Ranieri E, Paton B, Poulos A
Biochem J. 1986 Feb 1;233(3):763-72. doi: 10.1042/bj2330763.
Activator protein (AP), which stimulated fibroblast sphingomyelinase activity, was isolated from the spleen of a patient with Gaucher's disease type I by the combined techniques of heat and alcohol denaturation, DEAE-cellulose column chromatography, gel filtration, preparative polyacrylamide-gel electrophoresis and decyl-agarose chromatography. Urea/sodium dodecyl sulphate (SDS)/polyacrylamide-gel electrophoresis showed two bands, one with an Mr of approx. 3,000 and the other with an Mr of 5,000-6,500. Similarly, SDS/polyacrylamide-gel electrophoresis performed in the absence of urea revealed the presence of two components, one of which adsorbed to a concanavalin A (Con A) column. Both components stimulated sphingomyelinase activity. On a non-denaturing polyacrylamide gel containing Triton X-100, four major components, two of which bound to Con A, were detected with the dye Stains-All. Cross-reacting material (CRM) to polyclonal Gaucher spleen AP antibodies was detected in normal fibroblasts and in fibroblasts from patients with sphingomyelinase and beta-glucocerebrosidase deficiency states (Niemann-Pick and Gaucher's diseases respectively). CRM in normal fibroblasts adsorbed to Con A columns and had the same mobility on SDS/polyacrylamide-gel electrophoresis as Con A-adsorbing Gaucher spleen AP. Normal AP was not observed in mucolipidosis type II (I-cell disease) fibroblasts; instead, extracts from these cells revealed the presence of two closely migrating bands with higher Mr values than normal fibroblast CRM. Furthermore, extracts of media from I-cell fibroblast cultures, but not from control or Gaucher fibroblast cultures, contained AP activity towards sphingomyelinase and beta-glucocerebrosidase. Fibroblasts from a patient with mucolipidosis type III (pseudo-Hurler polydystrophy) showed an intermediate pattern consisting of normal as well as the higher-Mr CRM. Our data provide evidence for the existence of AP in cultured skin fibroblasts and suggest that these proteins may be targetted to the lysosome by post-translational modification in a similar manner to that reported for lysosomal enzymes.
通过加热和乙醇变性、DEAE-纤维素柱色谱、凝胶过滤、制备性聚丙烯酰胺凝胶电泳和癸基琼脂糖色谱等联合技术,从一名I型戈谢病患者的脾脏中分离出了刺激成纤维细胞鞘磷脂酶活性的激活蛋白(AP)。尿素/十二烷基硫酸钠(SDS)/聚丙烯酰胺凝胶电泳显示有两条带,一条的Mr约为3000,另一条的Mr为5000 - 6500。同样,在无尿素条件下进行的SDS/聚丙烯酰胺凝胶电泳显示存在两种成分,其中一种能吸附到伴刀豆球蛋白A(Con A)柱上。两种成分均能刺激鞘磷脂酶活性。在含有Triton X-100的非变性聚丙烯酰胺凝胶上,用“全染”染料检测到四个主要成分,其中两个能与Con A结合。在正常成纤维细胞以及鞘磷脂酶和β-葡萄糖脑苷脂酶缺乏状态(分别为尼曼-皮克病和戈谢病)患者的成纤维细胞中检测到了与多克隆戈谢脾脏AP抗体发生交叉反应的物质(CRM)。正常成纤维细胞中的CRM能吸附到Con A柱上,并且在SDS/聚丙烯酰胺凝胶电泳上与吸附Con A的戈谢脾脏AP具有相同的迁移率。在II型粘脂贮积症(I-细胞病)成纤维细胞中未观察到正常AP;相反,这些细胞的提取物显示存在两条迁移紧密且Mr值高于正常成纤维细胞CRM的带。此外,I-细胞成纤维细胞培养物的培养基提取物(而非对照或戈谢成纤维细胞培养物的培养基提取物)含有对鞘磷脂酶和β-葡萄糖脑苷脂酶具有活性的AP。III型粘脂贮积症(假胡尔勒氏多营养不良)患者的成纤维细胞显示出一种中间模式,包括正常的以及更高Mr的CRM。我们的数据为培养的皮肤成纤维细胞中存在AP提供了证据,并表明这些蛋白质可能通过与溶酶体酶类似的翻译后修饰方式被靶向运输到溶酶体。