Asako NAKAMURAProfessor
■Researcher basic information
Organization
- College of Science Department of Sciences Biological Sciences
- Graduate School of Science and Engineering（Master's Program） Major in Quantum Bean Science
- Graduate School of Science and Engineerin（Doctoral Program） Major in Quantum Bean Science
- Faculty of Basic Natural Science Domain of Biological Sciences
Research Areas
Career
Member History
- Jul. 2024 - Present, 広報出版委員会副委員長, 日本放射線影響学会
- Jul. 2023 - Present, SITプログラム小委員会, 日本放射線影響学会
- Jun. 2020 - Present, 学術評議員, 日本放射線影響学会
- May 2020 - Mar. 2026, 北茨城市創生推進会議委員, 北茨城市
- Sep. 2023 - Mar. 2025, 那珂市特産品ブランド推進協議会委員, 那珂市
- Aug. 2023 - Mar. 2024, 日立市におけるリカレント教育体制構築に係る事業アドバイザー, 日立市
- Mar. 2023 - Mar. 2024, 茨城県リスキリング推進協議会幹事会委員, 茨城県
- Apr. 2022 - Mar. 2024, 京都大学大学院生命科学研究科附属放射線生物研究センター運営委員会委員, 京都大学大学院生命科学研究科附属放射線生物研究センター
- Mar. 2022 - Mar. 2024, ダイバーシティ社会に向けたチャレンジ委員会委員, 茨城県水戸生涯学習センター
- May 2020 - Mar. 2024, 茨城県地場産業等総合支援事業補助金審査会委員, 茨城県
- Apr. 2020 - Mar. 2024, いばらき子ども大学実行委員会委員, 茨城県教育委員会
- Apr. 2020 - Mar. 2024, 水戸黄門まつり実行委員会委員, 水戸市
- Apr. 2020 - Mar. 2024, 茨城県圏央道沿線地域産業・交流活性化協議会幹事, 茨城県
- Apr. 2020 - Mar. 2024, 第60回水戸黄門まつり実行委員会委員, 水戸市
- Aug. 2023 - Nov. 2023, 令和5年度漁港施設等指定管理者選定委員, 茨城県農林水産部
- May 2020 - Mar. 2023, 関東近県生涯学習・社会教育実践研究交流会実行委員会委員, 茨城県
- Jul. 2022 - Oct. 2022, 令和4年度漁港施設等指定管理者選定委員会委員, 茨城県農林水産部
- Aug. 2020 - Jun. 2022, SITワークショップ準備検討小委員会委員, 日本放射線影響学会
- Jun. 2020 - Jun. 2022, 論文紹介企画小委員会委員, 日本放射線影響学会
- Jun. 2020 - Jun. 2022, キャリアパス・男女共同参画委員会, 日本放射線影響学会
- Apr. 2016 - Mar. 2022, 水戸第二高等学校SSH高大接続委員会委員, 水戸第二高等学校
- Nov. 2020 - Mar. 2021, アリーナを核としたスマートシティ推進協議会委員長, アリーナを核としたスマートシティ推進協議会
- Oct. 2016 - Nov. 2020, 重粒子線がん治療装置等共同利用運営委員会・議題採択評価部会委員, 量子科学技術研究開発機構
- Apr. 2016 - Mar. 2020, 共同利用・共同研究専門委員会委員, 京都大学放射線生物研究センター
Message from Researchers
(Message from Researchers)
Professional profile,•Radiation cellular biologist specializing in the mechanisms of genome integrity, DNA double-strand break repair and mammalian aging with more than fifteen years experience and more than 45 publications. ,•Involved in the development of an assay for a new pharmacodynamics biomarker in response to chemo- and radio-therapeutic treatments in cancer patients. ,•Co-developing a sensitive and accurate biomarker for exposure to radiation and genotoxic substances.,•Reviewer of several international journals (Oncogene, Journal of Nucleic Acid, Medical Molecular Morphology, and Journal of Radiation Research, etc.).,•Strong interest in pursuing translational studies which improve human health based on basic research ,•Highly motivated individual with abilities to communicate both in English and Japanese, to adapt to new environments (flexibility), to think critically, and to solve scientific problems.,•Mentor for the National Institutes of Health summer student program.,•Teaching for anatomy and histology at Osaka Medical College.,•Teaching for cellular biology at Ibaraki University.,,Education,•PhD of Pharmaceutical Science, Hiroshima University (Professor; Toshinori Ide and Kenshi Komatsu)(2002),Research project: The function of Nijmegen Breakage syndrome (NBS1) protein in telomere maintenance and genome stability. ,•MS of Pharmaceutical Science, Hiroshima University (Professor; Toshinori Ide and Kenshi Komatsu)(1999),Research project: The genomic mutation analysis of Fanconi Anemia (FA) patients and the study of function of FA proteins in DNA repair mechanism.,•Awarded the degree of Pharmacist (Registration No. 327562) (1997),•BA of Pharmaceutical Science, Hiroshima University (Professor; Toshinori Ide and Kenshi Komatsu)(1997),Research project: The identification of response gene for radiation sensitivity in Chinese hamster ovary (CHO) mutant cells, xrs-2.,,Professional Training,•Professor of Ibaraki University, College of Science (2017-current),•Associate Professor of Ibaraki University, College of Science (2013- 2017),•Junior Associate Professor of Osaka Medical College, Department of Anatomy and Cell Biology (Professor; Yoshinori Otsuki),(2011-2013),•Research Fellow of National Institutes of Health, National Cancer Institute, Laboratory of Molecular Pharmacology (Principal Investigator; William Bonner) (2009-2011),•Visiting Fellow of National Institutes of Health, National Cancer Institute, Laboratory of Molecular Pharmacology (Principal Investigator; William Bonner) (2007-2009),•Special volunteer of the Japan Society for Promotion of Science for Japanese Biomedical and Behavioral Researchers at NIH (Principal Investigator; William Bonner) (2004-2007),•Post Doctoral Research Fellow of the Japan Society for the Promotion of Science (Professor; Kenshi Komatsu) (2002-2004)
