SPARQL | HTML5 RDFa and Microdata document 
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      http://www.w3.org/1999/02/22-rdf-syntax-ns#type   
          http://www.w3.org/2004/02/skos/core#Collection 
          http://vocabularies.wikipathways.org/wp#Pathway 
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          http://purl.obolibrary.org/obo/PW_0000006 
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          http://vocabularies.wikipathways.org/wp#Curation:CPTAC 
          http://vocabularies.wikipathways.org/wp#Curation:PancCanNet 
          http://vocabularies.wikipathways.org/wp#Curation:AnalysisCollection 
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         http://purl.org/dc/elements/1.1/source   http://purl.org/dc/elements/1.1/title   http://purl.org/dc/terms/description   
          Ras proteins are small GTPases and are involved in transmitting signals within cells. In this way, Ras signaling controls many downstream processes, including cell proliferation, survival, growth, migration and differentiation. 
Ras proteins exists in two states, inactive while bound to GDP and active while bound to GTP. The exchange of GTP for GDP on RAS proteins is regulated by guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs). Activated RAS regulates cellular functions through a set of effector molecules, including Raf, phosphatidylinositol 3-kinase (PI3K) and Ral guanine nucleotide-dissociation stimulator (RALGDS).
Mutations in Ras genes can lead to the production of permanently activated Ras proteins. Because these signals result in cell growth and division, overactive Ras signaling can ultimately lead to cancer. The 3 Ras genes in humans (HRas, KRas, and NRas) are the most common oncogenes in human cancer; mutations that permanently activate Ras are found in 20% to 25% of all human tumors and up to 90% in certain types of cancer. 
Proteins on this pathway have targeted assays available via the [CPTAC Assay Portal](https://assays.cancer.gov/available_assays?wp_id=WP4223). 
         http://purl.org/dc/terms/identifier