2013
p16INK4a protects against dysfunctional telomere–induced ATR-dependent DNA damage responses
Wang Y, Sharpless N, Chang S. p16INK4a protects against dysfunctional telomere–induced ATR-dependent DNA damage responses. Journal Of Clinical Investigation 2013, 123: 4489-4501. PMID: 24091330, PMCID: PMC3784543, DOI: 10.1172/jci69574.Peer-Reviewed Original ResearchMeSH KeywordsAgingAnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsBone Marrow TransplantationCell ProliferationCells, CulturedCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21DNA DamageDNA RepairDNA-Binding ProteinsFemaleHematopoiesisHematopoietic Stem CellsIntestine, SmallMaleMiceMice, SCIDMice, TransgenicProtein StabilitySequence DeletionSpleenTelomereTelomere HomeostasisTumor Suppressor Protein p53ConceptsHematopoietic cellsDeletion of p21P21-dependent cell cycle arrestOrgan impairmentTelomere dysfunctionCell cycle arrestMouse modelDNA damage responseSmall intestineFunctional defectsCell functionProliferative capacityP53-dependent apoptosisCycle arrestDysfunctional telomeresCellular senescenceDysfunctionP53-dependent DNA damage responseProliferative cellsHematopoietic systemProtective functionTumor suppressorProliferative defectP53 stabilizationCells
2010
The telomere protein tankyrase 1 regulates DNA damage responses at telomeres
Chang S. The telomere protein tankyrase 1 regulates DNA damage responses at telomeres. Aging 2010, 2: 639-642. PMID: 21076181, PMCID: PMC2993793, DOI: 10.18632/aging.100221.Peer-Reviewed Original Research
2006
GCN5 Functions in Telomere Maintenance and Neural Development
Dent S, Evrard Y, Lin W, Bu P, Phan H, Chang S, Multani A. GCN5 Functions in Telomere Maintenance and Neural Development. The FASEB Journal 2006, 20: a1472-a1472. DOI: 10.1096/fasebj.20.5.a1472-e.Peer-Reviewed Original ResearchMutant embryosNeural developmentTelomere maintenanceDouble mutant embryosCatalytic site mutationsNeural tube closureGcn5 functionsTelomere defectsTelomere fusionEmbryonic lethalityHypomorphic alleleProper expressionGCN5Tube closureSite mutationSimilar defectsEnd associationEmbryosFirst evidenceApoptosisBrain developmentP53CellsTelomeresGenes
2005
Elevated telomere-telomere recombination in WRN-deficient, telomere dysfunctional cells promotes escape from senescence and engagement of the ALT pathway
Laud PR, Multani AS, Bailey SM, Wu L, Ma J, Kingsley C, Lebel M, Pathak S, DePinho RA, Chang S. Elevated telomere-telomere recombination in WRN-deficient, telomere dysfunctional cells promotes escape from senescence and engagement of the ALT pathway. Genes & Development 2005, 19: 2560-2570. PMID: 16264192, PMCID: PMC1276730, DOI: 10.1101/gad.1321305.Peer-Reviewed Original ResearchConceptsWerner syndromeSister chromatidsT-SCETelomere sister chromatid exchangeElevated recombination ratesActivation of ALTWRN functionAberrant recombinationGenomic instabilityALT pathwayChromosomal aberrationsChromosomal instabilityTelomeresPremature agingDysfunctional cellsTumor formationChromatidsSister chromatid exchangesPathwayChromatid exchangesRecombinationRecombination rateCellsWRNMutantsModeling aging and cancer in the telomerase knockout mouse
Chang S. Modeling aging and cancer in the telomerase knockout mouse. Mutation Research/Fundamental And Molecular Mechanisms Of Mutagenesis 2005, 576: 39-53. PMID: 15927211, DOI: 10.1016/j.mrfmmm.2004.08.020.Peer-Reviewed Original ResearchConceptsTelomere dysfunctionRole of telomeresTelomerase-null miceTelomerase knockout miceTelomerase-deficient miceOrganismal agingSomatic cellsMammalian organismsTight regulationCellular responsesTelomerase activityNull miceKnockout miceTelomeresMouse modelTelomeraseOrganismsMiceDeficient miceRegulationAgingCellsCancer