■Research activity information
Award
- 2019, 第６回バイオテックグランプリ ロート賞
Japan society - 2019, 第６回バイオテックグランプリ 吉野家賞
Japan society - Nov. 2018, 第３回茨城テックプラングランプリ 日本メクトロン賞
Japan society - Nov. 2018, 第3回茨城テックプラングランプリ オーディエンス賞
- 2018, 平成30年度茨城大学学長学術表彰奨励賞
- 2018, 第３回茨城テックプランター 日本メクトロン賞
Japan society - 2017, 平成29年度日本放射線影響学会岩崎民子賞
- 2015, 平成27年度茨城大学学長学術表彰奨励賞
- 2014, 平成26年度日本放射線影響学会奨励賞, 日本放射線影響学会
Paper
- A novel microfluidic chip for on-site radiation risk evaluation.
Kenta Takahashi; Takahiro Tamura; Kosuke Yamada; Kaisei Suga; Yuri Aoki; Ryota Sano; Kentaro Koyama; Asako J Nakamura; Takaaki Suzuki, Corresponding, This paper proposes a microfluidic chip for on-site radiation risk evaluation using immunofluorescence staining for the DNA double-strand break (DSB) marker phosphorylated histone, H2AX (γ-H2AX). The proposed microfluidic chip separates lymphocytes, the cells of the DNA DSB evaluation target, from whole blood based on their size and traps them in the trap structure. The subsequent DNA DSB evaluation, γ-H2AX assay, can be performed on a chip, which saves space and simplifies the complicated operation of the assay, which conventionally requires a large experimental space. Therefore, this chip will enable the biological effect evaluation of radiation exposure to be completed on-site. Bead experiments with samples containing 10 μm and 27 μm diameter beads showed that the proposed chip introduced the sample into the flow channel only by centrifugal force and passively separated the two types of beads by the structure in the flow channel. In addition, bead experiments showed that isolated 10 μm diameter beads were trapped in more than 95% of the 1000 lymphocyte trap structures (LTSs). The feasibility of the proposed method for on-site radiation risk evaluation was demonstrated through cell-based experiments by performing the γ-H2AX assay in human lymphoblastoid TK6 cells. The experiment shows that LTSs in the flow channel are capable of trapping TK6 cells, and γ-H2AX foci which are markers of DNA DSBs are observed in the TK6 cells on the chip. Thus, the results suggest that the proposed microfluidic chip simplifies the γ-H2AX assay protocol and provides a novel method to perform the assay on-site, which is conventionally impracticable.
The Analyst, 02 Dec. 2024, [Reviewed] - Senescence-Associated Heterochromatin Foci Suppress γ-H2AX Focus Formation Induced by Radiation Exposure.
Takashi Oizumi; Tomoya Suzuki; Junya Kobayashi; Asako J Nakamura, Last, DNA damage is induced by both endogenous and exogenous factors. Repair of DNA double-strand break (DSB), a serious damage that threatens genome stability, decreases with senescence. However, the molecular mechanisms underlying the decline in DNA repair capacity during senescence remain unclear. We performed immunofluorescence staining for phosphorylated histone H2AX (γ-H2AX) in normal human fetal lung fibroblasts and human skin fibroblasts of different ages after chronic irradiation (total dose, 1 Gy; dose rate, 1 Gy/day) to investigate the effect of cellular senescence and organismal aging on DSB repair. Accumulation of DSBs was observed with cellular senescence and organismal aging, probably caused by delayed DSB repair. Importantly, the formation of γ-H2AX foci, an early event in DSB repair, is delayed with cellular senescence and organismal aging. These results suggest that the delay in γ-H2AX focus formation might delay the overall DSB repair. Interestingly, immediate γ-H2AX foci formation was suppressed in cells with senescence-associated heterochromatin foci (SAHF). To investigate the relationship between the γ-H2AX focus formation and SAHF, we used LiCl to relax the SAHFs, followed by irradiation. We demonstrated that LiCl rescued the delayed γ-H2AX foci formation associated with cellular senescence. This indicates that SAHF interferes with γ-H2AX focus formation and inhibits DSB repair in radiation-induced DSB. Our results suggest that therapeutic targeting of SAHFs have potential to resolve DSB repair dysfunction associated with cellular senescence.
