Office: CP 338B
Lab: AHC3-510A and AHC3-508
Oxidative DNA damage is involved in development of many human diseases that include cancer, neurodegenerative diseases, atherosclerosis, and diabetes, among others. Oxidative DNA damage may result in genomic and epigenomic instability that subsequently leads to initiation and progression of human diseases. To combat the adverse effects of oxidative DNA damage, human cells have evolved a robust DNA repair pathway, DNA base excision repair (BER). Thus, understanding the molecular mechanisms by which oxidative DNA damage and BER may cause and prevent genomic and epigenomic instability is the key for further understanding the initiation and progression of human cancer and neurodegenerative diseases. Current research in our laboratory focuses on understanding the molecular mechanisms underlying oxidative DNA damage-induced genomic and epigenomic instability via BER and their applications in disease prevention, diagnosis, treatment and drug discovery.
Yaou was awarded the Student and New Investigator Travel Award to present his research at the 48th Annual Meeting of the Environmental Mutagenesis and Genomics Society in Raleigh, NC during September 9-13.
Yaou had a research paper published in the journal PLOS ONE, titled "Modulation of Trinucleotide Repeat Instability by DNA Polymerase b Polymorphic Variant R137Q".
Zhongliang was award the Student and New Investigator Travel Award to present his research at the 47th Annual Meeting of the Environmental Mutagenesis and Genomics Society in Kansas City September 24-28.