Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.1.21 (thymidine kinase)
 7,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Karyotype, mitochondrial ultrastructure and several enzymatic activities were studied in two clones, D22 and D27, from SV40-transformed rabbit chondrocytes. Similar chromosome alterations, with recurrent losses and gains were observed at the various passages. Mitochondria were rare, with increase in size and crest alterations. By comparison to non-transformed rabbit chondrocytes, activities of superoxide dismutase 1 and 2 (SOD) and glutathione peroxidase were increased, those of glutathione reductase, glucose-6-phosphate dehydrogenase and glutathione-S-transferase fluctuated according to passages, thymidylate synthase decreased, thymidine kinase and hypoxanthine-phosphoribosyl-transferase increased and the ratio lactate dehydrogenase B/A increased. In most cases, these variations were correlated with the number of chromosomes carrying the genes encoding for corresponding enzymes. These results, compared to those obtained in SV40-transformed human fibroblasts, demonstrate that the two cell types behave differently for detoxication systems against oxygen radicals, in particular for SOD2 activity, and have opposite imbalances of chromosomes carrying the corresponding genes.
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PMID:Chromosomal, mitochondrial and metabolic alterations in SV40-transformed rabbit chondrocytes. 131 10

PEG-mediated fusion between mouse Cl1d cells and primary Chinese hamster spleen cells produced interspecific hybrids which slowly and nonrandomly segregated Chinese hamster chromosomes. Cytogenetic and isozyme analysis (31 loci) of HAT and BrdU selected hybrid clones and subclones and of members of a hybrid clone panel retaining different combinations of Chinese hamster chromosomes enabled provisional assignment of the following enzyme loci on Chinese hamster chromosomes: thymidine kinase, galactokinase, and acid phosphatase-1 to chromosome 7; galactose-1-phosphate uridyltransferase to chromosome 2; and adenosine kinase, esterase D, glutathione reductase, glyoxalase, nucleoside phosphorylase, peptidases B and S, and phosphoglucomutase (PGM) 2 to chromosome 1. Assignments of PGM1, 6-phosphogluconate dehydrogenase, and enolase 1 to chromosome 2 were confirmed, and a chromosome 2 deletion (q23-q33) enabled the provisional assignment of PGM1 to that region. The assignments provide markers for the study of the genetic consequences of chromosomal rearrangements in Chinese hamster cell lines and support the concept of conservation of mammalian autosomal linkage groups.
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PMID:Confirmational, provisional, and/or regional assignment of 15 enzyme loci onto Chinese hamster autosomes 1, 2, and 7. 732 47

Five human melanoma cell lines were investigated for their antioxidant activities. These metabolic data were correlated with cytogenetic analysis giving the relative numbers of chromosomes or chromosomal segments carrying the gene encoding for each enzyme. Particular attention was focused on the expression of superoxide dismutase 2 (SOD2), whose gene, located on the long arm of chromosome 6 (6q), has been proposed as a tumour suppressor gene. The activity of glutathione peroxidase (GPX), glutathione reductase (GSR) and catalase appeared to be unrelated to the relative number of 3q, 8p and 11p arms which, respectively, carry their encoding genes. GPX activity paralleled that of total SOD activity, and GSR variations followed those of GPX, suggesting possible metabolic regulation. Both the activity and the amount of SOD1 immunoreactive protein correlated with the number of chromosomes 21, suggesting a gene dosage effect. The three cell lines with deletions of the 6q arm had lower SOD2 activity and less immunoreactive protein than the two cell lines without 6q deletion. In addition, they demonstrated high thymidine kinase and thymidylate synthetase activities, which are directly linked to the cell proliferation rate. These results strengthen the hypothesis that SOD2 has a function as a tumour suppressor gene, but also suggest that the expression of other antioxidant enzymes might be altered in human melanomas.
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PMID:Modifications of the antioxidant enzymes in relation to chromosome imbalances in human melanoma cell lines. 976 8