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)

Simian virus 40 (SV40) infection of human diploid cells failed to cause an enhanced production of thymidine kinase during the first 10 days after infection. Thymidine kinase activities from extracts of SV40-transformed cultures (human or simian) were considerably higher than the activity levels in extracts from the normal cells of origin. In addition, whereas the kinase activities obtained for human diploid cultures decreased as the cell sheet became confluent, the kinase activities for SV40-transformed human cells remained high after confluence was reached. Antisera obtained from hamsters bearing SV40 or adeno-7-SV40 hybrid virus tumors selectively inhibited enzyme from transformed sources (human or simian). Also, the antisera selectively inhibited enzyme extracted from SV40-lytically infected monkey cells. Sera from normal animals or from hamsters bearing polyoma tumors failed to inhibit enzymes from normal, SV40-transformed, or SV40-lytically infected cells. The Michaelis constant of partially purified enzyme from SV40-transformed cells was two to five times as high as that obtained for partially purified enzyme from human diploid cell cultures.
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PMID:Thymidine kinase from normal, simian virus 40-transformed and simian virus 40-lytically infected cells. 431 40

The P3HR-1 line of human lymphoblastoid cells that is Epstein-Barr virus positive was made resistant to 5-bromodeoxyuridine. Epstein-Barr virus-associated antigens, but not virus particles, were produced in P3HR-1(BU) cells maintained on 5-bromodeoxyuridine. However, virus particles did appear within 4 days after removal of the drug. Thymidine kinase activity was limited to P3HR-1(BU) cells producing viral antigen, whereas all control P3HR-1 cells showed thymidine kinase activity regardless of viral antigen synthesis. Cellular DNA in most P3HR-1(BU) cells was made via pathways that did not involve thymidine kinase. In cells having a pathway that involved thymidine kinase, a second DNA of density 1.71 g/cm(3), corresponding to Epstein-Barr virus, was detected.IT WAS CONCLUDED THAT: (a) a repressed Epstein-Barr virus genome persists in P3HR-1(BU) cells that do not contain thymidine kinase, with activation of the viral genome being accompanied by productive infection and the appearance of enzyme, and (b) thymidine kinase activity in P3HR-1(BU) cells could be used as a marker for viral genome expression.
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PMID:Persistence of a repressed Epstein-Barr virus genome in Burkitt lymphoma cells made resistant to 5-bromodeoxyuridine. 433 12

Thymidine kinase (EC 2.7.1.21)-deficient mouse cells were infected with inactivated herpes simplex virus, after which "transformed" cells that produce viral thymidine kinase were isolated. Shortly after transformation, the expression of the viral enzyme could be suppressed and reactivated with high efficiency. On continued multiplication in nonselective medium, the proportion of cells producing the viral enzyme decayed exponentially. This decay seemed to represent a change in the expression of the viral gene for thymidine kinase rather than the loss of the gene from the cells, since the viral enzyme could be apparently reactivated in every cell, albeit at a very low frequency.
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PMID:Herpes simplex virus as a source of thymidine kinase for thymidine kinase-deficient mouse cells: suppression and reactivation of the viral enzyme. 435 62

Cytoplasmic thymidine kinase from cardiac muscle of the rat has been characterized. It has a pH optimum of 9.0 and a K(m) value for thymidine of 1.6mum. The sedimentation coefficient of this enzyme in sucrose gradients is 4.5S, which represents a molecular weight of approx. 69000. Thymidine kinase prepared from cardiac muscle of foetal, neonatal and adult rats is inhibited by dTTP and dTDP; there is neither inhibition nor stimulation by dTMP, dCTP, dATP, dGTP or cyclic AMP. The activity of thymidine kinase in differentiating cardiac muscle of foetal and neonatal rats declines progressively with development, reaching adult values of almost zero by the fifteenth to seventeenth day of postnatal development. This represents a 70-fold decrease in enzyme activity from 3 days before birth to 17 days after birth. The loss of thymidine kinase activity in differentiating cardiac muscle correlates temporally with the cessation of DNA biosynthesis and the loss of cytoplasmic DNA polymerase activity in this tissue.
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PMID:Thymidine kinase activity in cardiac muscle during embryomic and postnatal development. 437 15

Thymidine kinase positive (TK(+)) N type cell lines that had been transformed by spleen focus-forming virus were established by transformation with NB tropic Friend virus complex. Thymidine kinase deficient (TK(-)) cell clones were isolated. Some of these cell clones release 1000- to 100,000-fold reduced amounts of Friend virus complex as compared to the TK(+) parental cell clone. TK(-) clones were grown in medium without BrdUrd. Some of these TK(-) clones can be induced to release endogenous helper virus and transforming spleen focus-forming virus on reexposure to 10(-6)-10(-4) M BrdUrd. The induced Friend virus complex is of N host range as expected with induced endogenous virus in N-type cells. Before the induction of the endogenous virus spleen focus-forming virus complex, an induction of thymidine kinase (ATP:thymidine 5'-phosphotransferase, EC 2.7.1.75) activity is observed. The latter is possibly a prerequisite for the induction of endogenous virus in TK(-) cells. Induction of thymidine kinase activity and of endogenous virus is transient and always correlated. The role of BrdUrd and another thymidine analogue, azidothymidine, in interfering with C-type virus release in virus positive cells is discussed. Azidothymidine is unable to induce endogenous virus. Induction of endogenous virus by BrdUrd and inhibition of virus release in virus positive cells is apparently not caused by the same mechanism.
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PMID:Induction of endogenous virus and of thymidine kinase by bromodeoxyuridine in cell cultures transformed by Friend virus. 453 Oct 31

