2023
Telomeres cooperate with the nuclear envelope to maintain genome stability
Rai R, Sodeinde T, Boston A, Chang S. Telomeres cooperate with the nuclear envelope to maintain genome stability. BioEssays 2023, 46: e2300184. PMID: 38047499, DOI: 10.1002/bies.202300184.Peer-Reviewed Original ResearchNuclear envelopeGenome stabilityNuclear envelope ruptureKu70/Ku80Homology-directed recombinationMammalian telomeresChromosome stabilityNuclear laminsShelterin componentsProtein TRF2Envelope ruptureRepair proteinsTelomeresRap1Recent findingsProteinFunction resultsRecombinationDNA sensingForm structuresLaminsTRF2Ku80DNAHomeostasisHomology directed telomere clustering, ultrabright telomere formation and nuclear envelope rupture in cells lacking TRF2B and RAP1
Rai R, Biju K, Sun W, Sodeinde T, Al-Hiyasat A, Morgan J, Ye X, Li X, Chen Y, Chang S. Homology directed telomere clustering, ultrabright telomere formation and nuclear envelope rupture in cells lacking TRF2B and RAP1. Nature Communications 2023, 14: 2144. PMID: 37059728, PMCID: PMC10104862, DOI: 10.1038/s41467-023-37761-w.Peer-Reviewed Original ResearchConceptsDouble-strand breaksNuclear envelopeDistinct DNA repair mechanismsNuclear envelope ruptureKu70/Ku80DNA repair mechanismsDNA-RNA hybridsBRCT domainGenome stabilityPhosphomimetic mutantTelomere formationGenotoxic stressEnvelope ruptureDysfunctional telomeresBasic domainRap1Aberrant laminTelomeresRepair mechanismsLaminsTRF2HomologyProteinShelterinADAR1p110
2021
Distinct functions of POT1 proteins contribute to the regulation of telomerase recruitment to telomeres
Gu P, Jia S, Takasugi T, Tesmer VM, Nandakumar J, Chen Y, Chang S. Distinct functions of POT1 proteins contribute to the regulation of telomerase recruitment to telomeres. Nature Communications 2021, 12: 5514. PMID: 34535663, PMCID: PMC8448735, DOI: 10.1038/s41467-021-25799-7.Peer-Reviewed Original ResearchConceptsDNA damage responseTelomerase recruitmentPOT1 proteinsDamage responseATR-dependent DNA damage responseNon-homologous end-joining DNA repair pathwayRecruitment of telomeraseC-strand fillAmino acidsDNA repair pathwaysUnique amino acidsTEN1 (CST) complexTelomere extensionCTC1-STN1Stable heterodimerRepair pathwaysC-terminusDistinct functionsPOT1bPOT1aTelomeresC-strandG-strandTPP1Protein
2012
RPA and POT1
Flynn RL, Chang S, Zou L. RPA and POT1. Cell Cycle 2012, 11: 652-657. PMID: 22373525, PMCID: PMC3318101, DOI: 10.4161/cc.11.4.19061.Peer-Reviewed Original ResearchConceptsReplication protein ATelomere maintenanceDNA replicationProtein complex shelterinTTAGGG telomeric repeatsTelomeric ssDNACheckpoint responseTelomeric repeatsPOT1Ataxia telangiectasiaCell cycleAberrant accumulationCycling cellsSpecific mannerInteresting modelTelomeresProtein ACritical roleProteinRecent studiesReplicationShelterinRad3KinaseRepeats
2010
Defending the end zone: Studying the players involved in protecting chromosome ends
Chan SS, Chang S. Defending the end zone: Studying the players involved in protecting chromosome ends. FEBS Letters 2010, 584: 3773-3778. PMID: 20579983, PMCID: PMC3657741, DOI: 10.1016/j.febslet.2010.06.016.Peer-Reviewed Original Research
2009
Multiple roles for MRE11 at uncapped telomeres
