CaMKII: claiming center stage in postsynaptic function and organization.
CaMKII: claiming center stage in postsynaptic function and organization.
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DOI：
10.1016/j.neuron.2013.12.024
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发表时间：
2014-01-22
期刊：
影响因子：
16.2
通讯作者：
Hell JW
中科院分区：
文献类型：
--
作者：
Hell JW
虽然CaMKII长期以来一直被认为是突触可塑性和学习所必需的，但最近的工作指出了CaMKII在神经系统中功能的新维度，揭示了CaMKII在突触组织中也起着重要作用。Ca2+触发的CaMKII的自磷酸化不仅通过在长期可塑性（LTP）和学习期间延长CaMKII活性来提供分子记忆，而且还代表了CaMKII的多方面蛋白质对接功能的自激活机制。关于CaMKIIα和CaMKIIβ在突触稳态中的不同作用的新细节也正在出现，进一步说明了CaMKII参与突触调节的多层和复杂性质。在这里，我审查新的分子和功能的洞察力CaMKII如何支持突触功能。
While CaMKII has long been known to be essential for synaptic plasticity and learning, recent work points to new dimensions of CaMKII function in the nervous system, revealing that CaMKII also plays an important role in synaptic organization. Ca2+-triggered autophosphorylation of CaMKII not only provides molecular memory by prolonging CaMKII activity during long-term plasticity (LTP) and learning but also represents a mechanism for autoactivation of CaMKII’s multifaceted protein docking functions. New details are also emerging about the distinct roles of CaMKIIα and CaMKIIβ in synaptic homeostasis, further illustrating the multilayered and complex nature of CaMKII’s involvement in synaptic regulation. Here, I review novel molecular and functional insight into how CaMKII supports synaptic function.