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Ras is the first protein in the apoptosis cascade, activated by tyrosine kinase receptors in response to growth factor stimulation from the extra cellular matrix. Ras is an oncogene, meaning it promotes cell cycle activity, driving cell replication, the main characteristic of cancerous tumours.
Ras has a binding site for GTP and hydrolyses it as part of its signal to downstream molecules such as raf and ARF. When there is a point mutation in the GTP binding site, the hydrolysis signal to raf and ARF becomes continuous instead of transient, and allows for uncontrolled cell replication.
Because of this behaviour, Ras has become a target for oncology researchers looking for treatments (http://www.bioportfolio.com/resources/pmarticle/394718/Targeting-The-Ras-Oncogene.html). As well as growth factors, scientists have found other compounds that interact with Ras, and have found one errant protein, Galectin-3 which promotes chronic activation of Ras, a sure tumour risk. Indeed, Galectin-3 activated Ras has been found in anaplastic thyroid carcinomas. Ras activity is also enhanced by other molecules called ASPP1 and ASPP2. By collecting the bigger picture of Ras activity, researchers have a greater number of options to try and modify Ras activity, and design therapeutics to inhibit it.
Ras mutations are one of the most common mutations found in cancer (http://www.bioportfolio.com/resources/pmarticle/361871/Interplay-Between-Oncogenic-K-ras-And-Wild-type-H-ras-In-Caco2.html) and implicated in a wide range of cancers affecting all organs and systems in the body. Therefore Ras is a prime target for oncology therapeutic research, to inhibit its’ devastating effects of the cell cycle.