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Lack of adenosine deaminase deficiency in the mutant mouse wasted
Author(s) -
Geiger J.D.,
Nagy J.I.
Publication year - 1986
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(86)81063-8
Subject(s) - adenosine deaminase , adenosine , spleen , mutant , adenosine deaminase deficiency , chemistry , metabolism , endocrinology , medicine , biology , biochemistry , gene
The possibility that the mutant mouse wasted (wst/wst) may serve as an animal model for studies of severe combined immunodeficiency disease (SCID) and the role of adenosine deaminase (ADA, EC 3.5.4.4) in adenosine metabolism were investigated. The specific activity of ADA in wst/wst compared with control mice was significantly lower by 26% in thymus, but significantly higher by 18% in spleen and 32% in cerebellum. V max values of ADA in spleens were 4356 higher in wst/wst mice and no changes were observed in K m values. In contrast, the V max of ADA was unchanged in erythrocytes from wst/wst mice, but the K m for adenosine was significantly elevated. Thus, based on ADA measurements alone, it may be premature to consider wst/wst mice as a model for ADA deficiency and SCID in humans.