Article
Biochemistry & Molecular Biology
Lingyu Qiu, Wenchao Xu, Xiaopeng Lu, Feng Chen, Yongcan Chen, Yuan Tian, Qian Zhu, Xiangyu Liu, Yongqing Wang, Xin-Hai Pei, Xingzhi Xu, Jun Zhang, Wei-Guo Zhu
Summary: HDAC6 regulates DNA damage signaling by controlling the mismatch repair and nucleotide excision repair pathways. It negatively regulates DNA double-strand break (DSB) repair in an enzyme activity-independent manner. HDAC6 interacts with H2A/H2A.X to prevent its interaction with the E3 ligase RNF168, and DSBs lead to the degradation of HDAC6 and the restoration of the interaction between RNF168 and H2A/H2A.X, facilitating the recruitment of DSB repair factors to chromatin and subsequent DNA repair.
NUCLEIC ACIDS RESEARCH
(2023)
Article
Biochemistry & Molecular Biology
Chao Dong, Liwei An, Cheng-han Yu, Michael S. Y. Huen
Summary: The DYRK1B kinase plays a crucial role in maintaining rDNA stability, nucleolar reorganization, and inhibition of rRNA synthesis. Inhibition of DYRK1B results in sustained nucleolar transcription, hypersensitivity to DSBs at rDNA arrays, and requirement for DSB repair and rDNA copy number maintenance. These findings highlight the importance of DYRK1B as a key signaling intermediate in coordinating DSB repair and rDNA transcriptional activities within the nucleolus.
NUCLEIC ACIDS RESEARCH
(2021)
Article
Biochemistry & Molecular Biology
Stavroula Tsaridou, Georgia Velimezi, Frances Willenbrock, Maria Chatzifrangkeskou, Waheba Elsayed, Andreas Panagopoulos, Dimitris Karamitros, Vassilis Gorgoulis, Zoi Lygerou, Vassilis Roukos, Eric O'Neill, Dafni Eleftheria Pefani
Summary: This study identified a novel role for the tumor suppressor RASSF1A at rDNA break sites, providing mechanistic insight into how the DNA damage response is organized in a chromatin context and further evidence for how silencing of the RASSF1A tumor suppressor contributes to genome instability.
Article
Cell Biology
Zachary Mirman, Nanda Kumar Sasi, Ashleigh King, J. Ross Chapman, Titia de Lange
Summary: The primary function of the shieldin complex in double-strand break repair in BRCA1-deficient cells is to recruit the CST-Pol alpha-primase complex for fill-in synthesis. The effectiveness of poly(ADP)-ribose polymerase 1 inhibition (PARPi) in BRCA1-deficient cells depends on 53BP1 and shieldin, which limit single-stranded DNA at double-strand breaks through blocking resection and/or fill-in by CST-Pol alpha-primase. CST-Pol alpha-primase promotes radial chromosome formation and BrdU incorporation at DSBs in PARPi-treated BRCA1-deficient cells, and shieldin acts primarily by recruiting CST for radial formation.
NATURE CELL BIOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Xiaopeng Lu, Min Xu, Qian Zhu, Jun Zhang, Ge Liu, Yantao Bao, Luo Gu, Yuan Tian, He Wen, Wei-Guo Zhu
Summary: Histone methyltransferase KMT5A interacts with E3 ligases RNF8 and RNF168 to establish histone modification status for DNA damage repair. KMT5A increases H4K20 monomethylation at DSBs and enhances RNF168's activity in catalyzing H2A ubiquitination, linking the two processes. The interaction between H2A acidic patch and KMT5A residues R188/R189 is crucial for KMT5A-mediated regulation of H2A ubiquitination.
Review
Cell Biology
Bo-Ruei Chen, Barry P. Sleckman
Summary: DNA double-strand breaks (DSBs) are constantly generated and repaired in cells, and the choice of repair pathway (homologous recombination or non-homologous end joining) depends on the structure of the broken DNA ends. Additionally, the chromatin state also affects the DNA end resection process.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2022)
Article
Obstetrics & Gynecology
Wei Le, Fang Zhou, Jun Xiang, Yiming Weng, Denglong Wu, Jun Xu, Jinfu Zhang
Summary: This study reveals the specific mechanism of 53BP1 in the DNA damage repair process of germline stem cells, providing new theoretical basis and insights for the diagnosis and treatment of male infertility.
