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Filamin A and Big2: A shared endocytic pathway

机译：Filamin A和Big2：共享的内吞途径

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Neural proliferation, migration and differentiation require reorganization of the actin cytoskeleton and regulation of vesicle trafficking to provide stability in maintaining cell adhesions, allow for changes in cell shape, and establishing cell polarity. Human disorders involving the actin-binding Filamin A (FLNA) and vesicle trafficking Brefeldin-associated guanine exchange factor 2 (BIG2 is encoded by the ARFGEF2 gene) proteins are implicated in these various developmental processes, resulting ina malformation of cortical development called periventricular heterotopia (nodules along the ventricular lining) and microcephaly (small brain). Here we discuss several recent reports from our laboratory that demonstrate a shared role for both proteins in actin-associated vesicle trafficking, which is required to maintain the expression and stability of cell adhesion and cell cycle associated molecules during cortical development. While changes in FLNA and BIG2 have first been linked to disorders involving the central nervous system, increasing reports suggest they are associated with aberrant development of various other organ systems in the body. These studies suggest that vesicle trafficking defects in FLN-GEF dependent pathways may contribute to amuch broader phenotype than previously realized.
机译：神经的增殖，迁移和分化需要肌动蛋白细胞骨架的重组和囊泡运输的调节，以提供维持细胞黏附的稳定性，允许细胞形状的改变并建立细胞极性。涉及肌动蛋白结合纤维蛋白A（FLNA）和囊泡运输布雷菲德菌素相关鸟嘌呤交换因子2（BIG2由ARFGEF2基因编码）蛋白的人类疾病与这些各种发育过程有关，导致称为脑室周围异位症的皮质发育畸形（沿室壁的结节）和小头畸形（小脑）。在这里，我们讨论了我们实验室的一些最新报告，这些报告证明了两种蛋白在肌动蛋白相关囊泡运输中的共同作用，这是在皮层发育过程中维持细胞粘附和细胞周期相关分子的表达和稳定性所必需的。虽然FLNA和BIG2的变化首先与涉及中枢神经系统的疾病有关，但越来越多的报道表明它们与体内其他各种器官系统的异常发育有关。这些研究表明，FLN-GEF依赖性途径中的囊泡运输缺陷可能导致比以前认识到的更广泛的表型。

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