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Dimerization of human immunodeficiency virus type 1 reverse transcriptase as an antiviral target

Current pharmaceutical design, 2006-05, Vol.12 (15), p.1879

2006

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Molecular mechanisms of HIV-1 resistance to nucleoside reverse transcriptase inhibitors (NRTIs)

Cellular and molecular life sciences : CMLS, 2000-09, Vol.57 (10), p.1408-1422

2000

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Relationship between enzyme activity and dimeric structure of recombinant HIV-1 reverse transcriptase

Proteins, structure, function, and bioinformatics, 2005-07, Vol.60 (1), p.5-13

2005

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B cells mediate R5-Tropic HIV infection of CCR5neg naive CD4 T cells

Journal of Virus Eradication, 2019-12, Vol.5, p.36

2019

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NNRTIs reduce HIV-1 production from latently infected resting CD4 + T cells

Journal of Virus Eradication, 2015-12, Vol.1, p.19-19

2015

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Persistence of antigen presenting cell-mediated HIV trans infection during cART

Journal of Virus Eradication, 2017-12, Vol.3, p.38

2017

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Mechanisms of inhibition of HIV replication by non-nucleoside reverse transcriptase inhibitors

Virus research, 2008-06, Vol.134 (1), p.147-156

2008

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Disulfiram reactivates latent HIV-1 expression through depletion of the phosphatase and tensin homolog

AIDS (London), 2013-01, Vol.27 (2), p.F7-F11

2013

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28 Dendritic cells programmed by inflammatory mediators can effectively induce both the immunologic ‘kick’ and ‘kill’ of latent HIV-1

Journal of Virus Eradication, 2016-07, Vol.2, p.18-18

2016

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Conformational stability of pGEX‐expressed Schistosoma japonicum glutathione S‐transferase: A detoxification enzyme and fusion‐protein affinity tag

Protein science, 1997-02, Vol.6 (2), p.399-406

1997

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Molecular mechanisms of bidirectional antagonism between K65R and thymidine analog mutations in HIV-1 reverse transcriptase

AIDS (London), 2007-07, Vol.21 (11), p.1405-1414

2007

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Conformational changes in HIV-1 reverse transcriptase induced by nonnucleoside reverse transcriptase inhibitor binding

Current HIV research, 2004-10, Vol.2 (4), p.323

2004

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N348I in HIV-1 reverse transcriptase decreases susceptibility to tenofovir and etravirine in combination with other resistance mutations

AIDS (London), 2010-01, Vol.24 (2), p.317-319

2010

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N348I in reverse transcriptase provides a genetic pathway for HIV-1 to select thymidine analogue mutations and mutations antagonistic to thymidine analogue mutations

AIDS (London), 2010-03, Vol.24 (5), p.659-667

2010

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Destabilization of the HIV-1 Reverse Transcriptase Dimer upon Interaction with N-Acyl Hydrazone Inhibitors

Molecular pharmacology, 2002-08, Vol.62 (2), p.398-405

2002

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Resistance complexities: the emerging profile of cross-resistance among NNRTIs

Antiviral therapy, 2014-01, Vol.19, p.A24-A24

Sluis-Cremer, N

2014

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Efavirenz enhances the proteolytic processing of an HIV-1 pol polyprotein precursor and reverse transcriptase homodimer formation

FEBS letters, 2005-01, Vol.579 (2), p.379-384

2005

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Proteolytic processing of an HIV-1 pol polyprotein precursor: insights into the mechanism of reverse transcriptase p66/p51 heterodimer formation

The international journal of biochemistry & cell biology, 2004-09, Vol.36 (9), p.1836-1847

2004

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Substrate mimicry: HIV-1 reverse transcriptase recognizes 6-modified-3'-azido-2',3'-dideoxyguanosine-5'-triphosphates as adenosine analogs

Nucleic acids research, 2012-01, Vol.40 (1), p.381

2012

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Stereo‐selectivity of HIV‐1 reverse transcriptase toward isomers of thymidine‐5′‐O‐1‐thiotriphosphate

