Ph.D. 1987, Kyoto University Postgraduate School of Medicine, Japan
Postdoctoral training 1987-1989 Stanford University School of Medicine
Postdoctoral training 1989-1991 Scripps Research Institute
Lecturer 1991-1996 Nagoya University, Japan
Associate Professor 1996-2004 Nagoya University, Japan
Associate Professor 2004-Present UMDNJ-Rutgers-New Jersey Medical School
My NCBI Collections
PHD, 1987, Kyoto University Postgraduate School of Medicine, Japan M.D., 1983, Hiroshima University School of Medicine, Japan
Biswas H, Goto G, Wang W, Sung P, and Sugimoto K (2019)
Ddc2 promotes Mec1 activation at RPA-covered ssDNA tracts.
PLOS Genetics: e1008294; PMID: 31369547
Goto GH, Ogi H, Biswas H, Ghosh A, Tanaka S, and Sugimoto K (2017)
Two separate pathways regulate protein stability of ATM/ATR-related protein kinases Mec1 and Tel1 in
budding yeast PLOS Genetics: PMID: 28827813
Ogi H, Goto G, Ghosh A, Zencir S, Henry E and Sugimoto K (2015)
Requirement of the FATC domain of protein kinase Tel1 for localization to DNA ends and target protein
Mol Biol Cell. PMID: 26246601
Goto G, Zencir S, Hirano Y, Ogi H, Ivessa A. and Sugimoto K (2015)
Binding of multiple Rap1 proteins stimulates chromosome breakage induction during DNA replication.
Bandhu, A., Kang, J., Fukunaga, K., Goto, G., Sugimoto, K. (2014)
Ddc2 mediates Mec1 activation through a Ddc1- or Dpb11-independent mechanism.
PLOS Genetics: e1004136 PMID: 24586187
Areas Of Interest
DNA damage repair and telomere homeostasis
We are aiming to understand how DNA damage is recognized by the DNA damage checkpoint machinery and how the
checkpoint machinery initiates DNA damage signaling using budding yeast as a model system.
DNA is continually subjected to damaging agents produced inside cells and penetrated from the environment. DNA
damage checkpoint control is devoted to the surveillance of damaged DNA. It is important to study DNA damage
checkpoint for two reasons. First, it is the front line defense against DNA damage. Unprocessed DNA damage can
lead to mutations that can accumulate to cause cancer. Second, some of the compounds used in cancer
chemotherapy and radiotherapy work by damaging DNA. The success of therapy with such agents is affected by DNA
damage checkpoint control in normal and tumor tissues. A deeper understanding of DNA damage checkpoint should
allow us to modulate the process in tumors in ways that could improve cancer therapy.