keyword
MENU ▼
Read by QxMD icon Read
search

53bp1

keyword
https://www.readbyqxmd.com/read/28943310/asf1a-promotes-non-homologous-end-joining-repair-by-facilitating-phosphorylation-of-mdc1-by-atm-at-double-strand-breaks
#1
Kyung Yong Lee, Jun-Sub Im, Etsuko Shibata, Anindya Dutta
Double-strand breaks (DSBs) of DNA in eukaryotic cells are predominantly repaired by non-homologous end joining (NHEJ). The histone chaperone anti-silencing factor 1a (ASF1a) interacts with MDC1 and is recruited to sites of DSBs to facilitate the interaction of phospho-ATM with MDC1 and phosphorylation of MDC1, which are required for the recruitment of RNF8/RNF168 histone ubiquitin ligases. Thus, ASF1a deficiency reduces histone ubiquitination at DSBs, decreasing the recruitment of 53BP1, and decreases NHEJ, rendering cells more sensitive to DSBs...
September 13, 2017: Molecular Cell
https://www.readbyqxmd.com/read/28930533/53bp1-a-guardian-for-centrosomal-integrity
#2
Haeyoung Kim, Hyungshin Yim
53BP1 is known as a mediator in DNA damage response and a regulator of DNA double-stranded breaks (DSBs) repair. 53BP1 was recently reported to be a centrosomal protein and a binding partner of mitotic polo-like kinase 1 (Plk1). The stability of 53BP1, in response to DSBs, is regulated by its phosphorylation, deubiquitination, and ubiquitination. During mitosis, 53BP1 is stabilized by phosphorylation at S380, a putative binding region with polo-box domain of Plk1, and deubiquitination by ubiquitin-specific protease 7 (USP7)...
January 1, 2018: Frontiers in Bioscience (Landmark Edition)
https://www.readbyqxmd.com/read/28919440/structural-insight-into-blm-recognition-by-topbp1
#3
Luxin Sun, Yuhao Huang, Ross A Edwards, Sukmin Yang, Andrew N Blackford, Wojciech Niedzwiedz, J N Mark Glover
Topoisomerase IIβ binding protein 1 (TopBP1) is a critical protein-protein interaction hub in DNA replication checkpoint control. It was proposed that TopBP1 BRCT5 interacts with Bloom syndrome helicase (BLM) to regulate genome stability through either phospho-Ser304 or phospho-Ser338 of BLM. Here we show that TopBP1 BRCT5 specifically interacts with the BLM region surrounding pSer304, not pSer338. Our crystal structure of TopBP1 BRCT4/5 bound to BLM reveals recognition of pSer304 by a conserved pSer-binding pocket, and interactions between an FVPP motif N-terminal to pSer304 and a hydrophobic groove on BRCT5...
September 1, 2017: Structure
https://www.readbyqxmd.com/read/28904335/brca2-suppresses-replication-stress-induced-mitotic-and-g1-abnormalities-through-homologous-recombination
#4
Weiran Feng, Maria Jasin
Mutations in the tumor suppressor BRCA2 predominantly predispose to breast cancer. Paradoxically, while loss of BRCA2 promotes tumor formation, it also causes cell lethality, although how lethality is triggered is unclear. Here, we generate BRCA2 conditional non-transformed human mammary epithelial cell lines using CRISPR-Cas9. Cells are inviable upon BRCA2 loss, which leads to replication stress associated with under replication, causing mitotic abnormalities, 53BP1 nuclear body formation in the ensuing G1 phase, and G1 arrest...
September 13, 2017: Nature Communications
https://www.readbyqxmd.com/read/28879461/perinatal-exposure-to-the-cyanotoxin-%C3%AE-n-m%C3%A3-thylamino-l-alanine-bmaa-results-in-long-lasting-behavioral-changes-in-offspring-potential-involvement-of-dna-damage-and-oxidative-stress
#5
Anthony Laugeray, Asma Oummadi, Clément Jourdain, Justyne Feat, Géraldine Meyer-Dilhet, Arnaud Menuet, Karen Plé, Marion Gay, Sylvain Routier, Stéphane Mortaud, Gilles J Guillemin
We recently demonstrated that perinatal exposure to the glutamate-related herbicide, glufosinate ammonium, has deleterious effects on neural stem cell (NSC) homeostasis within the sub-ventricular zone (SVZ), probably leading to ASD-like symptoms in offspring later in life. In the present study, we aimed to investigate whether perinatal exposure to another glutamate-related toxicant, the cyanobacterial amino acid β-N-methylamino-L-alanine (BMAA), might also trigger neurodevelopmental disturbances. With this aim, female mice were intranasally exposed to low doses of BMAA, 50 mg kg(-1) three times a week from embryonic days 7-10 to postnatal day 21...
