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首页> 外文期刊>Neuron >MAX-1, a Novel PH/MyTH4/FERM Domain Cytoplasmic Protein Implicated in Netrin-Mediated Axon Repulsion.
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MAX-1, a Novel PH/MyTH4/FERM Domain Cytoplasmic Protein Implicated in Netrin-Mediated Axon Repulsion.

机译:MAX-1,一种新型的PH / MyTH4 / FERM域胞质蛋白,涉及Netrin介导的轴突排斥。

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摘要

The netrin UNC-6 repels motor axons by activating the UNC-5 receptor alone or in combination with the UNC-40/DCC receptor. In a genetic screen for C. elegans mutants exhibiting partial defects in motor axon projections, we isolated the max-1 gene (required for motor neuron axon guidance). max-1 loss-of-function mutations cause fully penetrant but variable axon guidance defects. Mutations in unc-5 and unc-6, but not in unc-40, dominantly enhance the mutant phenotypes of max-1, whereas overexpression of unc-5 or unc-6, but not of unc-40, bypasses the requirement for max-1. MAX-1 proteins contain PH, MyTH4, and FERM domains and appear to be localized to neuronal processes. Human MAX-1 and UNC5H2 colocalize in discrete subcellular regions of transfected cells. Our results suggest a possible role for MAX-1 in netrin-induced axon repulsion by modulating the UNC-5 receptor signaling pathway.
机译:netrin UNC-6通过单独或与UNC-40 / DCC受体结合激活UNC-5受体来排斥运动轴突。在秀丽隐杆线虫突变体在运动轴突投射中显示部分缺陷的遗传筛选中,我们分离了max-1基因(运动神经元轴突指导所必需)。 max-1功能丧失突变会导致完全渗透但可变的轴突引导缺陷。 unc-5和unc-6中的突变(而非unc-40中的突变)主要增强max-1的突变表型,而unc-5或unc-6的过表达(而不是unc-40的过表达)绕过了对max的要求-1。 MAX-1蛋白包含PH,MyTH4和FERM域,似乎位于神经元过程中。人MAX-1和UNC5H2在转染细胞的离散亚细胞区域共定位。我们的结果表明,通过调节UNC-5受体信号传导途径,MAX-1在网蛋白诱导的轴突排斥中可能发挥作用。

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