2012
CTC1 deletion results in defective telomere replication, leading to catastrophic telomere loss and stem cell exhaustion
Gu P, Min J, Wang Y, Huang C, Peng T, Chai W, Chang S. CTC1 deletion results in defective telomere replication, leading to catastrophic telomere loss and stem cell exhaustion. The EMBO Journal 2012, 31: 2309-2321. PMID: 22531781, PMCID: PMC3364752, DOI: 10.1038/emboj.2012.96.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDNA ReplicationGene DeletionMiceMice, KnockoutStem CellsTelomereTelomere-Binding ProteinsConceptsMammalian CSTTelomere lossDefective telomere replicationDeletion resultsG2/M checkpointComplete bone marrow failureStem cell exhaustionTelomere deprotectionGenome stabilityTEN1 (CST) complexTelomere replicationReplication forksTelomere maintenanceLength maintenanceCTC1-STN1Efficient restartM checkpointVivo functionCTC1TelomeresAcute deletionBone marrow failureProliferative defectEfficient replicationEssential role
2008
Critical and Distinct Roles of p16 and Telomerase in Regulating the Proliferative Life Span of Normal Human Prostate Epithelial Progenitor Cells*
Bhatia B, Jiang M, Suraneni M, Patrawala L, Badeaux M, Schneider-Broussard R, Multani AS, Jeter CR, Calhoun-Davis T, Hu L, Hu J, Tsavachidis S, Zhang W, Chang S, Hayward SW, Tang DG. Critical and Distinct Roles of p16 and Telomerase in Regulating the Proliferative Life Span of Normal Human Prostate Epithelial Progenitor Cells*. Journal Of Biological Chemistry 2008, 283: 27957-27972. PMID: 18662989, PMCID: PMC2562067, DOI: 10.1074/jbc.m803467200.Peer-Reviewed Original ResearchConceptsProliferative life spanNHP cellsMolecular mechanismsProgenitor cellsSuppression of p16Normal human prostate epithelial cellsGene expression profilesLife spanProstate epithelial progenitor cellsHuman prostate epithelial cellsRegulation of p16Activation of p53Prostate epithelial cellsEpithelial progenitor cellsCell proliferative capacityExpression profilesBasal-like cellsProgenitor markersMultilineage differentiationTelomerase expressionDistinct rolesCell life spanCell marker CD44P16 inhibitionEpithelial cells
2004
Endogenous oncogenic K-rasG12D stimulates proliferation and widespread neoplastic and developmental defects
Tuveson D, Shaw A, Willis N, Silver D, Jackson E, Chang S, Mercer K, Grochow R, Hock H, Crowley D, Hingorani S, Zaks T, King C, Jacobetz M, Wang L, Bronson R, Orkin S, DePinho R, Jacks T. Endogenous oncogenic K-rasG12D stimulates proliferation and widespread neoplastic and developmental defects. Cancer Cell 2004, 5: 375-387. PMID: 15093544, DOI: 10.1016/s1535-6108(04)00085-6.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell CycleCell DivisionCell Transformation, NeoplasticCellular SenescenceCongenital AbnormalitiesCrosses, GeneticCyclin-Dependent Kinase Inhibitor p16Embryo, MammalianFemaleFibroblastsGene Expression Regulation, DevelopmentalGenes, rasIntegrasesMaleMiceMice, Inbred C57BLMice, TransgenicMutationNeoplasmsStem CellsTumor Suppressor Protein p14ARFTumor Suppressor Protein p53Viral ProteinsConceptsCanonical Ras effectorRas effectorsOncogenic RasEmbryonic developmentAbnormal cellular proliferationDevelopmental defectsRas oncogeneGenetic lesionsConditional expressionWidespread expressionK-RasG12DCellular proliferationFurther genetic abnormalitiesEnhanced proliferationOncogeneProliferationExpressionGenetic abnormalitiesEffectorsMutationsAllelesRegulationPathwayFibroblastsFrank malignancy