Stimulation of Deoxycytidine Kinase Results in Prolonged Maintenance of the Enzyme Activity

A number of genotoxic and antiproliferative agents such as 2-chlorodeoxyadenosine (Cladribine; CdA) and aphidicolin (APC) have been shown to stimulate the activity of deoxycytidine kinase, the main deoxynucleoside salvage enzyme in lymphocytes. Here we show that enzyme activation could be prevented...

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Bibliographic Details
Published in:Nucleosides, nucleotides & nucleic acids nucleotides & nucleic acids, 2004-10, Vol.23 (8-9), p.1357-1361
Main Authors: Keszler, G., Spasokoukotskaja, T., Virga, S., Sasvari-Szekely, M., Staub, M.
Format: Article
Language:English
Subjects:
2-Chlorodeoxyadenosine
Aphidicolin - metabolism
BAPTA-AM
Calcium - metabolism
Calcium chelation
Chelating Agents - pharmacology
Child
Child, Preschool
Cladribine - chemistry
Deoxycytidine kinase
Deoxycytidine Kinase - metabolism
Egtazic Acid - analogs & derivatives
Egtazic Acid - pharmacology
Enzyme Activation
Humans
Lymphocytes - enzymology
Lymphocytes - metabolism
Time Factors
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Summary:A number of genotoxic and antiproliferative agents such as 2-chlorodeoxyadenosine (Cladribine; CdA) and aphidicolin (APC) have been shown to stimulate the activity of deoxycytidine kinase, the main deoxynucleoside salvage enzyme in lymphocytes. Here we show that enzyme activation could be prevented by treating cells with the membrane-permeant calcium chelator BAPTA-AM. Long-term incubations demonstrated that CdA and APC not only stimulated but also sustained deoxycytidine kinase activity in the cellular context, as compared to the control and BAPTA-AM treated enzyme activities.
ISSN:1525-7770
1532-2335
DOI:10.1081/NCN-200027618