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149 results on '"Tauchi, Hiroshi"'

1. Establishment and activity of the planning and acting network for low dose radiation research in Japan (PLANET): 2016–2023.

Author

Yamada, Yutaka, Imaoka, Tatsuhiko, Iwasaki, Toshiyasu, Kobayashi, Junya, Misumi, Munechika, Sakai, Kazuo, Sugihara, Takashi, Suzuki, Keiji, Tauchi, Hiroshi, Yasuda, Hiroshi, Yoshinaga, Shinji, Sasatani, Megumi, Tanaka, Satoshi, Doi, Kazutaka, Tomita, Masanori, Iizuka, Daisuke, Kakinuma, Shizuko, Sasaki, Michiya, and Kai, Michiaki

Subjects
RADIATION carcinogenesis, ANIMAL experimentation, SCHEDULING, STEM cells, RADIATION doses
Abstract

The Planning and Acting Network for Low Dose Radiation Research in Japan (PLANET) was established in 2017 in response to the need for an all-Japan network of experts. It serves as an academic platform to propose strategies and facilitate collaboration to improve quantitative estimation of health risks from ionizing radiation at low-doses and low-dose-rates. PLANET established Working Group 1 (Dose-Rate Effects in Animal Experiments) to consolidate findings from animal experiments on dose-rate effects in carcinogenesis. Considering international trends in this field as well as the situation in Japan, PLANET updated its priority research areas for Japanese low-dose radiation research in 2023 to include (i) characterization of low-dose and low-dose-rate radiation risk, (ii) factors to be considered for individualization of radiation risk, (iii) biological mechanisms of low-dose and low-dose-rate radiation effects and (iv) integration of epidemiology and biology. In this context, PLANET established Working Group 2 (Dose and Dose-Rate Mapping for Radiation Risk Studies) to identify the range of doses and dose rates at which observable effects on different endpoints have been reported; Working Group 3 (Species- and Organ-Specific Dose-Rate Effects) to consider the relevance of stem cell dynamics in radiation carcinogenesis of different species and organs; and Working Group 4 (Research Mapping for Radiation-Related Carcinogenesis) to sort out relevant studies, including those on non-mutagenic effects, and to identify priority research areas. These PLANET activities will be used to improve the risk assessment and to contribute to the revision of the next main recommendations of the International Commission on Radiological Protection. [ABSTRACT FROM AUTHOR]

Published
2024
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6. Mechanistic insights into the survival curve of HeLa cells with a short shoulder and their S phase-specific sensitivity.

Author

Komatsu, Kenshi and Tauchi, Hiroshi

Abstract

HeLa cells are a cell line with two unique cellular features: a short-shouldered survival curve and two peaks of radioresistance during the cell cycle phase, while their underlying mechanisms remain unclear. We herein proposed that these radiobiological features are due to a common mechanism by which radiation suppresses homologous recombination repair (HRR) in a dose-dependent manner. This radio-suppression of HRR is mediated by an intra-S checkpoint and reduces survivals of cells in S phase, especially early S phase, resulting in both short shoulder and radioresistance with two peaks in the cell cycle. This new explanation may not be limited to HeLa cells since a similar close association of these features is also observed in other type of cells. [ABSTRACT FROM AUTHOR]

Published
2024
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14. Nbs1 is essential for DNA repair by homologous recombination in higher vertebrate cells

Author

Tauchi, Hiroshi, Kobayashi, Junya, Morishima, Ken-ichi, van Gent, Dik C., Shiraishi, Takahiro, Verkaik, Nicole S., vanHeems, Diana, Ito, Emi, Nakamura, Asako, Sonoda, Eiichiro, Takata, Minoru, Takeda, Shunichi, Matsuura, Shinya, and Komatsu, Kenshi

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): Hiroshi Tauchi (corresponding author) [1]; Junya Kobayashi [2]; Ken-ichi Morishima [2]; Dik C. van Gent [3]; Takahiro Shiraishi [2]; Nicole S. Verkaik [3]; Diana vanHeems [3]; Emi Ito [2]; [...]

Published
2002
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22. Mitotic cells can repair DNA double-strand breaks via a homology-directed pathway.

