摘要
In this report, mutual effect of alpha-synuclein and GPX-1 is investigated to unveil their involvement in the PD pathogenesis in terms of cellular defense mechanism against oxidative stress. Biochemical and immunocytochemical studies showed that a-synuclein enhanced the GPX-1 activity with Kd of 17.3 nM and the enzyme in turn markedly enhanced in vitro fibrillation of alpha-synuclein. Transmission electron microscopy revealed the fibrillar meshwork of alpha-synuclein containing GPX-1 located in locally concentrated islets. The entrapped enzyme was demonstrated to be protected in a latent form and its activity was fully recovered as released from the matrix. Therefore, novel defensive roles of alpha-synuclein and its amyloid fibrils against oxidative stress are suggested as the GPX-1 stimulator and the active depot for the enzyme, respectively.
- 出版日期2013-6