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Tctex1 plays a key role in the α-synuclein autophagy lysosomal degradation pathway.

Neurosci. Lett.2017 Nov 20;661:90-95. Epub 2017 Sep 29
Shuangshuang Dong 1 , Yongjin Zhang 1 , Jingfeng Ming 1 , Xinzhi Zhang 1 , Xiuming Li 1 , Jing Xu 1 , Zhenjie Sun 1 , Zenglin Cai 2 , Xiaomin Li 3
Shuangshuang Dong 1 , Yongjin Zhang 1 , Jingfeng Ming 1 , Xinzhi Zhang 1 , Xiuming Li 1 , Jing Xu 1 , Zhenjie Sun 1 , Zenglin Cai 2 , Xiaomin Li 3
+ et al

[No authors listed]

Author information
  • 1 Department of Neurology, Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, China.
  • 2 Department of Neurology, Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, China. Electronic address: caizengling@hotmail.com.
  • 3 Department of Emergency, Affiliated Lianyungang Hospital of Xuzhou Medical University, Lianyungang, China. Electronic address: lyglxm1@163.com.

摘要


Tctex1 is an important structure of dynein light chain in mammalian cells, clarifying the role of Tctex1 in α-synuclein autophagy lysosomal degradation may offer insights into the formation of Lewy bodies and neuronal death. We constructed dsRED-N1-Tctex1 overexpression, pDsRED2-N1-Tctex1(T94E) mutation and transfected into SH-SY5Y cells. Relative protein expression was measured by and mRNA levels were measured by real-time quantitative PCR. Confocal microscopy was used to observe their sublocalizations in cells. We found that: WST assay results show that cell activity decreased after Tctex1 mutation (T94E), while Tctex1 overexpression increased cell activity. In Tctex1 mutation transfected cell lines Tctex1 and dynein protein levels decreased; α-synuclein, LC3-II and LAMP2 protein increased. However, α-synuclein, LC3-II and LAMP2 proteins were reduced in Tctex1 overexpression cell lines, with the same trend was found in mRNA levels. In Tctex1 mutation transfected cell lines Tctex1 fluorescence intensity weakened; α-synuclein, LC3-II and LAMP2 fluorescence was enhanced, while α-synuclein, LC3-II and LAMP2 weakened in Tctex1 overexpressing cells. Our results suggest that Tctex1 mutants interference lead to Tctex1 downregulation and dysfunction. Tctex1 overexpression promoted autophagy lysosome fusion and effectively degraded α-synuclein with increased cell activity. Thus, Tctex1 plays an important role in α-synuclein autophagic degradation.

KEYWORDS: Autophagy, Parkinson’s disease, Tctex1, α-Synuclein