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. 2022 Jan 5;11:780655. doi: 10.3389/fonc.2021.780655

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Copyright © 2022 Shen, Qi, Ren, Lv and Yang

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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KRAS function and its main downstream pathways. This diagram is a summary of KRAS oncogenic mutations that impair its activity to hydrolyze GTP, thereby activating three major signaling pathways that mediate basic cellular processes. KRAS, kirsten rat sarcoma viral oncogene homolog; Gh2, growth hormone 2; SOS, Son of Sevenless; GTP, guanosine triphosphate; GDP, guanosine diphosphate; GAPs, GTPase-activating proteins; PI3K, phosphoinositide 3-kinase; Akt/PKB, protein kinase B; BAD, BCL-2/BCL-XL-associated death promoter; CASP9, Recombinant Caspase 9; PIP3, phosphatidyl inositol triphosphate; PDK1, 3-phosphoinositide dependent kinase-1; RASSF1, Ras association domain family 1; MST1, human macrophage stimulation 1; Raf, rat fibrosarcoma; MEK, mitogen-activated protein kinase kinase; ERK, extracellular regulated kinase; NORE1A, Ras-association domain family 5.