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dc.contributor.authorBettencourt-Dias, Men_US
dc.contributor.authorMittnacht, Sen_US
dc.contributor.authorBrockes, JPen_US
dc.date.accessioned2018-09-12T11:45:28Z
dc.date.issued2003-10en_US
dc.identifier.citationJournal of cell science, 2003, 116 (Pt 19), pp. 4001 - 4009en_US
dc.identifier.issn0021-9533en_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/2653
dc.identifier.eissn1477-9137en_US
dc.identifier.doi10.1242/jcs.00698en_US
dc.description.abstractAdult newt cardiomyocytes, in contrast to their mammalian counterparts, can proliferate after injury and contribute to the functional regeneration of the heart. In order to understand the mechanisms underlying this plasticity we performed longitudinal studies on single cardiomyocytes in culture. We find that the majority of cardiomyocytes can enter S phase, a process that occurs in response to serum-activated pathways and is dependent on the phosphorylation of the retinoblastoma protein. However, more than half of these cells stably arrest at either entry to mitosis or during cytokinesis, thus resembling the behaviour observed in mammalian cardiomyocytes. Approximately a third of the cells progress through mitosis and may enter successive cell divisions. When cardiomyocytes divided more than once, the proliferative behaviour of sister cells was significantly correlated, in terms of whether they underwent a subsequent cell cycle, and if so, the duration of that cycle. These observations suggest a mechanism whereby newt heart regeneration depends on the retention of proliferative potential in a subset of cardiomyocytes. The regulation of the remaining newt cardiomyocytes is similar to that described for their mammalian counterparts, as they arrest during mitosis or cytokinesis. Understanding the nature of this block and why it arises in some but not other newt cardiomyocytes may lead to an augmentation of the regenerative potential in the mammalian heart.en_US
dc.formatPrint-Electronicen_US
dc.format.extent4001 - 4009en_US
dc.languageengen_US
dc.language.isoengen_US
dc.rights.urihttp://www.rioxx.net/licenses/all-rights-reserveden_US
dc.subjectMyocardiumen_US
dc.subjectMyocytes, Cardiacen_US
dc.subjectAnimalsen_US
dc.subjectSalamandridaeen_US
dc.subjectRetinoblastoma Proteinen_US
dc.subjectRegenerationen_US
dc.subjectCell Divisionen_US
dc.subjectS Phaseen_US
dc.subjectCell Differentiationen_US
dc.subjectPhosphorylationen_US
dc.subjectModels, Biologicalen_US
dc.titleHeterogeneous proliferative potential in regenerative adult newt cardiomyocytes.en_US
dc.typeJournal Article
rioxxterms.versionofrecord10.1242/jcs.00698en_US
rioxxterms.licenseref.startdate2003-10en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfJournal of cell scienceen_US
pubs.issuePt 19en_US
pubs.notesNot knownen_US
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Closed research teams/Anti Oncogene
pubs.volume116en_US
pubs.embargo.termsNot knownen_US
icr.researchteamAnti Oncogeneen_US
dc.contributor.icrauthorMittnacht, Sibylleen_US


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