Onset of Quiescence Following p53 Mediated Down-Regulation of H2AX in Normal Cells 英文参考文献.docVIP

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Onset of Quiescence Following p53 Mediated Down-Regulation of H2AX in Normal Cells 英文参考文献.doc

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Onset of Quiescence Following p53 Mediated Down-Regulation of H2AX in Normal Cells 英文参考文献

OnsetofQuiescenceFollowingp53MediatedDown- RegulationofH2AXinNormalCells YukoAtsumi1.,HiroakiFujimori1,3.,HirokazuFukuda2.,AkiInase2,KeitaroShinohe3 ,Yoshiko Yoshioka3,MimaShikanai3,YosukeIchijima3,JunyaUnno4,ShukiMizutani4,NaotoTsuchiya2, YoshitakaHippo2,HitoshiNakagama2,MitsukoMasutani1,HirobumiTeraoka3,Ken-ichiYoshioka1,3* 1Division of Genome Stability Research, National Cancer Center Research Institute, Tokyo, Japan, 2Division of Cancer Development System, National Cancer Center ResearchInstitute,Tokyo,Japan,3DepartmentofPathologicalBiochemistry,MedicalResearchInstitute,TokyoMedicalandDentalUniversity,Tokyo,Japan,4Department ofPediatricsandDevelopmentalBiology,GraduateSchoolofMedicalandDentalSciences,TokyoMedicalandDentalUniversity,Tokyo,Japan Abstract Normalcells,bothinvivoandinvitro,becomequiescentafterserialcellproliferation.Duringthisprocess,cellscandevelop immortalitywithgenomicinstability,althoughthemechanismsbywhichthisisregulatedareunclear.Here,weshowthata growth-arrested cellular status is produced by the down-regulation of histone H2AX in normal cells. Normal mouse embryonic fibroblast cells preserve an H2AX diminished quiescent status through p53 regulation and stable-diploidy maintenance. However, such quiescence is abrogated under continuous growth stimulation, inducing DNA replication stress. Because DNA replication stress-associated lesions are cryptogenic and capable of mediating chromosome-bridge formation and cytokinesis failure, this results in tetraploidization. Arf/p53 module-mutation is induced during tetraploidization with the resulting H2AX recovery and immortality acquisition. Thus, although cellular homeostasis is preserved under quiescence with stable diploidy, tetraploidization induced under growth stimulation disrupts the homeostasisandtriggersimmortalityacquisition. Citation:AtsumiY,FujimoriH,FukudaH,InaseA,ShinoheK,etal.(2011)OnsetofQuiescenceFollowingp53MediatedDown-RegulationofH2AXinNormal Cells.PLoSONE6(8):e23432.doi:10.137