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https://www.readbyqxmd.com/read/29763736/generating-a-recombinant-phosphothreonine-binding-domain-for-a-phosphopeptide-of-the-human-transcription-factor-c-myc
#1
Leon A Venegas, Stefanie L Kall, Oluwadamilola Bankole, Arnon Lavie, Brian Kay
Transcription factor c-Myc is an oncoprotein that is regulated at the post-translational level through phosphorylation of two conserved residues, Serine 62 (Ser62) and Threonine 58 (Thr58). A highly specific tool capable of recognizing Myc via pThr58 is needed to monitor activation and localization. Through phage display, we have isolated 10 engineered Forkhead-associated (FHA) domains that selectively bind to a phosphothreonine (pThr)-containing peptide (53-FELLPpTPPLSPS-64) segment of human c-Myc. One domain variant was observed to bind to the Myc-pThr58 peptide with a KD value of 800 nM and had >1,000-fold discrimination between the phosphorylated and non-phosphorylated peptide...
May 12, 2018: New Biotechnology
https://www.readbyqxmd.com/read/29581097/spatial-separation-between-replisome-and-template-induced-replication-stress-signaling
#2
Néstor García-Rodríguez, Magdalena Morawska, Ronald P Wong, Yasukazu Daigaku, Helle D Ulrich
Polymerase-blocking DNA lesions are thought to elicit a checkpoint response via accumulation of single-stranded DNA at stalled replication forks. However, as an alternative to persistent fork stalling, re-priming downstream of lesions can give rise to daughter-strand gaps behind replication forks. We show here that the processing of such structures by an exonuclease, Exo1, is required for timely checkpoint activation, which in turn prevents further gap erosion in S phase. This Rad9-dependent mechanism of damage signaling is distinct from the Mrc1-dependent, fork-associated response to replication stress induced by conditions such as nucleotide depletion or replisome-inherent problems, but reminiscent of replication-independent checkpoint activation by single-stranded DNA Our results indicate that while replisome stalling triggers a checkpoint response directly at the stalled replication fork, the response to replication stress elicited by polymerase-blocking lesions mainly emanates from Exo1-processed, postreplicative daughter-strand gaps, thus offering a mechanistic explanation for the dichotomy between replisome- versus template-induced checkpoint signaling...
March 26, 2018: EMBO Journal
https://www.readbyqxmd.com/read/29420790/structurally-distinct-mre11-domains-mediate-mrx-functions-in-resection-end-tethering-and-dna-damage-resistance
#3
Corinne Cassani, Elisa Gobbini, Jacopo Vertemara, Weibin Wang, Antonio Marsella, Patrick Sung, Renata Tisi, Giuseppe Zampella, Maria Pia Longhese
Sae2 cooperates with the Mre11-Rad50-Xrs2 (MRX) complex to initiate resection of DNA double-strand breaks (DSBs) and to maintain the DSB ends in close proximity to allow their repair. How these diverse MRX-Sae2 functions contribute to DNA damage resistance is not known. Here, we describe mre11 alleles that suppress the hypersensitivity of sae2Δ cells to genotoxic agents. By assessing the impact of these mutations at the cellular and structural levels, we found that all the mre11 alleles that restore sae2Δ resistance to both camptothecin and phleomycin affect the Mre11 N-terminus and suppress the resection defect of sae2Δ cells by lowering MRX and Tel1 association to DSBs...
April 6, 2018: Nucleic Acids Research
https://www.readbyqxmd.com/read/29383801/preserving-salivary-gland-physiology-against-genotoxic-damage-the-tousled-way
#4
Gulshan Sunavala-Dossabhoy
Tousled and its homologs are evolutionarily conserved serine/threonine kinases present in plants and animals. Human Tousled-like kinases, TLK1 and TLK2, are implicated in chromatin assembly during DNA replication, chromosome segregation during mitosis, as well as in DNA damage response and repair. They share a high degree of sequence similarity, but have few non-redundant functions. Our lab has studied TLK1, and found that it increases the resistance of cells to ionizing radiation (IR) damage through expedited double strand break (DSB) repair...
