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dc.contributor.authorSbirkov, Y
dc.contributor.authorKwok, C
dc.contributor.authorBhamra, A
dc.contributor.authorThompson, AJ
dc.contributor.authorGil, V
dc.contributor.authorZelent, A
dc.contributor.authorPetrie, K
dc.date.accessioned2021-12-01T09:52:06Z
dc.date.available2021-12-01T09:52:06Z
dc.date.issued2017-07-05
dc.identifier.citationInternational journal of molecular sciences, 2017, 18 (7)
dc.identifier.issn1422-0067
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/4909
dc.identifier.eissn1422-0067
dc.identifier.doi10.3390/ijms18071440
dc.description.abstractAlterations to the gene encoding the EZH2 (KMT6A) methyltransferase, including both gain-of-function and loss-of-function, have been linked to a variety of haematological malignancies and solid tumours, suggesting a complex, context-dependent role of this methyltransferase. The successful implementation of molecularly targeted therapies against EZH2 requires a greater understanding of the potential mechanisms by which EZH2 contributes to cancer. One aspect of this effort is the mapping of EZH2 partner proteins and cellular targets. To this end we performed affinity-purification mass spectrometry in the FAB-M2 HL-60 acute myeloid leukaemia (AML) cell line before and after all- trans retinoic acid-induced differentiation. These studies identified new EZH2 interaction partners and potential non-histone substrates for EZH2-mediated methylation. Our results suggest that EZH2 is involved in the regulation of translation through interactions with a number of RNA binding proteins and by methylating key components of protein synthesis such as eEF1A1. Given that deregulated mRNA translation is a frequent feature of cancer and that eEF1A1 is highly expressed in many human tumours, these findings present new possibilities for the therapeutic targeting of EZH2 in AML.
dc.formatElectronic
dc.languageeng
dc.language.isoeng
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.subjectCell Line, Tumor
dc.subjectHL-60 Cells
dc.subjectHumans
dc.subjectCarrier Proteins
dc.subjectHistones
dc.subjectProtein Interaction Mapping
dc.subjectComputational Biology
dc.subjectAmino Acid Sequence
dc.subjectProtein Conformation
dc.subjectProtein Binding
dc.subjectMethylation
dc.subjectModels, Molecular
dc.subjectMass Spectrometry
dc.subjectLeukemia, Myeloid, Acute
dc.subjectWorkflow
dc.subjectProtein Interaction Maps
dc.subjectGene Ontology
dc.subjectEnhancer of Zeste Homolog 2 Protein
dc.titleSemi-Quantitative Mass Spectrometry in AML Cells Identifies New Non-Genomic Targets of the EZH2 Methyltransferase.
dc.typeJournal Article
dcterms.dateAccepted2017-06-29
rioxxterms.versionVoR
rioxxterms.versionofrecord10.3390/ijms18071440
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by/4.0
rioxxterms.licenseref.startdate2017-07-05
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfInternational journal of molecular sciences
pubs.issue7
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/Cancer Biomarkers
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/Cancer Biomarkers
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.publication-statusPublished
pubs.volume18
pubs.embargo.termsNot known
icr.researchteamCancer Biomarkers
icr.researchteamPaediatric Solid Tumour Biology and Therapeutics
dc.contributor.icrauthorKwok, Colinen_US
dc.contributor.icrauthorGil, Veronicaen_US


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Except where otherwise noted, this item's license is described as https://creativecommons.org/licenses/by/4.0