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http://hdl.handle.net/10261/60127
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dc.contributor.author | Moretó, Jemina | - |
dc.contributor.author | Santos de Dios, Eugenio | - |
dc.date.accessioned | 2012-11-13T12:51:44Z | - |
dc.date.available | 2012-11-13T12:51:44Z | - |
dc.date.issued | 2009 | - |
dc.identifier | doi: 10.1016/j.cellsig.2009.07.018 | - |
dc.identifier | issn: 0898-6568 | - |
dc.identifier.citation | Cellular Signalling 21(12): 1827-1836 (2009) | - |
dc.identifier.uri | http://hdl.handle.net/10261/60127 | - |
dc.description.abstract | We have previously demonstrated that inhibition of calmodulin (CaM) and the concomitant reduction of PI3K interfere with H-Ras-mediated activation of Raf-1 [1]. In the present study, we show that CaM has completely opposite effects on K-Ras-mediated Raf-1 activation. The differential contribution of CaM in the regulation of Raf-1 kinase activity via K- or H-Ras correlates with the stimulatory or inhibitory effect of CaM on MAPK phosphorylation depending on the cell type analyzed. FRET microscopy and biochemical analysis show that inhibition of CaM increases K-Ras-GTP levels and consequently its association with Raf-1. Though inhibition of CaM, using the CaM antagonist W-13, significantly increased Raf-1 activation by K-Ras-GTP, MAPK activation downstream K-Ras/Raf-1 was strongly reduced in COS-1 and several other cell lines. In contrast, in other cell lines such as NIH3T3-wt8, W-13-mediated inhibition of CaM increased Raf-1 activity, but resulted in an increase in MAPK phosphorylation. These findings suggest that modulation of K-Ras activity via CaM regulates MAPK signaling only in certain cell types. In support of this hypothesis, the comparison of H- and K-Ras expression, GTP loading and Raf-1 interaction in COS-1 and NIH3T3-wt8 suggests that the overall role of CaM in MAPK signal output is determined by the ratio of activated H- and K-Ras and the cell-specific contribution of each isoform in Raf-1 activation. © 2009 Elsevier Inc. All rights reserved. | - |
dc.description.sponsorship | This study was supported by grants BFU2007-67652 from Ministerio de Educación y Ciencia (MEC) of Spain to F.T.; BFU2006-01151 (MEC), RTICC program (Instituto de Salud Carlos III, Spain) and PI040236 from Maratò TV3 to C.E.; BFU2008-00345 (MEC) to A. P.; and grants 510293, 510294 from the National Health andMedical Research Council of Australia) to T. G.M.V-Q. is a recipient of a pre-doctoral RTICC program fellowship. | - |
dc.language.iso | eng | - |
dc.publisher | Elsevier | - |
dc.rights | closedAccess | - |
dc.title | Differential involvement of H- and K-Ras in Raf-1 activation determines the role of calmodulin in MAPK signaling | - |
dc.type | artículo | - |
dc.identifier.doi | 10.1016/j.cellsig.2009.07.018 | - |
dc.date.updated | 2012-11-13T12:51:44Z | - |
dc.description.version | Peer Reviewed | - |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.openairetype | artículo | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | No Fulltext | - |
item.languageiso639-1 | en | - |
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