January 30, 2018: Oral Diseases
https://www.readbyqxmd.com/read/29361157/ape2-promotes-dna-damage-response-pathway-from-a-single-strand-break
#5
Yunfeng Lin, Liping Bai, Steven Cupello, Md Akram Hossain, Bradley Deem, Melissa McLeod, Jude Raj, Shan Yan
As the most common type of DNA damage, DNA single-strand breaks (SSBs) are primarily repaired by the SSB repair mechanism. If not repaired properly or promptly, unrepaired SSBs lead to genome stability and have been implicated in cancer and neurodegenerative diseases. However, it remains unknown how unrepaired SSBs are recognized by DNA damage response (DDR) pathway, largely because of the lack of a feasible experimental system. Here, we demonstrate evidence showing that an ATR-dependent checkpoint signaling is activated by a defined plasmid-based site-specific SSB structure in Xenopus HSS (high-speed supernatant) system...
March 16, 2018: Nucleic Acids Research
https://www.readbyqxmd.com/read/29301856/rad9-53bp1-protects-stalled-replication-forks-from-degradation-in-mec1-atr-defective-cells
#6
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...
February 2018: EMBO Reports
https://www.readbyqxmd.com/read/28912563/a-cell-cycle-independent-mode-of-the-rad9-dpb11-interaction-is-induced-by-dna-damage
#7
Giulia di Cicco, Susanne C S Bantele, Karl-Uwe Reusswig, Boris Pfander
Budding yeast Rad9, like its orthologs, controls two aspects of the cellular response to DNA double strand breaks (DSBs) - signalling of the DNA damage checkpoint and DNA end resection. Rad9 binds to damaged chromatin via modified nucleosomes independently of the cell cycle phase. Additionally, Rad9 engages in a cell cycle-regulated interaction with Dpb11 and the 9-1-1 clamp, generating a second pathway that recruits Rad9 to DNA damage sites. Binding to Dpb11 depends on specific S/TP phosphorylation sites of Rad9, which are modified by cyclin-dependent kinase (CDK)...
September 14, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28629935/a-dicre-recombinase-based-system-for-inducible-expression-in-leishmania-major
#8
Renato E R S Santos, Gabriel L A Silva, Elaine V Santos, Samuel M Duncan, Jeremy C Mottram, Jeziel D Damasceno, Luiz R O Tosi
Here we present the establishment of an inducible system based on the dimerizable Cre recombinase (DiCre) for controlled gene expression in the protozoan parasite Leishmania. Rapamycin-induced DiCre activation promoted efficient flipping and expression of gene products in a time and dose-dependent manner. The DiCre flipping activity induced the expression of target genes from both integrated and episomal contexts broadening the applicability of the system. We validated the system by inducing the expression of both full length and truncated forms of the checkpoint protein Rad9, which revealed that the highly divergent C-terminal domain of Rad9 is necessary for proper subcellular localization...
June 16, 2017: Molecular and Biochemical Parasitology
https://www.readbyqxmd.com/read/28546384/systematic-analysis-of-the-dna-damage-response-network-in-telomere-defective-budding-yeast
#9
Eva-Maria Holstein, Greg Ngo, Conor Lawless, Peter Banks, Matthew Greetham, Darren Wilkinson, David Lydall
Functional telomeres are critically important to eukaryotic genetic stability. Scores of proteins and pathways are known to affect telomere function. Here, we report a series of related genome-wide genetic interaction screens performed on budding yeast cells with acute or chronic telomere defects. Genetic interactions were examined in cells defective in Cdc13 and Stn1, affecting two components of CST, a single stranded DNA (ssDNA) binding complex that binds telomeric DNA. For comparison, genetic interactions were also examined in cells with defects in Rfa3, affecting the major ssDNA binding protein, RPA, which has overlapping functions with CST at telomeres...
July 5, 2017: G3: Genes—Genomes—Genetics
https://www.readbyqxmd.com/read/28341832/mir-2425-5p-targets-rad9a-and-myog-to-regulate-the-proliferation-and-differentiation-of-bovine-skeletal-muscle-derived-satellite-cells
#10
Hui Li Tong, Run Ying Jiang, Wei Wei Zhang, Yun Qin Yan
Our group previously identified miR-2425-5p, a unique bovine miRNA; however, its biological function and regulation in muscle-derived satellite cells (MDSCs) remain unclear. Herein, stem-loop RT-PCR results showed that miR-2425-5p increased during MDSCs proliferation, but decreased during differentiation. Cell proliferation was examined using EdU assays, cyclin B1 (CCNB1) and proliferating cell nuclear antigen (PCNA) western blot (WB) and flow cytometry analysis. These results showed that miR-2425-5p mimics (miR-2425-M) enhanced MDSCs proliferation, whereas, miR-2425-5p inhibitor (miR-2425-I) had opposite effect...
