HIV-1 reverse transcriptase connection subdomain mutations reduce template RNA degradation and enhance AZT excision
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HIV-1 Reverse Transcriptase (RT) Polymorphism 172K Suppresses the Effect of Clinically Relevant Drug Resistance Mutations to Both Nucleoside and Non-nucleoside RT InhibitorsComplexes of HIV-1 RT, NNRTI and RNA/DNA hybrid reveal a structure compatible with RNA degradationZidovudine (AZT) monotherapy selects for the A360V mutation in the connection domain of HIV-1 reverse transcriptaseA novel molecular mechanism of dual resistance to nucleoside and nonnucleoside reverse transcriptase inhibitors.N348I in reverse transcriptase provides a genetic pathway for HIV-1 to select thymidine analogue mutations and mutations antagonistic to thymidine analogue mutationsThe Role of Nucleotide Excision by Reverse Transcriptase in HIV Drug Resistance.Structure and function of HIV-1 reverse transcriptase: molecular mechanisms of polymerization and inhibition.N348I in HIV-1 reverse transcriptase can counteract the nevirapine-mediated bias toward RNase H cleavage during plus-strand initiation.HIV-1 Ribonuclease H: Structure, Catalytic Mechanism and Inhibitors.The "Connection" Between HIV Drug Resistance and RNase HThe N348I mutation at the connection subdomain of HIV-1 reverse transcriptase decreases binding to nevirapine.Convergent evolution of ribonuclease h in LTR retrotransposons and retroviruses.Phenotypic characterization of drug resistance-associated mutations in HIV-1 RT connection and RNase H domains and their correlation with thymidine analogue mutations.The evolution of HIV-1 reverse transcriptase in route to acquisition of Q151M multi-drug resistance is complex and involves mutations in multiple domains.Mechanisms and factors that influence high frequency retroviral recombinationGenotypic resistance at viral rebound among patients who received lopinavir/ritonavir-based or efavirenz-based first antiretroviral therapy in South Africa.The effects of RNase H inhibitors and nevirapine on the susceptibility of HIV-1 to AZT and 3TC.In vitro resistance profile of the candidate HIV-1 microbicide drug dapivirineHIV-1 and HIV-2 reverse transcriptases: different mechanisms of resistance to nucleoside reverse transcriptase inhibitors.N348I in HIV-1 reverse transcriptase counteracts the synergy between zidovudine and nevirapine.Clinical relevance of substitutions in the connection subdomain and RNase H domain of HIV-1 reverse transcriptase from a cohort of antiretroviral treatment-naïve patients.Connection subdomain mutations in HIV-1 subtype-C treatment-experienced patients enhance NRTI and NNRTI drug resistanceEvolving uses of oral reverse transcriptase inhibitors in the HIV-1 epidemic: from treatment to preventionSubtype-specific differences in the human immunodeficiency virus type 1 reverse transcriptase connection subdomain of CRF01_AE are associated with higher levels of resistance to 3'-azido-3'-deoxythymidine.Mechanism by which a glutamine to leucine substitution at residue 509 in the ribonuclease H domain of HIV-1 reverse transcriptase confers zidovudine resistance.A novel mutation, D404N, in the connection subdomain of reverse transcriptase of HIV-1 CRF08_BC subtype confers cross-resistance to NNRTIs.Mechanisms involved in the selection of HIV-1 reverse transcriptase thumb subdomain polymorphisms associated with nucleoside analogue therapy failure.A role of template cleavage in reduced excision of chain-terminating nucleotides by human immunodeficiency virus type 1 reverse transcriptase containing the M184V mutation.Altered strand transfer activity of a multiple-drug-resistant human immunodeficiency virus type 1 reverse transcriptase mutant with a dipeptide fingers domain insertion.AZT resistance alters enzymatic properties and creates an ATP-binding site in SFVmac reverse transcriptase.Mutations in the C-terminal region of the HIV-1 reverse transcriptase and their correlation with drug resistance associated mutations and antiviral treatment.Inhibition of the DNA polymerase and RNase H activities of HIV-1 reverse transcriptase and HIV-1 replication by Brasenia schreberi (Junsai) and Petasites japonicus (Fuki) components.Clinical, virological and biochemical evidence supporting the association of HIV-1 reverse transcriptase polymorphism R284K and thymidine analogue resistance mutations M41L, L210W and T215Y in patients failing tenofovir/emtricitabine therapy
P2860
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P2860
HIV-1 reverse transcriptase connection subdomain mutations reduce template RNA degradation and enhance AZT excision
description
2008 nî lūn-bûn
@nan
2008 թուականի Յուլիսին հրատարակուած գիտական յօդուած
@hyw
2008 թվականի հուլիսին հրատարակված գիտական հոդված
@hy
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
name
HIV-1 reverse transcriptase co ...... ation and enhance AZT excision
@ast
HIV-1 reverse transcriptase co ...... ation and enhance AZT excision
@en
HIV-1 reverse transcriptase co ...... ation and enhance AZT excision
@nl
type
label
HIV-1 reverse transcriptase co ...... ation and enhance AZT excision
@ast
HIV-1 reverse transcriptase co ...... ation and enhance AZT excision
@en
HIV-1 reverse transcriptase co ...... ation and enhance AZT excision
@nl
prefLabel
HIV-1 reverse transcriptase co ...... ation and enhance AZT excision
@ast
HIV-1 reverse transcriptase co ...... ation and enhance AZT excision
@en
HIV-1 reverse transcriptase co ...... ation and enhance AZT excision
@nl
P2093
P2860
P356
P1476
HIV-1 reverse transcriptase co ...... ation and enhance AZT excision
@en
P2093
Abhay Jere
Galina N Nikolenko
John M Coffin
Krista A Delviks-Frankenberry
Paul L Boyer
Vinay K Pathak
P2860
P304
10943-10948
P356
10.1073/PNAS.0804660105
P407
P577
2008-07-30T00:00:00Z