Figure 1.

A simplified model of Ras signaling. Ras signaling pathways originate from growth factor binding and activation of its receptor such as the epidermal growth factor [EGF] binding to its receptor, EGF-R. The activation of the EGF-R by EGF primes the autophosphorylation of the cytoplasmic domain of EGF-R (P) and the recruitment of adapter proteins, Grb2 and Sos. Sos is a primary Ras-GEF that will promote GTP loading of Ras and subsequent Ras activation. Ras can then continue the signaling cascade to Raf-MAPKK (MEK)-MAPK (ERK) and eventually to the activation of the transcription factor Elk-1. Once activated by phosphorylation, Elk-1 can then acquire DNA binding competency to activate gene transcription to drive proliferation. Elk-1 is just one of many transcription factors modulated by Ras signaling and is only shown here for simplicity. There is evidence for Ras activation of cell death and it is thought to proceed through the RA SSF family of proteins. In the bottom right corner of this figure is a limited list of diseases that are a direct result of abnormal Ras signaling (the RASopathies).