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. 2017 Jan 1;25(1):26–43. doi: 10.4062/biomolther.2016.186

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Copyright ©2017, The Korean Society of Applied Pharmacology

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 6. — Roles of Arf6 in regulating GPCR endocytosis. Studies of β₂AR indicated β-arrestin involvement in recruiting ARNO to convert GDP-bound Arf to the GTP-bound form. GTP-bound Arf6 regulates different routes of receptor endocytosis. For example, by recruiting NM23-H1, Arf6 converts GDP-dynamin to GTP-dynamin to enhance receptor endocytosis. GTP-Arf6 activates PI(4)P5K to convert PI(4)P to PI(4,5)P2. Arf6 protein also can activate PI4K to convert PI to PI(4)P. Additionally, GTP-Arf6 activates PLD2 to produce PA. ADP, adenosine diphosphate; Arf, ADP-ribosylation factor; ARNO, Arf nucleotide-binding-site opener; GDP, guanosine diphosphate; GTP, guanosine triphosphate; PI, phosphatidylinositol; PI(4)P, phosphatidylinositol 4-phosphate; PI(4)P5K, phosphatidylinositol 4-phosphate 5-kinase; PI(4,5)P2, phosphatidylinositol 4,5-bisphosphate; PI4K, phosphatidylinositol 4-kinase; NM23-H1, nucleoside diphosphate kinase; PA, phosphatidic acid; GPCR, G protein-coupled receptor; GTP, guanosine triphosphate; PLD, phospholipase D.