2017
DNA polymerase beta participates in DNA End-joining
Ray S, Breuer G, DeVeaux M, Zelterman D, Bindra R, Sweasy JB. DNA polymerase beta participates in DNA End-joining. Nucleic Acids Research 2017, 46: 242-255. PMID: 29161447, PMCID: PMC5758893, DOI: 10.1093/nar/gkx1147.Peer-Reviewed Original ResearchConceptsDouble-strand breaksAlternative NHEJHomologous recombinationDNA polymerasePol βX-family DNA polymerasesFamily DNA polymerasesDNA polymerase betaDNA pol βDeleterious lesionsDNA endsGenomic instabilityNHEJ pathwayDNA proteinProcessing enzymesDefective repairCellular sensitivityCell deathStrand breaksPolymerase betaSubunit inhibitorPolymeraseSmall deletionsMechanistic insightsNHEJ
2016
A single double-strand break system reveals repair dynamics and mechanisms in heterochromatin and euchromatin
Janssen A, Breuer GA, Brinkman EK, van der Meulen AI, Borden SV, van Steensel B, Bindra RS, LaRocque JR, Karpen GH. A single double-strand break system reveals repair dynamics and mechanisms in heterochromatin and euchromatin. Genes & Development 2016, 30: 1645-1657. PMID: 27474442, PMCID: PMC4973294, DOI: 10.1101/gad.283028.116.Peer-Reviewed Original ResearchConceptsDNA double-strand breaksHomologous recombinationGenome stabilityHeterochromatic DSBsEuchromatic DSBsSingle DNA double-strand breakMain DSB repair pathwaysDifferent chromatin domainsLarval imaginal discsDistinct nuclear domainsRepetitive DNA sequencesDSB repair pathwaysDouble-strand breaksChromatin contextChromatin domainsEuchromatic lociPericentromeric heterochromatinChromatin regionsHomologous chromosomesHR templateImaginal discsDSB repairDNA sequencesNuclear domainsRepair pathways
2015
Identification of Novel Radiosensitizers in a High-Throughput, Cell-Based Screen for DSB Repair Inhibitors
Goglia AG, Delsite R, Luz AN, Shahbazian D, Salem AF, Sundaram RK, Chiaravalli J, Hendrikx PJ, Wilshire JA, Jasin M, Kluger HM, Glickman JF, Powell SN, Bindra RS. Identification of Novel Radiosensitizers in a High-Throughput, Cell-Based Screen for DSB Repair Inhibitors. Molecular Cancer Therapeutics 2015, 14: 326-342. PMID: 25512618, PMCID: PMC4326563, DOI: 10.1158/1535-7163.mct-14-0765.Peer-Reviewed Original ResearchConceptsDSB repair inhibitorsDouble-strand breaksDSB repairHomologous recombinationRepair inhibitorsCell-based small molecule screenSuccessful DSB repairDNA-damaging agentsPlate-based formatCell-based screenSmall-molecule screenGenomic integrityTumor cell survivalMammalian cellsHR repairDNA repairMolecule screenReporter systemSecondary assaysCell survivalDNA damageCancer cell linesTumor cellsNovel hitsMost cancer therapies
2014
Development of a novel method to create double-strand break repair fingerprints using next-generation sequencing
Soong CP, Breuer GA, Hannon RA, Kim SD, Salem AF, Wang G, Yu R, Carriero NJ, Bjornson R, Sundaram RK, Bindra RS. Development of a novel method to create double-strand break repair fingerprints using next-generation sequencing. DNA Repair 2014, 26: 44-53. PMID: 25547252, DOI: 10.1016/j.dnarep.2014.12.002.Peer-Reviewed Original ResearchConceptsHomologous recombinationNHEJ repairChromosomal lociDSB repair pathway choiceDNA double-strand break repairEndogenous chromosomal locusEfficient DNA double-strand break repairDouble-strand break repairDSB repair proteinsRepair pathway choiceDNA damaging agentsSequencing-based approachesDSB repair activityNext-generation sequencing-based approachChromatin interactionsGenomic integrityDSB repairMammalian cellsNext-generation sequencingBreak repairPathway choiceRepair proteinsReporter geneDamaging agentsRepair assays
2013
Development of an assay to measure mutagenic non-homologous end-joining repair activity in mammalian cells
