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dc.contributor.authorBüchel, G
dc.contributor.authorCarstensen, A
dc.contributor.authorMak, K-Y
dc.contributor.authorRoeschert, I
dc.contributor.authorLeen, E
dc.contributor.authorSumara, O
dc.contributor.authorHofstetter, J
dc.contributor.authorHerold, S
dc.contributor.authorKalb, J
dc.contributor.authorBaluapuri, A
dc.contributor.authorPoon, E
dc.contributor.authorKwok, C
dc.contributor.authorChesler, L
dc.contributor.authorMaric, HM
dc.contributor.authorRickman, DS
dc.contributor.authorWolf, E
dc.contributor.authorBayliss, R
dc.contributor.authorWalz, S
dc.contributor.authorEilers, M
dc.date.accessioned2018-02-19T16:31:02Z
dc.date.issued2017-12
dc.identifier.citationCell reports, 2017, 21 (12), pp. 3483 - 3497
dc.identifier.issn2211-1247
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.
dc.formatPrint
dc.format.extent3483 - 3497
dc.languageeng
dc.language.isoeng
dc.subjectCell Line, Tumor
dc.subjectHumans
dc.subjectDNA Topoisomerases, Type II
dc.subjectRNA Polymerase II
dc.subjectTranscription Factors, TFIII
dc.subjectNuclear Proteins
dc.subjectPhosphoproteins
dc.subjectDNA, Intergenic
dc.subjectS Phase
dc.subjectProtein Binding
dc.subjectPromoter Regions, Genetic
dc.subjectTranscription Elongation, Genetic
dc.subjectAurora Kinase A
dc.subjectN-Myc Proto-Oncogene Protein
dc.titleAssociation with Aurora-A Controls N-MYC-Dependent Promoter Escape and Pause Release of RNA Polymerase II during the Cell Cycle.
dc.typeJournal Article
dcterms.dateAccepted2017-11-27
rioxxterms.versionofrecord10.1016/j.celrep.2017.11.090
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by-nc-nd/4.0
rioxxterms.licenseref.startdate2017-12en_US
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfCell reports
pubs.issue12
pubs.notesNot known
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.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-statusPublished
pubs.volume21en_US
pubs.embargo.termsNot known
icr.researchteamPaediatric Solid Tumour Biology and Therapeuticsen_US
dc.contributor.icrauthorChesler, Louisen
dc.contributor.icrauthorKwok, Colinen
dc.contributor.icrauthorMarsden,en
dc.contributor.icrauthorPoon, Evonen


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