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https://www.readbyqxmd.com/read/28732309/zebularine-induces-replication-dependent-double-strand-breaks-which-are-preferentially-repaired-by-homologous-recombination
#1
Manuel Luis Orta, Nuria Pastor, Estefanía Burgos-Morón, Inmaculada Domínguez, José Manuel Calderón-Montaño, Carlos Huertas Castaño, Miguel López-Lázaro, Thomas Helleday, Santiago Mateos
Zebularine is a second-generation, highly stable hydrophilic inhibitor of DNA methylation with oral bioavailability that preferentially target cancer cells. It acts primarily as a trap for DNA methyl transferases (DNMTs) protein by forming covalent complexes between DNMT protein and zebularine-substrate DNA. It's well documented that replication-blocking DNA lesions can cause replication fork collapse and thereby to the formation of DNA double-strand breaks (DSB). DSB are dangerous lesions that can lead to potentially oncogenic genomic rearrangements or cell death...
July 12, 2017: DNA Repair
https://www.readbyqxmd.com/read/28729862/rad51-interacts-with-non-structural-3-protein-of-hepatitis-c-virus-and-regulates-viral-production
#2
Kidong Son, Tram T T Nguyen, Jae-Woong Choi, Long V Pham, Trang T D Luong, Yun-Sook Lim, Soon B Hwang
Hepatitis C virus (HCV) is a leading cause of chronic liver disease affecting over 170 million people worldwide. Chronic infection with HCV progresses to liver fibrosis, cirrhosis, and hepatocellular carcinoma. HCV exploits host cellular factors for viral propagation. To investigate the cellular factors required for HCV propagation, we screened a siRNA library targeting human cell cycle genes using cell culture grown HCV-infected cells. In the present study, we selected and characterized a gene encoding Rad51...
2017: Frontiers in Microbiology
https://www.readbyqxmd.com/read/28729543/evaluation-of-atm-heterozygous-mutations-underlying-individual-differences-in-radiosensitivity-using-genome-editing-in-human-cultured-cells
#3
Ekaterina Royba, Tatsuo Miyamoto, Silvia Natsuko Akutsu, Kosuke Hosoba, Hiroshi Tauchi, Yoshiki Kudo, Satoshi Tashiro, Takashi Yamamoto, Shinya Matsuura
Ionizing radiation (IR) induces DNA double-strand breaks (DSBs), which are an initial step towards chromosomal aberrations and cell death. It has been suggested that there are individual differences in radiosensitivity within human populations, and that the variations in DNA repair genes might determine this heterogeneity. However, it is difficult to quantify the effect of genetic variants on the individual differences in radiosensitivity, since confounding factors such as smoking and the diverse genetic backgrounds within human populations affect radiosensitivity...
July 20, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28729231/cernunnos-deficiency-associated-with-bcg-adenitis-and-autoimmunity-first-case-from-the-national-iranian-registry-and-review-of-the-literature
#4
Reza Yazdani, Hassan Abolhassani, Javad Tafaroji, Gholamreza Azizi, Raif S Geha, Asghar Aghamohammadi
Non-homologous end-joining (NHEJ) is a pathway that repairs double-strand breaks (DSB) in DNA and plays a vital role in V(D)J recombination of immunoglobulin genes. Cernunnos is a DNA repair factor that is involved in nonhomologous end-joining (NHEJ) process. Impairment in Cernunnos leads to a genetic disease characterized by neural disorders, immunodeficiency and increased radiosensitivity. We herein describe a severe combined immunodeficiency (SCID) patient with T- B+ phenotype who had a mutation in Cernunnos gene and manifested recurrent infections, microcephaly and growth retardation with hypogammaglobulinemia...
July 17, 2017: Clinical Immunology: the Official Journal of the Clinical Immunology Society
https://www.readbyqxmd.com/read/28727736/persistent-damaged-bases-in-dna-allow-mutagenic-break-repair-in-escherichia-coli
#5
Jessica M Moore, Raul Correa, Susan M Rosenberg, P J Hastings
Bacteria, yeast and human cancer cells possess mechanisms of mutagenesis upregulated by stress responses. Stress-inducible mutagenesis potentially accelerates adaptation, and may provide important models for mutagenesis that drives cancers, host pathogen interactions, antibiotic resistance and possibly much of evolution generally. In Escherichia coli repair of double-strand breaks (DSBs) becomes mutagenic, using low-fidelity DNA polymerases under the control of the SOS DNA-damage response and RpoS general stress response, which upregulate and allow the action of error-prone DNA polymerases IV (DinB), II and V to make mutations during repair...