Protein science, 2005-07, Vol.14 (7), p.1929-1933

2005

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Development of a primary cell model of HIV-1 latency in naive CD4 super(+) T-cells

Antiviral therapy, 2013-01, Vol.18, p.A25-A25

2013

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The 3′-Azido Group Is Not the Primary Determinant of 3′-Azido-3′-deoxythymidine (AZT) Responsible for the Excision Phenotype of AZT-resistant HIV-1

The Journal of biological chemistry, 2005-08, Vol.280 (32), p.29047-29052

2005

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Mechanism by Which Phosphonoformic Acid Resistance Mutations Restore 3′-Azido-3′-deoxythymidine (AZT) Sensitivity to AZT-resistant HIV-1 Reverse Transcriptase

The Journal of biological chemistry, 2000-03, Vol.275 (13), p.9251-9255

2000

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Silent mutations are selected in HIV-1 reverse transcriptase and affect enzymatic efficiency

AIDS (London), 2008-11, Vol.22 (18), p.2501-2508

2008

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Radiation Target Analyses of DNA Template/Primer Complexes

Biophysical journal, 2006-05, Vol.90 (9), p.L61-L63

2006

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Dimerization of human immunodeficiency virus type 1 reverse transcriptase as an antiviral target

Molecular mechanisms of HIV-1 resistance to nucleoside reverse transcriptase inhibitors (NRTIs)

Relationship between enzyme activity and dimeric structure of recombinant HIV-1 reverse transcriptase

B cells mediate R5-Tropic HIV infection of CCR5neg naive CD4 T cells

NNRTIs reduce HIV-1 production from latently infected resting CD4 + T cells

Persistence of antigen presenting cell-mediated HIV trans infection during cART

Mechanisms of inhibition of HIV replication by non-nucleoside reverse transcriptase inhibitors

Disulfiram reactivates latent HIV-1 expression through depletion of the phosphatase and tensin homolog

28 Dendritic cells programmed by inflammatory mediators can effectively induce both the immunologic ‘kick’ and ‘kill’ of latent HIV-1

Conformational stability of pGEX‐expressed Schistosoma japonicum glutathione S‐transferase: A detoxification enzyme and fusion‐protein affinity tag

Molecular mechanisms of bidirectional antagonism between K65R and thymidine analog mutations in HIV-1 reverse transcriptase

Conformational changes in HIV-1 reverse transcriptase induced by nonnucleoside reverse transcriptase inhibitor binding

N348I in HIV-1 reverse transcriptase decreases susceptibility to tenofovir and etravirine in combination with other resistance mutations

N348I in reverse transcriptase provides a genetic pathway for HIV-1 to select thymidine analogue mutations and mutations antagonistic to thymidine analogue mutations

Destabilization of the HIV-1 Reverse Transcriptase Dimer upon Interaction with N-Acyl Hydrazone Inhibitors

Resistance complexities: the emerging profile of cross-resistance among NNRTIs

Efavirenz enhances the proteolytic processing of an HIV-1 pol polyprotein precursor and reverse transcriptase homodimer formation

Proteolytic processing of an HIV-1 pol polyprotein precursor: insights into the mechanism of reverse transcriptase p66/p51 heterodimer formation

Substrate mimicry: HIV-1 reverse transcriptase recognizes 6-modified-3'-azido-2',3'-dideoxyguanosine-5'-triphosphates as adenosine analogs

Stereo‐selectivity of HIV‐1 reverse transcriptase toward isomers of thymidine‐5′‐O‐1‐thiotriphosphate

Development of a primary cell model of HIV-1 latency in naive CD4 super(+) T-cells

The 3′-Azido Group Is Not the Primary Determinant of 3′-Azido-3′-deoxythymidine (AZT) Responsible for the Excision Phenotype of AZT-resistant HIV-1

Mechanism by Which Phosphonoformic Acid Resistance Mutations Restore 3′-Azido-3′-deoxythymidine (AZT) Sensitivity to AZT-resistant HIV-1 Reverse Transcriptase

Silent mutations are selected in HIV-1 reverse transcriptase and affect enzymatic efficiency

Radiation Target Analyses of DNA Template/Primer Complexes

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