International journal of molecular sciences, 15 Mar. 2024, [Reviewed] - Nanoparticle as a Carrier of Cationic Porphyrin and Ratiometric Fluorescence pH Sensor.
Shinoda H; Higano R; Oizumi T; Nakamura AJ; Kamijo T; Takahashi M; Nagaoka M; Sato Y; Yamaguchi A.
ACS Appl Bio Mater., 11 Jan. 2024, [Reviewed] - Prediction of late adverse events in pelvic cancer patients receiving definitive radiotherapy using radiation-induced gamma-H2AX foci assay.
Someya M; Hasegawa T; Nakamura AJ; Tsuchiya T; Kitagawa M; Gocho T; Mafune S; Ikeuchi Y; Tauchi H; Sakata KI.
J Radiat Res., 21 Nov. 2023, [Reviewed] - Identification of Novel Senescent Markers in Small Extracellular Vesicles.
Misawa T; Hitomi K; Miyata K; Tanaka Y; Fujii R; Chiba M; Loo TM; Hanyu A; Kawasaki H; Kato H; Maezawa Y; Yokote K; Nakamura AJ; Ueda K; Yaegashi N; Takahashi A., Senescent cells exhibit several typical features, including the senescence-associated secretory phenotype (SASP), promoting the secretion of various inflammatory proteins and small extracellular vesicles (EVs). SASP factors cause chronic inflammation, leading to age-related diseases. Recently, therapeutic strategies targeting senescent cells, known as senolytics, have gained attention; however, noninvasive methods to detect senescent cells in living organisms have not been established. Therefore, the goal of this study was to identify novel senescent markers using small EVs (sEVs). sEVs were isolated from young and senescent fibroblasts using three different methods, including size-exclusion chromatography, affinity column for phosphatidylserine, and immunoprecipitation using antibodies against tetraspanin proteins, followed by mass spectrometry. Principal component analysis revealed that the protein composition of sEVs released from senescent cells was significantly different from that of young cells. Importantly, we identified ATP6V0D1 and RTN4 as novel markers that are frequently upregulated in sEVs from senescent and progeria cells derived from patients with Werner syndrome. Furthermore, these two proteins were significantly enriched in sEVs from the serum of aged mice. This study supports the potential use of senescent markers from sEVs to detect the presence of senescent cells in vivo.
Int J Mol Sci., 26 Jan. 2023, [Reviewed] - 〔Major achievements〕An Enriched Environment Alters DNA Repair and Inflammatory Responses After Radiation Exposure
Sakama Sae; Kurusu Keisuke; Morita Mayu; Oizumi Takashi; Masugata Shinya; Oka Shohei; Yokomizo Shinya; Nishimura Mayumi; Morioka Takamitsu; Kakinuma Shizuko; Shimada Yoshiya; Nakamura Asako J., Last, After the Fukushima Daiichi Nuclear Power Plant accident, there is growing concern about radiation-induced carcinogenesis. In addition, living in a long-term shelter or temporary housing due to disasters might cause unpleasant stress, which adversely affects physical and mental health. It’s been experimentally demonstrated that “eustress”, which is rich and comfortable, has beneficial effects for health using mouse models. In a previous study, mice raised in the enriched environment (EE) has shown effects such as suppression of tumor growth and enhancement of drug sensitivity during cancer treatment. However, it’s not yet been evaluated whether EE affects radiation-induced carcinogenesis. Therefore, to evaluate whether EE suppresses a radiation-induced carcinogenesis after radiation exposure, in this study, we assessed the serum leptin levels, radiation-induced DNA damage response and inflammatory response using the mouse model. In brief, serum and tissues were collected and analyzed over time in irradiated mice after manipulating the raising environment during the juvenile or adult stage. To assess the radiation-induced DNA damage response, we performed immunostaining for phosphorylated H2AX which is a marker of DNA double-strand break. Focusing on the polarization of macrophages in the inflammatory reaction that has an important role in carcinogenesis, we performed analysis using tissue immunofluorescence staining and RT-qPCR. Our data confirmed that EE breeding before radiation exposure improved the responsiveness to radiation-induced DNA damage and basal immunity, further suppressing the chronic inflammatory response, and that might lead to a reduction of the risk of radiation-induced carcinogenesis., Frontiers Media SA
Frontiers in Immunology, 22 Oct. 2021, [Reviewed] - Decreased ionizing radiation-induced DNA damage repair function of cultured fibroblasts derived from patients with xeroderma pigmentosum variant
Toshihiro OTSUKA; Asako J. NAKAMURA; and Shinichi MORIWAKI
Bulletin of Osaka Medical and Pharmaceutical University, 17 Sep. 2021, [Reviewed] - Health effects triggered by tritium: how do we get public understanding based on scientifically supported evidence?
