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Gene Review

UL23  -  thymidine kinase

Cercopithecine herpesvirus 2

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Disease relevance of UL23

  • The thymidine kinase gene of herpes simplex virus 1 was mutated by inserting oligodeoxynucleotide linkers into the region of the gene corresponding to the 5' untranslated portion of the mRNA [1].
  • One of the cell lines is able to complement the functional defect found in two temperature-sensitive mutants of HSV 1, and reversion of the cells to a thymidine kinase-negative phenotype results in the loss of this capability [2].
  • Formation of infectious progeny virus after insertion of herpes simplex thymidine kinase gene into DNA of an avian retrovirus [3].
  • Introduction of the herpes simplex virus thymidine kinase gene into mouse cells using virus DNA or transformed cell DNA [2].
  • In converted tk+ cells, the fused thymidine kinase gene, like the wild-type gene, is stimulated by superinfection with the tk- virus [4].

Psychiatry related information on UL23


High impact information on UL23


Chemical compound and disease context of UL23


Biological context of UL23

  • To examine this phenomenon further, a plasmid containing HSV thymidine kinase and human alpha- and gamma-globin genes was transfected into mouse L cells [14].
  • Mouse L cells lacking the enzyme thymidine kinase (LMTK-) have been converted to a TK+ phenotype by infection with fragmented HSV2 strain 333 DNA [15].
  • The acquired phenotype was demonstrated to be donor-derived by analysis of the electrophoretic mobility of the tk activity, and the presence of HSV DNA sequences in the recipient cells was demonstrated [16].
  • In the first step of the procedure, the herpes simplex virus thymidine kinase is inserted into the genome at a specific site [17].
  • Transfection experiments with HSV 1 in which one uses herpes simplex virus (HSV) thymidine kinase (TK) as a selectable prototrophic marker yield two classes of transformed cells: stable and unstable [18].

Anatomical context of UL23

  • When DNA was delivered directly into the nuclei of LMTK-, a mouse cell line deficient in thymidine kinase activity, 50--100% of the cells expressed TK enzymatic activity [19].
  • We examined the molecular basis of modulation of transfected herpes simplex virus (HSV) thymidine kinase (tk) gene in mouse fibroblasts [20].
  • The recombinant virus carrying the thymidine kinase inserted into the gene 22 and viruses exhibiting 0.1 kb and 0.7 kb deletions in the gene 22 specify new alpha polypeptides with molecular weights approximately 30% of the wild-type gene 22 product and grown normally in Vero cell cultures [17].
  • In companion experiments, we used high molecular weight DNA derived from tissues and cultured cells of a variety of species to transfer tk activity [16].
  • A plasmid, designated pMK, containing the structural gene for thymidine kinase from herpes simplex virus (HSV) fused to the promoter/regulatory region of the mouse metallothionein-I gene, was injected into the pronucleus of fertilized one-cell mouse eggs; the eggs were subsequently reimplanted into the oviducts of pseudopregnant mice [21].

Associations of UL23 with chemical compounds

  • Two virus-coded enzymes are important in the mechanism of action of this drug: thymidine kinase (TK) which initiates its activation by converting it to the monophosphate and DNA polymerase whose action is inhibited by ACV triphosphate [10].
  • The induction of TK expression by 5-azacytidine was concentration-dependent, with maximal induction at 10 micromoles per liter [11].
  • Investigation into the mechanism of the acyclovir resistance revealed changes in the thymidine-kinase activity of both isolates [22].
  • Transfections of the cisplatin-sensitive cells resulted in no sensitization to ganciclovir with pMT-TK (IC(50) 200 microg/mL) and a high sensitization with pCD3-TK (IC(50) = 6 microg/mL) [23].
  • Discontinuous polyacrylamide gel electrophoresis studies demonstrated that the HSV-2-specific TK was the selected enzyme in the hybrids [12].

Regulatory relationships of UL23


Other interactions of UL23


Analytical, diagnostic and therapeutic context of UL23

  • Furthermore, autoradiography of the cells still expressing TK shows that 3H-thymidine incorporation is reduced [26].
  • Direct microinjection of DNA by glass micropipettes was used to introduce the Herpes simplex virus thymidine kinase gene into cultured mammalian cells [19].
  • The tk+ mouse cells transformed with human DNA were shown to express human type tk activity as determined by isoelectric focusing [16].
  • Southern blot analyses demonstrated that functional thymidine kinase genes were generated by homologous recombination between the two deletion mutants [27].
  • CONCLUSION: These studies suggest that pMT-TK gene therapy may provide an alternative treatment for cisplatin-refractory ovarian tumors [23].


