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The nucleoside analog-resistant E89G mutant of human immunodeficiency virus type 1 reverse transcriptase displays a broader cross-resistance that extends to nonnucleoside inhibitors.

The alteration of a glutamic acid (E) to a glycine (G) amino acid residue at position 89 (E89G alteration) in the human immunodeficiency virus type 1 reverse transcriptase confers decreased susceptibility to several nucleoside analog inhibitors. Because the nonnucleoside inhibitor-binding pocket is...

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Autori principali: Kew, Y, Salomon, H, Olsen, L R, Wainberg, M A, Prasad, V R
Natura: Artigo
Lingua:Inglês
Pubblicazione: 1996
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Accesso online:https://ncbi.nlm.nih.gov/pmc/articles/PMC163400/
https://ncbi.nlm.nih.gov/pubmed/8807067
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