September 6, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28875039/nucleolar-and-coiled-body-phosphoprotein-1-nolc1-regulates-the-nucleolar-retention-of-trf2
#6
Fuwen Yuan, Guodong Li, Tanjun Tong
Telomeric repeat-binding factor 2 (TRF2) was reported to localize in the nucleolus of human cells in a cell cycle-dependent manner; however, the underlying mechanism remains unclear. Here, we found that nucleolar and coiled-body phosphoprotein 1 (NOLC1) interacted with TRF2 and mediated the shuttling of TRF2 between the nucleolus and nucleus in human 293T and HepG2 cells. Ablation of NOLC1 expression increased the number of nuclear TRF2 foci and decreased the nucleolar level of TRF2. Conversely, NOLC1 overexpression promoted the nucleolar accumulation of TRF2...
2017: Cell Death Discovery
https://www.readbyqxmd.com/read/28844239/personal-samplers-of-bioavailable-pesticides-integrated-with-a-hair-follicle-assay-of-dna-damage-to-assess-environmental-exposures-and-their-associated-risks-in-children
#7
Pierre-Alexandre Vidi, Kim A Anderson, Haiying Chen, Rebecca Anderson, Naike Salvador-Moreno, Dana C Mora, Carolyn Poutasse, Paul J Laurienti, Stephanie S Daniel, Thomas A Arcury
Agriculture in the United States employs youth ages ten and older in work environments with high pesticide levels. Younger children in rural areas may also be affected by indirect pesticide exposures. The long-term effects of pesticides on health and development are difficult to assess and poorly understood. Yet, epidemiologic studies suggest associations with cancer as well as cognitive deficits. We report a practical and cost-effective approach to assess environmental pesticide exposures and their biological consequences in children...
October 2017: Mutation Research
https://www.readbyqxmd.com/read/28841214/tudor-domain-protein-phf20l1-reads-lysine-methylated-retinoblastoma-tumour-suppressor-protein
#8
Simon M Carr, Shonagh Munro, Cari A Sagum, Oleg Fedorov, Mark T Bedford, Nicholas B La Thangue
The retinoblastoma tumour suppressor protein (pRb) classically functions to regulate early cell cycle progression where it acts to enforce a number of checkpoints in response to cellular stress and DNA damage. Methylation at lysine (K) 810, which occurs within a critical CDK phosphorylation site and antagonises a CDK-dependent phosphorylation event at the neighbouring S807 residue, acts to hold pRb in the hypo-phosphorylated growth-suppressing state. This is mediated in part by the recruitment of the reader protein 53BP1 to di-methylated K810, which allows pRb activity to be effectively integrated with the DNA damage response...
August 25, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28820355/alpha-particles-and-x-rays-interact-in-inducing-dna-damage-in-u2os-cells
#9
Alice Sollazzo, Beata Brzozowska, Lei Cheng, Lovisa Lundholm, Siamak Haghdoost, Harry Scherthan, Andrzej Wojcik
Survivors of the atomic bombings of Hiroshima and Nagasaki are monitored for health effects within the Life Span Study (LSS). The LSS results represent the most important source of data about cancer effects from ionizing radiation exposure, which forms the foundation for the radiation protection system. One uncertainty connected to deriving universal risk factors from these results is related to the problem of mixed radiation qualities. The A-bomb explosions generated a mixed beam of the sparsely ionizing gamma radiation and densely ionizing neutrons...
August 18, 2017: Radiation Research
https://www.readbyqxmd.com/read/28806777/a-synthetic-sickness-screen-for-senescence-re-engagement-targets-in-mutant-cancer-backgrounds
#10
Claire J Cairney, Lauren S Godwin, Alan E Bilsland, Sharon Burns, Katrina H Stevenson, Lynn McGarry, John Revie, Jon D Moore, Ceri M Wiggins, Rebecca S Collinson, Clare Mudd, Elpida Tsonou, Mahito Sadaie, Dorothy C Bennett, Masashi Narita, Christopher J Torrance, W Nicol Keith
Senescence is a universal barrier to immortalisation and tumorigenesis. As such, interest in the use of senescence-induction in a therapeutic context has been gaining momentum in the past few years; however, senescence and immortalisation remain underserved areas for drug discovery owing to a lack of robust senescence inducing agents and an incomplete understanding of the signalling events underlying this complex process. In order to address this issue we undertook a large-scale morphological siRNA screen for inducers of senescence phenotypes in the human melanoma cell line A375P...
