Skip to main content
. Author manuscript; available in PMC: 2022 Sep 9.
Published in final edited form as: Cancer Metastasis Rev. 2021 Sep 9;40(3):819–835. doi: 10.1007/s10555-021-09990-2

Fig. 1. Schematic illustration of KRAS pathway and targeted preclinical and clinical agents.

Fig. 1

Receptors in the EGFR family upstream of KRAS transmit extracellular signals to activate KRAS. KRAS is activated via GDP to GTP exchange catalyzed by GEFs such as SOS, whereas GAPs catalyze the GTPase activity of KRAS. Downstream signaling pathways include the RAF/MEK/ERK and PI3K/AKT/mTOR pathways, which result in the expression of genes that promote survival, growth, and metastasis. Inhibitors or other targeted agents in the upstream or downstream of KRAS signaling have been depicted. RASGAPs RAS GTPase activating proteins, RASGEFs RAS guanine exchange factors, CRBN cereblon, PROTACs proteolysis targeting chimeras, VHL Von Hippel–Lindau tumor suppressor