- 作者: Shyan-Yuan Kao
- 作者服務機構: Eaton Peabody Laboratory, Massachusetts Eye and Ear Infirmary, MA., U.S.A.
- 中文摘要: --
- 英文摘要:
Parkinson's disease (PD) is the second most common form of human degenerative disorder.
Mutation of parkin is one of the most prevalent causes of autosomal recessive PD. Parkin is an E3
ubiquitin ligase that acts on a variety of substrates, resulting in polyubiquitination and degradation
by the proteasome or monoubiquitination and regulation of biological activity. However, the
cellular functions of parkin that relate to its pathological involvement in PD are not well
understood. Here I show that parkin translocates into nucleus upon DNA damage. Nuclear
translocation of parkin appears to be required to promote DNA repair. These findings suggest that
DNA damage induces nuclear translocation of parkin leading to the PCNA interaction and possibly
other nuclear proteins involved in DNA repair. These results suggest that parkin promotes DNA
repair and protects against genotoxicity, and implicate DNA damage as a potential pathogenic
mechanism in parkinsonism. - 中文關鍵字: --
- 英文關鍵字: --