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https://www.readbyqxmd.com/read/29335415/usp48-restrains-resection-by-site-specific-cleavage-of-the-brca1-ubiquitin-mark-from-h2a
#1
Michael Uckelmann, Ruth M Densham, Roy Baas, Herrie H K Winterwerp, Alexander Fish, Titia K Sixma, Joanna R Morris
BRCA1-BARD1-catalyzed ubiquitination of histone H2A is an important regulator of the DNA damage response, priming chromatin for repair by homologous recombination. However, no specific deubiquitinating enzymes (DUBs) are known to antagonize this function. Here we identify ubiquitin specific protease-48 (USP48) as a H2A DUB, specific for the C-terminal BRCA1 ubiquitination site. Detailed biochemical analysis shows that an auxiliary ubiquitin, an additional ubiquitin that itself does not get cleaved, modulates USP48 activity, which has possible implications for its regulation in vivo...
January 15, 2018: Nature Communications
https://www.readbyqxmd.com/read/29328365/nuclear-gsk3%C3%AE-induces-dna-double-strand-break-repair-by-phosphorylating-53bp1-in-glioblastoma
#2
Yong Yang, Tiantian Lei, Suya Du, Rongsheng Tong, Hailian Wang, Jiao Yang, Juan Huang, Minghan Sun, Yi Wang, Zhi Dong
Glioblastoma is the most malignant and lethal subtype brain tumors with high risk of recurrence and therapeutic resistance. Emerging evidence has indicated that glycogen synthesis kinase 3 (GSK3)β plays oncogenic roles in multiple tumor types; however, the underlying mechanisms remain largely unknown. It has also been demonstrated that p53 binding protein 1 (53BP1) plays a central role in DNA double-strand break (DSB) repair. This study aimed to reveal the significance of GSK3β translocation from the cytoplasm to the nucleus, and to determine whether GSK3β induces DNA DSB repair in the nuclei of glioblastoma cells via phospho-53BP1...
January 4, 2018: International Journal of Oncology
https://www.readbyqxmd.com/read/29311308/dna-double-strand-break-response-factors-influence-end-joining-features-of-igh-class-switch-and-general-translocation-junctions
#3
Rohit A Panchakshari, Xuefei Zhang, Vipul Kumar, Zhou Du, Pei-Chi Wei, Jennifer Kao, Junchao Dong, Frederick W Alt
Ig heavy chain (IgH) class switch recombination (CSR) in B lymphocytes switches IgH constant regions to change antibody functions. CSR is initiated by DNA double-strand breaks (DSBs) within a donor IgH switch (S) region and a downstream acceptor S region. CSR is completed by fusing donor and acceptor S region DSB ends by classical nonhomologous end-joining (C-NHEJ) and, in its absence, by alternative end-joining that is more biased to use longer junctional microhomologies (MHs). Deficiency for DSB response (DSBR) factors, including ataxia telangiectasia-mutated (ATM) and 53BP1, variably impair CSR end-joining, with 53BP1 deficiency having the greatest impact...
January 8, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29309426/gadolinium-enhanced-cardiac-mr-exams-of-human-subjects-are-associated-with-significant-increases-in-the-dna-repair-marker-53bp1-but-not-the-damage-marker-%C3%AE-h2ax
#4
Jennifer S McDonald, Robert J McDonald, Jacob B Ekins, Anthony S Tin, Sylvain Costes, Tamara M Hudson, Dana J Schroeder, Kevin Kallmes, Scott H Kaufmann, Philip M Young, Aiming Lu, Ramanathan Kadirvel, David F Kallmes
Magnetic resonance imaging is considered low risk, yet recent studies have raised a concern of potential damage to DNA in peripheral blood leukocytes. This prospective Institutional Review Board-approved study examined potential double-strand DNA damage by analyzing changes in the DNA damage and repair markers γH2AX and 53BP1 in patients who underwent a 1.5 T gadolinium-enhanced cardiac magnetic resonance (MR) exam. Sixty patients were enrolled (median age 55 years, 39 males). Patients with history of malignancy or who were receiving chemotherapy, radiation therapy, or steroids were excluded...
2018: PloS One
https://www.readbyqxmd.com/read/29301856/rad9-53bp1-protects-stalled-replication-forks-from-degradation-in-mec1-atr-defective-cells
#5
Matteo Villa, Diego Bonetti, Massimo Carraro, Maria Pia Longhese
Nucleolytic processing by nucleases can be a relevant mechanism to allow repair/restart of stalled replication forks. However, nuclease action needs to be controlled to prevent overprocessing of damaged replication forks that can be detrimental to genome stability. The checkpoint protein Rad9/53BP1 is known to limit nucleolytic degradation (resection) of DNA double-strand breaks (DSBs) in both yeast and mammals. Here, we show that loss of the inhibition that Rad9 exerts on resection exacerbates the sensitivity to replication stress of Mec1/ATR-defective yeast cells by exposing stalled replication forks to Dna2-dependent degradation...