July 20, 2017: PLoS Genetics
https://www.readbyqxmd.com/read/28725235/gateway-compatible-crispr-cas9-vectors-and-a-rapid-detection-by-high-resolution-melting-curve-analysis
#6
Cynthia J Denbow, Samantha Lapins, Nick Dietz, Raelynn Scherer, Zachary L Nimchuk, Sakiko Okumoto
CRISPR-Cas9 system rapidly became an indispensable tool in plant biology to perform targeted mutagenesis. A CRISPR-Cas9-mediated double strand break followed by non-homologous end joining (NHEJ) repair most frequently results in a single base pair deletion or insertions (indels), which is hard to detect using methods based on enzymes that detect heteroduplex DNA. In addition, somatic tissues of the T1 generation inevitably contain a mosaic population, in which the portion of cells carrying the mutation can be too small to be detected by the enzyme-based methods...
2017: Frontiers in Plant Science
https://www.readbyqxmd.com/read/28724724/brct-domain-protein-brit1-influences-class-switch-recombination
#7
Wei-Feng Yen, Ashutosh Chaudhry, Bharat Vaidyanathan, William T Yewdell, Joseph N Pucella, Rahul Sharma, Yulong Liang, Kaiyi Li, Alexander Y Rudensky, Jayanta Chaudhuri
DNA double-strand breaks (DSBs) serve as obligatory intermediates for Ig heavy chain (Igh) class switch recombination (CSR). The mechanisms by which DSBs are resolved to promote long-range DNA end-joining while suppressing genomic instability inherently associated with DSBs are yet to be fully elucidated. Here, we use a targeted short-hairpin RNA screen in a B-cell lymphoma line to identify the BRCT-domain protein BRIT1 as an effector of CSR. We show that conditional genetic deletion of BRIT1 in mice leads to a marked increase in unrepaired Igh breaks and a significant reduction in CSR in ex vivo activated splenic B cells...
July 19, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28723680/meiotic-recombination-in-the-giraffe-g-reticulata
#8
Miluse Vozdova, Jan Fröhlich, Svatava Kubickova, Hana Sebestova, Jiri Rubes
Recently, the reticulated giraffe (G. reticulata) was identified as a distinct species, which emphasized the need for intensive research in this interesting animal. To shed light on the meiotic process as a source of biodiversity, we analysed the frequency and distribution of meiotic recombination in 2 reticulated giraffe males. We used immunofluorescence detection of synaptonemal complex protein (SYCP3), meiotic double strand breaks (DSB, marked as RAD51 foci) in leptonema, and crossovers (COs, as MLH1 foci) in pachynema...
July 20, 2017: Cytogenetic and Genome Research
https://www.readbyqxmd.com/read/28722656/corrupting-the-dna-damage-response-a-critical-role-for-rad52-in-tumor-cell-survival
#9
Rachel Lieberman, Ming You
The DNA damage response enables cells to survive, maintain genome integrity, and to safeguard the transmission of high-fidelity genetic information. Upon sensing DNA damage, cells respond by activating this multi-faceted DNA damage response leading to restoration of the cell, senescence, programmed cell death, or genomic instability if the cell survives without proper repair. However, unlike normal cells, cancer cells maintain a marked level of genomic instability. Because of this enhanced propensity to accumulate DNA damage, tumor cells rely on homologous recombination repair as a means of protection from the lethal effect of both spontaneous and therapy-induced double-strand breaks (DSBs) in DNA...
July 15, 2017: Aging
https://www.readbyqxmd.com/read/28721947/removal-of-scatter-radiation-in-paediatric-cardiac-catheterisation-a-randomised-controlled-clinical-trial
#10
Richard Gould, Sonyia L McFadden, Andrew J Sands, Brian A McCrossan, Simon Horn, Kevin M Prise, Philip Doyle, Ciara M Hughes
This study sought to determine if DNA integrity was compromised by ionising radiation from paediatric cardiac catheterisations and if dose optimisation techniques allowed DNA integrity to be maintained. Materials and Methods: Children were imaged using either: (i) an anti-scatter grid (current departmental protocol), (ii) no anti-scatter grid or, (iii) no anti-scatter grid and a 15 cm air-gap between the child and the X-ray detector. Dose area product and image quality were assessed, lifetime attributable cancer risk estimates were calculated and DNA double-strand breakages quantified using the γH2AX assay...
