Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.1.21 (thymidine kinase)
7,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cellular levels of the purine catabolic enzymes adenosine deaminase (ADA) and purine nucleoside phosphorylase (PNP) and those for the pyrimidine activities thymidine phosphorylase and thymidine kinase isozymes have been measured concurrently in peripheral blood nucleated cells of patients with acute lymphoblastic leukaemia, chronic lymphocytic or prolymphocytic leukaemia and correlated with the spontaneous tritiated thymidine uptake of the isolated cells. Highest ADA levels occurred in T-ALL cells but considerable overlap of individual activities occurred for non-T, non-BALL, B-CLL and T-CLL cells. The levels of PNP showed no distinct discriminatory trend in cells of the lymphoid proliferative disorders examined. Thymidine phosphorylase activity was markedly reduced in T-ALL and T-CLL cells with a stepwise increase in the level of mean activities for non-T, non-B ALL, B-CLL and B-PLL cells to that of isolated normal peripheral blood lymphocytes. Spontaneous tritiated thymidine uptake of the abnormal lymphoid cells exhibited a correlation between cellular thymidine kinase isozyme 1 and elevated ADA levels. The use of ADA inhibitors together with thymidine infusion for the treatment of lymphoproliferative disorders is discussed.
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PMID:Purine and pyrimidine activities in acute and chronic lymphocytic leukaemia: relation to cellular proliferative status. 681 8

Oncofetal markers for colon carcinomas are CSAp, a nonsulfated mucin, a second trimester fetal antigen, an altered thymidine kinase, a monosialoganglioside, and glycolipid antigens. For gastric carcinoma, they are basic fetoprotein, a sulfoglycoprotein, and for pancreatic carcinomas--POA, an oncofetal pancreatic antigen, and designated as CAPI, an oncofetal antigen. Tumor-associated markers for colon carcinomas are: UDP-galactosyltransferase and zinc glycinate marker; for gastric carcinomas, sulfated glycoprotein and for pancreatic carcinomas, pancreas carcinoma-associated antigen, a polycytidylic acid-specific ribonuclease, and galactosyltransferase. Suggested as tumor-specific markers for colon carcinomas are an altered mucoprotein, basic antigen, beta 2-microglobulin-associated antigen, and a specific adenosine deaminase; for gastric carcinomas, a specific protein, an antigen with 3-oxyanthranilic acid, and an antigen of unknown origin in gastric secretions; for pancreatic carcinomas, an antigen with molecular weight of 380,000 daltons and an antigen suggested by tumor immunity.
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PMID:Gastrointestinal tumor markers, other than carcinoembryonic antigen, and alpha fetal protein. 688 74

By growing Aedes albopictus mosquito cells in media containing increasing concentrations of adenosine and subsequently plating low numbers of cells in the presence of EHNA (an inhibitor of adenosine deaminase), three clones were obtained which were resistant to adenosine. The adenosine-resistant clones contained level of adenosine and thymidine kinase similar to those in the parental cells, but were unable to incorporate labeled nucleotides (adenosine, uridine, thymidine, or guanosine) into TCA-precipitable material. The inability to incorporate nucleosides was also reflected in an enhanced resistance to several nucleoside analogs such as 5-fluorodeoxyuridine and tubercidin but not to the unribosylated base, 5-fluorouracil. Direct measurements over short time intervals indicated that the primary defect in these cells was at the level of nucleoside transport.
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PMID:Aedes albopictus cells resistant to adenosine because of a defect in nucleoside transport. 713 63

The nature of the defect of a female baby who died of severe combined immunodeficiency (SCID) disease associated with adenosine deaminase deficiency (ADA-) was investigated. Since tissue or tissue culture material was not available for subsequent studies, the expression of ADA in her cells was investigated in the somatic cell hybrid clones derived from a fusion between the lymphocytes from one of her two obligate heterozygote parents and thymidine kinase deficient Chinese hamster (a3) fibroblasts. The results of analyses of the human chromosomes and biochemical markers in 12 independent clones and 27 subclones indicated that the ADA deficiency in the patient is determined probably by a mutation in the structural gene for ADA in chromosome 20 leading either to the production of catalytically defective molecules or to the cessation of the production of ADA. Incidentally, the involvement of chromosome 2, which carries a gene for adenosine deaminase complexing protein (ADCP), in the causation of ADA deficiency was excluded. The in vitro approach through the cells from an obligate heterozygote described in this paper may have a general application in pursuing studies on other cases of inborn errors of metabolism whenever the material from the affected individuals (i.e., the homozygotes) is not available or not suitable for direct investigations.
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PMID:Basic defect in the expression of adenosine deaminase in ADA- SCID disease investigated through the cells of an obligate heterozygote. 723 21

