Deconstruction for Reconstruction: The Role of Proteolysis in Neural Plasticity and Disease

被引：233

作者：

Bingol, Baris ^{[1
]}

Shang, Morgan ^{[1
]}

机构：

[1] Genentech Inc, Dept Neurosci, San Francisco, CA 94080 USA

来源：

NEURON | 2011年 / 69卷 / 01期

关键词：

UBIQUITIN-PROTEASOME SYSTEM; LONG-TERM POTENTIATION; CHAPERONE-MEDIATED AUTOPHAGY; SYNAPTIC PROTEIN-DEGRADATION; ALZHEIMERS-DISEASE; ALPHA-SYNUCLEIN; ANGELMAN-SYNDROME; DENDRITIC SPINES; HIPPOCAMPAL-NEURONS; PARKINSONS-DISEASE;

D O I：

10.1016/j.neuron.2010.11.006

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The brain changes in response to experience and altered environment. This neural plasticity is largely mediated by morphological and functional modification of synapses, a process that depends on both synthesis and degradation of proteins. It is now clear that regulated proteolysis plays a critical role in the remodeling of synapses, learning and memory, and neurodevelopment. Here, we highlight the mechanisms and functions of proteolysis in synaptic plasticity and discuss its alteration in disease states.

引用

页码：22 / 32

页数：11

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