Overview

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
http://www.ncbi.nlm.nih.gov/myncbi/browse/collection/47409482/?sort=date&direction=descending

Education

PHD, 1987, Kyoto University Postgraduate School of Medicine, Japan
MD, 1983, Hiroshima University School of Medicine, Japan

Languages

Yiddish

Relevant Publications

Tomoki Tamai, Giordano Reginato, Ryusei Ojiri, Issei Morita, Alexandra Avrutis, Petr Cejka, Miki Shinohara, Katsunori Sugimoto (2024) "Sae2 controls Mre11 endo- and exonuclease activities by different mechanisms"

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 recognition. 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. PLOS Genetics:e1005283

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

https://www.ncbi.nlm.nih.gov/myncbi/1JkjpBJde7aku/bibliography/public/

Areas Of Interest

DNA damage repair

cancer

centromere

signal transduction

telomere

Course List

MBGC5071Q

Adv. Nucleic Acids: DNA

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.