PREFERENTIAL INHIBITION OF THE GROWTH OF VIRUS-TRANSFORMED CELLS IN CULTURE BY RIFAZONE-82, A NEW RIFAMYCIN DERIVATIVE

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Rifazone-8{sub 2} (R-8{sub 2}), a new rifamycin derivative, is shown to preferentially inhibit the growth of virus-transformed chick cells in culture. Macromolecular synthesis and glucose uptake of transformed cells are also appreciably decreased in the presence of low concentrations of R-8{sub 2} where the normal cells appear unaffected. While R-8{sub 2} is shown to be a selective inhibitor of RNA-directed DNA polymerase in vitro, its action on the growth of transformed cells may involve some other mechanism.

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23 p.

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Bissell, Mina J.; Hatie, Carroll; Tischler, Allan N. & Calvin, Melvin. March 28, 1974.

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Rifazone-8{sub 2} (R-8{sub 2}), a new rifamycin derivative, is shown to preferentially inhibit the growth of virus-transformed chick cells in culture. Macromolecular synthesis and glucose uptake of transformed cells are also appreciably decreased in the presence of low concentrations of R-8{sub 2} where the normal cells appear unaffected. While R-8{sub 2} is shown to be a selective inhibitor of RNA-directed DNA polymerase in vitro, its action on the growth of transformed cells may involve some other mechanism.

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23 p.

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  • Journal Name: Proceedings of the National Academy of Sciences

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  • Report No.: LBL-2685
  • Grant Number: DE-AC02-05CH11231
  • DOI: 10.1073/pnas.71.6.2520 | External Link
  • Office of Scientific & Technical Information Report Number: 939470
  • Archival Resource Key: ark:/67531/metadc901706

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Office of Scientific & Technical Information Technical Reports

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  • March 28, 1974

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  • Sept. 27, 2016, 1:39 a.m.

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  • Oct. 3, 2016, 4:28 p.m.

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Bissell, Mina J.; Hatie, Carroll; Tischler, Allan N. & Calvin, Melvin. PREFERENTIAL INHIBITION OF THE GROWTH OF VIRUS-TRANSFORMED CELLS IN CULTURE BY RIFAZONE-82, A NEW RIFAMYCIN DERIVATIVE, article, March 28, 1974; Berkeley, California. (digital.library.unt.edu/ark:/67531/metadc901706/: accessed January 16, 2018), University of North Texas Libraries, Digital Library, digital.library.unt.edu; crediting UNT Libraries Government Documents Department.