  1. Insertion mutagenesis to increase secondary structure within the 5' noncoding region of a eukaryotic mRNA reduces translational efficiency. Pelletier, J., Sonenberg, N. Cell (1985) [Pubmed]
  2. Introduction of the herpes simplex virus thymidine kinase gene into mouse cells using virus DNA or transformed cell DNA. Minson, A.C., Wildy, P., Buchan, A., Darby, G. Cell (1978) [Pubmed]
  3. Formation of infectious progeny virus after insertion of herpes simplex thymidine kinase gene into DNA of an avian retrovirus. Shimotohno, K., Temin, H.M. Cell (1981) [Pubmed]
  4. Regulation of alpha genes of herpes simplex virus: expression of chimeric genes produced by fusion of thymidine kinase with alpha gene promoters. Post, L.E., Mackem, S., Roizman, B. Cell (1981) [Pubmed]
  5. Chromatin structure is required to block transcription of the methylated herpes simplex virus thymidine kinase gene. Buschhausen, G., Wittig, B., Graessmann, M., Graessmann, A. Proc. Natl. Acad. Sci. U.S.A. (1987) [Pubmed]
  6. Herpes simplex virus type 1 DNA is present in specific regions of brain from aged people with and without senile dementia of the Alzheimer type. Jamieson, G.A., Maitland, N.J., Wilcock, G.K., Yates, C.M., Itzhaki, R.F. J. Pathol. (1992) [Pubmed]
  7. Enhancement of mRNA nuclear transport by promoter elements. de la Peña, P., Zasloff, M. Cell (1987) [Pubmed]
  8. Isomerization of herpes simplex virus 1 genome: identification of the cis-acting and recombination sites within the domain of the a sequence. Chou, J., Roizman, B. Cell (1985) [Pubmed]
  9. Two distinct transcription factors bind to the HSV thymidine kinase promoter in vitro. Jones, K.A., Yamamoto, K.R., Tjian, R. Cell (1985) [Pubmed]
  10. Altered substrate specificity of herpes simplex virus thymidine kinase confers acyclovir-resistance. Darby, G., Field, H.J., Salisbury, S.A. Nature (1981) [Pubmed]
  11. 5-Azacytidine-induced reactivation of a herpes simplex thymidine kinase gene. Clough, D.W., Kunkel, L.M., Davidson, R.L. Science (1982) [Pubmed]
  12. Association of herpes simplex thymidine kinase gene with chromosome No. 18 in transformed human cells. McKinlay, M.A., Wilson, D.E., Harrison, B., Povey, S. J. Natl. Cancer Inst. (1980) [Pubmed]
  13. Extensive vitiligo after ganciclovir treatment of GvHD in a patient who had received donor T cells expressing herpes simplex virus thymidine kinase. Aubin, F., Cahn, J.Y., Ferrand, C., Angonin, R., Humbert, P., Tiberghien, P. Lancet (2000) [Pubmed]
  14. Coordinate modulation of transfected HSV thymidine kinase and human globin genes. Roginski, R.S., Skoultchi, A.I., Henthorn, P., Smithies, O., Hsiung, N., Kucherlapati, R. Cell (1983) [Pubmed]
  15. Biochemical transformation of mouse cells by fragments of herpes simplex virus DNA. Maitland, N.J., McDougall, J.K. Cell (1977) [Pubmed]
  16. Biochemical transfer of single-copy eucaryotic genes using total cellular DNA as donor. Wigler, M., Pellicer, A., Silverstein, S., Axel, R. Cell (1978) [Pubmed]
  17. A generalized technique for deletion of specific genes in large genomes: alpha gene 22 of herpes simplex virus 1 is not essential for growth. Post, L.E., Roizman, B. Cell (1981) [Pubmed]
  18. A herpes simplex virus 1 integration site in the mouse genome defined by somatic cell genetic analysis. Smiley, J.R., Steege, D.A., Juricek, D.K., Summers, W.P., Ruddle, F.H. Cell (1978) [Pubmed]
  19. High efficiency transformation by direct microinjection of DNA into cultured mammalian cells. Capecchi, M.R. Cell (1980) [Pubmed]
  20. Modulation of transfected gene expression mediated by changes in chromatin structure. Davies, R.L., Fuhrer-Krusi, S., Kucherlapati, R.S. Cell (1982) [Pubmed]
  21. Somatic expression of herpes thymidine kinase in mice following injection of a fusion gene into eggs. Brinster, R.L., Chen, H.Y., Trumbauer, M., Senear, A.W., Warren, R., Palmiter, R.D. Cell (1981) [Pubmed]
  22. Treatment of resistant herpes simplex virus with continuous-infusion acyclovir. Engel, J.P., Englund, J.A., Fletcher, C.V., Hill, E.L. JAMA (1990) [Pubmed]
  23. Transactivation of the metallothionein promoter in cisplatin-resistant cancer cells: a specific gene therapy strategy. Vandier, D., Calvez, V., Massade, L., Gouyette, A., Mickley, L., Fojo, T., Rixe, O. J. Natl. Cancer Inst. (2000) [Pubmed]
  24. A conserved open reading frame that overlaps the herpes simplex virus thymidine kinase gene is important for viral growth in cell culture. Jacobson, J.G., Martin, S.L., Coen, D.M. J. Virol. (1989) [Pubmed]
  25. Herpes simplex virus DNA polymerase, thymidine kinase and deoxyribonuclease activities in cells infected with wild type, ultraviolet-irradiated and defective virus. Becker, Y., Gutter, B., Cohen, Y., Chejanovsky, N., Rabkin, S., Fridlender, B. Arch. Virol. (1979) [Pubmed]
  26. Inhibition of thymidine kinase gene expression by anti-sense RNA: a molecular approach to genetic analysis. Izant, J.G., Weintraub, H. Cell (1984) [Pubmed]
  27. Recombination during gene transfer into mouse cells can restore the function of deleted genes. Small, J., Scangos, G. Science (1983) [Pubmed]
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