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

ASAP1和FIP3是Arf和Rab小G蛋白的效应器和/或调节剂。本研究探讨了它们参与肌动蛋白细胞骨架调控和生长因子受体内吞作用的可能性。为此，以圆形背褶的形成和PDGF受体的内吞作用为模型系统。ASAP1被认为是CDR形成的负调控因子，因为它的过表达下调了CDR的形成。在这项工作中，FI P3是一种asap1相互作用蛋白，被确定为CDR形成和PDGF内吞的积极调节因子。部分Arf和Rab蛋白定位于cdr中。综上所述，FIP3可能作为关键分子之一在肌动蛋白重塑和受体内吞作用之间的串扰中发挥作用。

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.