Interplay of enzymatic and structural functions of CaMKII in long-term potentiation

被引：33

作者：

Kim, Karam ^{[1
,6
]}

Saneyoshi, Takeo ^{[1
]}

Hosokawa, Tomohisa ^{[1
]}

Okamoto, Kenichi ^{[2
,3
]}

Hayashi, Yasunori ^{[1
,4
,5
,7
]}

机构：

[1] RIKEN, Brain Sci Inst, Wako, Saitama 3510198, Japan

[2] Mt Sinai Hosp, Lunenfeld Tanenbaum Res Inst, Toronto, ON, Canada

[3] Univ Toronto, Dept Mol Genet, Fac Med, Toronto, ON, Canada

[4] Saitama Univ, Brain Sci Inst, Saitama, Japan

[5] South China Normal Univ, Sch Life Sci, Guangzhou, Guangdong, Peoples R China

[6] Univ Calif Davis, Dept Pharmacol, Davis, CA 95616 USA

[7] Kyoto Univ, Dept Pharmacol, Fac Med, Kyoto 6068501, Japan

来源：

JOURNAL OF NEUROCHEMISTRY | 2016年 / 139卷 / 06期

基金：

加拿大创新基金会;

关键词：

CaMKII; cytoskeleton; synaptic plasticity; PROTEIN-KINASE-II; DENDRITIC SPINE MORPHOLOGY; D-ASPARTATE RECEPTOR; POSTSYNAPTIC DENSITY PROTEIN; GTPASE-ACTIVATING PROTEIN; SYNAPTIC AMPA RECEPTORS; NMDA RECEPTOR; F-ACTIN; SUBUNIT COMPOSITION; ALPHA-ACTININ;

D O I：

10.1111/jnc.13672

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Since the discovery of long-term potentiation (LTP) about a half-century ago, Ca2+/CaM-dependent protein kinase II (CaMKII) has been one of the most extensively studied components of the molecular machinery that regulate plasticity. This unique dodecameric kinase complex plays pivotal roles in LTP by phosphorylating substrates through elaborate regulatory mechanisms, and is known to be both necessary and sufficient for LTP. In addition to acting as a kinase, CaMKII has been postulated to have structural roles because of its extraordinary abundance and diverse interacting partners. It now is becoming clear that these two functions of CaMKII cooperate closely for the induction of both functional and structural synaptic plasticity of dendritic spines.

引用

页码：959 / 972

页数：14

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