March 24, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28301324/response-of-alternative-splice-isoforms-of-osrad9-gene-from-oryza-sativa-to-environmental-stress
#11
Rui Li, Wenguo Wang, Fosheng Li, Qingwei Wang, Shenghua Wang, Ying Xu, Fang Chen
Rad9 protein plays an important role in cell-cycle checkpoint signal transduction in human and yeast cells, but knowledge about Rad9 in plants is limited. This study reports that the Rad9 gene of rice can generate the transcript products OsRad9.1 and OsRad9.2 through alternative splicing. OsRad9.1, with all nine exons, is the main cell-cycle checkpoint protein involved in the response of rice to genotoxic stresses (ultraviolet radiation and antibiotic stress), environmental stresses (drought, salt, and heavy metal stress), and auxin stimuli (2,4-D, IAA, and IBA)...
July 14, 2017: Zeitschrift Für Naturforschung. C, A Journal of Biosciences
https://www.readbyqxmd.com/read/28228534/topbp1-dpb11-plays-a-conserved-role-in-homologous-recombination-dna-repair-through-the-coordinated-recruitment-of-53bp1-rad9
#12
Yi Liu, José Renato Cussiol, Diego Dibitetto, Jennie Rae Sims, Shyam Twayana, Robert Samuel Weiss, Raimundo Freire, Federica Marini, Achille Pellicioli, Marcus Bustamante Smolka
Genome maintenance and cancer suppression require homologous recombination (HR) DNA repair. In yeast and mammals, the scaffold protein TOPBP1(Dpb11) has been implicated in HR, although its precise function and mechanism of action remain elusive. In this study, we show that yeast Dpb11 plays an antagonistic role in recombination control through regulated protein interactions. Dpb11 mediates opposing roles in DNA end resection by coordinating both the stabilization and exclusion of Rad9 from DNA lesions. The Mec1 kinase promotes the pro-resection function of Dpb11 by mediating its interaction with the Slx4 scaffold...
March 6, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28140789/p53-and-rad9-the-dna-damage-response-and-regulation-of-transcription-networks
#13
REVIEW
Howard B Lieberman, Sunil K Panigrahi, Kevin M Hopkins, Li Wang, Constantinos G Broustas
The way cells respond to DNA damage is important since inefficient repair or misrepair of lesions can have deleterious consequences, including mutation, genomic instability, neurodegenerative disorders, premature aging, cancer or death. Whether damage occurs spontaneously as a byproduct of normal metabolic processes, or after exposure to exogenous agents, cells muster a coordinated, complex DNA damage response (DDR) to mitigate potential harmful effects. A variety of activities are involved to promote cell survival, and include DNA repair, DNA damage tolerance, as well as transient cell cycle arrest to provide time for repair before entry into critical cell cycle phases, an event that could be lethal if traversal occurs while damage is present...
April 2017: Radiation Research
https://www.readbyqxmd.com/read/28089177/cell-cycle-dependent-positive-and-negative-functions-of-fun30-chromatin-remodeler-in-dna-damage-response
#14
Jasmine Siler, Bowen Xia, Carina Wong, Morgan Kath, Xin Bi
The evolutionally conserved Fun30 chromatin remodeler in Saccharomyces cerevisiae has been shown to contribute to cellular resistance to genotoxic stress inflicted by camptothecin (CPT), methyl methanesulfonate (MMS) and hydroxyurea (HU). Fun30 aids in extensive DNA resection of DNA double stranded break (DSB) ends, which is thought to underlie its role in CPT-resistance. How Fun30 promotes MMS- or HU-resistance has not been resolved. Interestingly, we have recently found Fun30 to also play a negative role in cellular tolerance to MMS and HU in the absence of the Rad5-dependent DNA damage tolerance pathway...
