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Modelling the onset of senescence at the G1/S cell cycle checkpoint

dc.contributor.authorMombach, José CM
dc.contributor.authorBugs, Cristhian A
dc.contributor.authorChaouiya, Claudine
dc.date.accessioned2015-10-01T16:44:50Z
dc.date.available2015-10-01T16:44:50Z
dc.date.issued2014-10-27
dc.description.abstractDNA damage (single or double-strand breaks) triggers adapted cellular responses. These responses are elicited through signalling pathways, which activate cell cycle checkpoints and basically lead to three cellular fates: cycle arrest promoting DNA repair, senescence (permanent arrest) or cell death. Cellular senescence is known for having a tumour-suppressive function and its regulation arouses a growing scientific interest. Here, we advance a qualitative model covering DNA damage response pathways, focusing on G1/S checkpoint enforcement, supposedly more sensitive to arrest than G2/M checkpoint.pt_PT
dc.description.sponsorshipInstituto Gulbenkian de Ciência (IGC), the Brazilian agency CNPq for financial support (grants 236673/2012-2, 304805/2012-2, 402547/2012-8).pt_PT
dc.identifier10.1186/1471-2164-15-S7-S7
dc.identifier.doi10.1186/1471-2164-15-S7-S7
dc.identifier.doi10.1186/1471-2164-15-S7-S7
dc.identifier.urihttp://hdl.handle.net/10400.7/339
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherBioMed Centralpt_PT
dc.relation.publisherversionhttp://www.biomedcentral.com/1471-2164/15/S7/S7pt_PT
dc.subjectSignalling networkpt_PT
dc.subjectLogical modellingpt_PT
dc.subjectSenescencept_PT
dc.subjectDNA-damagept_PT
dc.subjectCell fatept_PT
dc.subjectCell cycle checkpointpt_PT
dc.titleModelling the onset of senescence at the G1/S cell cycle checkpointpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage11pt_PT
oaire.citation.startPage1pt_PT
oaire.citation.titleBMC Genomicspt_PT
oaire.citation.volume15pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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