January 4, 2018: EMBO Reports
https://www.readbyqxmd.com/read/29282803/hair-follicle-stem-cell-faith-is-dependent-on-chromatin-remodeling-capacity-following-low-dose-radiation
#6
Nadine Schuler, Sara Timm, Claudia E Rübe
The main function of the skin, to protect against the environment, is supported by the activity of different stem cell populations. The main focus of this study was elucidating the coping mechanisms of stem cells against the stimulation of constant exposure to genotoxic stresses, both endogenous and exogenous, to ensure long-term function. Investigation of various mouse strains, differing in their DNA repair capacity, enables us to clarify fractionated low-dose irradiation (LDR)-induced consequences for different stem cell populations of the murine hair follicle in their physiological stem cell niche...
December 28, 2017: Stem Cells
https://www.readbyqxmd.com/read/29274141/acquired-resistance-of-pten-deficient-cells-to-parp-inhibitor-and-ara-c-mediated-by-53bp1-loss-and-samhd1-overexpression
#7
Yu-Ting Wang, Bo Yuan, Hua-Dong Chen, Lin Xu, Yu-Nan Tian, Ao Zhang, Jin-Xue He, Ze-Hong Miao
With increasing uses of PARP inhibitors (PARPis) for cancer therapy, understanding their resistance is becoming urgent. However, acquired PARPi resistance in the PTEN-deficient background is poorly understood. We generated 3 PARPi-resistant PTEN-deficient glioblastoma U251 variants separately with olaparib (U251/OP), talazoparib (U251/TP) and simmiparib (U251/SP). These variants displayed consistent resistance (2.46~71.78-fold) to all 5 PARPis including niraparib and rucaparib and showed higher degrees of resistance to the PARPis to which the parental cells were more sensitive...
December 22, 2017: Cancer Science
https://www.readbyqxmd.com/read/29243734/chemically-synthesized-histone-h2a-lys13-di-ubiquitination-promotes-binding-of-53bp1-to-nucleosomes
#8
Jia-Bin Li, Yun-Kun Qi, Qiao-Qiao He, Hua-Song Ai, San-Ling Liu, Jia-Xing Wang, Ji-Shen Zheng, Lei Liu, Changlin Tian
No abstract text is available yet for this article.
December 15, 2017: Cell Research
https://www.readbyqxmd.com/read/29233925/a20-regulates-the-dna-damage-response-and-mediates-tumor-cell-resistance-to-dna-damaging-therapy
#9
Chuanzhen Yang, Weicheng Zang, Zefang Tang, Yapeng Ji, Ruidan Xu, Yongfeng Yang, Aiping Luo, Bin Hu, Zemin Zhang, Zhihua Liu, Xiaofeng Zheng
A competent DNA damage response (DDR) helps prevent cancer, but once cancer has arisen DDR can blunt the efficacy of chemotherapy and radiotherapy which cause lethal DNA breakage in cancer cells. Thus, blocking DDR may improve the efficacy of these modalities. Here we report a new DDR mechanism that interfaces with inflammatory signaling and might be blocked to improve anticancer outcomes. Specifically, we report that the ubiquitin-editing enzyme A20 binds and inhibits the E3 ubiquitin ligase RNF168, which is responsible for regulating histone H2A turnover critical for proper DNA repair...
December 12, 2017: Cancer Research
https://www.readbyqxmd.com/read/29216538/tip60-contributes-to-porcine-embryonic-development-by-regulating-dna-damage-response
#10
Jing Guo, Wenjun Zhou, Ying-Jie Niu, Kyung-Tae Shin, Young Tae Heo, Nam-Hyung Kim, Xiang-Shun Cui
The acetyltransferase TIP60 (also known as Kat5) is a member of the MYST family of histone acetyltransferases and was initially identified as a cellular protein. TIP60 acetylates histone and non-histone proteins and is involved in diverse biological processes, including apoptosis, cell cycle, and DNA damage responses. In this study, a specific inhibitor of TIP60 was used to detect the function of TIP60 in porcine parthenogenetic embryos. The results showed that TIP60 inhibition impaired porcine parthenogenetic embryonic development...
December 2, 2017: Theriogenology
https://www.readbyqxmd.com/read/29212152/prpf8-is-important-for-brca1-mediated-homologous-recombination
#11
David O Onyango, Gabriella Lee, Jeremy M Stark
Disruption of RNA splicing causes genome instability, which could contribute to cancer etiology. Furthermore, RNA splicing is an emerging anti-cancer target. Thus, we have evaluated the influence of the spliceosome factor PRPF8 and the splicing inhibitor Pladienolide B (PlaB) on homologous recombination (HR). We find that PRPF8 depletion and PlaB treatment cause a specific defect in homology-directed repair (HDR), and single strand annealing (SSA), which share end resection as a common intermediate, and BRCA1 as a required factor...