February 2017: DNA Repair
https://www.readbyqxmd.com/read/27915243/signaling-pathways-of-replication-stress-in-yeast
#15
REVIEW
Benjamin Pardo, Laure Crabbé, Philippe Pasero
Eukaryotic cells activate the S-phase checkpoint in response to a variety of events affecting the progression of replication forks, collectively referred to as replication stress. This signaling pathway is divided in two branches: the DNA damage checkpoint (DDC) and the DNA replication checkpoint (DRC). Both pathways are activated by the sensor kinase Mec1 and converge on the effector kinase Rad53. However, the DDC operates throughout the cell cycle and depends on the checkpoint mediator Rad9 to activate Rad53, whereas the DRC is specific to S phase and is mediated by Mrc1 and other fork components to signal replication impediments...
March 1, 2017: FEMS Yeast Research
https://www.readbyqxmd.com/read/27723720/etaa1-acts-at-stalled-replication-forks-to-maintain-genome-integrity
#16
Thomas E Bass, Jessica W Luzwick, Gina Kavanaugh, Clinton Carroll, Huzefa Dungrawala, Gloria G Glick, Michael D Feldkamp, Reid Putney, Walter J Chazin, David Cortez
The ATR checkpoint kinase coordinates cellular responses to DNA replication stress. Budding yeast contain three activators of Mec1 (the ATR orthologue); however, only TOPBP1 is known to activate ATR in vertebrates. We identified ETAA1 as a replication stress response protein in two proteomic screens. ETAA1-deficient cells accumulate double-strand breaks, sister chromatid exchanges, and other hallmarks of genome instability. They are also hypersensitive to replication stress and have increased frequencies of replication fork collapse...
November 2016: Nature Cell Biology
https://www.readbyqxmd.com/read/27716774/ontogeny-of-unstable-chromosomes-generated-by-telomere-error-in-budding-yeast
#17
Tracey Beyer, Ted Weinert
DNA replication errors at certain sites in the genome initiate chromosome instability that ultimately leads to stable genomic rearrangements. Where instability begins is often unclear. And, early instability may form unstable chromosome intermediates whose transient nature also hinders mechanistic understanding. We report here a budding yeast model that reveals the genetic ontogeny of genome rearrangements, from initial replication error to unstable chromosome formation to their resolution. Remarkably, the initial error often arises in or near the telomere, and frequently forms unstable chromosomes...
October 2016: PLoS Genetics
https://www.readbyqxmd.com/read/27678521/prevention-of-dna-rereplication-through-a-meiotic-recombination-checkpoint-response
#18
Nicole A Najor, Layne Weatherford, George S Brush
In the budding yeast Saccharomyces cerevisiae, unnatural stabilization of the cyclin-dependent kinase inhibitor Sic1 during meiosis can trigger extra rounds of DNA replication. When programmed DNA double-strand breaks (DSBs) are generated but not repaired due to absence of DMC1, a pathway involving the checkpoint gene RAD17 prevents this DNA rereplication. Further genetic analysis has now revealed that prevention of DNA rereplication also requires MEC1, which encodes a protein kinase that serves as a central checkpoint regulator in several pathways including the meiotic recombination checkpoint response...
December 7, 2016: G3: Genes—Genomes—Genetics
https://www.readbyqxmd.com/read/27628486/costs-benefits-and-redundant-mechanisms-of-adaption-to-chronic-low-dose-stress-in-yeast
#19
Marta Markiewicz-Potoczny, David Lydall
All organisms live in changeable, stressful environments. It has been reported that exposure to low-dose stresses or poisons can improve fitness. However, examining the effects of chronic low-dose chemical exposure is challenging. To address this issue we used temperature sensitive mutations affecting the yeast cell division cycle to induce low-dose stress for 40 generation times, or more. We examined cdc13-1 mutants, defective in telomere function, and cdc15-2 mutants, defective in mitotic kinase activity...
October 17, 2016: Cell Cycle
https://www.readbyqxmd.com/read/27537368/the-transcriptional-response-to-dna-double-strand-breaks-in-physcomitrella-patens
#20
Yasuko Kamisugi, John W Whitaker, Andrew C Cuming
The model bryophyte Physcomitrella patens is unique among plants in supporting the generation of mutant alleles by facile homologous recombination-mediated gene targeting (GT). Reasoning that targeted transgene integration occurs through the capture of transforming DNA by the homology-dependent pathway for DNA double-strand break (DNA-DSB) repair, we analysed the genome-wide transcriptomic response to bleomycin-induced DNA damage and generated mutants in candidate DNA repair genes. Massively parallel (Illumina) cDNA sequencing identified potential participants in gene targeting...
2016: PloS One
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