MAP1B 1–126 interacts with tubulin isoforms and induces neurite outgrowth and neuronal death of cultured cortical neurons
MAP1B 1–126 interacts with tubulin isoforms and induces neurite outgrowth and neuronal death of cultured cortical neurons
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DOI：
10.1016/j.brainres.2011.11.028
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发表时间：
2012-01
期刊：
影响因子：
2.9
通讯作者：
F. Gomi;Y. Uchida
中科院分区：
文献类型：
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作者：
F. Gomi;Y. Uchida
先前我们曾报道，含有126个氨基酸的MAP1B过表达促进了神经元的死亡。在这里，我们通过双杂交和下拉实验鉴定了α-，β-和βIII-微管蛋白是与MAP1B1-126相互作用的蛋白质。转染实验表明，MAP1B1-126与微管相互作用，但程度远低于先前报道的两个微管结合域。MAP1B1-126过表达可导致轴突伸展和神经元死亡，提示MAP1B1-126可能参与了神经元的变性和异常萌发。
Previously we reported that overexpression of MAP1B containing N-terminal 126 amino acids promoted neuronal death. Here, we identified α-, β-, and βIII-tubulins as proteins interacting with MAP1B 1–126 by two-hybrid and pull-down assays. Transfection experiments indicated that MAP1B 1–126 interacts with microtubules, but to a much lesser extent than two previously reported microtubule-binding domains. Overexpression of MAP1B 1–126 induced both neurite extension and neuronal death, suggesting that MAP1B 1–126 could be involved in neuronal degeneration and aberrant sprouting.