2011
The 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
2006
Block of T cell development in P53-deficient mice accelerates development of lymphomas with characteristic RAG-dependent cytogenetic alterations
Haines BB, Ryu CJ, Chang S, Protopopov A, Luch A, Kang YH, Draganov DD, Fragoso MF, Paik SG, Hong HJ, DePinho RA, Chen J. Block of T cell development in P53-deficient mice accelerates development of lymphomas with characteristic RAG-dependent cytogenetic alterations. Cancer Cell 2006, 9: 109-120. PMID: 16473278, DOI: 10.1016/j.ccr.2006.01.004.Peer-Reviewed Original Research
2000
Telomere dysfunction impairs DNA repair and enhances sensitivity to ionizing radiation
Wong K, Chang S, Weiler S, Ganesan S, Chaudhuri J, Zhu C, Artandi S, Rudolph K, Gottlieb G, Chin L, Alt F, DePinho R. Telomere dysfunction impairs DNA repair and enhances sensitivity to ionizing radiation. Nature Genetics 2000, 26: 85-88. PMID: 10973255, DOI: 10.1038/79232.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell NucleusCell SurvivalChromosome AberrationsChromosomesDNA FragmentationDNA RepairDose-Response Relationship, RadiationFibroblastsGenotypeIn Situ Nick-End LabelingKineticsMiceMice, TransgenicModels, GeneticRadiation ToleranceRadiation, IonizingTelomereThymus GlandTime FactorsConceptsMouse embryonic fibroblastsTelomere functionOrganismal responsesLinear eukaryotic chromosomesDNA repair machineryTelomerase RNA geneNon-homologous endImpairs DNA repairRole of telomeraseTelomerase-deficient miceEukaryotic chromosomesRNA genesYeast telomeresNucleoprotein complexesRepair machineryDNA repairIntact telomeresCrypt stem cellsEmbryonic fibroblastsTelomere dysfunctionDe novo synthesisChromosomal repairGenetic instabilityPrimary thymocytesRate of apoptosis