November 7, 2017: Oncotarget
https://www.readbyqxmd.com/read/29207170/bmi-1-suppression-increases-the-radiosensitivity-of-oesophageal-carcinoma-via-the-pi3k-akt-signaling-pathway
#12
Xing-Xiao Yang, Ming Ma, Mei-Xiang Sang, Xue-Yuan Zhang, Zhi-Kun Liu, Heng Song, Shu-Chai Zhu
B-cell‑specific Moloney murine leukaemia virus integration site-1 (BMI-1) contributes to the growth of tumour cells post-irradiation (IR). The aim of the present study was to characterize the effects of BMI-1 on cell viability, radiosensitivity and its mechanisms of action in oesophageal squamous cell cancer (ESCC). Western blotting and immunohistochemistry were employed to evaluate the protein expression of BMI-1 in ESCC cells and specimens, respectively. Additionally, the protein expression levels of BMI-1, H2AK119ub and γH2AX in ESCC cells were detected following different doses of IR and at different times after IR...
December 5, 2017: Oncology Reports
https://www.readbyqxmd.com/read/29206178/around-and-beyond-53bp1-nuclear-bodies
#13
REVIEW
Anne Fernandez-Vidal, Julien Vignard, Gladys Mirey
Within the nucleus, sub-nuclear domains define territories where specific functions occur. Nuclear bodies (NBs) are dynamic structures that concentrate nuclear factors and that can be observed microscopically. Recently, NBs containing the p53 binding protein 1 (53BP1), a key component of the DNA damage response, were defined. Interestingly, 53BP1 NBs are visualized during G1 phase, in daughter cells, while DNA damage was generated in mother cells and not properly processed. Unlike most NBs involved in transcriptional processes, replication has proven to be key for 53BP1 NBs, with replication stress leading to the formation of these large chromatin domains in daughter cells...
December 5, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29203878/atm-and-cdk2-control-chromatin-remodeler-csb-to-inhibit-rif1-in-dsb-repair-pathway-choice
#14
Nicole L Batenburg, John R Walker, Sylvie M Noordermeer, Nathalie Moatti, Daniel Durocher, Xu-Dong Zhu
CSB, a member of the SWI2/SNF2 superfamily, is implicated in DNA double-strand break (DSB) repair. However, how it regulates this repair process is poorly understood. Here we uncover that CSB interacts via its newly identified winged helix domain with RIF1, an effector of 53BP1, and that this interaction mediates CSB recruitment to DSBs in S phase. At DSBs, CSB remodels chromatin by evicting histones, which limits RIF1 and its effector MAD2L2 but promotes BRCA1 accumulation. The chromatin remodeling activity of CSB requires not only damage-induced phosphorylation on S10 by ATM but also cell cycle-dependent phosphorylation on S158 by cyclin A-CDK2...
December 4, 2017: Nature Communications
https://www.readbyqxmd.com/read/29196784/parp1-protects-from-benzo-a-pyrene-diol-epoxide-induced-replication-stress-and-mutagenicity
#15
Jan M F Fischer, Tabea Zubel, Kirsten Jander, Jelena Fix, Irmela R E A Trussina, Daniel Gebhard, Jörg Bergemann, Alexander Bürkle, Aswin Mangerich
Poly(ADP-ribosyl)ation (PARylation) is a complex and reversible posttranslational modification catalyzed by poly(ADP-ribose)polymerases (PARPs), which orchestrates protein function and subcellular localization. The function of PARP1 in genotoxic stress response upon induction of oxidative DNA lesions and strand breaks is firmly established, but its role in the response to chemical-induced, bulky DNA adducts is understood incompletely. To address the role of PARP1 in the response to bulky DNA adducts, we treated human cancer cells with benzo[a]pyrene 7,8-dihydrodiol-9,10-epoxide (BPDE), which represents the active metabolite of the environmental carcinogen benzo[a]pyrene [B(a)P], in nanomolar to low micromolar concentrations...
December 1, 2017: Archives of Toxicology
https://www.readbyqxmd.com/read/29190394/acetylation-of-53bp1-dictates-the-dna-double-strand-break-repair-pathway
#16
Xiang Guo, Yongtai Bai, Meimei Zhao, Mei Zhou, Qinjian Shen, Cai-Hong Yun, Hongquan Zhang, Wei-Guo Zhu, Jiadong Wang
P53-binding protein 1 (53BP1) plays critical roles in DNA double strand break (DSB) repair by promoting non-homologous end joining (NHEJ), and loss of 53BP1 abolishes PARPi sensitivity in BRCA1-deficient cells by restoring homologous recombination (HR). 53BP1 is one of the proteins initially recruited to sites of DSBs via recognition of H4K20me2 through the Tudor-UDR domain and H2AK15ub through the UDR motif. Although extensive studies have been conducted, it remains unclear how the post-translational modification of 53BP1 affects DSB repair pathway choice...
