Modulation of human deoxycytidine kinase activity as a response to cellular stress induced by NaF

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Abstract

Deoxycytidine kinase (dCK) is one of the key enzymes of deoxynucleoside salvage supplying resting lymphocytes with DNA precursors for synthesis and repair. The level of dCK activity is especially important in chemotherapy with the use of deoxynucleoside analogues like arabinosyl cytosine (Citarabid, ara-C), or 2-chloro-deoxyadenosine (Cladribine, CdA). Previous results showed that Cladribine treatment of human lymphocytes increased several fold the activity of dCK without increasing the amount of dCK protein itself (Sasvári-Székely, et al., 1998, Biochem. Pharmacol. 56, 1175), and a possible post-translational modification was suggested. This theory was further investigated using NaF as an inhibitor of protein phosphatases. It was shown that NaF treatment of cells elevated dCK activity while inhibiting DNA synthesis. The possible mechanism of dCK activation/inactivation induced by exposure of cell cultures to different agents is discussed.

Original languageEnglish
Pages (from-to)251-256
Number of pages6
JournalActa Biochimica Polonica
Volume48
Issue number1
Publication statusPublished - Dec 1 2001

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Keywords

  • Deoxycytidine kinase
  • Lymphocytes
  • NaF
  • Tonsil

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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