July 19, 2017: Journal of Radiological Protection: Official Journal of the Society for Radiological Protection
https://www.readbyqxmd.com/read/28718816/complex-dna-damage-a-route-to-radiation-induced-genomic-instability-and-carcinogenesis
#11
REVIEW
Ifigeneia V Mavragani, Zacharenia Nikitaki, Maria P Souli, Asef Aziz, Somaira Nowsheen, Khaled Aziz, Emmy Rogakou, Alexandros G Georgakilas
Cellular effects of ionizing radiation (IR) are of great variety and level, but they are mainly damaging since radiation can perturb all important components of the cell, from the membrane to the nucleus, due to alteration of different biological molecules ranging from lipids to proteins or DNA. Regarding DNA damage, which is the main focus of this review, as well as its repair, all current knowledge indicates that IR-induced DNA damage is always more complex than the corresponding endogenous damage resulting from endogenous oxidative stress...
July 18, 2017: Cancers
https://www.readbyqxmd.com/read/28718433/mitotic-dna-damage-response-at-the-crossroads-of-structural-and-numerical-cancer-chromosome-instabilities
#12
REVIEW
Samuel F Bakhoum, Lilian Kabeche, Duane A Compton, Simon N Powell, Holger Bastians
DNA double-strand breaks (DSBs) prevent cells from entering mitosis allowing cells to repair their genomic damage. Little is known about the response to DSBs once cells have already committed to mitosis. Here, we review the genome-protective role of the mitotic DNA damage response (DDR) and evidence suggesting that its untimely activation induces chromosome segregation errors and paradoxically undermines genomic integrity. In contrast to normal cells, cancer cells coopt this pathway to propagate structural and numerical chromosomal instabilities...
March 2017: Trends in Cancer
https://www.readbyqxmd.com/read/28717992/melting-of-polymeric-dna-double-helix-at-elevated-temperature-a-molecular-dynamics-approach
#13
Sangeeta Kundu, Sanchita Mukherjee, Dhananjay Bhattacharyya
Genomic DNA of higher organisms exists as extremely long polymers, while in bacteria and other lower organisms it is circular with no terminal base pairs. Temperature-induced melting of the DNA double helix by localized strand separation has been unattainable by molecular dynamic simulations due to more rapid fraying of the terminal base pairs in oligomeric DNA. However, local-sequence-dependent unfolding of the DNA double helix is extremely important for understanding various biochemical phenomena, and can be addressed by simulating a model polymeric DNA duplex...
August 2017: Journal of Molecular Modeling
https://www.readbyqxmd.com/read/28716689/brg1-and-smarcal1-transcriptionally-co-regulate-drosha-dgcr8-and-dicer-in-response-to-doxorubicin-induced-dna-damage
#14
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 ncRNA 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 14, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28716507/a-novel-topoisomerase-2a-inhibitor-cryptotanshinone-suppresses-the-growth-of-pc3-cells-without-apparent-cytotoxicity
#15
Eun Ju Kim, Sun Young Kim, Sang-Man Kim, Minyoung Lee
DNA topoisomerase 2, which is ubiquitously expressed in eukaryotic cells, is an essential nuclear enzyme that promotes cell survival by regulating DNA topology and chromatid separation. This enzyme has been validated as a target for anticancer agent screening. It can be poisoned by common chemotherapeutics, such as etoposide and doxorubicin, which leads to the accumulation of cytotoxic enzyme-linked DNA double-stranded breaks. However, recent studies have suggested that the topoisomerase 2a isozyme is predominantly responsible for the carcinogenic side effects associated with etoposide and doxorubicin chemotherapy...
July 14, 2017: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/28715428/cip29-is-phosphorylated-following-activation-of-the-dna-damage-response-in-xenopus-egg-extracts
#16
Janet Holden, Elaine M Taylor, Howard D Lindsay
Acting through a complex signalling network, DNA lesions trigger a range of cellular responses including DNA repair, cell cycle arrest, altered gene expression and cell death, which help to limit the mutagenic effects of such DNA damage. RNA processing factors are increasingly being recognised as important targets of DNA damage signalling, with roles in the regulation of gene expression and also more directly in the promotion of DNA repair. In this study, we have used a Xenopus laevis egg extract system to analyse the DNA damage-dependent phosphorylation of a putative RNA export factor, Cip29...
