dc.creatorLopez Bergami, Pablo Roberto
dc.date.accessioned2017-09-18T17:59:13Z
dc.date.accessioned2018-11-06T14:57:10Z
dc.date.available2017-09-18T17:59:13Z
dc.date.available2018-11-06T14:57:10Z
dc.date.created2017-09-18T17:59:13Z
dc.date.issued2009-03
dc.identifierLopez Bergami, Pablo Roberto; The long arm of BRAF V600E gets to mTORC1 ; Wiley; Pigment Cell & Melanoma Research; 22; 3; 3-2009; 244-245
dc.identifier1755-1471
dc.identifierhttp://hdl.handle.net/11336/24468
dc.identifier1755-148X
dc.identifierCONICET Digital
dc.identifierCONICET
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1892063
dc.description.abstractDespite the disappointing results of early clinical studies, targeting the BRAF ⁄ MEK⁄ extracellular signal-regulated kinase (ERK), mitogen-activated protein kinase (MAPK) pathway is still a subject of investigation due to its biological relevance to melanoma. It is now evident that to antagonize redundant protein functions and compensatory signaling pathways BRAF inhibitors must be combined with inhibitors of other relevant pathways based on a strong rational basis. Thus, we must expand our understanding of MAPK effectors and how MAPK interacts with those other pathways.
dc.languageeng
dc.publisherWiley
dc.relationinfo:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1111/j.1755-148X.2009.00566.x/abstract
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1111/j.1755-148X.2009.00566.x
dc.relationinfo:eu-repo/semantics/altIdentifier/pmid/19338646
dc.rightshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectMELANOMA
dc.subjectTUMOR SUPPRESSOR PROTEINS
dc.subjectMAP KINASE SIGNALING SYSTEM
dc.subjectPROTEIN SERINE THREONINE KINASES
dc.titleThe long arm of BRAF V600E gets to mTORC1
dc.typeArtículos de revistas
dc.typeArtículos de revistas
dc.typeArtículos de revistas


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