Matsumoto H; Shimada Y; Nakamura AJ; Usami N; Ojima M; Kakinuma S; Shimada M; Sunaoshi M; Hirayama R; Tauchi H.
J Radiat Res., 28 Apr. 2021, [Reviewed] - Repair Kinetics of DNA Double Strand Breaks Induced by Simulated Space Radiation.
Oizumi T.; Ohno R.; Yamabe S.; Funayama T. and Nakamura A.J., Last, Radiation is unavoidable in space. Energetic particles in space radiation are reported to induce cluster DNA damage that is difficult to repair. In this study, normal human fibroblasts were irradiated with components of space radiation such as proton, helium, or carbon ion beams. Immunostaining for γ-H2AX and 53BP1 was performed over time to evaluate the kinetics of DNA damage repair. Our data clearly show that the repair kinetics of DNA double strand breaks (DSBs) induced by carbon ion irradiation, which has a high linear energy transfer (LET), are significantly slower than those of proton and helium ion irradiation. Mixed irradiation with carbon ions, followed by helium ions, did not have an additive effect on the DSB repair kinetics. Interestingly, the mean γ-H2AX focus size was shown to increase with LET, suggesting that the delay in repair kinetics was due to damage that is more complex. Further, the 53BP1 focus size also increased in an LET-dependent manner. Repair of DSBs, characterized by large 53BP1 foci, was a slow process within the biphasic kinetics of DSB repair, suggesting non-homologous end joining with error-prone end resection. Our data suggest that the biological effects of space radiation may be significantly influenced by the dose as well as the type of radiation exposure., MDPI
Life, 10 Dec. 2020, [Reviewed] - DNA damage regulates senescence-associated extracellular vesicle release via the ceramide pathway to prevent excessive inflammatory responses.
Kazuhiro Hitomi; Ryo Okada; Tze Mun Loo; Kenichi Miyata; Asako J Nakamura; Akiko Takahashi, DNA damage, caused by various oncogenic stresses, can induce cell death or cellular senescence as an important tumor suppressor mechanism. Senescent cells display the features of a senescence-associated secretory phenotype (SASP), secreting inflammatory proteins into surrounding tissues, and contributing to various age-related pathologies. In addition to this inflammatory protein secretion, the release of extracellular vesicles (EVs) is also upregulated in senescent cells. However, the molecular mechanism underlying this phenomenon remains unclear. Here, we show that DNA damage activates the ceramide synthetic pathway, via the downregulation of sphingomyelin synthase 2 (SMS2) and the upregulation of neutral sphingomyelinase 2 (nSMase2), leading to an increase in senescence-associated EV (SA-EV) biogenesis. The EV biogenesis pathway, together with the autophagy-mediated degradation pathway, functions to block apoptosis by removing cytoplasmic DNA fragments derived from chromosomal DNA or bacterial infections. Our data suggest that this SA-EV pathway may play a prominent role in cellular homeostasis, particularly in senescent cells. In summary, DNA damage provokes SA-EV release by activating the ceramide pathway to protect cells from excessive inflammatory responses.
Int J Mol Sci., 25 May 2020, [Reviewed] - Space Radiation Biology for “Living in Space”
Satoshi Furukawa; 1 Aiko Nagamatsu; 1 Mitsuru Nenoi; 2 Akira Fujimori; 2 Shizuko Kakinuma; 2 Takanori Katsube; 2 Bing Wang; 2 Chizuru Tsuruoka; 2 Toshiyuki Shirai; 2 Asako J. Nakamura; 3 Asako Sakaue-Sawano; 4 Atsushi Miyawaki; 4 Hiroshi Harada; 5 Minoru Kobayashi; 5 Junya Kobayashi; 5 Takekazu Kunieda; 6 Tomoo Funayama; 7 Michiyo Suzuki; 7 Tatsuo Miyamoto; 8 Jun Hidema; 10; 9 Yukari Yoshida; 11 and Akihisa Takahashi, Space travel has advanced significantly over the last six decades with astronauts spending up to 6 months at the International Space Station. Nonetheless, the living environment while in outer space is extremely challenging to astronauts. In particular, exposure to space radiation represents a serious potential long-term threat to the health of astronauts because the amount of radiation exposure accumulates during their time in space. Therefore, health risks associated with exposure to space radiation are an important topic in space travel, and characterizing space radiation in detail is essential for improving the safety of space missions. In the first part of this review, we provide an overview of the space radiation environment and briefly present current and future endeavors that monitor different space radiation environments. We then present research evaluating adverse biological effects caused by exposure to various space radiation environments and how these can be reduced. We especially consider the deleterious effects on cellular DNA and how cells activate DNA repair mechanisms. The latest technologies being developed, e.g., a fluorescent ubiquitination-based cell cycle indicator, to measure real-time cell cycle progression and DNA damage caused by exposure to ultraviolet radiation are presented. Progress in examining the combined effects of microgravity and radiation to animals and plants are summarized, and our current understanding of the relationship between psychological stress and radiation is presented. Finally, we provide details about protective agents and the study of organisms that are highly resistant to radiation and how their biological mechanisms may aid developing novel technologies that alleviate biological damage caused by radiation. Future research that furthers our understanding of the effects of space radiation on human health will facilitate risk-mitigating strategies to enable long-term space and planetary exploration.