2017: PloS One
https://www.readbyqxmd.com/read/28714954/c9orf72-expansion-disrupts-atm-mediated-chromosomal-break-repair
#17
Callum Walker, Saul Herranz-Martin, Evangelia Karyka, Chunyan Liao, Katherine Lewis, Waheba Elsayed, Vera Lukashchuk, Shih-Chieh Chiang, Swagat Ray, Padraig J Mulcahy, Mateusz Jurga, Ioannis Tsagakis, Tommaso Iannitti, Jayanth Chandran, Ian Coldicott, Kurt J De Vos, Mohamed K Hassan, Adrian Higginbottom, Pamela J Shaw, Guillaume M Hautbergue, Mimoun Azzouz, Sherif F El-Khamisy
Hexanucleotide repeat expansions represent the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, though the mechanisms by which such expansions cause neurodegeneration are poorly understood. We report elevated levels of DNA-RNA hybrids (R-loops) and double strand breaks in rat neurons, human cells and C9orf72 ALS patient spinal cord tissues. Accumulation of endogenous DNA damage is concomitant with defective ATM-mediated DNA repair signaling and accumulation of protein-linked DNA breaks...
July 17, 2017: Nature Neuroscience
https://www.readbyqxmd.com/read/28714850/high-resolution-mapping-of-heteroduplex-dna-formed-during-uv-induced-and-spontaneous-mitotic-recombination-events-in-yeast
#18
Yi Yin, Margaret Dominska, Eunice Yim, Thomas D Petes
In yeast, DNA breaks are usually repaired by homologous recombination (HR). An early step for HR pathways is formation of a heteroduplex, in which a single-strand from the broken DNA molecule pairs with a strand derived from an intact DNA molecule. If the two strands of DNA are not identical, there will be mismatches within the heteroduplex DNA (hetDNA). In wild-type strains, these mismatches are repaired by the mismatch repair (MMR) system, producing a gene conversion event. In strains lacking MMR, the mismatches persist...
July 17, 2017: ELife
https://www.readbyqxmd.com/read/28714549/increased-level-of-dna-damage-in-some-organs-of-obese-zucker-rats-by-%C3%AE-h2ax-analysis
#19
Alessia Azzarà, Anna Chiaramonte, Erika Filomeni, Barbara Pinto, Stefano Mazzoni, Simona Piaggi, Maria Angela Guzzardi, Fabrizio Bruschi, Patricia Iozzo, Roberto Scarpato
In a recent study, we showed that lymphocytes of obese Italian children/adolescents displayed levels of double strand breaks (DSB), assayed as serine 139-phosphorylated histone H2AX (γ-H2AX), about eightfold higher than normal weight controls, and that 30% of this damage-generated micronuclei. These findings suggested that obese children could be at increased risk of obesity-mediated cancer later in life. We therefore aimed to assess the level of γ-H2AX in a genetic animal model of obesity (Zucker rat) to identify a genotoxic/carcinogenic risk in some organs...
July 17, 2017: Environmental and Molecular Mutagenesis
https://www.readbyqxmd.com/read/28713155/hypoxia-induces-universal-but-differential-drug-resistance-and-impairs-anticancer-mechanisms-of-5-fluorouracil-in-hepatoma-cells
#20
Jing-Qiu Li, Xian Wu, Lu Gan, Xiang-Liang Yang, Ze-Hong Miao
Hepatocellular carcinoma (HCC) is one of the most refractory cancers. The mechanisms by which hypoxia further aggravates therapeutic responses of advanced HCC to anticancer drugs remain to be clarified. Here, we report that hypoxia (1% O2) caused 2.55-489.7-fold resistance to 6 anticancer drugs (sorafenib, 5-fluorouracil [5-FU], gemcitabine, cisplatin, adriamycin and 6-thioguanine) in 3 HCC cell lines (BEL-7402, HepG2 and SMMC-7721). Among the 6 drugs, sorafenib, the sole one approved for HCC therapy, inhibited proliferation with little influence from hypoxia and displayed the smallest variation among the 3 HCC cell lines tested...
July 17, 2017: Acta Pharmacologica Sinica
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