Dr Qian Wu

Profile

My group is studying the fundamental mechanism of how cells respond and deal with DNA damage. Human cells are under constant threat of damage from external and internal sources. One of the most dangerous forms of damage is to DNA. Accumulated DNA damages lead to cell death and genome instability, which can cause cancer, neurodegenerative disease and ageing. Maintaining the integrity of genetic information stored in DNA through various damage response and repair signalling pathways are critical for cellular function and cell survival. We focus on the structural determination of key protein complexes function in DNA damage response (DDR) and repair. Together with various biochemical/biophysical methods and cellular studies, we would like to work out the exact mechanisms in human DDR and repair network. 

After completing my undergraduate degree in Biochemistry, University of Bristol, I moved to the University of Cambridge, Department of Biochemistry for my PhD and then postdoc in structural biology (Prof. Sir Tom Blundell's group). During my PhD, I determined the structure and function of key protein complexes in NHEJ pathway, which is one of two major repair pathways for human DNA double-strand breaks.  For my postdoc time, I developed interest to study protein complexes, such as BRCA1 related complexes, in DNA damage response, which is earlier stage than repair pathway. In September 2018, I was awarded University Academic Fellowship to start my own group here. 

Research interests

We study DNA double-strand breaks (DSBs), which are the most toxic damages in cells. Human cells have two major pathways for repairing DSBs: Homologous Recombination (HR) and Non-Homologous End Joining (NHEJ). Cellular signaling network of DNA damage response (including BRCA1 and 53BP1) is responsible for regulating the function of HR and NHEJ pathways respectively. It is crucial to identify and understand the structural and functional mechanisms of proteins invovled in this network not only as individuals, but more importantly as complexes at DNA damage sites. We strongly believe that one of the core values of basic biomedical research is translation into tools and treatment to improve human health. Therefore, through our research, we would like to understand how these decisions go wrong in cancer cells compared with normal cells. This will enable us to identify suitable targets to develop small molecule compounds that modulate the DNA damage response and repair signaling for future drug discovery, medical applications and ultimately killing cancer cells specifically.

• Structural mechanism of DNA damage response on replicating chromatin

Qualifications

• Postdoc, University of Cambridge
• PhD, Structural biology, University of Cambridge
• BSc,Biochemistry, University of Bristol

Professional memberships

• Biochemistry Society