BioMed Research International, 08 Apr. 2020, [Reviewed] - Pilot clinical study of ascorbic acid treatment in cardiac catheterization.
Sun L; Igarashi T; Tetsuka R; Li YS; Kawasaki Y; Kawai K; Hirakawa H; Tsuboi K; Nakamura AJ; Moritake T.
J Radiat Res., 2018, [Reviewed] - The Causal Relationship between DNA Damage Induction in Bovine Lymphocytes and the Fukushima Nuclear Power Plant Accident
Asako J. Nakamura; Masatoshi Suzuki; Christophe E. Redon; Yoshikazu Kuwahara; Hideaki Yamashiro; Yasuyuki Abe; Shintaro Takahashi; Tomokazu Fukuda; Emiko Isogai; William M. Bonner; Manabu Fukumoto
RADIATION RESEARCH, May 2017, [Reviewed] - 抗酸化物質Tempolによる放射線誘発のDNA損傷抑制効果の検討
加藤 正尊; 飯岡 俊英; 丸山 里奈; 澤井 裕一; 中村 麻子; 笹谷 めぐみ; 神谷 研二; 小林 純也; 小松 賢志; 志村 勉, (一社)日本放射線影響学会
日本放射線影響学会大会講演要旨集, Oct. 2016 - Evidence for chromosome fragility at the frataxin locus in Friedreich ataxia.
Mutat Res., 2016, [Reviewed] - A Phase I Study of DMS612, a Novel Bi-functional Alkylating Agent.
Leonard J. Appleman; Sanjeeve Balasubramaniam; Robert A. Parise; Christine Bryla; Christophe E. Redon; Asako J. Nakamura; William M. Bonner; John J. Wright; Richard Piekarz; David R. Kohler; Yixing Jiang; Chandra P. Belani; Julie Eiseman; Edward Chu; Jan H. Beumer; Susan E. Bates
Clin Cancer Res., 2015, [Reviewed] - Systemic DNA damage accumulation under in vivo tumor growth can be inhibited by the antioxidant tempol.
Alexandros G. Georgakilas; Christophe E. Redon; Nicholas F. Ferguson; Thomas B. Kryston; Palak Parekh; Jennifer S. Dickey; Asako J. Nakamura; James B. Mitchell; William M. Bonner; Olga A. Martin
Cancer Lett., 2014, [Reviewed] - Mito-Tempol and Dexrazoxane Exhibit Cardioprotective and Chemotherapeutic Effects through Specific Protein Oxidation and Autophagy in a Syngeneic Breast Tumor Preclinical Model.
•Dickey JS; Gonzalez Y; Aryal B; Mog S; Nakamura AJ; Redon CE; Baxa U; Rosen E; Cheng G; Zielonka J; Parekh P; Mason KP; Joseph J; Kalyanaraman B; Bonner WM; Herman E; Shacter E; Rao VA.
PloS One, 2013, [Reviewed] - Qg-H2AX, an analysis method for partial-body radiation exposure using γ-H2AX in non-human primate lymphocytes.
Redon CE; Nakamura AJ; Gouliaeva K; Rahman A; Blakely WF and Bonner WM.
Radiat. Meas., 2011, [Reviewed] - Hypothermia postpones DNA damage repair in irradiated cells and protects against cell killing.
Jackson-Baird B; Dickey JS; Nakamura AJ; Redon CE; Parekh P; Griko YV; Aziz K; Georgakilas AG; Bonner WM; Sedelnikova OA.
Mutation Res., 2011, [Reviewed] - The use of γ-H2AX as a biodosimeter for total-body radiation exposure – application for acute partial-body exposure dose assessments.
Redon CE; Nakamura AJ; Gouliaeva K; Rahman A; Blakely WF and Bonner WM.
PLoS One, 2010, [Reviewed] - Tumors induce complex DNA damage in proliferative tissues in vivo.
Redon CE; Dickey JS; Nakamura AJ; Kareva IG; Naf D; Nowsheen S; Kalogerinis PK; Bonner WM; Georgakilas AG and Sedelnikova OA.
Proc. Natl. Acad. Sci. U. S. A., 2010, [Reviewed] - The complexity of phosphorylated H2AX foci formation and DNA repair assembly at DNA double-strand breaks.
Nakamura AJ; Rao AV; Pommier Y and Bonner WM., Lead
Cell Cycle, 2010, [Reviewed] - Expression of mutant RPA in human cancer cells causes telomere shortening.
Kobayashi Y; Sato K; Kibe T; Seimiya H; Nakamura A; Yukawa M; Tsuchiya E and Ueno M.
