Signaling to the microtubule cytoskeleton: an unconventional role for CaMKII.

Signaling to the microtubule cytoskeleton: an unconventional role for CaMKII.
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DOI:
10.1002/dneu.22227
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发表时间:
2015-04
影响因子:
3
通讯作者:
Dent, Erik W.
Dent, Erik W.
中科院分区:
医学3区
文献类型:
--
作者:
McVicker, Derrick P.;Millette, Matthew M.;Dent, Erik W.

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突触可塑性是神经系统的标志,被认为是学习和记忆等高级大脑功能的组成部分。作为第二信使的钙和钙/钙调蛋白依赖性激酶CaMKII是神经元可塑性的关键调节剂。鉴于肌动蛋白和微管(MT)细胞骨架在树突棘形态,组成和可塑性的重要性,这并不奇怪,这些细胞骨架元件的许多监管机构的CaMKII途径的下游。在这篇综述中,我们讨论了新出现的作用,钙和CaMKII在调节的MT和货物卸载突触可塑性。
Synaptic plasticity is a hallmark of the nervous system and is thought to be integral to higher brain functions such as learning and memory. Calcium, acting as a second messenger, and the calcium/calmodulin dependent kinase CaMKII are key regulators of neuronal plasticity. Given the importance of the actin and microtubule (MT) cytoskeleton in dendritic spine morphology, composition and plasticity, it is not surprising that many regulators of these cytoskeletal elements are downstream of the CaMKII pathway. In this review we discuss the emerging role of calcium and CaMKII in the regulation of MTs and cargo unloading during synaptic plasticity.
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