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组蛋白去乙酰化酶6与神经变性疾病 被引量:2

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摘要 神经变性疾病是一组由于中枢神经系统特定区域神经元发生变性而引起的慢性进行性疾病,主要包括帕金森病(Parkinson's disease,PD)、阿尔茨海默病(Alzheimer’s disease,AD)和亨廷顿舞蹈病(Huntington’s disease,HD)等,这些疾病均以异常蛋白质聚集和神经元选择性丢失为特征。虽然细胞自身具备清除这种蛋白质的途径,但是当其产生速度超过清除速度时,将会聚集并干扰细胞的正常功能。因此,寻找降解异常蛋白质的有效途径,对于治疗神经变性疾病具有重要意义。
出处 《中国神经精神疾病杂志》 CAS CSCD 北大核心 2013年第1期10-10,22,33,43,47,共5页 Chinese Journal of Nervous and Mental Diseases
基金 国家自然科学基金资助项目(编号:81000538)
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参考文献25

  • 1Pandey UB,Nie Z,Batlevi Y. HDAC6 rescues neurodegeneration and provides an essential link between autophagy and the UPS[J].Nature,2007,(7146):859-863.
  • 2Ding H,Dolan PJ,Johnson GV. Histone deacetylase 6 interacts with the microtubule-associated protein tau[J].Journal of Neurochemistry,2008,(05):2119-2130.
  • 3Du G,Liu X,Chen X. Drosophila histone deacetylase 6 protects dopaminergic neurons against α-synuclein toxicity by promoting inclusion formation[J].Molecular Biology of the Cell,2010,(13):2128-2137.
  • 4lwata A,Riley BE,Johnston JA. HDAC6 and microtubules are required for autophagic degradation of aggregated huntingtin[J].Journal of Biological Chemistry,2005,(48):40282-40292.
  • 5Kawaguchi Y,Kovacs JJ,McLaurin A. The deacetylase HDAC6 regulates aggresome formation and cell viability in response to misfolded protein stress[J].Cell,2003,(06):727-738.
  • 6Simms-Waldrip T,Rodriguez-Gonzalez A,Lin T. The aggresome pathway as a target for therapy in hematologic malignancies[J].Molecular Genetics and Metabolism,2008,(03):283-286.doi:10.1016/j.ymgme.2008.03.012.
  • 7Lee JY,Koga H,Kawaguchi Y. HDAC6 controls autophagosome maturation essential for ubiquitin-selective quality-control autophagy[J].EMBO Journal,2010,(05):969-980.doi:10.1038/emboj.2009.405.
  • 8Boyault C,Zhang Y,Fritah S. HDAC6 controls major cell response pathways to cytotoxic accumulation of protein aggregates[J].Genes and Development,2007,(17):2172-2181.
  • 9Seigneurin-Bemy D,Verdel A,Curtet S. Identification of components of the murine histone deacetylase 6 complex:link between acetylation and ubiquitination signaling pathways[J].Molecular and Cellular Biology,2001,(23):8035-8044.doi:10.1128/MCB.21.23.8035-8044.2001.
  • 10Uo T,Veenstra TD,Morrison RS. Histone deacetylase inhibitors prevent p53-dependent and p53-independent Bax-mediated neuronal apoptosis through two distinct mechanisms[J].The Journal of Neuroscience,2009,(09):2824-2832.

