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dc.contributor.authorPitolli, Consueloen
dc.contributor.authorWang, Yingen
dc.contributor.authorCandi, Eleonoraen
dc.contributor.authorShi, Yufangen
dc.contributor.authorMelino, Gerryen
dc.contributor.authorAmelio, Ivanoen
dc.date.accessioned2019-12-13T00:30:09Z
dc.date.available2019-12-13T00:30:09Z
dc.date.issued2019-12-09en
dc.identifier.issn2072-6694
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/299827
dc.description.abstractThe tumour suppressor p53 regulates different cellular pathways involved in cell survival, DNA repair, apoptosis and senescence. However, according to an increasing number of studies, the p53-mediated canonical DNA damage response is dispensable for tumour suppression. p53 is involved in mechanisms regulating many other cellular processes, including metabolism, autophagy, cell migration and invasion, and these pathways might crucially contribute to its tumour suppressor function. In this review we summarize the canonical and non-canonical functions of p53 in an attempt to provide an overview of the potentially crucial aspects related to its tumour suppressor activity.
dc.description.sponsorshipThis work is funded by the Medical Research Council and partially supported by AIRC (IG22206 to EC) and Ministry of Health (IDI-IRCCS)-MAECI (CN18GR09 to EC).
dc.format.mediumElectronicen
dc.languageengen
dc.publisherMDPI AG
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.titlep53-Mediated Tumor Suppression: DNA-Damage Response and Alternative Mechanisms.en
dc.typeArticle
prism.issueIdentifier12en
prism.publicationDate2019en
prism.publicationNameCancersen
prism.volume11en
dc.identifier.doi10.17863/CAM.46900
dcterms.dateAccepted2019-12-04en
rioxxterms.versionofrecord10.3390/cancers11121983en
rioxxterms.versionVoR
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2019-12-09en
dc.contributor.orcidShi, Yufang [0000-0001-8964-319X]
dc.contributor.orcidMelino, Gerry [0000-0001-9428-5972]
dc.contributor.orcidAmelio, Ivano [0000-0002-9126-5391]
dc.identifier.eissn2072-6694
rioxxterms.typeJournal Article/Reviewen


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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International