中国神经再生研究(英文版) ›› 2019, Vol. 14 ›› Issue (7): 1148-1151.doi: 10.4103/1673-5374.251193

• 综述:退行性病与再生 • 上一篇    下一篇

神经退行性疾病中的转录失调:谁使大脑阴阳因子1平衡?

  

  • 出版日期:2019-07-15 发布日期:2019-07-15

Transcriptional dysregulation in neurodegenerative diseases: who tipped the balance of Yin Yang 1 in the brain?

Zhefan Stephen Chen 1 , Ho Yin Edwin Chan 1, 2   

  1. 1 School of Life Sciences, Faculty of Science, The Chinese University of Hong Kong, Hong Kong Special Administration Region, China
    2 Gerald Choa Neuroscience Centre, The Chinese University of Hong Kong, Hong Kong Special Administration Region, China
  • Online:2019-07-15 Published:2019-07-15
  • Contact: Zhefan Stephen Chen, PhD, b140892@cuhk.edu.hk.
  • Supported by:

    This work was supported by the General Research Fund (14100714) of the Hong Kong Research Grants Council; The Chinese University of Hong Kong Vice-Chancellor’s One-Off Discretionary Fund (VCF2014011); The Chinese University of Hong Kong One-of Funding for Joint Lab/Research Collaboration (3132980); The Chinese University of Hong Kong Faculty of Science Strategic Development Fund (FACULTY-P17173); The Chinese University of Hong Kong Gerald Choa Neuroscience Centre (7105306); and donations from Chow Tai Fook Charity Foundation (6903898) and Hong Kong Spinocerebellar Ataxia Association (6903291). Zhefan Stephen Chen is supported by the Postdoctoral Fellowship in Clinical Neurosciences of The Chinese University of Hong Kong, China.

摘要:

orcid: 0000-0002-9276-0378 (Zhefan Stephen Chen)

Abstract:

Yin Yang 1 (YY1) is a multi-functional transcription factor that regulates gene expression in a range of cell types, including neurons. It controls neuronal differentiation, as well as neuronal specification and migration during the development of the mammalian nervous system. Besides, YY1 also mediates the transcription of genes that are required for neuronal survival. An impairment of the transcriptional function of YY1 causes neuronal death. This review summarizes recent research findings that unveil the dysfunction of YY1 in multiple neurodegenerative disorders. The expression of disease proteins perturbs the function of YY1 via distinct molecular mechanisms, including recruitment to protein aggregates, protein degradation and aberrant nuclear/cytoplasmic shuttling. Understanding the pathogenic roles of YY1 will further broaden our knowledge of the disease mechanisms in distinct neurodegenerative disorders.

Key words: Alzheimer’s disease, amyotrophic lateral sclerosis, neurodegeneration, protein aggregates recruitment, protein degradation, subcellular localization, transcriptional regulation, Yin Yang 1