Dialyzed extracts of Bacillus megaterium KM contain thymidine, deoxyadenosine, and deoxyguanosine kinase activities. Thymidine kinase activity is best with deoxyadenosine triphosphate or deoxyguanosine triphosphate (dGTP) as the phosphoryl donor, whereas the best deoxyadenosine kinase activity is obtained with dGTP or adenosine triphosphate. Deoxyguanosine kinase activity functions optimally with deoxycytidine triphosphate as the donor. Although the thymidine kinase activity of crude extracts does not have a demonstrable divalent cation requirement, the addition of Mg(2+) or Mn(2+) is necessary for the formation of thymidine di- and triphosphates. The synthesis of thymidine kinase appears to be partially derepressed by thymine starvation. Incubation of extracts with deoxyadenosine and dGTP results in the substantial accumulation of deoxyadenosine di- and triphosphates. Extracts deaminate deoxycytidine to deoxyuridine, presumably as a consequence of the action of deoxycytidine deaminase, and then convert deoxyuridine to deoxyuridylic acid. B. megaterium extracts do not contain any detectable deoxycytidine kinase activity.
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PMID:Deoxynucleoside kinases of Bacillus megaterium KM. 499 37

Thymidine kinase was induced after infection of an established strain of green monkey kidney cells (CV-1) with simian adenovirus SV15. Increased levels of thymidine kinase were first observed 8 to 10 hr postinoculation (PI), and the levels increased four- to eightfold by 16 to 24 hr PI. A transient increase (1.5- to 3-fold) of deoxyribonucleic acid (DNA) polymerase activity was also observed about 18 hr PI, but the level of deoxycytidylic deaminase was not enhanced. The inductions of thymidine kinase and DNA polymerase were not obtained when protein synthesis was inhibited with 10(-5) M cycloheximide. However, the enzyme increases did take place when infected cultures were treated with 1-beta-D-arabinofuranosylcytosine (ara-C), an inhibitor of DNA synthesis and SV15 replication. The incorporation of tritium-labeled thymidine (H(3)-dT) into DNA was also stimulated 8 to 24 hr after infection with SV15.
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PMID:Enzyme induction in green monkey kidney cultures infected with simian adenovirus. 562 53

The early steps in vaccinia virus infection were studied in HeLa cells which had been treated with actinomycin D (1 mug/ml) and then incubated for several hours in fresh medium prior to infection. Initiation of infection occurred in such cells even though the synthesis of cellular ribonucleic acid and deoxyribonucleic acid (DNA) was severely depressed. Thymidine kinase was synthesized in amounts that exceeded those found in untreated, infected cells. The breakdown of viral "cores" to liberate viral DNA and the synthesis of viral specific DNA-polymerase also occurred but were somewhat delayed. A deoxyribonuclease resembling an exonuclease was made by the infected, pretreated cells. The time course for these events suggested that the genetic code for synthesis of thymidine kinase can be expressed before "cores" are broken down, but the DNA-polymerase can be synthesized only after liberation of the viral DNA. The amount of viral specific DNA-polymerase which was made after infection was proportional to the total number of virus synthesizing sites even beyond the point where all the cells were infected with one infectious particle. A similar relationship was observed for the amount of thymidine kinase formed and for the rate of viral DNA synthesis from (3)H-thymidine.
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PMID:Initiation of vaccinia virus infection in actinomycin D-pretreated cells. 572 24

Thymidine kinase-deficient (TK-; ATP:thymidine 5'-phosphotransferase, EC 2.7.1.21)F9 teratocarcinoma stem cells have been transformed with a recombinant plasmid genome consisting of the pBR322 genome linked to a herpes simplex virus type 1 thymidine kinase gene (HSV-1 tk) and a simian virus 40 (SV40) genome. A clonal line of stem cells was obtained that contains only one copy of plasmid DNA, which is integrated into murine chromosomal DNA through a site on the pBRR322 genome. The HSV-1 tk gene, which is adjacent to the SV40 genome, is expressed in stem cells, whereas SV40 gene expression is not detectable. If differentiation of these stem cells is induced, the differentiated cells express SV40 early gene products. Thus, we have constructed a stem cell which contains a set of genes (SV40), the expression of which is regulated differently in stem and differentiated cells. This cell line could be used to determine the mechanism of suppression of expression of these genes in stem cells.
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PMID:DNA-transformed murine teratocarcinoma cells: regulation of expression of simian virus 40 tumor antigen in stem versus differentiated cells. 625 45

After the stimulation of quiescent density-inhibited BALB/c-3T3 cells with fresh bovine calf serum, uridine kinase activity measured in cellular extracts increased between hours 3 and 6 of incubation and remained elevated through 12 h after stimulation. The addition of either partially purified platelet-derived growth factor (PDGF) or platelet-poor plasma (PPP) also caused increased uridine kinase activity by 6 h, but the increased activity was not maintained and the activity returned to the prestimulated level by 12 h. However, when PDGF and PPP were added in combination an increased level of uridine kinase activity was maintained in a manner similar to that seen after the addition of serum. The components of PPP eluted in the void volume from Sephadex G-50 chromatography did not induce uridine kinase activity when present alone, although they did act synergistically with PDGF to allow the maintenance of elevated levels or uridine kinase activity over the period from 6 to 12 h after stimulation. Thymidine kinase activity was not induced by the addition of either PDGF or PPP alone, although either serum or the combination of PDGF and PPP did produce and induction of thymidine kinase activity in late G1.
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PMID:Regulation of uridine kinase activity in BALB/C-3T3 cells by serum components. 627 91


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