The oxidative DNA damage response: A review of research undertaken with Tsinghua and Xiangya students at the University of Pittsburgh
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Endogenous stress and exogenous toxicants (chemicals and UV light) alter genetic information either directly or indirectly through the production of reactive oxygen species (ROS), thereby driving genomic instability in cells and promoting tumorigenesis. All living cells try to faithfully preserve and transmit their genomic information from one generation to the next using DNA repair mechanisms to repair oxidative DNA damage to prevent cancer or premature aging. Oxidative DNA damage comprises a mixture of DNA lesions including base damage, DNA single strand breaks (SSBs), and DNA double strand breaks (DSBs). This review summarizes some of the studies on DNA damage response at a defined genome locus that are performed by students from the Tsinghua University School of Medicine and the School of Medicine of Central South University (Xiangya Hospital) at the University of Pittsburgh School of Medicine. A summary of their work highlights the continuous contribution of the students to a particular research program and exemplifies the achievements of this China-U.S. collaborative training program.
KeywordsDNA damage chromatin telomere DNA repair
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This work was supported in part by grants from the National Institutes of Health GM118833 to LL. This project used the UPMC Hillman Cancer Center Cytometry Facility, supported in part by National Institutes of Health P30CA047904.
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