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SOS GEFs in health and disease.

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dc.contributor.authorBaltanás, Fernando C
dc.contributor.authorZarich-Dimitrievich, Natasha
dc.contributor.authorRojas-Cabañeros, Jose Maria
dc.contributor.authorSantos, Eugenio
dc.contributor.funderInstituto de Salud Carlos III
dc.contributor.funderFundación Ramón Areces
dc.contributor.funderMinisterio de Economía y Competitividad (España)
dc.contributor.funderUnión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
dc.contributor.funderAsociación Española Contra el Cáncer
dc.date.accessioned2020-12-29T11:31:47Z
dc.date.available2020-12-29T11:31:47Z
dc.date.issued2020-12
dc.description.abstractSOS1 and SOS2 are the most universal and widely expressed family of guanine exchange factors (GEFs) capable or activating RAS or RAC1 proteins in metazoan cells. SOS proteins contain a sequence of modular domains that are responsible for different intramolecular and intermolecular interactions modulating mechanisms of self-inhibition, allosteric activation and intracellular homeostasis. Despite their homology, analyses of SOS1/2-KO mice demonstrate functional prevalence of SOS1 over SOS2 in cellular processes including proliferation, migration, inflammation or maintenance of intracellular redox homeostasis, although some functional redundancy cannot be excluded, particularly at the organismal level. Specific SOS1 gain-of-function mutations have been identified in inherited RASopathies and various sporadic human cancers. SOS1 depletion reduces tumorigenesis mediated by RAS or RAC1 in mouse models and is associated with increased intracellular oxidative stress and mitochondrial dysfunction. Since WT RAS is essential for development of RAS-mutant tumors, the SOS GEFs may be considered as relevant biomarkers or therapy targets in RAS-dependent cancers. Inhibitors blocking SOS expression, intrinsic GEF activity, or productive SOS protein-protein interactions with cellular regulators and/or RAS/RAC targets have been recently developed and shown preclinical and clinical effectiveness blocking aberrant RAS signaling in RAS-driven and RTK-driven tumors.es_ES
dc.description.peerreviewedSíes_ES
dc.description.sponsorshipES and FCB were supported by grants from ISCIII-MCUI (FIS PI19/00934), JCyL (SA264P18-UIC 076) and Areces Foundation (CIVP19A5942). JMRC and NZ received grant support from MINECO-FEDER (SAF2016-78852-R and Spanish Association against Cancer (AECC/CGB14142035THOM). ES and JMRC were also supported by ISCIII-CIBERONC (groups CB16/12/00352 and CB16/12/00273, respectively). Research co-financed by FEDER funds.es_ES
dc.format.number2es_ES
dc.format.page188445es_ES
dc.format.volume1874es_ES
dc.identifier.citationBiochim Biophys Acta Rev Cancer . 2020 Dec;1874(2):188445es_ES
dc.identifier.doi10.1016/j.bbcan.2020.188445es_ES
dc.identifier.e-issn1879-2561
dc.identifier.journalBiochimica et biophysica acta. Reviews on canceres_ES
dc.identifier.pubmedID33035641es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/11569
dc.language.isoenges_ES
dc.publisherElsevieres_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/FIS PI19/00934es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SA264P18-UIC 076es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/SAF2016-78852-Res_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/CB16/12/00352es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/ES/CB16/12/00273es_ES
dc.relation.publisherversionhttp://dx.doi.org/10.1016/j.bbcan.2020.188445es_ES
dc.repisalud.centroISCIII::Unidad Funcional de Investigación de Enfermedades Crónicas (UFIEC)es_ES
dc.repisalud.institucionISCIIIes_ES
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectSOS1es_ES
dc.subjectSOS2es_ES
dc.subjectRASGEFes_ES
dc.subjectRASes_ES
dc.subjectCanceres_ES
dc.subjectRasopathieses_ES
dc.titleSOS GEFs in health and disease.es_ES
dc.typejournal articlees_ES
dc.type.hasVersionVoRes_ES
dspace.entity.typePublication
relation.isAuthorOfPublication8a02c8b2-2b21-48f0-89b5-eabddf9b9b64
relation.isAuthorOfPublication370c9d7e-71b3-4b96-87ba-fe32e580397d
relation.isAuthorOfPublication.latestForDiscovery8a02c8b2-2b21-48f0-89b5-eabddf9b9b64
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