中国神经再生研究(英文版) ›› 2019, Vol. 14 ›› Issue (4): 588-590.doi: 10.4103/1673-5374.247460

• 观点:退行性病与再生 • 上一篇    下一篇

TRiC/含TCP1伴侣蛋白亚基调节tau蛋白磷酸化和逆行轴突运输-对神经退行性疾病的影响?

  

  • 出版日期:2019-04-15 发布日期:2019-04-15

Involvement of T-complex protein 1-ring complex/chaperonin containing T-complex protein 1 (TRiC/CCT) in retrograde axonal transport through tau phosphorylation

Xu-Qiao Chen   

  1. Department of Neurosciences, University of California San Diego, La Jolla, CA, USA)
  • Online:2019-04-15 Published:2019-04-15
  • Contact: Xu-Qiao Chen, PhD, q0chen@ucsd.edu.

摘要:

orcid: 0000-0001-9799-7246 (Xu-Qiao Chen)

Abstract:

The cytosolic chaperonin T-complex protein 1-ring complex (TRiC) or chaperonin containing T-complex protein 1 (CCT) is essential in de novo folding of approximately 10% of the eukaryotic, newly translated polypeptides as well as misfolded proteins. There is a close link between the TRiC/CCT cytosolic chaperonin and neurodegenerative diseases. A lot of research suggests that CCT plays neuroprotective roles in neurodegenerative diseases including Huntington’s disease. Either overexpression of a single or all eight subunits (CCT1-8) or treatment of the substrate-binding apical domain of yeast CCT1 (ApiCCT1) prevented mutant Huntingtin aggregation and improved cellular and neuronal functions. Importantly, our recent study has demonstrated that both CCT and ApiCCT could reduce mutant Huntingtin level and enhance both anterograde and retrograde axonal transport of brain-derived neurotrophic factor. These results led to restoration of the trophic status of striatal neurons from a bacterial artificial chromosome transgenic mouse model of Huntington’s disease.