研究者詳細 - 益谷　央豪

論文 - 益谷　央豪

分割表示 125 件中 1 - 20 件目／全件表示 >>

Novel mechanisms for the removal of strong replication-blocking HMCES- and thiazolidine-DNA adducts in humans. 査読有り

Sugimoto Y, Masuda Y, Iwai S, Miyake Y, Kanao R, Masutani C

Nucleic acids research 2023年4月

RFWD3 and translesion DNA polymerases contribute to PCNA modification-dependent DNA damage tolerance 査読有り

Rie Kanao, Hidehiko Kawai, Toshiyasu Taniguchi, Minoru Takata, Chikahide Masutani

Life Science Alliance 5 巻 ( 12 ) 2022年7月

Regulation of HLTF-mediated PCNA polyubiquitination by RFC and PCNA monoubiquitination levels determines choice of damage tolerance pathway. 査読有り

Masuda Y, Mitsuyuki S, Kanao R, Hishiki A, Hashimoto H, Masutani C

Nucleic acids research 2018年10月

USP7 is a suppressor of PCNA ubiquitination and oxidative-stress-induced mutagenesis in human cells. 査読有り

Kashiwaba, S., Kanao, R., Masuda, Y., Kusumoto-Matsuo, R., Hanaoka, F., Masutani, C.

Cell Reports 13 巻頁： 2072-2080 2015年12月

Different types of interaction between PCNA and PIP boxes contribute to distinct cellular functions of Y-family DNA polymerases 査読有り

Masuda Yuji, Kanao Rie, Kaji Kentaro, Ohmori Haruo, Hanaoka Fumio, Masutani Chikahide

NUCLEIC ACIDS RESEARCH 43 巻 ( 16 ) 頁： 7898 - 7910 2015年9月

担当区分：最終著者,　責任著者記述言語：英語掲載種別：研究論文（学術雑誌）出版者・発行元：Nucleic Acids Research

Translesion DNA synthesis (TLS) by the Y-family DNA polymerases Poln, Poli and Polk, mediated via interaction with proliferating cell nuclear antigen (PCNA), is a crucial pathway that protects human cells against DNA damage. We report that Poln has three PCNA-interacting protein (PIP) boxes (PIP1, 2, 3) that contribute differentially to two distinct functions, stimulation of DNA synthesis and promotion of PCNA ubiquitination. The latter function is strongly associated with formation of nuclear Poln foci, which co-localize with PCNA. We also show that Polk has two functionally distinct PIP boxes, like Poln, whereas Poli has a single PIP box involved in stimulation of DNA synthesis. All three polymerases were additionally stimulated by mono-ubiquitinated PCNA in vitro. The three PIP boxes and a ubiquitinbinding zinc-finger of Poln exert redundant and additive effects in vivo via distinct molecular mechanisms. These findings provide an integrated picture of the orchestration of TLS polymerases.

DOI： 10.1093/nar/gkv712

Web of Science

Scopus

PubMed

Relevance of Simultaneous Mono-Ubiquitinations of Multiple Units of PCNA Homo-Trimers in DNA Damage Tolerance 査読有り国際誌

Kanao Rie, Masuda Yuji, Deguchi Saori, Yumoto-Sugimoto Mayumi, Hanaoka Fumio, Masutani Chikahide

PLOS ONE 10 巻 ( 2 ) 頁： e0118775 2015年2月

担当区分：最終著者,　責任著者記述言語：日本語掲載種別：研究論文（学術雑誌）出版者・発行元：PLoS ONE

DNA damage tolerance (DDT) pathways, including translesion synthesis (TLS) and additional unknown mechanisms, enable recovery from replication arrest at DNA lesions. DDT pathways are regulated by post-translational modifications of proliferating cell nuclear antigen (PCNA) at its K164 residue. In particular, mono-ubiquitination by the ubiquitin ligase RAD18 is crucial for Polη-mediated TLS. Although the importance of modifications of PCNA to DDT pathways is well known, the relevance of its homo-trimer form, in which three K164 residues are present in a single ring, remains to be elucidated. Here, we show that multiple units of a PCNA homo-trimer are simultaneously mono-ubiquitinated in vitro and in vivo. RAD18 catalyzed sequential mono-ubiquitinations of multiple units of a PCNA homo-trimer in a reconstituted system. Exogenous PCNA formed hetero-trimers with endogenous PCNA in WI38VA13 cell transformants. When K164R-mutated PCNA was expressed in these cells at levels that depleted endogenous PCNA homo-trimers, multiple modifications of PCNA complexes were reduced and the cells showed defects in DDT after UV irradiation. Notably, ectopic expression of mutant PCNA increased the UV sensitivities of Polη-proficient, Polη-deficient, and REV1-depleted cells, suggesting the disruption of a DDT pathway distinct from the Polη- and REV1-mediated pathways. These results suggest that simultaneous modifications of multiple units of a PCNA homo-trimer are required for a certain DDT pathway in human cells.

DOI： 10.1371/journal.pone.0118775

Web of Science

Scopus

PubMed

Mechanisms of accurate translesion synthesis by human DNA polymerase h. 査読有り

Masutani, C., Kusumoto, R., Iwai, S., and Hanaoka, F.

EMBO J. 19 巻頁： 3100-3109 2000年

Xeroderma pigmentosum variant (XP-V) correcting protein from HeLa cells has a thymine dimer bypass DNA polymerase activity. 査読有り

Masutani, C., Araki, M., Yamada, A., Kusumoto, R., Nogimori, T., Maekawa, T., Iwai, S., and Hanaoka, F.

