Non-visual arrestins regulate the focal adhesion formation via small GTPases RhoA and Rac1 independently of GPCRs |
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| Affiliation: | 1. Department of Pharmacology, Vanderbilt University, Nashville, TN 37232, United States;2. Department of Medicine, Vanderbilt University, Nashville, TN 37232, United States;3. Department of Veterans Affairs Hospital, Nashville, TN, 37232, United States;1. Department of Structural and Functional Biology, Institute of Biology, State University of Campinas (UNICAMP), Campinas, SP, Brazil;2. Department of Internal Medicine, School of Medical Science, Hematology and Hemotherapy Center — Hemocentro, INCT Sangue, State University of Campinas (UNICAMP), Campinas, SP, Brazil |
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| Abstract: | Arrestins recruit a variety of signaling proteins to active phosphorylated G protein-coupled receptors in the plasma membrane and to the cytoskeleton. Loss of arrestins leads to decreased cell migration, altered cell shape, and an increase in focal adhesions. Small GTPases of the Rho family are molecular switches that regulate actin cytoskeleton and affect a variety of dynamic cellular functions including cell migration and cell morphology. Here we show that non-visual arrestins differentially regulate RhoA and Rac1 activity to promote cell spreading via actin reorganization, and focal adhesion formation via two distinct mechanisms. Arrestins regulate these small GTPases independently of G-protein-coupled receptor activation. |
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