November 28, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/29180822/damage-induced-lncrnas-control-the-dna-damage-response-through-interaction-with-ddrnas-at-individual-double-strand-breaks
#17
Flavia Michelini, Sethuramasundaram Pitchiaya, Valerio Vitelli, Sheetal Sharma, Ubaldo Gioia, Fabio Pessina, Matteo Cabrini, Yejun Wang, Ilaria Capozzo, Fabio Iannelli, Valentina Matti, Sofia Francia, G V Shivashankar, Nils G Walter, Fabrizio d'Adda di Fagagna
The DNA damage response (DDR) preserves genomic integrity. Small non-coding RNAs termed DDRNAs are generated at DNA double-strand breaks (DSBs) and are critical for DDR activation. Here we show that active DDRNAs specifically localize to their damaged homologous genomic sites in a transcription-dependent manner. Following DNA damage, RNA polymerase II (RNAPII) binds to the MRE11-RAD50-NBS1 complex, is recruited to DSBs and synthesizes damage-induced long non-coding RNAs (dilncRNAs) from and towards DNA ends...
December 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/29176614/inhibition-of-53bp1-favors-homology-dependent-dna-repair-and-increases-crispr-cas9-genome-editing-efficiency
#18
Marella D Canny, Nathalie Moatti, Leo C K Wan, Amélie Fradet-Turcotte, Danielle Krasner, Pedro A Mateos-Gomez, Michal Zimmermann, Alexandre Orthwein, Yu-Chi Juang, Wei Zhang, Sylvie M Noordermeer, Eduardo Seclen, Marcus D Wilson, Andrew Vorobyov, Meagan Munro, Andreas Ernst, Timothy F Ng, Tiffany Cho, Paula M Cannon, Sachdev S Sidhu, Frank Sicheri, Daniel Durocher
Programmable nucleases, such as Cas9, are used for precise genome editing by homology-dependent repair (HDR). However, HDR efficiency is constrained by competition from other double-strand break (DSB) repair pathways, including non-homologous end-joining (NHEJ). We report the discovery of a genetically encoded inhibitor of 53BP1 that increases the efficiency of HDR-dependent genome editing in human and mouse cells. 53BP1 is a key regulator of DSB repair pathway choice in eukaryotic cells and functions to favor NHEJ over HDR by suppressing end resection, which is the rate-limiting step in the initiation of HDR...
November 27, 2017: Nature Biotechnology
https://www.readbyqxmd.com/read/29167269/ring-finger-protein-126-rnf126-suppresses-ionizing-radiation-induced-p53-binding-protein-1-53bp1-foci-formation
#19
Nam Soo Lee, Hae Ryung Chang, Soomi Kim, Jae-Hoon Ji, Joorak Lee, Hyun Ji Lee, Yoojeong Seo, Misun Kang, Joo Seok Han, Kyungjae Myung, Yonghwan Kim, Hongtae Kim
Cells have evolved sophisticated mechanisms to maintain genomic integrity in response to DNA damage. Ionizing radiation (IR) induced DNA damage results in the formation of IR induced foci (iRIF) in the nucleus. The iRIF formation is part of the DNA damage response (DDR), which is an essential signaling cascade that must be strictly regulated because either the loss of or an augmented DDR leads to loss of genome integrity. Accordingly, negative regulation of the DDR is as critical as its activation. In this study, we have identified ring finger protein 126 (RNF126) as a negative regulator of the DDR from a screen of iRIF containing 53BP1...
November 22, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29161537/association-of-h3k79-monomethylation-an-epigenetic-signature-with-arsenic-induced-skin-lesions
#20
Pritha Bhattacharjee, Somnath Paul, Sandip Bhattacharjee, Ashok K Giri, Pritha Bhattacharjee
Arsenic, a non mutagenic carcinogen, poses a profound health risk upon prolonged exposure. The objective of the study was to analyze the post-translational modifications of the major histone H3 and the associated molecular crosstalk to identify the epigenetic signature of arsenic susceptibility. Herein, we identified significant upregulation of H3K79me1, in individuals with arsenic-induced skin lesion (WSL), and H3K79me1 was found to be regulated by the upstream methyltransferase DOT1L. Moreover, the downstream target molecule 53BP1, a tumor suppressor protein that has a docking preference for H3K79me1 at a site of a double-strand break (DSB), was downregulated, indicating greater DNA damage in the WSL group...
November 14, 2017: Mutation Research
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