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dc.contributor.authorMargalef, Pol
dc.contributor.authorFernández-Majada, Vanessa
dc.contributor.authorVillanueva, Alberto
dc.contributor.authorGarcia-Carbonell, Ricard
dc.contributor.authorIglesias, Mar
dc.contributor.authorLópez, Laura
dc.contributor.authorMartínez-Iniesta, María
dc.contributor.authorVillà-Freixa, Jordi
dc.contributor.authorMulero, Mari Carmen
dc.contributor.authorAndreu, Montserrat
dc.contributor.authorTorres, Ferran
dc.contributor.authorMayo, Marty W.
dc.contributor.authorBigas, Anna
dc.contributor.authorEspinosa, Lluis
dc.date.accessioned2020-10-28T15:11:14Z
dc.date.available2020-10-28T15:11:14Z
dc.date.issued2012-10-25
dc.identifier.citationMargalef, Pol; Fernández-Majada, Vanessa; Villanueva, Alberto [et al.]. A truncated form of IKKa is responsible for specific nuclear IKK activity in colorectal cancer. Cell Reports, 2012, 2(4), p. 840-854. Disponible en: <https://www.sciencedirect.com/science/article/pii/S2211124712002689?via%3Dihub>. Fecha de acceso: 28 oct. 2020. DOI: 10.1016/j.celrep.2012.08.028.ca
dc.identifier.issn2211-1247ca
dc.identifier.urihttp://hdl.handle.net/20.500.12328/1698
dc.description.abstractNuclear IKKα regulates gene transcription by phosphorylating specific substrates and has been linked to cancer progression and metastasis. However, the mechanistic connection between tumorigenesis and IKKα activity remains poorly understood. We have now analyzed 288 human colorectal cancer samples and found a significant association between the presence of nuclear IKK and malignancy. Importantly, the nucleus of tumor cells contains an active IKKα isoform with a predicted molecular weight of 45 kDa (p45-IKKα) that includes the kinase domain but lacks several regulatory regions. Active nuclear p45-IKKα forms a complex with nonactive IKKα and NEMO that mediates phosphorylation of SMRT and histone H3. Proteolytic cleavage of FL-IKKα into p45-IKKα is required for preventing the apoptosis of CRC cells in vitro and sustaining tumor growth in vivo. Our findings identify a potentially druggable target for treating patients with advance refractory CRC.ca
dc.format.extent15ca
dc.language.isoengca
dc.publisherElsevierca
dc.relation.ispartofCell Reportsca
dc.relation.ispartofseries2;4
dc.rights© 2012 The Authors. Published by Elsevier Inc. This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 Unported License (CC-BY-NC-ND; http://creativecommons.org/licenses/by-nc-nd/3.0/ legalcode)ca
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/3.0/
dc.subject.otherCòlon--Càncerca
dc.subject.otherMetàstasi
dc.subject.otherTumors
dc.subject.otherOncologia
dc.subject.otherCáncer de colon
dc.subject.otherMetástasis
dc.subject.otherTumores
dc.subject.otherOncología
dc.subject.otherColon cancer
dc.subject.otherMetastasis
dc.subject.otherTumors
dc.subject.otherOncology
dc.titleA truncated form of IKKa is responsible for specific nuclear IKK activity in colorectal cancerca
dc.typeinfo:eu-repo/semantics/articleca
dc.description.versioninfo:eu-repo/semantics/publishedVersionca
dc.rights.accessLevelinfo:eu-repo/semantics/openAccess
dc.embargo.termscapca
dc.subject.udc61ca
dc.subject.udc616ca
dc.identifier.doihttps://dx.doi.org/10.1016/j.celrep.2012.08.028ca


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© 2012 The Authors. Published by Elsevier Inc. This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 Unported License (CC-BY-NC-ND; http://creativecommons.org/licenses/by-nc-nd/3.0/
legalcode)
Except where otherwise noted, this item's license is described as https://creativecommons.org/licenses/by-nc-nd/3.0/