Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.4.1.2 (glutamate dehydrogenase)
 4,380 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cell-free extracts of rat brain catalyze the reactions of the purine nucleotide cycle. Ammonia is formed during the deamination but not the amination phase of the cycle. The activity of adenylate deaminase in brain is sufficient to account for the maximum rates of ammonia production that have been reported. The activity of glutamate dehydrogenase is not sufficient to account for these rates of ammonia production. The activities of adenylosuccinate synthetase and adenylosuccinase are nearly sufficient to account for the steady state rates of ammonia production observed in brain. Demonstration of the cycle in extracts of brain is complicated by the occurrence of side reactions, in particular those catalyzed by phosphomonoesterase, nucleoside phosphorylase, and guanase.
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PMID:Purine nucleotide cycle. Evidence for the occurrence of the cycle in brain. 0 96

Most chromosome aberrations in gliomas are numerical, resulting in either gains or deficiencies of whole chromosomes. In tumors of low malignancy, the karyotype is frequently normal or exhibits a loss of sex chromosome and a gain of chromosome 7. These two anomalies may not be directly related to malignancy. In the highly malignant cases, the two most frequent aberrations are the gain of chromosome 7 and the loss of chromosome 10, other anomalies such as losses or deletions of chromosomes, 9, 22, 6, 13 and 14 being detected at various frequencies. Several of these chromosomes carry important genes of adenine metabolism: AK1 and AK3 (adenylate kinase) and MTAP (methylthioadenosine phosphorylase) for chromosome 9; ADK (adenosine kinase) and mitochondrial ATPase for chromosome 10; ADSL (adenylosuccinate lyase) for chromosome 22, NP (nucleoside phosphorylase) for chromosome 14. We performed the corresponding assays of enzyme activity on both fresh tumors and tumors grafted on nude mice, which showed that these enzymes had a relatively low activity although the tumors were proliferating. However, chromosome losses do not seem to directly cause the metabolic alterations by gene dosage effect. Interestingly, chromosome 10, frequently deficient, also carries genes of importance for glycolysis (hexokinase) and glutamate metabolism (glutamate dehydrogenase and glutamate oxaloacetate transaminase). The deficiency for these genes could be taken into account for a better type of chemotherapy by antimetabolics.
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PMID:[Chromosome abnormalities and adenine metabolism in human glial tumors]. 144 60

Multilocus enzyme electrophoresis was developed to evaluate the genetic diversity of 71 human strains and 17 animal strains of Clostridium perfringens. Crude protein extracts, obtained by sonication of washed bacteria, were analyzed by polyacrylamide-agarose gel electrophoresis to characterize electrophoretic mobility variants of seven enzymes (esterase, glutamate dehydrogenase, glutamic-oxaloacetic transaminase, nucleoside phosphorylase, phosphoglucose isomerase, phosphoglucomutase, threonine dehydrogenase). Genetic diversity of the enzyme loci ranged from 0.340 to 0.813. Sixty-nine electrophoretic types were described among the 88 strains tested and the index of discrimination was 0.994. All strains were typable, and epidemiological relationships between isolates could be established. This method showed a fair correlation with esterase electrophoretic typing based on hydrolytic and electrophoretic polymorphism of esterases. This work demonstrates that multilocus enzyme polymorphism is a reliable and discriminant marker of genetic diversity of strains of C. perfringens.
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PMID:Multilocus enzyme typing of human and animal strains of Clostridium perfringens. 808 23