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长时程增强:从钙/钙调蛋白依赖性蛋白激酶II到α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体转运

Long-Term Potentiation: From CaMKII to AMPA Receptor Trafficking.

作者信息

Herring Bruce E, Nicoll Roger A

机构信息

Department of Cellular and Molecular Pharmacology and.

Department of Physiology, University of California, San Francisco, California 94143; email:

出版信息

Annu Rev Physiol. 2016;78:351-65. doi: 10.1146/annurev-physiol-021014-071753.

Abstract

For more than 20 years, we have known that Ca(2+)/calmodulin-dependent protein kinase (CaMKII) activation is both necessary and sufficient for the induction of long-term potentiation (LTP). During this time, tremendous effort has been spent in attempting to understand how CaMKII activation gives rise to this phenomenon. Despite such efforts, there is much to be learned about the molecular mechanisms involved in LTP induction downstream of CaMKII activation. In this review, we highlight recent developments that have shaped our current thinking about the molecular mechanisms underlying LTP and discuss important questions that remain in the field.

摘要

20多年来,我们已经知道,钙/钙调蛋白依赖性蛋白激酶(CaMKII)的激活对于长时程增强(LTP)的诱导既是必要的也是充分的。在此期间,人们花费了巨大努力试图理解CaMKII激活如何引发这一现象。尽管付出了这些努力,但对于CaMKII激活下游参与LTP诱导的分子机制仍有许多有待了解之处。在这篇综述中,我们重点介绍了塑造我们当前对LTP潜在分子机制认识的最新进展,并讨论了该领域仍然存在的重要问题。

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