Down-regulation of parkin protein in transient focal cerebral ischemia: A link between stroke and degenerative disease?
Down-regulation of parkin protein in transient focal cerebral ischemia: A link between stroke and degenerative disease?
复制标题
DOI：
10.1073/pnas.232588799
复制
发表时间：
2002-11-12
影响因子：
11.1
通讯作者：
Paschen, W
中科院分区：
文献类型：
--
作者：
Mengesdorf, T;Jensen, PH;Paschen, W
泛素化蛋白质聚集体是神经退行性疾病的特征性特征，其也在脑的急性病理状态如中风中发现。许多与神经退行性疾病相关的蛋白质在泛素-蛋白酶体途径中发挥作用。其中一种蛋白质（E3遍在蛋白连接酶帕金）的突变是常染色体隐性青少年帕金森病的原因。在这里，我们表明，短暂的局灶性脑缺血1小时的持续时间诱导明显的消耗parkin蛋白水平，60%，36%，33%和25%的控制后，1，3，6，和24小时的再灌注，但缺血不会导致较低的蛋白水平的E2泛素结合酶Ubc 6，Ubc 7，或Ubc 9。再灌注3小时后，当parkin蛋白水平已降至
Ubiquitylated protein aggregates are characteristic features of neurodegenerative disorders that are also found in acute pathological states of the brain such as stroke. Many of the proteins connected to neurodegenerative diseases play a role in the ubiquitin-proteasomal pathway. Mutation of one of these proteins, the E3 ubiquitin ligase parkin, is the cause of autosomal recessive juvenile Parkinson's disease. Here we show that transient focal cerebral ischemia of 1-h duration induces marked depletion of parkin protein levels, to 60%, 36%, 33%, and 25% of controls after 1, 3, 6, and 24 h of reperfusion, but that ischemia does not cause lower protein levels of E2 ubiquitin-conjugating enzymes Ubc6, Ubc7, or Ubc9. After 3 h of reperfusion, when parkin protein levels were already reduced to