Ubiquitination in Postsynaptic Function and Plasticity

被引：199

作者：

Mabb, Angela M. ^{[1
]}

Ehlers, Michael D. ^{[2
]}

机构：

[1] Duke Univ, Med Ctr, Dept Neurobiol, Durham, NC 27710 USA

[2] Duke Univ, Med Ctr, Howard Hughes Med Inst, Durham, NC 27710 USA

来源：

ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, VOL 26 | 2010年 / 26卷

关键词：

ubiquitin; neuron; synapse; glutamate; circuit; dendrite; DEPENDENT PROTEIN-KINASE; D-ASPARTATE RECEPTOR; METABOTROPIC GLUTAMATE RECEPTORS; LONG-TERM FACILITATION; ANAPHASE-PROMOTING COMPLEX; DENDRITIC SPINE MORPHOLOGY; VENTRAL NERVE CORD; LIGASE GENE UBE3A; PROTEASOME SYSTEM; C-ELEGANS;

D O I：

10.1146/annurev-cellbio-100109-104129

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Neurons are highly specialized cells whose connectivity at synapses subserves rapid information transfer in the brain. Proper information processing, learning, and memory storage in the brain requires continuous remodeling of synaptic networks. Such remodeling includes synapse formation, elimination, synaptic protein turnover, and changes in synaptic transmission. An emergent mechanism for regulating synapse function is posttranslational modification through the ubiquitin pathway at the postsynaptic membrane. Here, we discuss recent findings implicating ubiquitination and protein degradation in postsynaptic function and plasticity. We describe postsynaptic ubiquitination pathways and their role in brain development, neuronal physiology, and brain disorders.

引用

页码：179 / 210

页数：32

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