2015
Monitoring the DNA Damage Response at Dysfunctional Telomeres
Rai R, Chang S. Monitoring the DNA Damage Response at Dysfunctional Telomeres. Methods In Molecular Biology 2015, 1343: 175-180. PMID: 26420717, DOI: 10.1007/978-1-4939-2963-4_14.Peer-Reviewed Original ResearchConceptsDysfunctional telomeresDNA damage sensorDNA damage responseDNA damage fociSitu hybridization approachEukaryotic chromosomesShelterin componentsDNA repeatsGenomic stabilityDDR proteinsDamage responseTelomeric DNADDR pathwaysDamage fociChromosomal endsTelomere dysfunctionDamage sensorTelomeresDNA damageHybridization approachCellular viabilityPathwayProper maintenanceChromosomesRepeats
2011
Cytogenetic Analysis of Telomere Dysfunction
Multani A, Chang S. Cytogenetic Analysis of Telomere Dysfunction. Methods In Molecular Biology 2011, 735: 139-143. PMID: 21461818, PMCID: PMC3725757, DOI: 10.1007/978-1-61779-092-8_13.Peer-Reviewed Original ResearchAnimalsCells, CulturedCytogenetic AnalysisDNA Breaks, Double-StrandedDNA RepairFibroblastsIn Situ Hybridization, FluorescenceMiceRecombination, GeneticTelomereProbing the Telomere Damage Response
Rai R, Chang S. Probing the Telomere Damage Response. Methods In Molecular Biology 2011, 735: 145-150. PMID: 21461819, PMCID: PMC3690558, DOI: 10.1007/978-1-61779-092-8_14.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDNADNA DamageDNA RepairFibroblastsHEK293 CellsHumansIn Situ Hybridization, FluorescenceMiceRetroviridaeTelomereTripeptidyl-Peptidase 1ConceptsTelomere dysfunctionDNA damage response signalsDNA damage repair pathwaysTelomere damage responseΓ-H2AXDamage repair pathwaysCheckpoint sensorNbs1 complexReplicative attritionMre11-Rad50Shelterin componentsDamage responseTelomeric DNADysfunctional telomeresRepair pathwaysDownstream effectorsComplete deletionTelomeresDNAPathwayTRF2Chk2Chk1KinaseEffectorsThe RAG2 C terminus suppresses genomic instability and lymphomagenesis
Deriano L, Chaumeil J, Coussens M, Multani A, Chou Y, Alekseyenko AV, Chang S, Skok JA, Roth DB. The RAG2 C terminus suppresses genomic instability and lymphomagenesis. Nature 2011, 471: 119-123. PMID: 21368836, PMCID: PMC3174233, DOI: 10.1038/nature09755.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsChromosome DeletionChromosomes, MammalianDisease ProgressionDNA-Binding ProteinsGene Rearrangement, T-LymphocyteGenes, Immunoglobulin Heavy ChainGenes, p53Genomic InstabilityIn Situ Hybridization, FluorescenceKaplan-Meier EstimateLymphomaMiceProtein Serine-Threonine KinasesReceptors, Antigen, T-CellRecombination, GeneticThymus GlandTranslocation, GeneticTumor Suppressor ProteinsConceptsRAG2 C terminusGenomic instabilityC-terminusTCRα/δDNA double-strand breaksT-cell receptor lociDouble-strand breaksGenomic stabilityComplex chromosomal translocationReceptor locusChromosomal translocationsSimilar defectsLymphomagenesisThymic lymphomasTerminusLociRecombinaseTailRAG2TranslocationDeletionRecombinationRoleLymphoid malignanciesMice
2003
Telomere-based crisis: functional differences between telomerase activation and ALT in tumor progression
Chang S, Khoo C, Naylor M, Maser R, DePinho R. Telomere-based crisis: functional differences between telomerase activation and ALT in tumor progression. Genes & Development 2003, 17: 88-100. PMID: 12514102, PMCID: PMC195968, DOI: 10.1101/gad.1029903.Peer-Reviewed Original ResearchConceptsInk4a/Lung metastasesSubcutaneous tumorsTumor progressionTelomerase activationSubcutaneous tumor formationAdvanced human cancersTail vein injectionTelomere dysfunctionLate passagesMalignant endpointsTelomerase-independent alternative lengtheningImmunocompromised miceFunctional differencesCytogenetic profileMetastatic activityDysfunctionMetastasisCancer cell genomeTumor formationChromosomal aberrationsHuman cancersMarked increaseInitiated cellsMouse embryonic fibroblast cultures