|Yoshimichi Nakatsu||Last modified date：2020.06.30|
Reseacher Profiling Tool Kyushu University Pure
Department of Medical Biophysics and Radiation Biology, Faculty of Medical Sciences .
Doctor of Science
Country of degree conferring institution (Overseas)
Field of Specialization
Total Priod of education and research career in the foreign country
Research InterestsMembership in Academic Society
- Elucidation of environmental and genetic factors that enhance microsatellite instability in mismatch repair deficient human cells
keyword : Genomic destabilization, mismatch repair, colorectal cancer
- Biological effects of non-thermal atmospheric pressure plasma
keyword : ROS, cell death, mutation, DNA damages, epigenome
- Mutagenesis and carcinogenesis caused by the failure of the mechanisms for DNA damage response
keyword : oxidative stress DNA repair mismatch repair cell-death
- Molecular mechanisms for DNA damage response
keyword : mutation cell-death adaptive response mismatch repair
- Molecular mechanisms for prevention and elimination of oxidative DNA damages
keyword : oxidative DNA damages, nucleotide, mutagenesis, cell death, carcinogenesis, gene-knockout mice, transgenic mice
- Non-thermal atmospheric pressure plasma induces selective death for cancer cells and promotes endoderm formation in embryonic body derived from embryonic stem cells. Plasma-treatment of plant seeds also promotes germination and subsequent growth. Since plasma irradiation causes DNA damage responses, active molecular species generated by plasma act on chromatin, and It is possible that the resulting chromatin-modifications could cause cell death and epigenome changes leading to the promotion of endoderm formation in the embryoid body and the growth promotion of plants. In this study, we examine the possibility that non-thermal atmospheric pressure plasma can generate modified bases in genomic DNA and induce cell death and epigenome changes.
- The mutation rate and microsatellite sequence stability are analyzed in wild type and mutant human iPS cells, human cancer cell lines, and mouse fetal fibroblasts, cultured under hypoxic conditions.
- The short tandem repeat (STR) is a difficult-to-reproduce sequence in which errors frequently occur during DNA replication, but a large number of STR are distributed on the eukaryotic genome. The physiological function of STR is unknown so far, but its alterations are associated with some human cancers and neuromuscular diseases. With the aim of elucidating the molecular mechanism of STR changes and to identify the molecular abnormalities that lead to repeat instability, the mutations in DNA mismatch repair gene and DNA polymerase δ gene found in human diseases are introduced into human cells by means of genome editing technique, and the mutation rate, mutation spectrum and changes in microsatellite sequences of those cells are analyzed.
- Plasma exhibits wound healing and carcinostatic effects, but on the other hand, it may induce DNA damages and cause carcinogenesis and aging. For safety use of plasma medicine, it is necessary to establish safe dosage and usage. The purpose of this study is to analyze the DNA damages and mutations caused by plasma, and to provide a research base for the safety evaluation of plasma medicine.
- The MUTYH gene is known to be associated with Familial adenomatous polyposis (MAP: MUTYH -associated polyposis), and encodes a DNA repair protein that suppresses mutations caused by oxidative stress in mammalian cells. MUTYH is involved not only in the suppression of mutations but also in the cell death induced by oxidative stress. In this study, I investigate the role of MUTYH associated with mismatch repair proteins in the induction of cell death caused by oxidative stress.
- We developed an experimental system for oxidative stress-inducing mutagenesis and carcinogenesis in the intestine of mice. In oder to identify the common genes mutated in the adenomas/carcinomas induced by using this system, we analyze the genomes of adenomas/carcinomas induced in the same animals.
- Mutagenesis caused by oxidized nucleotides and it preventing mechanisms.
Analysis of cell death pathway evoked by oxidized nucleotides.
- Oxygen-induced DNA damage and its repair mechanism
|1.||Yoshimichi Nakatsu, Mutso Sekiguchi, Oxidative Damage to Nucleotide: Consequences and Preventive Mechanism, Imperial College Press, "Oxidative Stress, Disease and Cancer" Singh, KK (Ed), pp221-252, 2006.01.|
|1.||Tsuzuki T, Nakatsu Y, Nakabeppu Y, Significance of error-avoiding mechanisms for oxidative DNA damage in carcinogenesis, Cancer Science, 2007.08.|
- The Japanese Environmental Mutagen Society (JEMS)
- Genetic Society of Japan
- The Japan Radiation Research Society
- Japanese Cancer Association
- The Molecular Biology Society of Japan