Biosci Biotechnol Biochem., 2010, [Reviewed] - ATM activation by transcription- and topoisomerase I-induced DNA double-strand breaks.
Sordet O; Redon CE; Gourouilh-Barbat J; Smith S; Solier S; Douarre C; Conti C; Nakamura AJ; Das B; Nicolas E; Kohn K; Bonner WM and Pommier Y.
EMBO report, 2009, [Reviewed] - The role of DNA damage response pathways in chromosome fragility in Fragile X syndrome.
Kumari D; Somma V; Nakamura AJ; Bonner WM; D’Ambrosio E and Usdin K.
Nucleic Acids Res., 2009, [Reviewed] - Telomere-dependent and telomere-independent origins of endogenous DNA damage in tumor cells.
Nakamura AJ; Redon CE; Bonner WM and Sedelnikova OA., Lead
Aging, 2009, [Reviewed] - Association of ionizing radiation-induced foci of NBS1 with chromosomal instability and breast cancer susceptibility
Masanori Someya; Koh-ichi Sakata; Hiroshi Tauchi; Yoshihisa Matsumoto; Asako Nakamura; Kenshi Komatsu; Masato Hareyama
RADIATION RESEARCH, Oct. 2006, [Reviewed] - Nbs1 is essential for DNA repair by homologous recombination in higher vertebrate cells
H Tauchi; J Kobayashi; K Morishima; DC van Gent; T Shiraishi; NS Verkaik; D vanHeems; E Ito; A Nakamura; E Sonodo; M Takata; S Takeda; S Matsuura; K Komatsu
NATURE, Nov. 2002, [Reviewed] - NBS1 localizes to gamma-H2AX foci through interaction with the FHA/BRCT domain
J Kobayashi; H Tauchi; S Sakamoto; A Nakamura; K Morishima; S Matsuura; T Kobayashi; K Tamai; K Tanimoto; K Komatsu
CURRENT BIOLOGY, Oct. 2002, [Reviewed] - The forkhead-associated domain of NBS1 is essential for nuclear foci formation after irradiation but not essential for hRAD50 center dot hMRE11 center dot NBS1 complex DNA repair activity
H Tauchi; J Kobayashi; K Morishima; S Matsuura; A Nakamura; T Shiraishi; E Ito; D Masnada; D Delia; K Komatsu
JOURNAL OF BIOLOGICAL CHEMISTRY, Jan. 2001, [Reviewed] - Expression of full-length NBS1 protein restores normal radiation responses in cells from Nijmegen breakage syndrome patients
Atsushi Ito; Hiroshi Tauchi; Junya Kobayashi; Kenichi Morishima; Asako Nakamura; Yutaka Hirokawa; Shinya Matsuura; Katsuhide Ito; Kenshi Komatsu, Academic Press Inc.
Biochemical and Biophysical Research Communications, 30 Nov. 1999, [Reviewed] - Sequence analysis of an 800-kb genomic DNA region on chromosome 8q21 that contains the Nijmegen breakage syndrome gene, NBS1
H Tauchi; S Matsuura; M Isomura; T Kinjo; A Nakamura; S Sakamoto; N Kondo; S Endo; K Komatsu; Y Nakamura
GENOMICS, Jan. 1999, [Reviewed] - Four novel mutations of the Fanconi anemia group A gene (FAA) in Japanese patients
A Nakamura; S Matsuura; H Tauchi; R Hanada; H Ohashi; T Hasegawa; K Honda; M Masuno; K Imaizumi; K Sugita; T Ide; K Komatsu, Lead
JOURNAL OF HUMAN GENETICS, 1999, [Reviewed] - A polymorphic CA repeat marker at the human 27-kD calbindin (CALB1) locus
K Morishima; S Matsuura; H Tauchi; A Nakamura; K Komatsu
JOURNAL OF HUMAN GENETICS, 1999, [Reviewed] - Positional cloning of the gene for Nijmegen breakage syndrome
S Matsuura; H Tauchi; A Nakamura; N Kondo; S Sakamoto; S Endo; D Smeets; B Solder; BH Belohradsky; VMD Kaloustian; M Oshimura; M Isomura; Y Nakamura; K Komatsu
NATURE GENETICS, Jun. 1998, [Reviewed] - Genetic mapping using microcell-mediated chromosome transfer suggests a locus for Nijmegen breakage syndrome at chromosome 8q21-24
S Matsuura; C Weemaes; D Smeets; H Takami; N Kondo; S Sakamoto; N Yano; A Nakamura; H Tauchi; S Endo; M Oshimura; K Komatsu
AMERICAN JOURNAL OF HUMAN GENETICS, Jun. 1997, [Reviewed]
MISC
- Beyond visualization of DNA double-strand breaks after radiation exposure.
Int J Radiat Biol., 27 May 2021, [Reviewed] - Assessment of radiation-induced DNA damage level using phosphorylated H2AX.
