Abstract
Edward Seto received his bachelor’s degree from the University of California at Irvine and his PhD from the University of California at San Francisco. After completing an American Cancer Society Postdoctoral Fellowship in Thomas Shenk’s laboratory at Princeton University, Dr. Seto spent 4 years as an assistant professor at the University of Texas before moving his research group to the Moffitt Cancer Center at the University of South Florida. Dr. Seto currently holds the Ralph R. Kaul Endowed Professorship at the Moffitt Cancer Center and is the chairman of the Molecular Oncology Department.
Dr. Seto’s laboratory was the first to discover and clone HDAC2 and HDAC3 enzymes and to perform detailed analyses of these proteins. His laboratory was also the first to demonstrate that HDACs repress transcription when recruited to promoters. Over the last 16 years, his laboratory has been actively studying many different aspects of histone deacetylation, including the dissection of all 11 human class I and II HDACs. This work has led to seminal discoveries on the regulation of histone acetylation/deacetylation and identification of key nonhistone targets of the HDAC enzymes.
Recently, Dr. Seto extended his work to the class III sirtuin HDACs. His laboratory found that SIRT1 deacetylates the Nijmegen breakage syndrome 1 (NBS1) protein and has a positive role in promoting DNA double-strand break repair. Additionally, Dr. Seto’s laboratory discovered that the DNA methyltransferase 1 (DNMT1) enzyme is a SIRT1 substrate and that deacetylation of DNMT1 by SIRT1 enhances DNA methyltransferase activity. Finally, his laboratory reported the observation that SIRT1 negatively regulates the activities and functions of 2 acetyltransferases, hMOF and TIP60.
Dr. Seto has published over a hundred scientific articles and currently serves on several editorial and advisory boards. Together with Dr. Xiang-Jiao Yang (McGill University), he organized the 2007 FASEB Summer Research Conference on Histone Deacetylases.