首页> 美国卫生研究院文献>Wiley-Blackwell Online Open >MAP6 interacts with Tctex1 and Cav2.2/N‐type calcium channels to regulate calcium signalling in neurons
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MAP6 interacts with Tctex1 and Cav2.2/N‐type calcium channels to regulate calcium signalling in neurons

机译:MAP6与Tctex1和Cav2.2 / N型钙通道相互作用调节神经元中的钙信号传导

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摘要

MAP6 proteins were first described as microtubule‐stabilizing agents, whose properties were thought to be essential for neuronal development and maintenance of complex neuronal networks. However, deletion of all MAP6 isoforms in MAP6 KO mice does not lead to dramatic morphological aberrations of the brain but rather to alterations in multiple neurotransmissions and severe behavioural impairments. A search for protein partners of MAP6 proteins identified Tctex1 – a dynein light chain with multiple non‐microtubule‐related functions. The involvement of Tctex1 in calcium signalling led to investigate it in MAP6 KO neurons. In this study, we show that functional Cav2.2/N‐type calcium channels are deficient in MAP6 KO neurons, due to improper location. We also show that MAP6 proteins interact directly with both Tctex1 and the C‐terminus of Cav2.2/N‐type calcium channels. A balance of these two interactions seems to be crucial for MAP6 to modulate calcium signalling in neurons.
机译:MAP6蛋白首先被描述为微管稳定剂,其特性被认为对于神经元发育和复杂神经元网络的维持至关重要。但是,删除MAP6 KO小鼠中的所有MAP6亚型并不会导致大脑剧烈的形态畸变,而是会导致多种神经传递的改变和严重的行为障碍。对MAP6蛋白的蛋白伴侣的搜索确定了Tctex1 –一种具有多种非微管相关功能的达因轻链。 Tctex1参与钙信号传导导致在MAP6 KO神经元中对其进行研究。在这项研究中,我们表明,由于位置不正确,功能性Cav2.2 / N型钙通道在MAP6 KO神经元中缺乏。我们还表明,MAP6蛋白与Tctex1和Cav2.2 / N型钙通道的C末端直接相互作用。这两种相互作用的平衡对于MAP6调节神经元中的钙信号传导似乎至关重要。

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