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dc.contributor.authorAmato, Jussara
dc.contributor.authorMadanayake, Thushara W.
dc.contributor.authorIaccarino, Nunzia
dc.contributor.authorNovellino, Ettore
dc.contributor.authorRandazzo, Antonio
dc.contributor.authorHurley, Laurence H.
dc.contributor.authorPagano, Bruno
dc.date.accessioned2018-10-12T19:28:45Z
dc.date.available2018-10-12T19:28:45Z
dc.date.issued2018-09-04
dc.identifier.citationChem. Commun., 2018, 54, 9442en_US
dc.identifier.issn1359-7345
dc.identifier.issn1364-548X
dc.identifier.pmid30079419
dc.identifier.doi10.1039/C8CC03614D
dc.identifier.urihttp://hdl.handle.net/10150/630255
dc.description.abstractThis communication reports on a possible distinct role of HMGB1 protein. Biophysical studies revealed that HMGB1 binds and stabilizes the G-quadruplex of the KRAS promoter element that is responsible for most of the transcriptional activity. Biological data showed that inhibition of HMGB1 increases KRAS expression. These results suggest that HMGB1 could play a role in the gene transcriptional regulation via the functional recognition of the G-quadruplex.en_US
dc.description.sponsorshipNCI NIH HHS [R01 CA153821]en_US
dc.language.isoenen_US
dc.publisherROYAL SOC CHEMISTRYen_US
dc.relation.urlhttp://xlink.rsc.org/?DOI=C8CC03614Den_US
dc.rights© The Royal Society of Chemistry 2018en_US
dc.titleHMGB1 binds to the KRAS promoter G-quadruplex: a new player in oncogene transcriptional regulation?en_US
dc.typeArticleen_US
dc.contributor.departmentUniv Arizona, Coll Pharmen_US
dc.identifier.journalCHEMICAL COMMUNICATIONSen_US
dc.description.note12 month embargo; published online: 31 July 2018en_US
dc.description.collectioninformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.en_US
dc.eprint.versionFinal accepted manuscripten_US
dc.source.journaltitleChemical Communications
dc.source.volume54
dc.source.issue68
dc.source.beginpage9442
dc.source.endpage9445


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