Regulation of receptor trafficking and cytoskeleton by Arf small G proteins and their effectors

ASAP 1和FIP 3是Arf和Rab小G蛋白的效应子和/或调节子。本研究探讨了它们参与肌动蛋白细胞骨架调节和生长因子受体内吞的可能性。为此，使用圆形背褶形成和PDGF受体内吞作用作为模型系统。ASAP 1被认为是CDR形成的负调节因子，因为其过表达下调CDR形成。在这项工作中，FIP 3，这是一个ASAP 1相互作用的蛋白质，被确定为一个积极的调节CDR形成和PDGF的内吞作用。部分Arf和Rab蛋白定位于CDR区。总而言之，FIP 3可能作为关键分子之一在肌动蛋白重塑和受体内吞之间的相互作用中发挥作用。

ASAP1 and FIP3 are effectors and/or regulators of Arf and Rab small G proteins. In this study, the possibility that they are involved in actin cytoskeleton regulation and endocytosis of growth factor receptor was evaluated. For the purpose of this, circular dorsal ruffles formation and PDGF receptor endocytosis was used as a model system. ASAP1 has been proposed to be a negative regulator for CDR formation because its overexpression down -regulates CDR formation. In this work, FI P3, which is an ASAP1-interacting protein, was identified as a positive regulator for CDR formation and PDGF endocytosis. Some of Arf and Rab proteins were localized in CDRs. Taken together, FIP3 may play a role in a crosstalk between actin remodeling and receptor endocytosis as one of key molecules.