The role of the ubiquitin proteasome system in synapse remodeling and neurodegenerative diseases

被引:57
作者
Ding, Mei [1 ]
Shen, Kang [2 ]
机构
[1] Chinese Acad Sci, Inst Genet & Dev Biol, Beijing 100101, Peoples R China
[2] Stanford Univ, Howard Hughes Med Inst, Dept Biol, Stanford, CA 94305 USA
关键词
D O I
10.1002/bies.20843
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
The ubiquitin proteasome system is a potent regulatory mechanism used to control protein stability in numerous cellular processes, including neural development. Many neurodegenerative diseases are featured by the accumulation of UPS-associated proteins, suggesting the UPS dysfunction may be crucial for pathogenesis. Recent experiments have highlighted the UPS as a key player during synaptic development. Here we summarize recent discoveries centered on the role of the UPS in synapse remodeling and draw attention to the potential link between the synaptic UPS dysfunction and the pathology of neurodegenerative diseases. BioEssays 30:10751083, 2008. (C) 2008 Wiley Periodicals, Inc.
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收藏
页码:1075 / 1083
页数:9
相关论文
共 101 条
  • [1] Mechanism and function of deubiquitinating enzymes
    Amerik, AY
    Hochstrasser, M
    [J]. BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH, 2004, 1695 (1-3): : 189 - 207
  • [2] Drosophila Unc-13 is essential for synaptic transmission
    Aravamudan, B
    Fergestad, T
    Davis, WS
    Rodesch, CK
    Broadie, K
    [J]. NATURE NEUROSCIENCE, 1999, 2 (11) : 965 - 971
  • [3] Synaptic Drosophila UNC-13 is regulated by antagonistic G-protein pathways via a proteasome-dependent degradation mechanism
    Aravamudan, B
    Broadie, K
    [J]. JOURNAL OF NEUROBIOLOGY, 2003, 54 (03): : 417 - 438
  • [4] GABAA receptor cell surface number and subunit stability are regulated by the ubiquitin-like protein Plic-1
    Bedford, FK
    Kittler, JT
    Muller, E
    Thomas, P
    Uren, JM
    Merlo, D
    Wisden, W
    Triller, A
    Smart, TG
    Moss, SJ
    [J]. NATURE NEUROSCIENCE, 2001, 4 (09) : 908 - 916
  • [5] Global changes to the ubiquitin system in Huntington's disease
    Bennett, Eric J.
    Shaler, Thomas A.
    Woodman, Ben
    Ryu, Kwon-Yul
    Zaitseva, Tatiana S.
    Becker, Christopher H.
    Bates, Gillian P.
    Schulman, Howard
    Kopito, Ron R.
    [J]. NATURE, 2007, 448 (7154) : 704 - U11
  • [6] Proteasome impairment does not contribute to pathogenesis in R6/2 Huntington's disease mice:: exclusion of proteasome activator REGγ as a therapeutic target
    Bett, JS
    Goellner, GM
    Woodman, B
    Pratt, G
    Rechsteiner, M
    Bates, GP
    [J]. HUMAN MOLECULAR GENETICS, 2006, 15 (01) : 33 - 44
  • [7] Synaptic protein degradation by the ubiquitin proteasome system
    Bingol, B
    Schuman, EM
    [J]. CURRENT OPINION IN NEUROBIOLOGY, 2005, 15 (05) : 536 - 541
  • [8] Activity-dependent dynamics and sequestration of proteasomes in dendritic spines
    Bingol, Baris
    Schuman, Erin M.
    [J]. NATURE, 2006, 441 (7097) : 1144 - 1148
  • [9] The requirement for Phr1 in CNS axon tract formation reveals the corticostriatal boundary as a choice point for cortical axons
    Bloom, A. Joseph
    Miller, Bradley R.
    Sanes, Joshua R.
    DiAntonio, Aaron
    [J]. GENES & DEVELOPMENT, 2007, 21 (20) : 2593 - 2606
  • [10] BOWE MA, 1995, ANNU REV NEUROSCI, V18, P443