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  1. 1.   Structural Basis for the Role of the K65R Mutation in HIV-1 Reverse Transcriptase Polymerization, Excision Antagonism, and Tenofovir Resistance
  2. Das, K.; Bandwar, R. P.; White, K. L.; Feng, J. Y.; Sarafianos, S. G.; Tuske, S.; Tu, X. Y.; Clark, A. D.; Boyer, P. L.; Hou, X. R.; Gaffney, B. L.; Jones, R. A.; Miller, M. D.; Hughes, S. H.; Arnold, E.
  3. Journal of Biological Chemistry. 2009 284(50): 35092-35100.
  1. 2.   Mechanism for nucleoside analog-mediated abrogation of HIV-1 replication: Balance between RNase H activity and nucleotide excision
  2. Nikolenko, G. N.; Palmer, S.; Maldarelli, F.; Mellors, J. W.; Coffin, J. M.; Pathak, V. K.
  3. Proceedings of the National Academy of Sciences of the United States of America. 2005, FEB 8; 102(6): 2093-2098.
  1. 3.   Fixed conformation nucleoside analogs effectively inhibit excision-proficient HIV-1 reverse transcriptases
  2. Boyer, P. L.; Julias, J. G.; Marquez, V. E.; Hughes, S. H.
  3. Journal of Molecular Biology. 2005, JAN 21; 345(3): 441-450.
  1. 4.   Taking aim at a moving target: designing drugs to inhibit drug-resistant HIV-1 reverse transcriptases
  2. Sarafianos, S. G.; Das, K.; Hughes, S. H.; Arnold, E.
  3. Current Opinion in Structural Biology. 2004, DEC; 14(6): 716-730.
  1. 5.   Effects of the Delta 67 complex of mutations in human immunodeficiency virus type 1 reverse transcriptase on nucleoside analog excision
  2. Boyer, P. L.; Imamichi, T.; Sarafianos, S. G.; Arnold, E.; Hughes, S. H.
  3. Journal of Virology. 2004, SEP; 78(18): 9987-9997.
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