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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

In vitro biological activity of 9-beta-D-arabinofuranosyl-2-fluoroadenine and the biochemical actions of its triphosphate on DNA polymerases and ribonucleotide reductase from HeLa cells.

9-beta-D-Arabinofuranosyl-2-fluoroadenine (2-F-araA) inhibited the growth in vitro of HeLa cells by 50% at a concentration of 0.25 microM and depressed the replication of herpes simplex virus Types 1 and 2 by 99% at 25 microM. The analogue served as a substrate for cytoplasmic but not mitochondrial deoxycytidine (dCyd) kinase partially purified from human peripheral chronic lymphocytic leukemic blast cells. The Km values of dCyd and 2-F-araA for the cytoplasmic enzyme were 5 microM and 213 microM, respectively. However, at concentrations of 0.4 mM, the analogue was phosphorylated 2.9 times faster than dCyd. The 5'-triphosphate of 2-F-araA was examined for its biochemical effects on partially purified ribonucleotide reductase and highly purified DNA alpha- and beta-polymerases from HeLa cells. 2-F-araATP was a potent inhibitor of ribonucleotide reductase; the concentration required for 50% inhibition of ADP reduction (0.3 mM ADP; 5 mM GTP or dGTP) was 1 microM and for CDP reduction (0.15 mM CPD; 5 mM ATP) was 8.5 microM. Furthermore, 2-F-araATP was a competitive inhibition (Ki = 1.2 microM) with respect to dATP (Km = 3.8 microM) of DNA alpha-polymerase, whereas DNA beta-polymerase was relatively insensitive to the drug. The results suggest that the cytotoxic actions of 2-F-araA may be due, in part, to a "self-potentiating" inhibition of DNA synthesis. This is, by inhibiting the formation of competing dATP, 2-F-araATP may potentiate its inhibition of DNA synthesis.[1]


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