Vpr14-88-Apobec3G fusion protein is efficiently incorporated into Vif-positive HIV-1 particles and inhibits viral infection.
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Importin alpha3 interacts with HIV-1 integrase and contributes to HIV-1 nuclear import and replicationDriving DNA transposition by lentiviral protein transductionR88-APOBEC3Gm Inhibits the Replication of Both Drug-resistant Strains of HIV-1 and Viruses Produced From Latently Infected CellsInteractions of host APOBEC3 restriction factors with HIV-1 in vivo: implications for therapeutics.N-terminal hemagglutinin tag renders lysine-deficient APOBEC3G resistant to HIV-1 Vif-induced degradation by reduced polyubiquitination.HIV-1 accessory protein Vpr: relevance in the pathogenesis of HIV and potential for therapeutic interventionMultifaceted counter-APOBEC3G mechanisms employed by HIV-1 Vif.Characterization of anti-HIV activity mediated by R88-APOBEC3G mutant fusion proteins in CD4+ T cells, peripheral blood mononuclear cells, and macrophages.Inactivation of microbial infectiousness by silver nanoparticles-coated condom: a new approach to inhibit HIV- and HSV-transmitted infection.Running loose or getting lost: how HIV-1 counters and capitalizes on APOBEC3-induced mutagenesis through its Vif proteinCharacterization of antiviral activity of benzamide derivative AH0109 against HIV-1 infection.Binding of RNA by APOBEC3G controls deamination-independent restriction of retrovirusesIntracellular transport of human immunodeficiency virus type 1 genomic RNA and viral production are dependent on dynein motor function and late endosome positioningHost Factors and HIV-1 Replication: Clinical Evidence and Potential Therapeutic ApproachesActivation of HIV-1 expression in latently infected CD4+ T cells by the small molecule PKC412.Functional analysis and structural modeling of human APOBEC3G reveal the role of evolutionarily conserved elements in the inhibition of human immunodeficiency virus type 1 infection and Alu transposition.Gene therapy strategies to exploit TRIM derived restriction factors against HIV-1.Targeted genome editing by lentiviral protein transduction of zinc-finger and TAL-effector nucleasesThe cellular antiviral protein APOBEC3G interacts with HIV-1 reverse transcriptase and inhibits its function during viral replication.Inhibition of HIV-1 infection and replication by enhancing viral incorporation of innate anti-HIV-1 protein A3G: a non-pathogenic Nef mutant-based anti-HIV strategy.Contribution of host nucleoporin 62 in HIV-1 integrase chromatin association and viral DNA integrationHost protein Ku70 binds and protects HIV-1 integrase from proteasomal degradation and is required for HIV replicationMultiple Inhibitory Factors Act in the Late Phase of HIV-1 Replication: a Systematic Review of the Literature.
P2860
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P2860
Vpr14-88-Apobec3G fusion protein is efficiently incorporated into Vif-positive HIV-1 particles and inhibits viral infection.
description
2008 nî lūn-bûn
@nan
2008 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2008 թվականի ապրիլին 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
Vpr14-88-Apobec3G fusion prote ...... and inhibits viral infection.
@ast
Vpr14-88-Apobec3G fusion prote ...... and inhibits viral infection.
@en
Vpr14-88-Apobec3G fusion prote ...... and inhibits viral infection.
@nl
type
label
Vpr14-88-Apobec3G fusion prote ...... and inhibits viral infection.
@ast
Vpr14-88-Apobec3G fusion prote ...... and inhibits viral infection.
@en
Vpr14-88-Apobec3G fusion prote ...... and inhibits viral infection.
@nl
prefLabel
Vpr14-88-Apobec3G fusion prote ...... and inhibits viral infection.
@ast
Vpr14-88-Apobec3G fusion prote ...... and inhibits viral infection.
@en
Vpr14-88-Apobec3G fusion prote ...... and inhibits viral infection.
@nl
P2093
P2860
P1433
P1476
Vpr14-88-Apobec3G fusion prote ...... and inhibits viral infection.
@en
P2093
Xiaojian Yao
Yingfeng Zheng
P2860
P356
10.1371/JOURNAL.PONE.0001995
P407
P577
2008-04-16T00:00:00Z