Neurons extend long processes known as axons and dendrites, through which they communicate with each other. The neuronal circuits formed by the axons and dendrites are the structural basis of higher brain functions. The formation and maintenance of these processes are essential for physiological brain activities. Membrane components, both lipids, and proteins, that are required for process formation are supplied by vesicle transport. Intracellular membrane trafficking is regulated by a family of Rab small GTPases. A group of Rabs regulating endosomal trafficking has been studied mainly in nonpolarized culture cell lines, and little is known about their regulation in polarized neurons with long processes. As shown in our recent study, lemur tail (former tyrosine) kinase 1 (LMTK1), an as yet uncharacterized Ser/Thr kinase associated with Rab11-positive recycling endosomes, modulates the formation of axons, dendrites, and spines in cultured primary neurons. LMTK1 knockdown or knockout (KO) or the expression of a kinase-negative mutant stimulates the transport of endosomal vesicles in neurons, leading to the overgrowth of axons, dendrites, and spines. More recently, we found that LMTK1 regulates TBC1D9B Rab11 GAP and proposed the Cdk5/p35-LMTK1-TBC1D9B-Rab11 pathway as a signaling cascade that regulates endosomal trafficking. Here, we summarize the biochemical, cell biological, and physiological properties of LMTK1.

神经元扩展了称为轴突和树突的长过程，它们通过它们相互交流。轴突和树突形成的神经元回路是高级脑功能的结构基础。这些过程的形成和维持对于大脑的生理活动至关重要。形成过程所需的膜成分，包括脂质和蛋白质，都是通过囊泡运输提供的。细胞内膜运输受Rab小GTPases家族调节。一组Rabs调节内体运输的研究主要在非极化培养细胞系中进行，对它们在长过程的极化神经元中的调控了解甚少。如我们最近的研究所示，狐猴尾巴（前酪氨酸）激酶1（LMTK1）与Rab11阳性回收内体相关的尚未表征的Ser / Thr激酶，可调节培养的原代神经元中轴突，树突和棘的形成。LMTK1敲低或敲除（KO）或激酶阴性突变体的表达刺激内体小泡在神经元中的运输，导致轴突，树突和棘的过度生长。最近，我们发现LMTK1调节TBC1D9B Rab11 GAP，并提出Cdk5 / p35-LMTK1-TBC1D9B-Rab11途径作为调节内体运输的信号级联。在这里，我们总结了LMTK1的生物化学，细胞生物学和生理学特性。LMTK1敲低或敲除（KO）或激酶阴性突变体的表达刺激内体小泡在神经元中的运输，导致轴突，树突和棘的过度生长。最近，我们发现LMTK1调节TBC1D9B Rab11 GAP，并提出Cdk5 / p35-LMTK1-TBC1D9B-Rab11途径作为调节内体运输的信号级联。在这里，我们总结了LMTK1的生物化学，细胞生物学和生理学特性。LMTK1敲低或敲除（KO）或激酶阴性突变体的表达刺激内体小泡在神经元中的运输，导致轴突，树突和棘的过度生长。最近，我们发现LMTK1调节TBC1D9B Rab11 GAP，并提出Cdk5 / p35-LMTK1-TBC1D9B-Rab11途径作为调节内体运输的信号级联。在这里，我们总结了LMTK1的生物化学，细胞生物学和生理学特性。