二级参考文献21

  • 1Langston JW, Forno LS, Tetrud J, et al. Evidence of active nerve cell degeneration in the substantia nigra of humans year after 1 -methy- 4-pheny-1,2,3,6-tetrahydropyridine exposure. Ann Neurol, 1999,46(4) :598.
  • 2Fonck C, Baudry M. Rapid reduction of ATP synthesis and lack of free radical formation by MPP + in rat brain synaptosomes and mitochondria. Brain Res, 2003, 975( 1 -2):214.
  • 3Watanabe H, Muramatsu Y, Kurosaki R, et al. Protective effects of neuronal nitric oxide synthase inhibitor in mouse brain against MPTP neurotoxicity: an immunohistological study. Eur Neuropsychopharmacol, 2004, 14(2) :93.
  • 4Sugana S, Yang L, Cho BP, et al. Age-related microglial actvation in 1-methy4-pheny-1,2,3,6-tetrahydropyridine ( MPTP )-induced dopaminergic neurodegeneration in C57BL/6 mice. Brain Research, 2003, 964 ( 2 ) :288.
  • 5Irwin I, Finnegan KT, DeLanney LE, et al. The relationships between aging, monoamine oxidase, striatal dopamine and the effects of MPTP in C57BL/6 mice: a critical reassessment. Brain Res, 1992, 572(1-2) :224.
  • 6Irwin I, DeLanney LE, McNeill TH, et al. Aging and the nigrostriatal dopamine system: a non-human primate study. Neurodegeneration, 1994, 3(4) :251.
  • 7Jordi Bove, Delhaine Prou, Celine Perier, et al. Toxin-Induced Models of Parkinson's Disease. NeuroRx, 2005, 2(3) :484.
  • 8Vila M, Vukosavic S, Jackson-Lewis V, et al. α-synuclein up-regulation in substantia nigra dopaminergic neurons following administration of the parkinsonian toxin MPTP. Neurochem, 2000, 74 ( 2 ) : 721.
  • 9Meredith GE, Totterdell S, Petroske E et al. Lysosomal malfunction accompanies algha-synuclein aggregation in a progressive mouse model of Parkinson' disease. Brain Research, 2002, 956( 1 ) :156.
  • 10Fornai F, Schluter OM, Lenzi P, et al. Parkinson-like syndrome induced by continuous MPTP infusion : Convergent roles of the ubiquitin-proteasome system and α-synuclein. PNAS, 2005, 102 ( 9 ) :3413.

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  • 1Hisahara S, Chiba S, Matsumoto H, et al. Histone deacetylase SIRT1 modulates neuronal differentiation by its nuclear translo- cation[J]. Proc Natl Acad Sci U S A, 2008, 105(40): 15599-15604.
  • 2Prozorovski T, Schulze-Topphoff U, Glumm R, et al. Sirtl con- tributes critically to the redox-dependent fate of neural progeni- tors[J]. Nat Cell Biol, 2008, 10(4): 385-394.
  • 3Raval AP, Lin HW, Dave KR, et al. Resveratrol and ischemic preconditioning in the brain[J]. Curr Med Chem, 2008, 15(15): 1545-1551.
  • 4Li XH, Lv BL, Xie JZ, et al. AGEs induce Alzheimer-like tau pathology and memory deficit via RAGE-mediated GSK-3 acti- vation[J]. Neurobiol Aging, 2012, 33(7): 1400-1410.
  • 5Min SW, Cho SH, Zhou Y, et al. Acetylation of tau inhibits its degradation and contributes to tauopathy[J]. Neuron, 2010, 67 (6): 953-966.
  • 6Michan S, Li Y, Chou MM, et al. SIRT1 is essential for normal cognitive function and synaptic plasticity[J]. J Neurosci, 2010, 30(29): 9695-9707.
  • 7Lee IH, Cao L, Mostoslavsky R, et al. A role for the NAD-de- pendent deacetylase Sirtl in the regulation of autophagy[J]. Proc Natl Acad Sci USA, 2008, 105(9): 3374-3379.
  • 8颉宾芳,孙雯雯,刘卉,王佳冰,刘昕.大鼠脑组织中甲状腺素受体THRα1的表达与阿尔茨海默病的发病机制[J].中国神经精神疾病杂志,2012,38(9):530-534. 被引量:3
  • 9荆婧,王雪晶,马耀华,祝应俊,丁晓岚,滕军放.α-synuclein(A53T)蛋白调控自噬诱导神经元凋亡[J].中国神经精神疾病杂志,2013,39(2):102-106. 被引量:1
  • 10张冬梅.毛蕊异黄酮-7-O-β-D-葡萄糖苷对人宫颈癌HeLa细胞凋亡及Bcl-2/Bax表达的影响[J].中草药,2015,46(10):1498-1502. 被引量:25

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