Regular ArticleDual Mechanisms of 9-β--Arabinofuranosylguanine Resistance in CEM T-Lymphoblast Leukemia Cells☆
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Cited by (8)
Effects of 9-β-D-arabinofuranosylguanine on mitochondria in CEM T-lymphoblast leukemia cells
2003, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Cells were harvested after 2, 4 or 6 days and to the remaining cells were added fresh medium and drugs. Crude protein cell extracts were prepared as previously described [21] and stored at −80 °C until use. The protein concentrations in the crude cell extracts was determined using the BioRad protein assay reagent with bovine serum albumin as standard.
Resistance to mitochondrial- and Fas-mediated apoptosis in human leukemic cells with acquired resistance to 9-β-D-arabinofuranosylguanosine
2002, Biochemical and Biophysical Research CommunicationsLow level of mitochondrial deoxyguanosine kinase is the dominant factor in acquired resistance to 9-β-D-arabinofuranosylguanine cytotoxicity
2002, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Therefore we do not know if Ara-G can be phosphorylated in the mitochondria by dGK and then transported to the cytosol. Recent work demonstrates that Ara-G can induce resistance via more than one mechanism [16]. Primarily, a decrease in Ara-G incorporation into mitochondrial DNA was observed, followed by selection for dCK-deficient cells at high Ara-G concentration.
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Abbreviations used: dGK, deoxyguanosine kinase; dCK, deoxycytidine kinase; TK1, thymidine kinase 1; TK2, thymidine kinase 2; araG, 9-β--arabinofuranosylguanine; araC, 1-β--arabinofuranosylcytosine; araT, 1-β--arabinofuranosylthymine; CdA, 2-chloro-2′-deoxyadenosine; dThd, deoxythymidine; dCyd, deoxycytidine; dFdC, 2′,2′-difluorodeoxycytidine.
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