Vincent I J, Davies P
Department of Pathology and Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461.
Brain Res. 1990 Oct 29;531(1-2):127-35. doi: 10.1016/0006-8993(90)90765-4.
As a first step in understanding the function of the 68-kDa Alz-50 antigen (A68) in the pathophysiology of Alzheimer's disease (AD), we have reexamined preliminary observations in our laboratory (Wolozin and Davies, 1986) of a protein kinase activity associated with crude preparations of the protein. This study was undertaken to determine whether the kinase activity is an inherent property of the Alz-50 antigen, or is a property of an associated protein. Phosphorylation was therefore examined by incubating A68-enriched preparations with radiolabelled ATP. This resulted in the appearance of a labelled 68-kDa phosphoprotein, comigrating with the Alz-50 reactive A68 protein. The labelling of this 68-kDa protein occurred in the presence of 2% SDS, suggesting that it is more likely to represent an autophosphorylation than a transfer of phosphate mediated by another kinase. Upon further inspection, it was found that the autophosphorylated 68-kDa protein was not localized to regions of AD brain where A68 was detectable, but displayed a more ubiquitous distribution. In addition, this phosphoprotein was also observed to be present in similar preparations from normal brain, which lacked the Alz-50 antigen (Wolozin et al, 1986). These findings indicate that the auto-kinase activity at 68 kDa is not closely associated with the A68 protein, but with a comigrating contaminant in the preparation. Other experiments in this study indicate that A68 is not a substrate for in vitro phosphorylation. Following incubation of A68 preparations with radiolabelled ATP, immunoprecipitation of the antigen did not reveal any phosphate transfer to the protein. These results were unaffected by a prior incubation with alkaline phosphatase, even when the subsequent phosphorylation reactions were conducted in the presence of protein kinase activators. Incubation with alkaline phosphatase did not produce any alterations in electrophoretic mobility of A68, nor did it affect the binding of antibodies directed against phosphatase-sensitive epitopes with A68. Thus, despite the suggestion that A68 is a modified form of tau, the antigen exhibits remarkable differences from tau with regard to its sensitivity to kinases and to alkaline phosphatase.
作为了解68 kDa阿尔茨海默病相关蛋白50(Alz-50抗原,A68)在阿尔茨海默病(AD)病理生理学中功能的第一步,我们重新审视了我们实验室(Wolozin和Davies,1986年)对与该蛋白粗制品相关的蛋白激酶活性的初步观察。本研究旨在确定该激酶活性是Alz-50抗原的固有特性,还是相关蛋白的特性。因此通过将富含A68的制品与放射性标记的ATP一起孵育来检测磷酸化。这导致出现了一种标记的68 kDa磷蛋白,与Alz-50反应性A68蛋白迁移率相同。这种68 kDa蛋白的标记在2% SDS存在的情况下发生,这表明它更有可能代表自磷酸化而不是由另一种激酶介导的磷酸转移。进一步检查发现,自磷酸化的68 kDa蛋白并不定位于可检测到A68的AD脑区域,而是呈现出更广泛的分布。此外,在来自缺乏Alz-50抗原的正常脑的类似制品中也观察到了这种磷蛋白(Wolozin等人,1986年)。这些发现表明,68 kDa的自激酶活性与A68蛋白没有密切关联,而是与制品中一起迁移的污染物有关。本研究中的其他实验表明,A68不是体外磷酸化的底物。在将A68制品与放射性标记的ATP孵育后,对抗原进行免疫沉淀未发现有任何磷酸转移到该蛋白上。即使随后的磷酸化反应在蛋白激酶激活剂存在的情况下进行,这些结果也不受先前用碱性磷酸酶孵育的影响。用碱性磷酸酶孵育不会使A68的电泳迁移率发生任何改变,也不会影响针对磷酸酶敏感表位的抗体与A68的结合。因此,尽管有人认为A68是tau的一种修饰形式,但该抗原在对激酶和碱性磷酸酶的敏感性方面与tau表现出显著差异。