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Mihoko Kai, M.S., Ph.D.
Associate Professor of Radiation Oncology and Molecular Radiation Sciences
Research Interests: Induced neural cells; Stem cells; DNA damage response
Dr. Mihoko Kai is an assistant professor of radiation oncology and molecular radiation services and oncology at the Johns Hopkins University School of Medicine. Her research focuses on DNA damage response, stem cells and induced neural cells.
Dr. Kai’s lab focuses on the use of molecular and cellular biology and genetics to understand the mechanisms of DNA damage response pathways of cancer stem cells. The laboratory also developed methods to create human-induced neurons from adult somatic cells.
She received her undergraduate degree from the University of Tokyo. She earned a M.S. and Ph.D. from the University of Tokyo. She completed her postdoctoral fellowship in molecular biology at Stanford University School of Medicine. Prior to coming to Johns Hopkins, Dr. Kai was an instructor and a basic life science senior research scientist in the Department of Pathology at Stanford University. Dr. Kai joined the Johns Hopkins faculty in 2008.
- Associate Professor of Radiation Oncology and Molecular Radiation Sciences
- Assistant Professor of Oncology
Departments / Divisions
Centers & Institutes
- B.S., University of Tokyo (Japan) (1994)
- M.S., University of Tokyo (Japan) (1996)
- Ph.D., University of Tokyo (Japan) (1999)
Stanford University School of Medicine, Palo Alto, CA, 2003, Postdoctoral Fellow
Research & Publications
Dr. Kai’s research objectives focus on the use of molecular and cellular biology and genetics to understand the mechanisms of DNA damage response pathways of cancer stem cells. Her laboratory also developed methods to create human induced neurons from adult somatic cells.
The main focus of Dr. Kai’s laboratory is to understand how genome stability is maintained in cells.
Nature has evolved two highly conserved processes in order to cope with chromosomal perturbations: DNA repair and the cell cycle checkpoint. Mutations in repair and checkpoint genes have been implicated in cancer-prone syndromes in human cells. Improper coordination and control of these two mechanisms can lead to the accumulation of mutations and genome instability. But while the repair and checkpoint pathways have been separately well studied, understanding of the relationship between them has lagged.
Her laboratory is presently investigating four aspects of this relationship, employing a two-pronged research strategy that involves both yeast and human cells. This approach allows them to obtain fast and powerful results at the basic level, and also apply them rapidly to mammalian cell studies that are directly relevant to human diseases.
- Kai M, Furuya K, Paderi F, Carr AM, and Wang TSF. "Rad3-dependent phosphorylation of the checkpoint clamp regulates repair pathway choice." Nature Cell Biology, 2007; 9:691-697.
- Kai M, Boddy MN, Russell P, and Wang TS. "Replication checkpoint kinase Cds1 regulates Mus81 to preserve genome integrity during replication stress." Genes & Development. 2005; 19: 919-932.
- Kai M and Wang TS. "Checkpoint response to replication stalling: inducing tolerance and preventing mutagenesis (review)." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis. 2003 532: 59-73
- Kai M and Wang TSF. "Checkpoint activation regulates mutagenesis translesion synthesis." Genes & Development. 2003 17 (1): 64-76.
- Kai M, Tanaka H, and Wang TS. "Fission Yeast Rad17 Associates with Chromatin in Response to Aberrant Genomic Structures." Mol. Cell. Biol. 2001 May 15; 21(10):3289-3301.