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Virology & Mycology

Virology & Mycology
Open Access

ISSN: 2161-0517

+44 1223 790975

Jie Liu

Jie Liu

Jie Liu
Scientist, Heyer Lab
University of California, USA

Biography

Dr. Jie Liu received her Ph.D. degree from the Department of Biochemistry at the University of Vermont, working with Dr. Scott W. Morrical on the biochemical and biophysical characterizations of recombination proteins in Bacteriophage T4. After completing her graduate work, she obtained a postdoctoral fellowship and worked with Dr. Wolf-Dietrich Heyer at the University of California, Davis, on the functional analysis of human breast cancer tumor suppressor protein BRCA2 and yeast Rad51 paralogs Rad55-Rad57 through a multi-disciplinary approach combining genetics, biochemistry, and structural work. She was one of the first to purify and characterize full-length human BRCA2 protein, revealing its mechanistic function in DNA repair and cancer prevention. She is currently working in Department of Microbiology at the University of California, Davis. Her research interest is to investigate the molecular and cellular roles of key recombination protein factors from Bacteriophage to human using a multi-disciplinary approach.  

 

Research Interest

Human chromosomal DNA is under daily attack from environmental chemical and radiation exposures, as well as from internal metabolic products. Homologous recombination is a high-fidelity DNA repair pathway cells utilize to recover lost genetic information after damages and to maintain stability and integrity of the chromosomes. Presynaptic filament is a critical intermediate to initiate recombinational repair, which involves the filament formation of RecA/Rad51 family of proteins on the ssDNA substrate. I am interested in exploring the mechanistic steps and cellular regulation of this repair process using different systems varying from bacteriophage to human. In particular, I am currently pursuing how presynaptic filament, a meta-stable reversible intermediate, is regulated in cells to ensure legitimate repair events at the correct cellular context. 

 

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