Ras GTPases are important hubs in signalling networks that regulate cell proliferation and survival. Ras pathway nodes are commonly mutated in developmental disorders and cancers; and Ras mutants are found in ~20% of all cancer patients. Cells express four closely related isoforms of Ras called HRAS, KRAS4A, KRAS4B and NRAS. Ras isoforms and different activating Ras mutations differentially contribute to normal and disease associated Ras biology; however, the mechanisms underpinning these observations are poorly understood. I鈥檒l be discussing our recent work investigating Ras variant biology to try to understand how they differ and why KRAS is so oncogenic. Using models to probe endogenous Ras biology we find that Ras variant outputs are context dependent and do not conform to the prevailing dogma derived from over-expression studies.
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