McKinnon P J, Burgoyne L A
Exp Cell Res. 1985 Jun;158(2):413-22. doi: 10.1016/0014-4827(85)90465-3.
In a number of lymphoblastoid cell lines from individuals with the genetic disease ataxia-telangiectasia (A-T), a decrease in the levels of actin and a concomitant increase in the levels of a protein species of 37K has been observed to occur following high cell density. In this paper we describe ataxia-telangiectasia lymphoblastoid lines that show this response constitutively, and demonstrate that this 37K protein is most likely an actin-derived peptide. This is because of extensive similarity between the two proteins in the spectrum of peptides produced by proteolytic fingerprinting. It appears likely that this 37K protein is similar to the well documented protease-resistant actin fragments produced by protease digestion of actin in vitro. Examination of a number of possible initiators found no clear signal that promoted this response, although the response is clearly very dependent on cell culture conditions. The possible involvement of a cytoskeletal anomaly in ataxia-telangiectasia is discussed.
在一些来自患有遗传性疾病共济失调毛细血管扩张症（A-T）个体的淋巴母细胞系中，在高细胞密度后，观察到肌动蛋白水平下降，同时一种37K蛋白质种类的水平相应增加。在本文中，我们描述了组成性表现出这种反应的共济失调毛细血管扩张症淋巴母细胞系，并证明这种37K蛋白质很可能是一种肌动蛋白衍生肽。这是因为在通过蛋白水解指纹图谱产生的肽谱中，这两种蛋白质之间存在广泛的相似性。看起来这种37K蛋白质类似于体外通过蛋白酶消化肌动蛋白产生的、有充分记录的抗蛋白酶肌动蛋白片段。尽管这种反应显然非常依赖于细胞培养条件，但对多种可能的引发剂进行检测时，未发现促进这种反应的明确信号。本文还讨论了细胞骨架异常在共济失调毛细血管扩张症中可能的作用。
