Dr. Fotedar's laboratory is working on cell cycle checkpoints and how they link DNA damage and repair, cell cycle progression, and apoptosis
Dr. Fotedar received her Ph.D. in Immunology from the University of Alberta, Canada.
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Distinct p21 requirements for regulating normal and self-reactive T cells through IFN-γ production.
Daszkiewicz L, Vázquez-Mateo C, Rackov G, Ballesteros-Tato A, Weber K, Madrigal-Avilés A, Di Pilato M, Fotedar A, Fotedar R, Flores JM, Esteban M, Martínez-A C, Balomenos D
Sci Rep. 2015;5:7691
Rati Fotedar's Research Focus
Eukaryotic cells have elaborate pathways to detect and repair DNA damage in order to prevent alterations in their genetic material. In response to DNA damage, cells arrest at distinct points during the cell cycle, called checkpoints, to facilitate DNA repair. Defects in these regulatory mechanisms lead to resumption of the cell cycle and cell division in the presence of DNA damage, thereby contributing to genomic instability. The integrity of the checkpoints in normal and tumor cells will influence the outcome of radiotherapy and chemotherapy. Therefore knowledge of the molecular basis of these regulatory mechanisms may provide a conceptual framework for discovering effective strategies to improve cancer therapy. Our research focus is to gain a better understanding of the cell cycle checkpoints and how they link the detection of DNA damage to cell cycle progression, DNA repair, senescence and apoptosis.
About Rati Fotedar
Dr. Fotedar received her Ph.D. in Immunology from the University of Alberta, Canada. Following postdoctoral training in the cell cycle at the Fred Hutchinson Cancer Research Center in Seattle, she was appointed as Assistant Professor at the Institut de Biologie Structurale, Grenoble, France in 1992 and promoted to Professor in 2003. Dr. Fotedar moved to the Sidney Kimmel Cancer Center in San Diego in 2006 as Professor in the Division of Cancer Cell Biology. In 2009, she was appointed as Professor in the Tumor Development Program at Sanford-Burnham.