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. 2020 Apr 8;8:201. doi: 10.3389/fcell.2020.00201

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Copyright © 2020 Maldonado, Medina, Velazquez and Dharmawardhane.

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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Receptor tyrosine kinases (RTKs), G-protein coupled receptors (GPCRs) and Integrin pathways converge in the activation of Rac and Cdc42 GEFs. Cell surface receptors activate GEFs by a variety of mechanisms, involving phosphoinside 3-kinase (PI3-K)-mediated production of phosphatidyl-inositol (3,4,5) tris phosphate (PIP3), which activates GEFs such as P-Rex1, DOCKs, and Vavs; Ras, which activates Tiam-1; and Focal adhesion kinase (FAK)/ signaling to activate ELMO a partner for DOCK1. Upregulation of Rac and Cdc42 can lead to resistance to cell surface receptor targeted therapies (eg. Trastuzumab, Lapatinib, Gefitinib, Eroltinib). Rac/Cdc42-interaction inhibitors are shown in blue boxes. Color-coding of GEFs represent Rac-exclusive GEFs, Cdc42-exclusive GEFs, and GEFs that interact with both Rac and Cdc42.