Three isomers of trifluoromethylaniline (TFMA) were investigated for their possible different toxic effects on the hematopoietic system in male Wistar rats. The effects of isomeric 2-, 3- and 4-TFMA were compared with those of aniline, the prototypic drug. Strong leukocytosis manifested by considerable increase in the number of all respective white blood elements was observed in the peripheral blood 1 day after the administration of 4-TFMA. In contrast, erythropoiesis, as ascertained by erythrocyte count and hemoglobin concentration, was inhibited by 4-TFMA. The determination of the ED50 revealed lymphocytes to be the most responsive elements towards 4-TFMA administration. Besides hyperemic and proliferative splenomegaly the histological changes in maturation of immunocompetent cells following the 4-TFMA administration were found also in thymus. In accord with an enhanced incorporation of [3H]thymidine, the specific activity of thymidine kinase (TdK) in spleen was increased after a single dose of 4-TFMA. Activities of the catabolic enzymes adenosine deaminase (ADA) and inosine phosphorylase (IP) decreased in both organs with the exception of IP activity in thymus. The effects evoked by the 3-TFMA isomer were regularly less pronounced, and 2-TFMA was nearly inactive.
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PMID:Effects of trifluoromethylaniline isomers on enzyme activities in lymphatic organs and hematology of the rat. 794 May 66

Chromosomal aberrations in human gliomas are principally numerical. In tumours of low malignancy, karyotypes are frequently normal, but occasionally an excess of chromosome 7 and a loss of sex chromosome are observed. In highly malignant tumours, the most frequent aberrations are gain of chromosome 7, loss of chromosome 10 and less frequently losses or deletions of chromosomes 9, 22, 6, 13 and 14 or gains of chromosomes 19 and 20. To understand the meaning of these chromosome imbalances, the relationships between chromosome abnormalities and metabolic disturbances were studied. The losses or deletions observed affected principally chromosomes carrying genes encoding enzymes involved in purine metabolism. The activities of ten enzymes were measured: adenosine kinase, adenine phosphoribosyltransferase, adenylate kinase, methylthioadenosine phosphorylase, hypoxanthine phosphoribosyltransferase, adenylosuccinate lyase, inosine monophosphate dehydrogenase, adenosine deaminase, nucleoside phosphorylase and adenosine monophosphate deaminase. In parallel, two enzymes involved in pyrimidine metabolism, thymidine kinase and thymidylate synthase (TS), were studied. The activities of all these enzymes were measured on samples from 30 human primary glial tumours with low or high malignancy, six xenografted tumours at different passages, four portions of normal brain tissue and four non-glial brain neoplasms. As suggested by cytogenetic data, the enzymatic results showed a relatively low activity of purine metabolism in glial tumours when compared with normal brain and non-glial brain neoplasms. Considering the two enzymes involved in pyrimidine metabolism, only TS had higher activity in glial tumours of high malignancy than in normal brain. In comparison with normal brain, the balance between salvage and de novo pathways changes in gliomas, and even more in grafted tumours, in favour of de novo synthesis. The relation between chromosomes and metabolic imbalances does not correspond to a simple gene dosage effect in these tumours. These data suggest that the decrease of adenosine metabolism occurs before chromosomal aberrations appear, since it is observed in tumours of low malignancy when most karyotypes are still normal, and that the de novo pathway increases with tumour progression.
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PMID:Purine and pyrimidine metabolism in human gliomas: relation to chromosomal aberrations. 805 68

