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. 2019 Dec 18;10(12):955. doi: 10.1038/s41419-019-2192-y

Fig. 1. Downstream canonical signaling pathways of oncogenic RAS effectors.

Fig. 1

RAS signaling is initiated by upstream growth factor receptors and receptors tyrosine kinase (RTK) activation, leading to recruitment of guanine nucleotide exchange factor (GEF) by Src homology 2 domain containing transforming protein (SHC) and growth factor receptor-bound protein 2 (GRB2), which substitutes GDP with GTP to activate RAS. Once in its active state, or in the case of activating mutations, RAS can engage its downstream effectors including but not limited to phosphoinositide 3-kinase (PI3K), rapidly accelerated fibrosarcoma proto-oncogene (RAF), Ral guanine nucleotide dissociation stimulator (RALGDS) and phospholipase C-epsilon (PLCε).