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dc.contributor.authorKizilors, Aytug*
dc.contributor.authorPickard, Mark R.*
dc.contributor.authorSchulte, Cathleen E.*
dc.contributor.authorYacqub-Usman, Kiren*
dc.contributor.authorMcCarthy, Nicola J.*
dc.contributor.authorGan, Shu-Uin*
dc.contributor.authorDarling, David*
dc.contributor.authorGäken, Joop*
dc.contributor.authorWilliams, Gwyn T.*
dc.contributor.authorFarzaneh, Farzin*
dc.date.accessioned2017-09-25T13:00:55Z
dc.date.available2017-09-25T13:00:55Z
dc.date.issued14/08/2017
dc.identifier.citationKizilors, A., et al. (2017). Retroviral insertional mutagenesis implicates E3 ubiquitin ligase RNF168 in the control of cell proliferation and survival. Bioscience Reports, 37(4), BSR20170843. DOI: 10.1042/BSR20170843
dc.identifier.doi10.1042/BSR20170843
dc.identifier.urihttp://hdl.handle.net/10034/620626
dc.description.abstractThe E3 ubiquitin ligase RNF168 is a ring finger protein that has previously been identified to play an important regulatory role in the repair of double-strand DNA breaks. In the present study, an unbiased forward genetics functional screen in mouse granulocyte/ macrophage progenitor cell line FDCP1 has identified E3 ubiquitin ligase RNF168 as a key regulator of cell survival and proliferation. Our data indicate that RNF168 is an important component of the mechanisms controlling cell fate, not only in human and mouse haematopoietic growth factor-dependent cells, but also in the human breast epithelial cell line MCF-7. These observations therefore suggest that RNF168 provides a connection to key pathways controlling cell fate, potentially through interaction with PML nuclear bodies and/or epigenetic control of gene expression. Our study is the first to demonstrate a critical role for RNF168 in the in the mechanisms regulating cell proliferation and survival, in addition to its well-established role in DNA repair.
dc.language.isoenen
dc.publisherPortland Press
dc.relation.urlhttp://www.bioscirep.org/content/37/4/BSR20170843en
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en
dc.subjectRetroviral Insertional Mutagenesisen
dc.subjectUbiquitinen
dc.subjectApoptosisen
dc.subjectCell proliferationen
dc.subjectCell survivalen
dc.titleRetroviral insertional mutagenesis implicates E3 ubiquitin ligase RNF168 in the control of cell proliferation and survivalen
dc.typeArticleen
dc.identifier.eissn1573-4935
dc.contributor.departmentKings College London; Keele University; University of Chester; University of Nottingham; National University of Singapore
dc.identifier.journalBioscience reportsen
dc.date.accepted2017-07-27
or.grant.openaccessYesen
rioxxterms.funderBloodwise; Breast Cancer Now; Rosetrees Trust; National Institute for Health Research (NIHR) Biomedical Research Centre (BRC)en
rioxxterms.identifier.projectNon-RCUK externally funded research to Kings College London & Keele Universityen
rioxxterms.versionAMen
rioxxterms.licenseref.startdate2017-08-14
refterms.dateFCD2019-07-17T08:51:57Z
refterms.versionFCDAM
html.description.abstractThe E3 ubiquitin ligase RNF168 is a ring finger protein that has previously been identified to play an important regulatory role in the repair of double-strand DNA breaks. In the present study, an unbiased forward genetics functional screen in mouse granulocyte/ macrophage progenitor cell line FDCP1 has identified E3 ubiquitin ligase RNF168 as a key regulator of cell survival and proliferation. Our data indicate that RNF168 is an important component of the mechanisms controlling cell fate, not only in human and mouse haematopoietic growth factor-dependent cells, but also in the human breast epithelial cell line MCF-7. These observations therefore suggest that RNF168 provides a connection to key pathways controlling cell fate, potentially through interaction with PML nuclear bodies and/or epigenetic control of gene expression. Our study is the first to demonstrate a critical role for RNF168 in the in the mechanisms regulating cell proliferation and survival, in addition to its well-established role in DNA repair.


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