August 2017: PLoS Genetics
https://www.readbyqxmd.com/read/28796249/rho-inhibition-by-lovastatin-affects-apoptosis-and-dsb-repair-of-primary-human-lung-cells-in-vitro-and-lung-tissue-in-vivo-following-fractionated-irradiation
#11
Verena Ziegler, Christian Henninger, Ioannis Simiantonakis, Marcel Buchholzer, Mohammad Reza Ahmadian, Wilfried Budach, Gerhard Fritz
Thoracic radiotherapy causes damage of normal lung tissue, which limits the cumulative radiation dose and, hence, confines the anticancer efficacy of radiotherapy and impacts the quality of life of tumor patients. Ras-homologous (Rho) small GTPases regulate multiple stress responses and cell death. Therefore, we investigated whether pharmacological targeting of Rho signaling by the HMG-CoA-reductase inhibitor lovastatin influences ionizing radiation (IR)-induced toxicity in primary human lung fibroblasts, lung epithelial and lung microvascular endothelial cells in vitro and subchronic mouse lung tissue damage following hypo-fractionated irradiation (4x4 Gy)...
August 10, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28781144/regulation-of-repair-pathway-choice-at-two-ended-dna-double-strand-breaks
#12
REVIEW
Atsushi Shibata
A DNA double-strand break (DSB) is considered to be a critical DNA lesion because its misrepair can cause severe mutations, such as deletions or chromosomal translocations. For the precise repair of DSBs, the repair pathway that is optimal for the particular circumstance needs to be selected. Non-homologous end joining (NHEJ) functions in G1/S/G2 phase, while homologous recombination (HR) becomes active only in S/G2 phase after DNA replication. DSB end structure is another factor affecting the repair pathway...
July 29, 2017: Mutation Research
https://www.readbyqxmd.com/read/28753066/a-single-exposure-to-low-or-high-let-radiation-induces-persistent-genomic-damage-in-mouse-epithelial-cells-in-vitro-and-in-lung-tissue
#13
Erica Werner, Ya Wang, Paul W Doetsch
Exposures to low- and high-linear energy transfer (LET) radiation induce clustered damage in DNA that is difficult to repair. These lesions are manifested as DNA-associated foci positive for DNA repair proteins and have been shown to persist in vitro and in vivo for days in several cell types and tissues in response to low-LET radiation. Although in some experimental conditions these residual foci have been linked with genomic instability and chromosomal aberrations, it remains poorly understood what type of damage they represent...
July 28, 2017: Radiation Research
https://www.readbyqxmd.com/read/28751496/nup153-and-nup50-promote-recruitment-of-53bp1-to-dna-repair-foci-by-antagonizing-brca1-dependent-events
#14
Douglas R Mackay, Amanda C Howa, Theresa L Werner, Katharine S Ullman
DNA double strand breaks are typically repaired through either the high-fidelity process of homologous recombination (HR), in which BRCA1 plays a key role, or the more error-prone process of non-homologous end joining (NHEJ), which relies on 53BP1. The balance between NHEJ and HR depends, in part, on whether 53BP1 predominates in binding to damage sites, where it protects the DNA ends from resection. The nucleoporin Nup153 has been implicated in the DNA damage response, attributed to a role in promoting nuclear import of 53BP1...
July 27, 2017: Journal of Cell Science
https://www.readbyqxmd.com/read/28747595/nac-ameliorates-dental-composite-induced-dna-double-strand-breaks-and-chromatin-condensation
#15
Panorea Styllou, Marianthi Styllou, Reinhard Hickel, Christof Högg, Franz Xaver Reichl, Harry Scherthan
Released (co)monomers from dental composite components can induce DNA damage of which DNA double-strand breaks (DSBs) threaten genome integrity. Here, we tested whether the administration of the antioxidant N-acetylcysteine (NAC) is able to reduce the dental composite-induced DSBs in primary human gingiva fibroblasts. The dental composites Bis-GMA (bisphenol-A-glycerolate dimethacrylate), GMA (glycidyl methacrylate), HEMA (2-hydroxyethyl methacrylate) and TEGDMA (triethyleneglycol dimethacrylate) were found to induce co-localizing microscopic nuclear foci numbers of the DSB markers γ-H2AX and 53BP1 per cell in the order: GMA>Bis-GMA>TEGDMA>HEMA...
