Abstract
These studies with wild-type and mutant cells defective in IMP dehydrogenase and the previous data with the adenylosuccinate synthetase-deficient cell line suggest that among the clinical population with dominantly inherited hyperuricemia, patients with partial deficiencies in these enzymes exist. It is hoped that these pharmacogenetic cell culture models for overproduction hyperuricemia will lead to the initiation of a search for hyperuricemia patients with either of these deficiencies. If such patients are found it may be possible to design chemotherapeutic regimens by which effectors (inhibitors) of purine synthesis might ameliorate the overproduction of purines by the de novo pathway.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 373-379 |
| Number of pages | 7 |
| Journal | Advances in Experimental Medicine and Biology |
| Volume | 165 Pt A |
| State | Published - 1984 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
Cite this
IMP dehydrogenase mutants : cell culture model for hyperuricemia. / Ullman, Buddy.
In: Advances in Experimental Medicine and Biology, Vol. 165 Pt A, 1984, p. 373-379.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - IMP dehydrogenase mutants
T2 - cell culture model for hyperuricemia.
AU - Ullman, Buddy
PY - 1984
Y1 - 1984
N2 - These studies with wild-type and mutant cells defective in IMP dehydrogenase and the previous data with the adenylosuccinate synthetase-deficient cell line suggest that among the clinical population with dominantly inherited hyperuricemia, patients with partial deficiencies in these enzymes exist. It is hoped that these pharmacogenetic cell culture models for overproduction hyperuricemia will lead to the initiation of a search for hyperuricemia patients with either of these deficiencies. If such patients are found it may be possible to design chemotherapeutic regimens by which effectors (inhibitors) of purine synthesis might ameliorate the overproduction of purines by the de novo pathway.
AB - These studies with wild-type and mutant cells defective in IMP dehydrogenase and the previous data with the adenylosuccinate synthetase-deficient cell line suggest that among the clinical population with dominantly inherited hyperuricemia, patients with partial deficiencies in these enzymes exist. It is hoped that these pharmacogenetic cell culture models for overproduction hyperuricemia will lead to the initiation of a search for hyperuricemia patients with either of these deficiencies. If such patients are found it may be possible to design chemotherapeutic regimens by which effectors (inhibitors) of purine synthesis might ameliorate the overproduction of purines by the de novo pathway.
UR - http://www.scopus.com/inward/record.url?scp=0021297691&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0021297691&partnerID=8YFLogxK
M3 - Article
C2 - 6144250
AN - SCOPUS:0021297691
VL - 165 Pt A
SP - 373
EP - 379
JO - Advances in Experimental Medicine and Biology
JF - Advances in Experimental Medicine and Biology
SN - 0065-2598
ER -