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p62-induced protein sequestration and autophagy in Parkinson's disease pathogenesis

p62-induced protein sequestration and autophagy in Parkinson's disease pathogenesis
帕金森病发病机制中 p62 诱导的蛋白隔离和自噬
批准号:
20590999
负责人:
NAKASO Kazuhiro
金额:
$3.0万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2008
资助国家:
日本
项目状态:
已结题
起止时间:
2008 至 2010

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中文摘要
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英文摘要
Most neurodegenerative diseases such as Parkinson's disease (PD) show neuronal inclusion body in the patient's brain. p62(A170) is one of the component proteins of the inclusion body, and it is believed that it plays an important role in the step of protein sequestration and induces unfolded proteins to the proteolysis by autophagy. In the present study, we clarified that p62(A170) was induced in the transcription level by proteasome inhibition or overexpression of alpha-synuclein. Furthermore, autophagy-related molecules, such as LC3, were colocalized with p62(A170) existing inclusion body.
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会议论文
Endogenous catecholamine enhances the dysfunction of unfolded protein response and alpha-synuclein oligomerization in PC12 cells overexpressing human alpha-synuclein.
内源性儿茶酚胺增强了过度表达人 α-突触核蛋白的 PC12 细胞中未折叠蛋白反应和 α-突触核蛋白寡聚化的功能障碍。
DOI: --
发表时间: 2009
期刊: Neurosci Res. inpress(in press)
影响因子: --
作者: [Ito S, Nakaso K, Imamura K, Takeshima T, Nakashima K]
通讯作者: Nakashima K
Toxicity of Alpha-synuclein in Dopaminergic Cells : A Candidate of Therapeutic Target for Parkinson's Disease
多巴胺能细胞中α-突触核蛋白的毒性:帕金森病的候选治疗靶点
DOI: --
发表时间: 2010
期刊:
影响因子: --
作者: [Ikeuchi, et al., 中曽一裕]
通讯作者: 中曽一裕
Toxicity, Oligomerization and Accumulation of alpha-synuclein in Catecholaminergic cells
儿茶酚胺能细胞中α-突触核蛋白的毒性、寡聚化和积累
DOI: --
发表时间: 2009
期刊:
影响因子: --
作者: [中曽一裕, 伊藤悟, 中島健二]
通讯作者: 中島健二
Parkin protects dopaminergic neurons against microtuble-depolymerizing toxins by attenuating microtubule-associated protein kinase activation.
Parkin 通过减弱微管相关蛋白激酶的激活来保护多巴胺能神经元免受微管解聚毒素的侵害。
DOI: --
发表时间: 2009
期刊: J Biol Chem. 284
影响因子: --
作者: [Ren Y, Jiang H, Yang F, Nakaso K, Feng J.]
通讯作者: Feng J.
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