EMBO J. 18 巻頁： 3491-3501 1999年

The XPV (xeroderma pigmentosum variant) gene encodes human DNA polymerase h. 査読有り

Masutani, C., Kusumoto, R., Yamada, A., Dohmae, N., Yokoi, M., Yuasa, M., Araki, M., Iwai, S., Takio, K., and Hanaoka, F.

Nature 399 巻頁： 700-704 1999年

Acetaldehyde induces NER repairable mutagenic DNA lesions. 査読有り

Sonohara Y, Takatsuka R, Masutani C, Iwai S, Kuraoka I

Carcinogenesis 2021年9月

Stepwise multipolyubiquitination of p53 by the E6AP-E6 ubiquitin ligase complex 査読有り

Masuda Yuji, Saeki Yasushi, Arai Naoko, Kawai Hidehiko, Kukimoto Iwao, Tanaka Keiji, Masutani Chikahide

JOURNAL OF BIOLOGICAL CHEMISTRY 294 巻 ( 41 ) 頁： 14860 - 14875 2019年10月

Spatiotemporal regulation of PCNA ubiquitination in damage tolerance pathways 査読有り

Masuda Yuji, Masutani Chikahide

CRITICAL REVIEWS IN BIOCHEMISTRY AND MOLECULAR BIOLOGY 54 巻 ( 5 ) 頁： 418 - 442 2019年9月

Preferential digestion of PCNA-ubiquitin and p53-ubiquitin linkages by USP7 to remove polyubiquitin chains from substrates. 査読有り

Masuda Y, Kanao R, Kawai H, Kukimoto I, Masutani C

The Journal of biological chemistry 2019年1月

Regulation of DNA damage tolerance in mammalian cells by post-translational modifications of PCNA 査読有り

Kanao Rie, Masutani Chikahide

MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS 803 巻頁： 82 - 88 2017年10月

Biochemical analysis of HLTF, a human homologue of SWI/SNF-related ubiquitin ligase RAD5

Masuda Yuji, Kanao Rie, Masutani Chikahide

GENES & GENETIC SYSTEMS 91 巻 ( 6 ) 頁： 366 - 366 2016年12月

Stimulation of human DNA polymerase eta by PCNA

Masuda Yuji, Kanao Rie, Masutani Chikahide

GENES & GENETIC SYSTEMS 90 巻 ( 6 ) 頁： 368 - 368 2015年12月

The BAH domain of BAF180 is required for PCNA ubiquitination. 査読有り

Niimi A, Hopkins SR, Downs JA, Masutani C

Mutation Research 779 巻頁： 16-23 2015年6月

UV-induced mutations in epidermal cells of mice defective in DNA polymerase η and/or ι. 査読有り

Kanao R., Yokoi M., Ohkumo T., Sakurai Y., Dotsu K., Kura S., Nakatsu Y., Tsuzuki T., Masutani C., Hanaoka F.

DNA Repair (Amst) 29 巻頁： 139-146 2015年5月

UV-induced mutations in epidermal cells of mice defective in DNA polymerase eta and/or iota

Kanao Rie, Yokoi Masayuki, Ohkumo Tsuyoshi, Sakurai Yasutaka, Dotsu Kantaro, Kura Shinobu, Nakatsu Yoshimichi, Tsuzuki Teruhisa, Masutani Chikahide, Hanaoka Fumio

DNA REPAIR 29 巻頁： 139 - 146 2015年5月

記述言語：日本語掲載種別：研究論文（学術雑誌）出版者・発行元：DNA Repair

Xeroderma pigmentosum variant (XP-V) is a human rare inherited recessive disease, predisposed to sunlight-induced skin cancer, which is caused by deficiency in DNA polymerase η (Polη). Polη catalyzes accurate translesion synthesis (TLS) past pyrimidine dimers, the most prominent UV-induced lesions. DNA polymerase ι (Polι) is a paralog of Polη that has been suggested to participate in TLS past UV-induced lesions, but its function in vivo remains uncertain. We have previously reported that Polη-deficient and Polη/Polι double-deficient mice showed increased susceptibility to UV-induced carcinogenesis. Here, we investigated UV-induced mutation frequencies and spectra in the epidermal cells of Polη- and/or Polι-deficient mice. While Polη-deficient mice showed significantly higher UV-induced mutation frequencies than wild-type mice, Polι deficiency did not influence the frequencies in the presence of Polη. Interestingly, the frequencies in Polη/Polι double-deficient mice were statistically lower than those in Polη-deficient mice, although they were still higher than those of wild-type mice. Sequence analysis revealed that most of the UV-induced mutations in Polη-deficient and Polη/Polι double-deficient mice were base substitutions at dipyrimidine sites. An increase in UV-induced mutations at both G:C and A:T pairs associated with Polη deficiency suggests that Polη contributes to accurate TLS past both thymine- and cytosine-containing dimers in vivo. A significant decrease in G:C to A:T transition in Polη/Polι double-deficient mice when compared with Polη-deficient mice suggests that Polι is involved in error-prone TLS past cytosine-containing dimers when Polη is inactivated.

DOI： 10.1016/j.dnarep.2015.02.006

Web of Science

Scopus

PubMed

Relevance of simultaneous mono-ubiquitnations of multiple units of PCNA homo-trimers in DNA damage tolerance. 査読有り

Kanao R, Masuda Y, Deguchi S, Yumoto-Sugimoto M, Hanaoka F, Masutani C

PLoS One 10 巻 ( 2 ) 頁： e0118775 2015年2月

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