中村 麻子
Rad. Biol. Res. Commun., 2012
Lead - Use of the γ-H2AX assay to monitor DNA damage and repair in translational cancer research.
Ivashkevich A; Redon CE; Nakamura AJ; Martin RF; Martin OA.
Cancer Lett., 2012 - Systemic DNA damage related to cancer.
Martin OA; Redon CE; Nakamura AJ; Dickey JS; Georgakilas AG; Bonner WM.
Cancer Res., 2011 - Para-inflammation mediates systemic DNA damage in response to tumor growth.
Martin OA; Redon CE; Dickey JS; Nakamura AJ and Bonner WM.
Commun. Integr. Biol., 2011 - Recent developments in the use of γ-H2AX as a quantitative DNA double-strand break biomarker.
Redon CE; Nakamura AJ; Martin OA; Parekh PR; Weyemi US; Bonner WM.
Aging, 2011 - Histone γ-H2AX and poly(ADP ribose) as clinical pharmacodynamics biomarker.
Redon CE; Nakamura AJ; Zhang Y; Jiz J; Bonner WM; Kinders RJ; Parchments R; Doroshow JH and Pommier Y
Clinical Cancer Res., 2010 - DNA double-strand breakes and ATM activation by transcription-blocking DNA lesions.
Sordet O; Nakamura AJ; Redon CE and Pommier Y.
Cell Cycle, 2010 - H2AX: functional role and potential applications.
Dickey JS; Redon CE; Nakamura AJ; Baird BJ; Bonner WM and Sedelnikova OA.
Chromosoma, 2009 - Where did they come from? The origins of endogenous γ-H2AX foci in tumor cells.
Nakamura AJ; Redon CE and Sedelnikova OA.
Cell Cycle, 2009
Lead - γ-H2AX and cancer.
Bonner WM; Redon CE; Dickey JS; Nakamura AJ; Sedelnikova OA; Solier S; Pommier; Y.
Nature Review Cancer, 2008
Books and other publications
- 知ってるつもりの放射線読本―放射線の基礎知識から、福島第一原発事故による放射線影響、単位㏜の理解まで
福本学, Contributor
三輪書店, 20 Apr. 2023
9784895907774 - 宇宙生命科学の進歩と医学応用への展望,宇宙環境における生物リスク評価のためのDNA損傷検出デバイス
中村麻子・高橋健太, Contributor
医歯薬出版, 06 Nov. 2021 - 放射線医科学の事典: 放射線および紫外線・電磁波・超音波
大西 武雄 (監修); 松本 英樹 (編集); 甲斐 倫明 (編集); 宮川 清 (編集); 柿沼 志津子 (編集); 西村 恭昌 (編集); 近藤 隆 (編集), Contributor
朝倉書店, 05 Dec. 2019
9784254301175 - Methods for the assessment of telomere status.
Single work
Cell Senescence. Methods Mol. Biol., 2013 - γ-H2AX formation and chromatin structure.
Nakamura AJ; Parekh P; martin OA; Bonner WM and Redon CE., Joint work
Advances in Genet. Res., 2012 - H2AX and DNA damage response.
Redon CE; Dickey JS; Nakamura AJ; Sedelnikova OA and Bonner WM., Joint work
Current Cancer Research: Molecular Determinants of Radiation Response, 2011 - γ-H2AX detection peripheral blood lymphocytes, splenocytes, bone marrow, xenografts, and skin.
Redon CE; Nakamura AJ; Sordet O; Dickey JS; Gouliaeva K; Tabb B; Lawrence S; Kinders RJ; Bonner WM and Sedelnikova OA., Joint work
Methods Mol. Biol., 2011 - Stress and γ-H2AX.
Dickey JS; Redon CE; Nakamura AJ; Baird BJ; Sedelnikova OA and Bonner WM., Joint work
Handbook of cell signaling, Regulation of organelle and Cell compartment Signalling., 2010 - Techniques for γ-H2AX detection.
Nakamura A; Sedelnikova OA; Redon C; Pilch DR; Sinogeeva NI; Shroff R; Michael L; and Bonner WM, Joint work
Methods in Enzymology, 2006 - The gene for Nijmegen breakage syndrome and its function in rejoining double-strand break.
中村麻子; 小松賢志, Joint work
共立出版, Jun. 2001
Lectures, oral presentations, etc.
- DNA二本鎖切断レベルのモニタリングを利用したがん治療評価および有害事象リスク予測の将来展望
中村麻子
第34回日本乳癌検診学会学術総会, 29 Nov. 2024, [Invited]
20241129, 20241130 - 植物残渣抽出成分の放射線防護剤としての有用性検討
鈴木 智也; 大泉 昂之; 舟山 知夫; 中村 麻子1
QST高崎サイエンスフェスタ2022, 16 Dec. 2022 - Age dependence of radiation-induced cellular and tissue responses in mouse.
Takashi Oizumi; Rika Shitomi; Yi Shang; Shizuko Kakinuma; Asako J Nakamura
日本放射線影響学会第65回大会, 17 Sep. 2022
20220915, 20220917 - Analysis of the protective effect of Tempol against radiation-induced DNA damage and inflammatory responses in mice.
