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首页> 外文期刊>Neuron >VEGF Mediates Commissural Axon Chemoattraction through Its Receptor Flk1.
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VEGF Mediates Commissural Axon Chemoattraction through Its Receptor Flk1.

机译:VEGF通过其受体Flk1介导连合轴突趋化性。

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摘要

Growing axons are guided to their targets by attractive and repulsive cues. In the developing spinal cord, Netrin-1 and Shh guide commissural axons toward the midline. However, the combined inhibition of their activity in commissural axon turning assays does not completely abrogate turning toward floor plate tissue, suggesting that additional guidance cues are present. Here we show that the prototypic angiogenic factor VEGF is secreted by the floor plate and is a chemoattractant for commissural axons in vitro and in vivo. Inactivation of Vegf in the floor plate or of its receptor Flk1 in commissural neurons causes axon guidance defects, whereas Flk1 blockade inhibits turning of axons to VEGF in vitro. Similar to Shh and Netrin-1, VEGF-mediated commissural axon guidance requires the activity of Src family kinases. Our results identify VEGF and Flk1 as a novel ligand/receptor pair controlling commissural axon guidance.
机译:不断增长的轴突通过引人入胜和排斥的信号被引导至目标。在发育中的脊髓中,Netrin-1和Shh将连合轴突导向中线。然而,在连合轴突转向试验中对它们活性的综合抑制不能完全消除向底板组织的转向,这表明存在其他指导提示。在这里,我们显示了原型血管生成因子VEGF是由底板分泌的,并且是体外和体内连合轴突的化学吸引剂。地板中的Vegf或其连合神经元中的受体Flk1失活会导致轴突导向缺陷,而Flk1的阻滞作用在体外抑制轴突转向VEGF。类似于Shh和Netrin-1,VEGF介导的连合轴突引导需要Src家族激酶的活性。我们的研究结果确定VEGF和Flk1作为控制连合轴突指导的新型配体/受体对。

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