REPRODUCTIVE SCIENCES
(2023)
Article
Biochemistry & Molecular Biology
Laura Furia, Simone Pelicci, Mirco Scanarini, Pier Giuseppe Pelicci, Mario Faretta
Summary: 53BP1 protein plays an important role in sustaining the activity of the p53-regulated transcriptional program. This study uses an automated-microscopy protocol to analyze the evolution of the DNA-Damage Response (DDR) and demonstrates the movement of 53BP1 protein from damaged sites to the nucleoplasm, where it interacts with p53 and enhances the transcriptional regulation of the guardian of the genome protein.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Biochemistry & Molecular Biology
Linke Tang, Weifeng Yuan, Shitao Li, Xiuyan Ding, Liqian Zhu
Summary: In this study, the interaction between UV-primed global DDR and BoHV-1 productive infection was demonstrated. UV-primed global DDR differentially modulated the transcription of virus genes and stabilization of virus protein. Vice versa, the virus infection may affect UV-primed DDR signaling.
Review
Oncology
Caroline Molinaro, Alain Martoriati, Katia Cailliau
Summary: Cells respond to genotoxic stress through complex protein pathways called DNA damage response (DDR), ensuring genomic integrity and activating processes like DNA repair, cell cycle regulation, and programmed cell death. Alterations in DDR network proteins can lead to various diseases, including cancer. Recent technological advancements have allowed for the exploitation of DDR vulnerabilities to improve cancer treatments through DNA damage strategies and combination therapies.
Article
Oncology
Jianfeng He, Caihu Huang, Yanmin Guo, Rong Deng, Lian Li, Ran Chen, Yanli Wang, Jian Huang, Junke Zheng, Xian Zhao, Jianxiu Yu
Summary: SUMOylated PTEN promotes homologous recombination (HR) repair and represses nonhomologous end joining (NHEJ) repair. It dephosphorylates TP53-binding protein 1 (53BP1) to regulate HR repair. Furthermore, SUMOylated PTEN directly and specifically dephosphorylates a specific site on 53BP1, facilitating DNA end resection and ongoing HR repair.
MOLECULAR ONCOLOGY
(2023)
Article
Cell Biology
Takehiko Usui, Akira Shinohara
Summary: This study reveals that meiotic cells activate Rad53 in response to exogenous DSBs, dependent on histone H3K79 methylation, but Rad9 is insensitive to meiotic programmed DSBs due to its inability to bind to DSBs. Artifical tethering of Rad9 to meiotic DSBs activates Rad53, leading to decreased repair of meiotic DSBs.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Multidisciplinary Sciences
Ines Paniagua, Zainab Tayeh, Mattia Falcone, Santiago Hernandez Perez, Aurora Cerutti, Jacqueline J. L. Jacobs
Summary: MAD2L2, a member of the shieldin complex, protects stalled replication forks from excessive resection. Its loss leads to uncontrolled DNA resection, causing genomic damage. MAD2L2 functions independently of shieldin and cooperates with REV3L and REV1 to promote fork stability.
NATURE COMMUNICATIONS
(2022)
Article
Microbiology
Weiyin Xu, Ping Yan, Ziyan Zhou, Jingting Yao, Haochun Pan, Luyao Jiang, Zongyi Bo, Bo Ni, Mingxia Sun, Song Gao, Changchao Huan
Summary: Pseudorabies virus (PRV) infection in swine can cause high morbidity and mortality, leading to significant economic losses. In this study, the role of histone deacetylase 6 (HDAC6) in PRV infection was investigated. The inhibition of HDAC6 significantly decreased PRV replication, while its overexpression promoted PRV replication. PRV infection induced DNA damage response (DDR), and HDAC6 inhibition and knockout decreased DDR, suggesting that HDAC6 may be a crucial factor in promoting PRV replication.
MICROBIOLOGY SPECTRUM
(2023)
Article
Radiology, Nuclear Medicine & Medical Imaging
S. Schumann, H. Scherthan, K. Pfestroff, S. Schoof, A. Pfestroff, P. Hartrampf, N. Hasenauer, A. K. Buck, M. Luster, M. Port, M. Lassmann, U. Eberlein
Summary: This study provides novel data on ex vivo DSB repair in internally irradiated PBMCs of patients before radionuclide therapy, showing efficient repair occurs after internal irradiation with 50 mGy absorbed dose, and that the induction and repair rate after I-131 exposure is comparable to that of external irradiation with gamma- or X-rays.
EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
(2022)
Article
Biochemistry & Molecular Biology
Ryo Sakasai, Kuniyoshi Iwabuchi
GENES & GENETIC SYSTEMS
(2015)
Editorial Material
Multidisciplinary Sciences
Bennett W. Fox, Randal S. Tibbetts
Article
Biochemistry & Molecular Biology
Sang Hwa Kim, Anthony T. Trinh, Michele Campaigne Larsen, Adam S. Mastrocola, Colin R. Jefcoate, Pierre R. Bushel, Randal S. Tibbetts
NUCLEIC ACIDS RESEARCH
(2016)
Article
Multidisciplinary Sciences
Makoto Iimori, Sugiko Watanabe, Shinichi Kiyonari, Kazuaki Matsuoka, Ryo Sakasai, Hiroshi Saeki, Eiji Oki, Hiroyuki Kitao, Yoshihiko Maehara
NATURE COMMUNICATIONS
(2016)
Article
Biochemistry & Molecular Biology
Sang Hwa Kim, Shannon G. Stiles, Joseph M. Feichtmeier, Nandini Ramesh, Lihong Zhan, Mark A. Scalf, Lloyd M. Smith, Udai Bhan Pandey, Randal S. Tibbetts
HUMAN MOLECULAR GENETICS
(2018)
Article
Oncology
Yumi Sunatani, Radhika Pankaj Kamdar, Mukesh Kumar Sharma, Tadashi Matsui, Ryo Sakasai, Mitsumasa Hashimoto, Yasuhito Ishigaki, Yoshihisa Matsumoto, Kuniyoshi Iwabuchi
EXPERIMENTAL CELL RESEARCH
(2018)
Article
Biochemistry & Molecular Biology
Yusuke Okamoto, Watal M. Iwasaki, Kazuto Kugou, Kazuki K. Takahashi, Arisa Oda, Koichi Sato, Wataru Kobayashi, Hidehiko Kawai, Ryo Sakasai, Akifumi Takaori-Kondo, Takashi Yamamoto, Masato T. Kanemaki, Masato Taoka, Toshiaki Isobe, Hitoshi Kurumizaka, Hideki Innan, Kunihiro Ohta, Masamichi Ishiai, Minoru Takata
NUCLEIC ACIDS RESEARCH
(2018)
Article
Biochemistry & Molecular Biology
Lihong Zhan, Qijing Xie, Randal S. Tibbetts
HUMAN MOLECULAR GENETICS
(2015)
Article
Biochemistry & Molecular Biology
Adam S. Mastrocola, Sang Hwa Kim, Anthony T. Trinh, Lance A. Rodenkirch, Randal S. Tibbetts
JOURNAL OF BIOLOGICAL CHEMISTRY
(2013)
Article
Biochemistry & Molecular Biology
Anthony T. Trinh, Sang Hwa Kim, Hae-yoon Chang, Adam S. Mastrocola, Randal S. Tibbetts
JOURNAL OF BIOLOGICAL CHEMISTRY
(2013)
Article
Biochemistry & Molecular Biology
Yuko Atsumi, Aki Inase, Tomoyuki Osawa, Eiji Sugihara, Ryo Sakasai, Hiroaki Fujimori, Hirobumi Teraoka, Hideyuki Saya, Masamoto Kanno, Fumio Tashiro, Hitoshi Nakagama, Mitsuko Masutani, Ken-ichi Yoshioka
JOURNAL OF BIOLOGICAL CHEMISTRY
(2013)
Article
Multidisciplinary Sciences
Ryo Sakasai, Mayu Isono, Mitsuo Wakasugi, Mitsumasa Hashimoto, Yumi Sunatani, Tadashi Matsui, Atsushi Shibata, Tsukasa Matsunaga, Kuniyoshi Iwabuchi
SCIENTIFIC REPORTS
(2017)
Article
Oncology
Misaki Matsui, Ryo Sakasai, Masako Abe, Yusuke Kimura, Shoki Kajita, Wakana Torii, Yoko Katsuki, Masamichi Ishiai, Kuniyoshi Iwabuchi, Minoru Takata, Ryotaro Nishi
Article
Cell Biology
Teppei Shibata, Masahito Ikawa, Ryo Sakasai, Yasuhito Ishigaki, Etsuko Kiyokawa, Kuniyoshi Iwabuchi, Dhirendra P. Singh, Hiroshi Sasaki, Eri Kubo
Summary: Tpm1 is important for lens development and homeostasis, as its deficiency can lead to lens abnormalities and potentially cataract formation.
MECHANISMS OF AGEING AND DEVELOPMENT
(2021)
Article
Genetics & Heredity
Ryo Sakasai, Mitsuo Wakasugi, Tadashi Matsui, Yumi Sunatani, Masafumi Saijo, Tsukasa Matsunaga, Kuniyoshi Iwabuchi
Summary: This study analyzed the combined effect of CPT and cisplatin or UV and found that CPT suppresses transcription recovery after UV damage and induces the disappearance of the CSB protein. The CSB ubiquitination caused by CPT is regulated differently from the UV response. However, CPT enhances cisplatin or UV sensitivity regardless of TC-NER status. These results suggest that CPT blocks the repair of cisplatin or UV-induced DNA damage through alternative repair pathways.