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dc.creatorCalvo Baltanás, Fernandoes
dc.creatorGarcía Navas, Rósulaes
dc.creatorSantos, Eugenioes
dc.date.accessioned2022-12-15T16:32:06Z
dc.date.available2022-12-15T16:32:06Z
dc.date.issued2021-06-21
dc.identifier.citationCalvo Baltanás, F., García Navas, R. y Santos, E. (2021). SOS2 Comes to the Fore: Differential Functionalities in Physiology and Pathology. International Journal of Molecular Sciences, 22 (12), 6613. https://doi.org/10.3390/ijms22126613.
dc.identifier.issn1422-0067es
dc.identifier.urihttps://hdl.handle.net/11441/140531
dc.description.abstractThe SOS family of Ras-GEFs encompasses two highly homologous and widely expressed members, SOS1 and SOS2. Despite their similar structures and expression patterns, early studies of constitutive KO mice showing that SOS1-KO mutants were embryonic lethal while SOS2-KO mice were viable led to initially viewing SOS1 as the main Ras-GEF linking external stimuli to downstream RAS signaling, while obviating the functional significance of SOS2. Subsequently, different genetic and/or pharmacological ablation tools defined more precisely the functional specificity/redundancy of the SOS1/2 GEFs. Interestingly, the defective phenotypes observed in concomitantly ablated SOS1/2-DKO contexts are frequently much stronger than in single SOS1-KO scenarios and undetectable in single SOS2-KO cells, demonstrating functional redundancy between them and suggesting an ancillary role of SOS2 in the absence of SOS1. Preferential SOS1 role was also demonstrated in different RASopathies and tumors. Conversely, specific SOS2 functions, including a critical role in regulation of the RAS–PI3K/AKT signaling axis in keratinocytes and KRAS-driven tumor lines or in control of epidermal stem cell homeostasis, were also reported. Specific SOS2 mutations were also identified in some RASopathies and cancer forms. The relevance/specificity of the newly uncovered functional roles suggests that SOS2 should join SOS1 for consideration as a relevant biomarker/therapy target.es
dc.formatapplication/pdfes
dc.format.extent14 p.es
dc.language.isoenges
dc.publisherMDPIes
dc.relation.ispartofInternational Journal of Molecular Sciences, 22 (12), 6613.
dc.rightsAtribución 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectson of sevenlesses
dc.subjectSOS1es
dc.subjectSOS2es
dc.subjectRAS signalinges
dc.subjectGEFses
dc.titleSOS2 Comes to the Fore: Differential Functionalities in Physiology and Pathologyes
dc.typeinfo:eu-repo/semantics/articlees
dcterms.identifierhttps://ror.org/03yxnpp24
dc.type.versioninfo:eu-repo/semantics/publishedVersiones
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.contributor.affiliationUniversidad de Sevilla. Departamento de Fisiología Médica y Biofísicaes
dc.relation.projectIDCIVP19A5942es
dc.relation.projectIDCB16/12/00352es
dc.relation.projectIDFIS PI19/00934es
dc.relation.projectIDSA264P18 UIC 076es
dc.relation.projectIDFS/32-2020es
dc.relation.publisherversionhttps://www.mdpi.com/1422-0067/22/12/6613es
dc.identifier.doi10.3390/ijms22126613es
dc.journaltitleInternational Journal of Molecular Scienceses
dc.publication.volumen22es
dc.publication.issue12es
dc.publication.initialPage6613es
dc.contributor.funderFundación Ramón Areces CIVP19A5942es
dc.contributor.funderEuropean Commission (EC). Fondo Europeo de Desarrollo Regional (FEDER)es
dc.contributor.funderInstituto de Salud Carlos III CB16/12/00352; FIS PI19/00934es
dc.contributor.funderGobierno regional de Castilla y León SA264P18 UIC 076es
dc.contributor.funderFundación Memoria de D. Samuel Solorzano Barruso FS/32-2020es

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Except where otherwise noted, this item's license is described as: Atribución 4.0 Internacional