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泛素-蛋白酶体系统在神经退行性疾病中的研究 被引量:8

The Research of Ubiquitin-proteasome System in Neurodegenerative Diseases
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摘要 泛素-蛋白酶体系统(UPS)是真核细胞内蛋白质降解的主要信号通路,UPS在降解细胞内错误折叠受损的蛋白也起着重要作用。神经退行性疾病的共同特征是中枢神经系统的细胞内或细胞外异常聚集着突变或损伤的蛋白,如帕金森病(PD)、阿尔茨海默病(AD)、亨廷顿病(Huntington)等。而且UPS成分的突变也可导致神经退行性疾病[1]。因此,UPS的功能异常影响着神经退行性疾病的发生发展。 Ubiquitin-proteasome system( UPS) is the main signal path of protein degradation in the eukaryotic cells. UPS plays an important role in the degradation of misfolded damaged cell proteins. Common feature of neurodegenerative diseases is the central nervous system cells or extracellular abnormal accumulation of mutations or damage of proteins,such as Parkinson’s disease( PD),Alzheimer’s disease( AD),Huntington’s disease( Huntington),etc. Mutations of UPS component may also lead to neurodegenerative diseases. Therefore,UPS dysfunction affects the development of neurodegenerative diseases.
作者 金雪佳
出处 《药物生物技术》 CAS 2015年第4期366-368,共3页 Pharmaceutical Biotechnology
关键词 泛素-蛋白酶体系统 神经退行性疾病 帕金森病 阿尔茨海默病 亨廷顿病 肌萎缩侧索硬化 Ubiquitin-proteasome system Neurodegenerative disease Parkinson’ s disease Alzheimer’ s disease Huntington’ s disease Amyotrophi
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  • 1Cieehanover A, Brundin. P The ubiquitin proteasome system in neurodegenerative diseases : sometimes the chicken, sometimes the egg [ J ]. Neuron, 2003,40 ( 2 ) :427- 446.
  • 2Bassermann F, Eichner R, Pagano M. The ubiquitin proteasome system-Implications for cell cycle control and the targeted treat-ment of cancer[ J]. Biochim Biophys Acta ,2013.
  • 3Whitby F G,Masters E I,Kramer L,et al. Structural basis for the activation of 20S proteasomes by 11S regulators [ J ]. Nature, 2000,408(6808) :115-120.
  • 4Ito K, Carracedo A, Weiss D, et al. A PML-PPAR-deha pathway for fatty acid oxidation regulates hematopoietic stem cell mainte- nance[J]. Nat Med,2012 ,18( 9 ) :1350-1358.
  • 5Nussbaum A K, Dick T P, Keilholz W, et al. Cleavage motifs of the yeast 20S proteasome beta subunits deduced from digests of enolase 1 [J]. Proc Natl Acad Sci USA, 1998, 95 (21): 12504-12509.
  • 6Dick T P, Nussbaum A K, Deeg M,et al. Contribution of proteaso- mal beta-subunits to the cleavage of peptide substrates analyzed with yeast mutants [ J ]. J Biol Chem, 1998, 273 ( 40 ) : 25637 -25646.
  • 7Seemuller E, Lupas A, Stock D, et al. Proteasome from Thermo- plasma acidophilum : a threonine protease [ J ]. Science, 1995,268 (5210) :579-582.
  • 8Song X, Mott J D, von Kampen J, et al. A model for the quaternary structure of the proteasome activator PA28 [ J]. J Biol Chem, 1996,271 (42) :26410-26417.
  • 9Mayer R J. From neurodegeneration to neurohomeostasis:the role of ubiquitin [ J ]. Drug News Perspect, 2003,16 ( 2 ) : 103-108.
  • 10Pankratz N, Foroud T. Genetics of Parkinson disease [ J ]. Neu- roRx ,2004 ,1 ( 2 ) : 235 -242.

同被引文献76

  • 1Riederer BM, Leuba G, Vernay A, et al. The role of the ubiquitin proteasome system in Alzheimer's disease[J]. Exp Biol Med(Maywood), 2011, 236(3):268-276.
  • 2Lopez Salon M, Pasquini L, Besio Moreno M, et al. Relationship between β-amyloid degradation and the 26S proteasome in neural cells[J]. Exp Neurol, 2003, 180(2):131-143.
  • 3Sulistio YA, Heese K. The Ubiquitin-proteasome system and molecular chaperone deregulation in Alzheimer's disease[J].Mol Neurobiol, 2016, 53(2):905-931.
  • 4Panmanee J, Nopparat C, Chawanich N, et al. Melatonin regulates the transcription of βAPP-cleaving secretases mediated through melatonin receptors in human neuroblastoma SH-SY5Y cells[J]. J Pineal Res, 2015, 59(3):308-320.
  • 5Shen D, Coleman J, Chan E, et al. Novel cell- and tissue-based assays for detecting misfolded and aggregated protein accumulation within aggresomes and inclusion bodies[J]. Cell Biochem Biophys, 2011, 60(3):173-185.
  • 6Wang H, Yu Y, Chen W, et al. PLTP deficiency impairs learning and memory capabilities partially due to alteration of amyloid-beta metabolism in old mice[J]. J Alzheimers Dis, 2014, 39(1):79-88.
  • 7Wuwongse S, Cheng SS, Wong GT, et al. Effects of corticosterone and amyloid-beta on proteins essential for sy-naptic function: implications for depression and Alzheimer's disease[J]. Biochim Biophys Acta, 2013, 1832(12):2245-2256.
  • 8Xiao Q, Yan P, Ma X, et al. Neuronal-targeted TFEB accelerates lysosomal degradation of APP, reducing Aβ ge-neration and amyloid plaque pathogenesis[J]. J Neurosci, 2015, 35(35):12137-12151.
  • 9Ullrich C, Mlekusch R, Kuschnig A, et al. Ubiquitin enzymes ubiquitin and proteasome activity in blood mononuclear cells of MCI, Alzheimer and Parkinson patients[J]. Curr Alzheimer Res, 2010, 7(6):549-555.
  • 10Keck S, Nitsch R, Grune T, et al. Proteasome inhibition by paired helical filament-tau in brains of patients with Alzheimer's disease[J]. J Neurochem, 2003, 85(1):115-122.

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