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. 2022 Oct 17;12(10):1503. doi: 10.3390/biom12101503

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

The mechanism by which KRAS proto-oncogene and GTPase (KRAS) mutations affect downstream signaling in the pancreatic ductal adenocarcinoma (PDAC). KRAS, KRAS Proto-Oncogene and GTPase; PI3Kl, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha; PIP2, phosphatidylinositol-4, 5-bisphosphate; PIP3, phosphatidylinositol-3, 4, 5-triphosphate; AKT, v-Akt murine thymoma viral oncogene homolog 1; mTOR, mechanistic target of rapamycin kinase. Under the control of KRAS, PI3 kinases catalyze the production of PIP3 by PIP2, although the downstream of mTOR has been studied for complete understanding.