Deng Y, Guo X, Ferguson DO, Chang S. Multiple roles for MRE11 at uncapped telomeres. Nature 2009, 460: 914-918. PMID: 19633651, PMCID: PMC2760383, DOI: 10.1038/nature08196.Peer-Reviewed Original ResearchMeSH KeywordsAllelesAnimalsAtaxia Telangiectasia Mutated ProteinsATP-Binding Cassette TransportersCell Cycle ProteinsCell LineChromosomal Proteins, Non-HistoneChromosome AberrationsDNA DamageDNA Ligase ATPDNA LigasesDNA Repair EnzymesDNA-Binding ProteinsFibroblastsIntracellular Signaling Peptides and ProteinsMiceMRE11 Homologue ProteinNuclear ProteinsShelterin ComplexTelomereTelomere-Binding ProteinsTelomeric Repeat Binding Protein 2Tumor Suppressor p53-Binding Protein 1Tumor Suppressor ProteinsConceptsMRN complexLinear eukaryotic chromosomesDNA double-strand breaksDNA damage repair pathwaysDouble-strand breaksDamage repair pathwaysGenome integrityEukaryotic chromosomesUncapped telomeresTelomere maintenanceRepair factorsDNA endsRepair pathwaysTelomeric endNuclease activityTelomeresMultiple rolesMre11Major playersPathogenic lesionsMre1ChromosomesComplexesProteinAlleles
2008
Telomere dysfunction and tumour suppression: the senescence connection
Deng Y, Chan SS, Chang S. Telomere dysfunction and tumour suppression: the senescence connection. Nature Reviews Cancer 2008, 8: 450-458. PMID: 18500246, PMCID: PMC3688269, DOI: 10.1038/nrc2393.Peer-Reviewed Original ResearchConceptsTelomere dysfunctionDysfunctional telomeresDNA damage responseKey PointsTelomeresEukaryotic chromosomesGenome instabilityShelterin complexApoptotic programDamage responseRepetitive sequencesCellular senescenceTelomeric endTumor suppressionProtein resultsP53 pathwayMutant p53TelomeresSpontaneous tumorigenesisSenescenceTumorigenesisMouse modelChromosomesDysfunctionProteinApoptosisInitiation of Genomic Instability, Cellular Senescence, and Organismal Aging by Dysfunctional Telomeres
Chang S. Initiation of Genomic Instability, Cellular Senescence, and Organismal Aging by Dysfunctional Telomeres. 2008, 57-75. DOI: 10.1007/978-3-540-73709-4_4.Peer-Reviewed Original ResearchDysfunctional telomeresOrganismal agingCellular senescenceDNA damage responseLinear chromosomesShelterin complexDamage responseTelomeric repeatsGenomic instabilityTelomeric structureTelomeresSenescenceFunction resultsProteinImportant roleChromosomesMouse modelRepeatsTelomeraseDNAProgressive lossP53ActivationComplexesAging
2007
WRN at telomeres: implications for aging and cancer
Multani AS, Chang S. WRN at telomeres: implications for aging and cancer. Journal Of Cell Science 2007, 120: 713-721. PMID: 17314245, DOI: 10.1242/jcs.03397.Peer-Reviewed Original ResearchConceptsWerner syndromeHuman Werner syndromePremature aging syndromesRecent genetic evidenceAge-related pathologiesGenome stabilityWRN deficiencyTelomere maintenanceDNA replicationGenetic evidenceSingle gene defectsTelomere dysfunctionCellular senescenceAging syndromesMolecular levelPremature agingEarly cancer onsetWRNGene defectsCancer onsetMajor roleTelomeresSenescenceRapid onsetProtein
2001
Rescue of a telomere length defect of Nijmegen breakage syndrome cells requires NBS and telomerase catalytic subunit
Ranganathan V, Heine W, Ciccone D, Rudolph K, Wu X, Chang S, Hai H, Ahearn I, Livingston D, Resnick I, Rosen F, Seemanova E, Jarolim P, DePinho R, Weaver D. Rescue of a telomere length defect of Nijmegen breakage syndrome cells requires NBS and telomerase catalytic subunit. Current Biology 2001, 11: 962-966. PMID: 11448772, DOI: 10.1016/s0960-9822(01)00267-6.Peer-Reviewed Original ResearchConceptsNijmegen breakage syndromeNBS fibroblastsNBS patientsCatalytic subunitChromosome instabilityNijmegen breakage syndrome cellsDNA repair complexRare human diseasesTRF proteinsTelomere extensionNBS cellsTelomere endsRepair complexAccessory proteinsBreakage syndromeGrowth cessationHuman diseasesCancer predispositionLength defectsTelomeresPremature growth cessationProliferative capacitySubunitsProteinGamma irradiation damage