Mutants of mouse T-lymphoma S49 cells lacking thymidine kinase activity of deficient in nucleoside transport were selected by growth in the presence of 5′-fluorodeoxyuridine and their sensitivity to interferon tested. All five thymidine kinase and both transport deficient mutants were sensitive to the antiproliferative effects of interferon. The replication of encephalomyocarditis virus was also inhibited by interferon, and the intracellular levels of (2′-5′)oligo-adenylate synthetase were elevated in all mutants tested. These results suggest that an intact nucleoside transport system or thymidine kinase activity are not essential for the expression of interferon sensitivity in these cells.
|Number of pages||7|
|Journal||Biochemical and Biophysical Research Communications|
|Publication status||Published - 13 Jan 1984|