Author

Sakamoto, Yuki, Kokuta, Tetsuya, Teshigahara, Ai, Iijima, Kenta, Kitao, Hiroyuki, Takata, Minoru, and Tauchi, Hiroshi

Subjects
HOMOLOGY theory, METAPHASE (Mitosis)
Abstract

The choice of repair pathways of DNA double-strand breaks (DSBs) is dependent upon the cell cycle phases. While homologous recombination repair (HRR) is active between the S and G2 phases, its involvement in mitotic DSB repair has not been examined in detail. In the present study, we developed a new reporter assay system to detect homology-directed repair (HDR), a major pathway used for HRR, in combination with an inducible DSB-generation system. As expected, the maximal HDR activity was observed in the late S phase, along with minimal activity in the G1 phase and at the G1/S boundary. Surprisingly, significant HDR activity was observed in M phase, and the repair efficiency was similar to that observed in late S phase. HDR was also confirmed in metaphase cells collected with continuous colcemid exposure. ChIP assays revealed the recruitment of RAD51 to the vicinity of DSBs in M phase. In addition, the ChIP assay for gamma-H2AX and phosphorylated DNA-PKcs indicated that a part of M-phase cells with DSBs could proceed into the next G1 phase. These results provide evidence showing that a portion of mitotic cell DSBs are undoubtedly repaired through action of the HDR repair pathway. [ABSTRACT FROM AUTHOR]

Published
2021
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24. Effects of depletion of dihydropyrimidine dehydrogenase on focus formation and RPA phosphorylation

Author

Someya, Masanori, Sakata, Koh-ichi, Matsumoto, Yoshihisa, Tauchi, Hiroshi, Hareyama, Masato, and et.al

Subjects
enzymes and coenzymes (carbohydrates)
Abstract

Gimeracil, an inhibitor of dihydropyrimidine dehydrogenase (DPYD), partially inhibits homologous recombination (HR) repair and has a radiosensitizing effect as well as enhanced sensitivity to Camptothecin (CPT). DPYD is the target protein for radiosensitization by Gimeracil. We investigated the mechanisms of sensitization of radiation and CPT by DPYD inhibition using DLD-1 cells treated with siRNA for DPYD. We investigated the focus formation of various kinds of proteins involved in HR and examined the phosphorylation of RPA by irradiation using Western blot analysis. DPYD depletion by siRNA significantly restrained the formation of radiation-induced foci of Rad51 and RPA, whereas it increased the number of foci of NBS1. The numbers of colocalization of NBS1 and RPA foci in DPYD-depleted cells after radiation were significantly smaller than in the control cells. These results suggest that DPYD depletion is attributable to decreased single-stranded DNA generated by the Mre11/Rad50/NBS1 complex-dependent resection of DNA double-strand break ends. The phosphorylation of RPA by irradiation was partially suppressed in DPYD-depleted cells, suggesting that DPYD depletion may partially inhibit DNA repair with HR by suppressing phosphorylation of RPA. DPYD depletion showed a radiosensitizing effect as well as enhanced sensitivity to CPT. The radiosensitizing effect of DPYD depletion plus CPT was the additive effect of DPYD depletion and CPT. DPYD depletion did not have a cell-killing effect, suggesting that DPYD depletion may not be so toxic. Considering these results, the combination of CPT and drugs that inhibit DPYD may prove useful for radiotherapy as a method of radiosensitization.

Published
2012

25. Two major factors involved in the reverse dose-rate effect for somatic mutation induction are the cell cycle position and LET value

Author

Tauchi, Hiroshi, Iwata, Yoshiyuki, Komatsu, Kenshi, Furusawa, Yoshiya, Eguchi-Kasai, Kiyomi, Tachibana, Akira, and et.al

Abstract

To study mechanisms which could be involved in the reverse dose rate effect observed during mutation induction after exposure to high LET radiation, synchronized mouse L5178Y cells were exposed to carbon 290 MeV/n beams with different LET values at the G2/M, G1, G1/S or S phases in the cell cycle. The frequency of Hprt-deficient (6-thioguanine-resistant) mutant induction was subsequently determined. The results showed that after exposure to high LET value radiation (50.8 and 76.5 keV/μm), maximum mutation frequencies were seen at the G2/M phase, but after exposure to lower LET radiation (13.3 keV/μm), the highest mutation frequencies were observed at the G1 phase. The higher LET beam always produced higher mutation frequencies in the G2/M phase than in the G1 phase, regardless of radiation dose. These results suggest that cells in the G2/M phase is hyper-sensitive for mutation induction from high LET radiation, but not to mutation induction from low LET radiation. Molecular analysis of mutation spectra showed that large deletions (which could include almost entire exons) of the mouse Hprt gene were most efficiently induced in G2/M cells irradiated with high LET radiation. These entire exon deletions were not as frequent in cells exposed to lower LET radiation. This suggests that inappropriate recombination repair might have occurred in response to condensed damage in condensed chromatin in the G2/M phase. In addition, by using a hyper-sensitive mutation detection system (GM06318-10 cells), a reverse dose-rate effect was clearly observed after exposure to carbon beams with higher LET values (66 keV/μm), but not after exposure to beams with lower LET values (13.3 keV/μm). Thus, G2/M sensitivity towards mutation induction, and the dependence on radiation LET values could both be major factors involved in the reverse dose rate effect produced by high LET radiation.

