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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 431-434 |
| Number of pages | 4 |
| Journal | FEBS Letters |
| Volume | 208 |
| Issue number | 2 |
| DOIs | |
| State | Published - Nov 24 1986 |
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Keywords
- Adenosine deaminase Adenosine Animal model Severe combined immunodeficiency disease
ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Molecular Biology
Cite this
Lack of adenosine deaminase deficiency in the mutant mouse wasted. / Geiger, J. D.; Nagy, J. I.
In: FEBS Letters, Vol. 208, No. 2, 24.11.1986, p. 431-434.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Lack of adenosine deaminase deficiency in the mutant mouse wasted
AU - Geiger, J. D.
AU - Nagy, J. I.
PY - 1986/11/24
Y1 - 1986/11/24
N2 - 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.
AB - 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.
KW - Adenosine deaminase Adenosine Animal model Severe combined immunodeficiency disease
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U2 - 10.1016/0014-5793(86)81063-8
DO - 10.1016/0014-5793(86)81063-8
M3 - Article
C2 - 3780980
AN - SCOPUS:0023032947
VL - 208
SP - 431
EP - 434
JO - FEBS Letters
JF - FEBS Letters
SN - 0014-5793
IS - 2
ER -