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dc.contributor.authorBüchel, Gen_US
dc.contributor.authorCarstensen, Aen_US
dc.contributor.authorMak, K-Yen_US
dc.contributor.authorRoeschert, Ien_US
dc.contributor.authorLeen, Een_US
dc.contributor.authorSumara, Oen_US
dc.contributor.authorHofstetter, Jen_US
dc.contributor.authorHerold, Sen_US
dc.contributor.authorKalb, Jen_US
dc.contributor.authorBaluapuri, Aen_US
dc.contributor.authorPoon, Een_US
dc.contributor.authorKwok, Cen_US
dc.contributor.authorChesler, Len_US
dc.contributor.authorMaric, HMen_US
dc.contributor.authorRickman, DSen_US
dc.contributor.authorWolf, Een_US
dc.contributor.authorBayliss, Ren_US
dc.contributor.authorWalz, Sen_US
dc.contributor.authorEilers, Men_US
dc.coverage.spatialUnited Statesen_US
dc.date.accessioned2018-02-19T16:31:02Z
dc.date.issued2017-12-19en_US
dc.identifierhttps://www.ncbi.nlm.nih.gov/pubmed/29262328en_US
dc.identifierS2211-1247(17)31757-6en_US
dc.identifier.citationCell Rep, 2017, 21 (12), pp. 3483 - 3497en_US
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/1323
dc.identifier.eissn2211-1247en_US
dc.identifier.doi10.1016/j.celrep.2017.11.090en_US
dc.description.abstractMYC proteins bind globally to active promoters and promote transcriptional elongation by RNA polymerase II (Pol II). To identify effector proteins that mediate this function, we performed mass spectrometry on N-MYC complexes in neuroblastoma cells. The analysis shows that N-MYC forms complexes with TFIIIC, TOP2A, and RAD21, a subunit of cohesin. N-MYC and TFIIIC bind to overlapping sites in thousands of Pol II promoters and intergenic regions. TFIIIC promotes association of RAD21 with N-MYC target sites and is required for N-MYC-dependent promoter escape and pause release of Pol II. Aurora-A competes with binding of TFIIIC and RAD21 to N-MYC in vitro and antagonizes association of TOP2A, TFIIIC, and RAD21 with N-MYC during S phase, blocking N-MYC-dependent release of Pol II from the promoter. Inhibition of Aurora-A in S phase restores RAD21 and TFIIIC binding to chromatin and partially restores N-MYC-dependent transcriptional elongation. We propose that complex formation with Aurora-A controls N-MYC function during the cell cycle.en_US
dc.format.extent3483 - 3497en_US
dc.languageengen_US
dc.language.isoengen_US
dc.subjectAurora-Aen_US
dc.subjectMYCen_US
dc.subjectN-MYCen_US
dc.subjectRAD21en_US
dc.subjectTFIIICen_US
dc.subjectneuroblastomaen_US
dc.subjectpause releaseen_US
dc.subjectAurora Kinase Aen_US
dc.subjectCell Line, Tumoren_US
dc.subjectDNA Topoisomerases, Type IIen_US
dc.subjectDNA, Intergenicen_US
dc.subjectHumansen_US
dc.subjectN-Myc Proto-Oncogene Proteinen_US
dc.subjectNuclear Proteinsen_US
dc.subjectPhosphoproteinsen_US
dc.subjectPromoter Regions, Geneticen_US
dc.subjectProtein Bindingen_US
dc.subjectRNA Polymerase IIen_US
dc.subjectS Phaseen_US
dc.subjectTranscription Elongation, Geneticen_US
dc.subjectTranscription Factors, TFIIIen_US
dc.titleAssociation with Aurora-A Controls N-MYC-Dependent Promoter Escape and Pause Release of RNA Polymerase II during the Cell Cycle.en_US
dc.typeJournal Article
dcterms.dateAccepted2017-11-27en_US
rioxxterms.versionofrecord10.1016/j.celrep.2017.11.090en_US
rioxxterms.licenseref.startdate2017-12-19en_US
rioxxterms.typeJournal Article/Reviewen_US
dc.relation.isPartOfCell Repen_US
pubs.issue12en_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/Cancer Therapeutics
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Therapeutics/Paediatric Solid Tumour Biology and Therapeutics
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Paediatric Solid Tumour Biology and Therapeutics
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Molecular Pathology/Paediatric Solid Tumour Biology and Therapeutics
pubs.organisational-group/ICR/Primary Group/Royal Marsden Clinical Units
pubs.publication-statusPublisheden_US
pubs.volume21en_US
pubs.embargo.termsNot knownen_US
icr.researchteamPaediatric Solid Tumour Biology and Therapeuticsen_US
dc.contributor.icrauthorChesler, Louisen_US
dc.contributor.icrauthorKwok, Colinen_US
dc.contributor.icrauthorMarsden,en_US
dc.contributor.icrauthorPoon, Evonen_US


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