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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 (Sasvari-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 activa- tion/inactivation induced by exposure of cell cultures to different agents is discussed.
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p.251-256,fig.
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- Semmelweis University, H-1444 Budapest-8, POB 260, Hungary
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Bibliografia
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- 6.Eriksson, S., Kierdaszuk, B., Munch-Petersen, B., Oberg, B. & Johansson, N.G. (1991) Comparison of substrate specificities of human thymidine kinase 1 and 2 and deoxycytidine kinase toward antiviral and cytostatic nucleoside analogues. Biochem. Biophys. Res. Commun. 176, 586-592.
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- 20.Spasokoukotskaja, T., Sasvari-Szekely, M., Keszler, G., Albertioni, F., Eriksson, S. & Staub, M. (1999) Treatment of normal and malignant cells with nucleoside analogues and etoposide enhances deoxycytidine kinase activity. Eur. J. Cancer 35, 1862-1867.
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Bibliografia
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bwmeta1.element.agro-article-00f1552f-31a9-479e-91e0-97dc68082b2f