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dc.contributor.authorO'BYRNE, KENen
dc.date.accessioned2017-05-24T14:10:00Z
dc.date.available2017-05-24T14:10:00Z
dc.date.issued2016en
dc.date.submitted2016en
dc.identifier.citationBox J.K, Paquet N, Adams M.N, Boucher D, Bolderson E, O'Byrne K.J, Richard D.J, Nucleophosmin: From structure and function to disease development, BMC Molecular Biology, 17, 1, 2016, 19-en
dc.identifier.otherYen
dc.description.abstractNucleophosmin (NPM1) is a critical cellular protein that has been implicated in a number of pathways including mRNA transport, chromatin remodeling, apoptosis and genome stability. NPM1 function is a critical requirement for normal cellular biology as is underlined in cancer where NPM1 is commonly overexpressed, mutated, rearranged and sporadically deleted. Consistent with a multifunctional role within the cell, NPM1 can function not only as a proto- oncogene but also as a tumor suppressor. The aim of this review is to look at the less well-described role of NPM1 in the DNA repair pathways as well as the role of NPM1 in the regulation of apoptosis and its mutation in cancers.en
dc.description.sponsorshipThis work was supported by a NHMRC project Grant (1066550), an ARC project Grant (D.J.R, DP 120103099) and by a Queensland Health Senior Clinical Research Fellowship (K.J.O.). M.A. holds a NHMRC Early Career Fellowship (1091589). E.B. is supported by an Advance Queensland Research Fellowship.en
dc.format.extent19en
dc.relation.ispartofseriesBMC Molecular Biologyen
dc.relation.ispartofseries17en
dc.relation.ispartofseries1en
dc.rightsYen
dc.subjectNucleophosmin 1 DNA repair Cancer Apoptosisen
dc.subject.lcshNucleophosmin 1 DNA repair Cancer Apoptosisen
dc.titleNucleophosmin: From structure and function to disease developmenten
dc.typeJournal Articleen
dc.type.supercollectionscholarly_publicationsen
dc.type.supercollectionrefereed_publicationsen
dc.identifier.peoplefinderurlhttp://people.tcd.ie/obyrnekeen
dc.identifier.rssinternalid156634en
dc.identifier.doihttp://dx.doi.org/10.1186/s12867-016-0073-9en
dc.rights.ecaccessrightsopenAccess
dc.identifier.rssurihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-84983260759&doi=10.1186%2fs12867-016-0073-9&partnerID=40&md5=3b0bcc59a72a8fff0d488b4862cd5cc8en
dc.identifier.urihttp://hdl.handle.net/2262/80214


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