Lack of adenosine deaminase deficiency in the mutant mouse wasted

J. D. Geiger; J. I. Nagy

doi:10.1016/0014-5793(86)81063-8

Lack of adenosine deaminase deficiency in the mutant mouse wasted

J. D. Geiger, J. I. Nagy

Great Plains IDeA-CTR

Research output: Contribution to journal › Article

3 Scopus citations

Abstract

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.

Original language	English (US)
Pages (from-to)	431-434
Number of pages	4
Journal	FEBS Letters
Volume	208
Issue number	2
DOIs	https://doi.org/10.1016/0014-5793(86)81063-8
Publication status	Published - Nov 24 1986

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Keywords

Adenosine deaminase Adenosine Animal model Severe combined immunodeficiency disease

ASJC Scopus subject areas

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

Cite this

Geiger, J. D., & Nagy, J. I. (1986). Lack of adenosine deaminase deficiency in the mutant mouse wasted. FEBS Letters, 208(2), 431-434. https://doi.org/10.1016/0014-5793(86)81063-8

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abstract = "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 4356 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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10.1016/0014-5793(86)81063-8