We selected the common shrew (Sorex araneus) to generate the first insectivore gene map. Shrew-Chinese hamster and shrew- mouse somatic cell hybrid cells were constructed. When the 119 shrew-rodent clones were characterized, only shrew chromosomes were found to have segregated. A panel of hybrid clones was selected for gene assignment. The genes for hypoxanthine phosphoribosyl transferase (HPRT), glucose-6- phosphate dehydrogenase (G6PD), and malate dehydrogenase 1 (MDH1) were assigned to shrew Chromosome (Chr) de [which is the product of a tandem fusion between the 'original' mammalian X Chromosome (Chr) and an autosome], the gene for adenosine deaminase (ADA) and 6-phosphogluconate dehydrogenase se (PGD) to Chromosome jl, the gene for thymidine kinase (TK) to Chromosome hn, and the gene for lactate dehydrogenase (LDHA) to chromosome ik. Further studies in progress.
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PMID:Gene mapping in the common shrew (Sorex araneus; Insectivora) by shrew-rodent cell hybrids: chromosome localization of the loci for HPRT, TK, LDHA, MDH1, G6PD, PGD, and ADA. 859 34

As has been shown earlier by us, the metabolism of extracellular deoxycytidine (dCyd) is 2-3 times higher in follicular and in PNA+ cells than in other cells. Deoxycytidine kinase (dCK) is one of the most important target enzymes for anti-proliferative drugs such as arabinosile-cytosine (ara-C), 2-Cl-deoxyadenosine (CdA). Neither the dCK activity nor the polypeptide correlates with the S phase of the cells, as thymidine kinase (TK1) does in tonsils. The newly developed anti-leukemic drug CdA, and also BrdA, are also phosphorylated by dCK and both effectively inhibit the 3H-dThd incorporation into DNA in tonsillar lymphocytes. A new molecular mechanism has been developed for CdA; it inhibits the interconversion of dCyd into dThd nucleotides. Analysis of the pools after 3H-dCyd labeling showed a decrease of the dUMP labeling. The inhibition of dCMP deaminase by the corresponding monophosphates (Cl-dAMP) in the cells has been suggested. CdA cannot be deaminated by adenosine deaminase (ADA), thus providing a good tool to investigate the importance of that enzyme during differentiation of the lymphoid cells. Elucidation of the nucleoside metabolism during the normal differentiation process might be the only way to get information about the same pathways in malignant transformations, i.e., in leukemias.
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PMID:Human tonsillar lymphocytes as targets for immunosuppressive and anticancer drugs. 908 56

The activity of thymidine kinase, thymidine phosphorylase, adenosine deaminase and 5'-nucleotedase of AMP was studied in tissues, blood serum and lymphocytes of 60 healthy females and 50 females with fibrocavernous mastopathy aged 23-70. It was revealed that age-related changes in the activity of thymidine kinase in blood serum reflect the analogous changes in enzyme activity in tissues of healthy women. A direct correlation was established between thymidine kinase activity and age both in healthy females and those with mastopathy. A significant decrease in activity of thymidine phosphorylase was demonstrated in blood serum of patients with mastopathy aged 46-60. Determined 4-fold increase in activity of adenosine deaminase in serum was accompanied by decreased enzyme activity in lymphocytes and decreased Lymphocyte Blast Transformation Index in the same age range. The revealed metabolic changes in DNA-precursors' metabolism in patients with mastopathy aged 46-60 might be one of the reasons of increased risk of oncological diseases in this age group.
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PMID:[Age-related changes in metabolism of DNA precursors in patients with mastopathy]. 931 43

The activity of thymidine kinase, thymidine phosphorylase, adenosine deaminase and 5'-nucleotidase of AMP was studied in tissues of 39 healthy females, as well as blood serum and lymphocytes of 60 healthy females, as well as in 50 patients with fibrocavernous mastopathy aged as 23-70. Comparative determination of adenosine metabolism enzymes activity in lymphocytes was carried out simultaneously with studying some immunological indexes in the organism of the same-aged healthy females and ones with mastopathy. It was revealed that age-related changes in the activity of thymidine kinase in blood serum reflected the analogous changes in enzyme activity in tissues of the healthy women. A direct correlation was established between thymidine kinase activity and age both in the healthy females and those with mastopathy. A significant decrease in activity of thymidine phosphorylase was demonstrated in blood serum of the patients with mastopathy in the age 46-60. Determined 4-fold increase in the activity of adenosine deaminase in serum was accompanied by decreased enzyme activity in lymphocytes and decreased Lymphocyte Blast Transformation Index in the same age range. Changes of immunological status are more expressed in T-system of immunity. The revealed metabolic changes in DNA-precursors metabolism in the patients with mastopathy aged as 46-60 might be one of the reasons of increased risk of oncological disease in this age group.
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PMID:[Metabolism of adenosine and thymidine in healthy females of different ages and females with mastopathies]. 1060 30


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