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Publication : Lack of adenosine deaminase deficiency in the mutant mouse wasted.

First Author  Geiger JD Year  1986
Journal  FEBS Lett Volume  208
Issue  2 Pages  431-4
PubMed ID  3780980 Mgi Jnum  J:12932
Mgi Id  MGI:61146 Doi  10.1016/0014-5793(86)81063-8
Citation  Geiger JD, et al. (1986) Lack of adenosine deaminase deficiency in the mutant mouse wasted. FEBS Lett 208(2):431-4
abstractText  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. Vmax values of ADA in spleens were 43% higher in wst/wst mice and no changes were observed in Km values. In contrast, the Vmax of ADA was unchanged in erythrocytes from wst/wst mice, but the Km 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.
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