Published
2009

26. The Japan Radiation Research Society

Author

Kobayashi, Junya, Iwabuchi, Kuniyoshi, Miyagawa, Kiyoshi, Sonoda, Eiichiro, Suzuki, Keiji, Takata, Minoru, and Tauchi, Hiroshi

Subjects
enzymes and coenzymes (carbohydrates), cells, DNA repair, biological phenomena, cell phenomena, and immunity, Homologous recombination, Non-homologous end joining, Nuclear foci
Abstract

DNA double strand break (DSB) is one of the most critical types of damage which is induced by ionizing radiation. In this review, we summarize current progress in investigations on the function of DSB repair-related proteins. We focused on recent findings in the analysis of the function of proteins such as 53BP1, histone H2AX, Mus81-Eme1, Fanc complex, and UBC13, which are found to be related to homologous recombination repair or to non-homologous end joining. In addition to the function of these proteins in DSB repair, the biological function of nuclear foci formation following DSB induction is discussed.

Published
2008

30. Mutations in the FHA-domain of ectopically expressed NBS1 lead to radiosensitization and to no increase in somatic mutation rates via a partial suppression of homologous recombination

Author

Ohara, Maki, primary, Funyu, Yumi, additional, Ebara, Shunsuke, additional, Sakamoto, Yuki, additional, Seki, Ryota, additional, Iijima, Kenta, additional, Ohishi, Akiko, additional, Kobayashi, Junya, additional, Komatsu, Kenshi, additional, Tachibana, Akira, additional, and Tauchi, Hiroshi, additional

Published
2014
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31. This title is unavailable for guests, please login to see more information.

Author

30301302, 70423051, 80124577, Yanagihara, Hiromi, Kobayashi, Junya, Tateishi, Satoshi, Kato, Akihiro, Matsuura, Shinya, Tauchi, Hiroshi, Yamada, Kouichi, Takezawa, Jun, Sugasawa, Kaoru, Masutani, Chikahide, Hanaoka, Fumio, Weemaes, Corry M, Mori, Toshio, Zou, Lee, Komatsu, Kenshi, 30301302, 70423051, 80124577, Yanagihara, Hiromi, Kobayashi, Junya, Tateishi, Satoshi, Kato, Akihiro, Matsuura, Shinya, Tauchi, Hiroshi, Yamada, Kouichi, Takezawa, Jun, Sugasawa, Kaoru, Masutani, Chikahide, Hanaoka, Fumio, Weemaes, Corry M, Mori, Toshio, Zou, Lee, and Komatsu, Kenshi

Published
2011

41. Chk2 Activation Dependence on Nbs1 after DNA Damage

Author

Buscemi, Giacomo, primary, Savio, Camilla, additional, Zannini, Laura, additional, Miccichè, Francesca, additional, Masnada, Debora, additional, Nakanishi, Makoto, additional, Tauchi, Hiroshi, additional, Komatsu, Kenshi, additional, Mizutani, Shuki, additional, Khanna, KumKum, additional, Chen, Phil, additional, Concannon, Patrick, additional, Chessa, Luciana, additional, and Delia, Domenico, additional

Published
2001
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45. Neutron Generator (HIRRAC) and Dosimetry Study.

Author

ENDO, SATORU, primary, HOSHI, MASAHARU, additional, TAKADA, JUN, additional, TAUCHI, HIROSHI, additional, MATSUURA, SHINYA, additional, TAKEOKA, SEIJI, additional, KITAGAWA, KAZUHIDE, additional, SUGA, SHINJI, additional, and KOMATSU, KENSHI, additional

Published
1999
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49. Genetic Mapping Using Microcell-Mediated Chromosome Transfer Suggests a Locus for Nijmegen Breakage Syndrome at Chromosome 8q21-24

Author

Matsuura, Shinya, primary, Weemaes, Corry, additional, Smeets, Dominique, additional, Takami, Hideki, additional, Kondo, Noriko, additional, Sakamoto, Shuuichi, additional, Yano, Nozomi, additional, Nakamura, Asako, additional, Tauchi, Hiroshi, additional, Endo, Satoru, additional, Oshimura, Mitsuo, additional, and Komatsu, Kenshi, additional

Published
1997
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