Bindra RS, Goglia AG, Jasin M, Powell SN. Development of an assay to measure mutagenic non-homologous end-joining repair activity in mammalian cells. Nucleic Acids Research 2013, 41: e115-e115. PMID: 23585275, PMCID: PMC3675474, DOI: 10.1093/nar/gkt255.Peer-Reviewed Original ResearchConceptsMammalian cellsHomologous recombinationDouble-strand break repair pathwayNon-homologous end-joining repairSite-specific DSBsEnd-joining activityBreak repair pathwayEnd-joining repairPrevention of tumorigenesisSerum-deprived cellsGenomic integrityIntrachromosomal locusI-SceIHR repairProtein stabilityCanonical NHEJRepair pathwaysRepair assaysNHEJ repairMutagenic NHEJCellular localizationDSB inductionLiving cellsNHEJRepair activity
2005
Hypoxia-Induced Down-regulation of BRCA1 Expression by E2Fs
Bindra RS, Gibson SL, Meng A, Westermark U, Jasin M, Pierce AJ, Bristow RG, Classon MK, Glazer PM. Hypoxia-Induced Down-regulation of BRCA1 Expression by E2Fs. Cancer Research 2005, 65: 11597-11604. PMID: 16357170, DOI: 10.1158/0008-5472.can-05-2119.Peer-Reviewed Original ResearchMeSH KeywordsBRCA1 ProteinBreast NeoplasmsCell HypoxiaChromatin ImmunoprecipitationColonic NeoplasmsDNA RepairDown-RegulationE2F Transcription FactorsGene Expression Regulation, NeoplasticHumansHypoxia-Inducible Factor 1, alpha SubunitLuciferasesLung NeoplasmsPromoter Regions, GeneticRecombination, GeneticReverse Transcriptase Polymerase Chain ReactionRNA, MessengerTranscription, GeneticTumor Cells, CulturedConceptsHomologous recombinationBRCA1 expressionGenetic instabilityError-prone NHEJ pathwayAdjacent E2F sitesHomologous recombination pathwayImpaired homologous recombinationNonhomologous end-joining repair pathwayGenetic mutationsTranscriptional repressionE2F sitePromoter occupancyTranscriptional responseDNA repairNHEJ pathwayRepair pathwaysNovel linkE2FRecombination pathwayBRCA1 promoterSporadic cancersIntriguing mechanismBRCA1 inactivationDynamic redistributionRepressionAlterations in DNA Repair Gene Expression under Hypoxia: Elucidating the Mechanisms of Hypoxia‐Induced Genetic Instability
BINDRA RS, SCHAFFER PJ, MENG A, WOO J, MÅSEIDE K, ROTH ME, LIZARDI P, HEDLEY DW, BRISTOW RG, GLAZER PM. Alterations in DNA Repair Gene Expression under Hypoxia: Elucidating the Mechanisms of Hypoxia‐Induced Genetic Instability. Annals Of The New York Academy Of Sciences 2005, 1059: 184-195. PMID: 16382054, DOI: 10.1196/annals.1339.049.Peer-Reviewed Original ResearchConceptsGenetic instabilityHomologous recombinationRAD51 expressionDNA repair gene expressionSuch genetic instabilityPost-hypoxic cellsDNA repair genesRepair gene expressionNumerous cell linesExpression of RAD51HR pathwayHR repairHypoxia-inducible factorGene expressionCell cycleRepair genesNovel mechanismHypoxic stressIndependent mannerPost-hypoxic periodCell linesCancer cellsCritical mediatorGenesExpression
2004
Down-Regulation of Rad51 and Decreased Homologous Recombination in Hypoxic Cancer Cells
Bindra RS, Schaffer PJ, Meng A, Woo J, Måseide K, Roth ME, Lizardi P, Hedley DW, Bristow RG, Glazer PM. Down-Regulation of Rad51 and Decreased Homologous Recombination in Hypoxic Cancer Cells. Molecular And Cellular Biology 2004, 24: 8504-8518. PMID: 15367671, PMCID: PMC516750, DOI: 10.1128/mcb.24.19.8504-8518.2004.Peer-Reviewed Original ResearchMeSH KeywordsCell CycleDNA RepairDNA-Binding ProteinsDown-RegulationFemaleGene Expression RegulationHumansHypoxiaHypoxia-Inducible Factor 1Hypoxia-Inducible Factor 1, alpha SubunitIronMaleNuclear ProteinsProstatic NeoplasmsRecombination, GeneticRNA, MessengerTranscription FactorsTranscription, GeneticUterine Cervical NeoplasmsConceptsHomologous recombinationExpression of RAD51RAD51 expressionGenetic instabilityCancer cellsCritical DNA repair pathwaysDNA damage responseMultiple cancer cell typesDNA repair pathwaysLevels of RAD51Homologous recombination pathwayGene promoter activityTranscriptional repressionCell cycle profileCancer cell typesDamage responseMammalian cellsHypoxia-inducible factorDNA repairProtein stabilityRepair pathwaysAberrant regulationPromoter activityRAD51Hypoxic cancer cells