Masugata Shinya; Megumi Sasatani; Asako J. Nakamura
日本放射線影響学会第65回大会, 16 Sep. 2022
20220915, 20220917 - Evaluation of the radioprotective effect of Sugarcane extract and Hesperetin.
Tomoya Suzuki; Takashi Oizumi; Tomoo Funayama; Asako J. Nakamura
日本放射線影響学会第65回大会, 16 Sep. 2022
20220915, 20220917 - Analysis of the effects of housing in enriched environments on radiation carcinogenesis processes.
Yuri Matsugano; Shinya Yokomizo; Mayumi Nishimura,Takamitsu Morioka,Shizuko Kakinuma,Yoshiya Shimada,Asako J. Nakamura
日本放射線影響学会第65回大会, 16 Sep. 2022
20220915, 20220917 - Development of portable biodosimetry device using PDMS micro-fluidic chip.
Kenta Takahashi; Yuma Chihara; Takayuki Komori; Naohiro Fujisawa; Asako J. Nakamura
日本放射線影響学会第65回大会, 15 Sep. 2022
20220915, 20220917 - DNA二本鎖切断の検出から可視化する放射線の影響
第59回アイソトープ・放射線研究発表会, 07 Jul. 2022, [Invited] - 宇宙環境における生物の健康影響評価のためのDNA損傷検出デバイスと宇宙環境ヘルケアビジネスへの展開
中村麻子
2022年AMO討論会, 10 Jun. 2022, [Invited]
Affiliated academic society
Research Themes
- 光線力学を利用した新規がん診断・治療のためのセラノスティクスシステム開発およびがんリスク制御のための分子基盤確立
Oct. 2023 - Mar. 2028 - 現場における生体内DNA損傷モニタリング手法を用いた放射線がん治療後の有害事象リスク予測システムの構築
Apr. 2020 - Mar. 2021 - 大規模放射線災害に対応できる複数の生物学的指標を組み合わせた線量推定システムの技術基盤構築
放射線健康管理・健康不安対策事業（放射線の健康影響に係る研究調査事業）
Apr. 2018 - Mar. 2021 - 長期的視点に立った放射線に関する科学リテラシー涵養とリスクコミュニケーション人材育成のための小中学校における「目で見る」放射線科学教育の実践研究
放射線健康管理・健康不安対策事業（放射線の健康影響に係る研究調査事業）
Apr. 2020 - 低線量放射線は循環器疾患のリスクを上げるか？低線量率放射線は？放射線関連循環器疾患の機序の解明
放射線健康管理・健康不安対策事業（放射線の健康影響に係る研究調査事業）
Apr. 2016 - Mar. 2019 - Assessment of biological effect of low-dose radiation by phosphorylated H2AX in vivo
Grant-in-Aid for Young Scientists (B)
Apr. 2012 - Mar. 2014 - DNA損傷によるストレスの解剖とストレスの見える化
Social Contribution Activities
- 令和5年度常陸大宮市市民大学講座「DNAのキズが見えると何が分かる？」
lecturer
常陸大宮市, 05 Jul. 2023 - 29 Jul. 2023 - 令和4年度IBARAKIドリームパスAWARD
commentator
18 Feb. 2023 - 茨城県高等学校長協会研修会
lecturer
26 Sep. 2022 - 茨城大学図書館 土曜アカデミー「大学発ベンチャー立ち上げました：DNAのキズの見える化で何ができるか」
lecturer
30 Jul. 2022 - 令和3年度IBARAKIドリームパスAWARD
commentator
30 Jan. 2022 - 高崎市立高崎経済大学附属高等学校 オンライン系統別模擬授業
lecturer
07 Jul. 2021 - 水戸第三高等学校出前授業
lecturer
25 Jun. 2021 - 2020年度IBARAKIドリームパス中間発表会講演
lecturer
20 Dec. 2020 - 紫西グローバルチャレンジII事業 下館第一高等学校 大学実験講座
lecturer
21 Nov. 2020 - 22 Nov. 2020 - 令和2年度茨城高校イバダイ特別講座
lecturer
19 Sep. 2020 - 茨城テックプランター2020キックオフイベント
lecturer
株式会社リバネス, 16 Sep. 2020 - 紫西グローバルチャレンジII事業 下館第一高等学校 大学実験講座
lecturer
07 Sep. 2019 - 08 Sep. 2019 - 緑岡高校出前授業
lecturer
13 Oct. 2016 - 女子高校生サイエンス＆テクノロジー教室
lecturer
03 Sep. 2016 - 土浦第三高等学校出前授業
lecturer
15 Jun. 2016 - 下妻第一高等学校出前授業
lecturer
12 Nov. 2015 - 青少年のための科学の祭典 第6回ひたちなか大会
lecturer
02 Nov. 2014 - 夢ナビライブ学びステーション
advisor
12 Jul. 2014
Academic Contribution Activities
