Daddona P E, Kelley W N
Biochim Biophys Acta. 1981 Apr 14;658(2):280-90. doi: 10.1016/0005-2744(81)90298-9.
An inherited deficiency of adenosine deaminase (adenosine aminohydrolase, EC 3.5.4.4) is associated with an autosomal recessive form of severe combined immunodeficiency disease. Affected patients exhibit markedly reduced or absent adenosine deaminating activity in various tissues. In this study we have demonstrated the presence of a low level aminohydrolase activity in 11 different normal and adenosine deaminase-deficient lymphoblast cell lines which is apparently distinct from normal adenosine deaminase. Based on enzymatic, physical and immunoreactive properties, this lymphoblast aminohydrolase does not appear to be related to adenosine deaminase and is most likely coded for by a different gene locus. In future investigations designed to characterize mutant forms of adenosine deaminase, it will be important to distinguish this lymphoblast aminohydrolase activity from putative products of the adenosine deaminase gene locus.
腺苷脱氨酶(腺苷氨基水解酶,EC 3.5.4.4)的遗传性缺乏与常染色体隐性遗传形式的严重联合免疫缺陷病相关。受影响的患者在各种组织中表现出明显降低或缺乏的腺苷脱氨活性。在本研究中,我们已经证实在11种不同的正常和腺苷脱氨酶缺陷的淋巴母细胞系中存在低水平的氨基水解酶活性,这显然与正常腺苷脱氨酶不同。基于酶学、物理和免疫反应特性,这种淋巴母细胞氨基水解酶似乎与腺苷脱氨酶无关,很可能由不同的基因位点编码。在未来旨在鉴定腺苷脱氨酶突变形式的研究中,将这种淋巴母细胞氨基水解酶活性与腺苷脱氨酶基因位点的推定产物区分开来将很重要。