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 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.
Keszler
G
G
Institute of Medical Chemistry, Molecular Biology and Pathobiochemistry, Semmelweis University, Budapest, Hungary.
Spasokoukotskaja
T
T
Virga
S
S
Sasvari-Szekely
M
M
Staub
M
M
D016590:Aphidicolin / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism; D002614:Chelating Agents / Q000494:pharmacology; D002648:Child; D002675:Child, Preschool; D017338:Cladribine / Q000737:chemistry*; D003842:Deoxycytidine Kinase / Q000378:metabolism*; D004533:Egtazic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D004789:Enzyme Activation; D006801:Humans; D008214:Lymphocytes / Q000201:enzymology / Q000378:metabolism; D013997:Time Factors
D002614:Chelating Agents; C070379:1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester; D016590:Aphidicolin; D017338:Cladribine; D004533:Egtazic Acid; D003842:Deoxycytidine Kinase; D002118:Calcium