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About Yue Zou

Research interests of my laboratory focus on mechanistic understanding of DNA damage, repair, and checkpoints, as well as the interactions between these pathways. Today one of the greatest challenges to the human health today is the voluntary and involuntary exposure to a variety of ubiquitous genotoxic agents (typically UV irradiation and environmental carcinogens) which potentially cause DNA damage, mutations, genome instability and thus cancers. To cope with genetic stress induced by DNA damage, cells launch a series of cellular responses primarily including DNA repair and DNA damage checkpoints. As a cellular defense system against DNA damage for maintaining the integrity of genetic materials, DNA repair recognizes and removes DNA lesions, while activation of DNA damage checkpoints leads to the arrest of cell cycle progression to allow sufficient time for DNA repair. Nucleotide excision repair (NER) is one of the major DNA repair pathways in cells. It removes a large variety of DNA lesions induced by various environmental pollutants and carcinogens. We are particularly interested in DNA damage recognition, structure and function of repair proteins, and the relationship of NER with DNA damage checkpoints, particularly ATR and ATM signaling pathways. Our work includes characterization of xeroderma pigmentosum group A (XPA) and replication protein A (RPA) for their role in NER and checkpoint regulation in cellular responses to DNA damage. In addiction, the involvement of NER in removal of a variety of carcinogenic DNA adducts has been examined.
Another major effort in my lab is to determine the molecular basis of DNA damage, particularly DNA double-strand breaks (DSBs), accumulation in laminopathy-based premature aging and normal aging. While aging that governs human lifespan is a normal but complex biological process, individuals who have the rare disease Hutchinson-Gilford progeria syndrome (HGPS) suffer from premature aging. Recent evidence links HGPS to deficiency in maturation of lamin A protein, a major inner component of the nuclear envelope and skeleton. The accelerated aging phenotypes may result from genomic instability induced by DSB accumulation, an observation similar to that in normal aging. However, how these DSBs form as the result of the lamin A deficiency and why they are resistant to repair and thus accumulate remain unknown. Our goal is to delineate the underlying mechanism and its potential implication in normal aging. Such understanding may provide molecular basis for development of potential new therapeutic strategies for better treatment of the devastating disease.


Present Professor, East Tennessee State University Biomedical Sciences, Quillen College of Medicine


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Contact Information

Room B029, Building 178, VA Campus
Lab-(423) 439-2123
Office-(423) 439-2124
FAX: (423) 439-2030


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