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Zhigang Wang, Ph.D.

Graduate Center for Toxicology

Mailing Address:

Graduate Center for Toxicology
1095 V.A. Drive
306 Health Sciences Research Building
Lexington, KY  40536-0305
Office: 340 HSRB
Phone: (859) 323-5784
Fax: (859) 323-1059
Web site:

Research Interests

Dr. Wang's laboratory is interested in two closely related areas: (i) DNA damage-induced mutagenesis; and (ii) DNA excision repair.

Damage-induced mutagenesis. Endogenous and environmental agents frequently attack DNA. DNA damage can cause mutations during replication. Mutagenesis is an important factor during the initiation and progression of human cancers. In the yeast Saccharomyces cerevisiae, it appears that the majority of damage-induced mutations and some spontaneous mutations are generated through the damage-induced mutagenesis pathway. A similar mutagenesis pathway is most likely operational in humans. Hence, understanding damage-induced mutagenesis is a key to the understanding of carcinogenesis. Furthermore, this mutagenesis pathway offers an exciting novel target for cancer prevention and suppression through therapeutic inhibition of the pathway. Our objectives in this area are (a) to understand the molecular mechanism of the damage-induced mutagenesis pathway; and (b) to explore this mutagenesis pathway as a target for cancer prevention and suppression.

DNA excision repair. DNA excision repair is a major cellular response to DNA damage. It consists of base excision repair (BER) and nucleotide excision repair (NER). Defects in NER can lead to a predisposition to cancers as manifested in the human hereditary disease xeroderma pigmentosum (XP). We face two challenges in the area of excision repair: (a) repair of nucleosomal DNA; and (b) transcription-coupled repair. Our studies of excision repair rely on the eukaryotic model organism, the yeast S. cerevisiae. We are using molecular, biochemical, and genetic techniques to study the mechanism of DNA excision repair in this model system.

For a list of Dr. Wang's publications, please visit the PubMed web site.

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