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                  <mods:namePart>Rojas-Cabañeros, Jose Maria</mods:namePart>
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                  <mods:namePart>Oliva-Martinez, Jose Luis</mods:namePart>
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                  <mods:namePart>Junta de Castilla y León (España)</mods:namePart>
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               <mods:identifier type="citation">Genes Cancer. 2011;2(3):298-305</mods:identifier>
               <mods:identifier type="doi">10.1177/1947601911408078</mods:identifier>
               <mods:identifier type="e-issn">1947-6027</mods:identifier>
               <mods:identifier type="issn">1947-6019</mods:identifier>
               <mods:identifier type="journal">Genes &amp; cancer</mods:identifier>
               <mods:identifier type="other">https://pmc.ncbi.nlm.nih.gov/articles/PMC3128634/</mods:identifier>
               <mods:identifier type="pubmedID">21779500</mods:identifier>
               <mods:identifier type="uri">http://hdl.handle.net/20.500.12105/7002</mods:identifier>
               <mods:abstract>The Son of Sevenless (Sos) factors were originally discovered 2 decades ago as specialized Ras activators in signaling pathways controlling the process of R7 cell development in the eye of Drosophila melanogaster. The 2 known members of the mammalian Sos family (Sos1 and Sos2) code for ubiquitously expressed, highly homologous (69% overall) proteins involved in coupling signals originated by cell surface receptor tyrosine kinases (RTKs) to downstream, Ras-dependent mitogenic signaling pathways. Mechanistically, the Sos proteins function as enzymatic factors interacting with Ras proteins in response to upstream stimuli to promote guanine nucleotide exchange (GDP/GTP) and subsequent formation of the active Ras-GTP complex. In this review, we summarize current knowledge on structural, regulatory, and functional aspects of the Sos family, focusing on specific aspects of Sos biology such as structure-function relationship, crosstalk with different signaling pathways, and in vivo functional significance as deduced from phenotypic characterization of Sos knockout mice and human genetic syndromes caused by germline hSos1 mutations.</mods:abstract>
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               <mods:subject>
                  <mods:topic>RTK</mods:topic>
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                  <mods:topic>Ras</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Ras-GEF</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Sos</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>signaling</mods:topic>
               </mods:subject>
               <mods:titleInfo>
                  <mods:title>Mammalian son of sevenless Guanine nucleotide exchange factors: old concepts and new perspectives</mods:title>
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