskatoon on December 1, 2011. The award in the New Investigator Establishment Grants – Biomedical category went to Yuliang Wu, from the department of biochemistry in the College of Medicine. Wu aims to understand how protein changes can lead to breast cancer and Fanconi anemia, a genetic disease that often leads to leukemia and other types of cancer. Wu and his team are looking at the Fanconi anemia group J protein, which contributes to DNA repair. He has identified changes, or mutations, in the protein in cases of breast cancer or Fanconi anemia and is conducting further research to determine the potential structural defects. This knowledge is an important step toward possible  therapies that target the mutated protein. (OCN December 6, 2011)

Publications

1.  Wu,Y. (2012) Unwinding and rewinding: double faces of helicase? J Nucleic Acids., 2012:140601. (PMID: 22888405).

2.  Wu,Y., Sommers,J.A., Loiland,J.A., Kitao,H., Kuper,J., Kisker,C. and Brosh,R.M. (2012) The Q Motif of FANCJ DNA Helicase Regulates its Dimerization, DNA Binding, and DNA Repair Function. J Biol Chem., 287, 21699-21716.

3.  Wu,Y. and Brosh,R.M., Jr. (2012) DNA helicase and helicase-nuclease enzymes with a conserved iron-sulfur cluster. Nucleic Acids Res., 40, 4247-4260.

4.  Wu,Y., Sommers,J., Khan,I., de,W.J. and Brosh,R. (2011) Biochemical characterization of Warsaw Breakage Syndrome helicase. J Biol Chem., 287, 1007-1021.

5. Wu,Y., Sommers,J.A., Suhasini,A.N., Leonard,T., Deakyne,J.S., Mazin,A.V., Shin-ya,K., Kitao,H. and Brosh,R.M., Jr. (2010) Fanconi anemia group J mutation abolishes its DNA repair function by uncoupling DNA translocation from helicase activity or   disruption of protein-DNA complexes. Blood, 116, 3780-3791.

6.  Wu,Y., Shin-ya,K. and Brosh,R.M., Jr. (2008) FANCJ helicase defective in Fanconia anemia and breast cancer unwinds G-quadruplex DNA to defend genomic stability. Mol. Cell Biol., 28, 4116-4128.

7.  Wu,Y., Dai,X.Q., Li,Q., Chen,C.X., Mai,W., Hussain,Z., Long,W., Montalbetti,N., Li,G., Glynne,R. et al. (2006) Kinesin-2 mediates physical and functional interactions between polycystin-2 and fibrocystin. Hum. Mol. Genet., 15, 3280-3292.

    For more publication information please visit PubMed.