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Rac3-induced Neuritogenesis Requires Binding to Neurabin I

机译:RAC3诱导的神经发生需要与Neurabin I结合

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Rac3, a neuronal GTP-binding protein of the Rho family, induces neuritogenesis in primary neurons. Using yeast two-hybrid analysis, we show that Neurabin I, the neuronal F-actin binding protein, is a direct Rac3-interacting molecule. Biochemical and light microscopy studies indicate that Neurabin I copartitions and colocalizes with Rac3 at the growth cones of neurites, inducing Neurabin I association to the cytoskeleton. Moreover, Neurabin I antisense oligonucleotides abolish Rac3-induced neuritogenesis, which in turn is rescued by exogenous Neurabin I but not by Neurabin I mutant lacking the Rac3-binding domain. These results show that Neurabin I mediates Rac3-induced neuritogenesis, possibly by anchoring Rac3 to growth cone F-actin.
机译:RAC3是RHO家族的神经元GTP结合蛋白,在原发性神经元中诱导神经生成。使用酵母双杂化分析,我们表明神经角蛋白I,神经元F-肌动蛋白结合蛋白是直接RAC3相互作用的分子。生物化学和光学显微镜研究表明,Neurabin I在神经疾病的生长锥中与RAC3结合,诱导神经杂蛋白I结合到细胞骨架。此外,Neurabin I反义寡核苷酸废除RAC3诱导的神经发生,这反过来被外源神经内蛋白I拯救,但不是神经蛋白I突变体缺乏RAC3结合结构域。这些结果表明,Neurabin I介导RAC3诱导的神经发生,可能是通过将RAC3锚固至生长锥F-肌动蛋白。

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