July 26, 2017: Dental Materials Journal
https://www.readbyqxmd.com/read/28747557/%C3%AE-h2ax-53bp1-and-rad51-protein-foci-changes-in-mesenchymal-stem-cells-during-prolonged-x-ray-irradiation
#16
Anastasia Tsvetkova, Ivan V Ozerov, Margarita Pustovalova, Anna Grekhova, Petr Eremin, Natalia Vorobyeva, Ilya Eremin, Andrey Pulin, Vadim Zorin, Pavel Kopnin, Sergey Leonov, Alex Zhavoronkov, Dmitry Klokov, Andreyan N Osipov
At high exposure levels ionizing radiation is a carcinogen. Little is known about how human stem cells, which are known to contribute to tumorigenesis, respond to prolonged radiation exposures. We studied formation of DNA double strand breaks, accessed as γH2AX and 53BP1 foci, in human mesenchymal stem cells (MSCs) exposed to either acute (5400 mGy/h) or prolonged (270 mGy/h) X-irradiation. We show a linear γH2AX and 53BP1 dose response for acute exposures. In contrast, prolonged exposure resulted in a dose-response curve that had an initial linear portion followed by a plateau...
July 12, 2017: Oncotarget
https://www.readbyqxmd.com/read/28746371/ionizing-radiation-response-of-primary-normal-human-lens-epithelial-cells
#17
Nobuyuki Hamada
Whilst the cataractogenic potential of ionizing radiation has been known for over the past 120 years, little is known about radiation responses of lens cells. Our previous work was the first to evaluate the radiosensitivity of lens cells with the clonogenic assay, documenting that the survival of HLEC1 human lens epithelial cells is comparable to that of WI-38 human lung fibroblasts. Moreover, HLEC1 cells were found to contain subsets where irradiation stimulates proliferation or facilitates formation of abortive colonies with fewer cells than human fibroblasts...
2017: PloS One
https://www.readbyqxmd.com/read/28731465/pr-set7-deficiency-limits-uterine-epithelial-population-growth-hampering-postnatal-gland-formation-in-mice
#18
Tongtong Cui, Bo He, Shuangbo Kong, Chan Zhou, Hangxiao Zhang, Zhangli Ni, Haili Bao, Jingtao Qiu, Qiliang Xin, Danny Reinberg, John P Lydon, Jinhua Lu, Haibin Wang
Formation of secretary endometrial glands in the uterus known as adenogenesis is a typical process of branching morphogenesis involving dynamic epithelial growth and differentiation. Unsuccessful adenogenesis often leads to female infertility. However, it remains largely unexplored so far regarding the epigenetic machinery governing normal endometrial gland formation. Here, we demonstrated that PR-Set7, an epigenetic regulator for H4K20me1 modification, was extensively expressed in the postnatal uteri, and its conditional deletion resulted in a complete lack of endometrial glands and infertility in mice...
July 21, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28716689/brg1-and-smarcal1-transcriptionally-co-regulate-drosha-dgcr8-and-dicer-in-response-to-doxorubicin-induced-dna-damage
#19
Ketki Patne, Radhakrishnan Rakesh, Vijendra Arya, Upasana Bedi Chanana, Ramesh Sethy, Pynskhem Bok Swer, Rohini Muthuswami
Recent investigations have emphasized the role of miRNA biogenesis proteins in the synthesis of non-coding RNA when double-strand DNA breaks are induced by ionizing radiations. However, the role of these non-coding RNA and their regulation in response to doxorubicin-induced DNA damage is not known. In this paper, BRG1 and SMARCAL1, members of the ATP-dependent chromatin remodelling family, are shown to co-regulate the transcription of DROSHA, DGCR8, and DICER in response to double-strand DNA breaks induced by doxorubicin...
July 15, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28700933/inhibition-of-rif1-by-scai-allows-brca1-mediated-repair
#20
Shin-Ya Isobe, Koji Nagao, Naohito Nozaki, Hiroshi Kimura, Chikashi Obuse
DNA double-strand breaks (DSBs) are repaired by either the homology-directed repair (HDR) or the non-homologous end-joining (NHEJ) pathway. RIF1 (RAP1-interacting factor homolog) was recently shown to stimulate NHEJ through an interaction with 53BP1 (p53-binding protein 1) phosphorylated at S/TQ sites, but the molecular mechanism underlying pathway choice remains unclear. Here, we show that SCAI (suppressor of cancer cell invasion) binds to 53BP1 phosphorylated at S/TP sites and facilitates HDR. Upon DNA damage, RIF1 immediately accumulates at damage sites and then gradually dissociates from 53BP1 and is subsequently replaced with SCAI...
July 11, 2017: Cell Reports
keyword
keyword
22934
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"