The cell cycle independence of HIV infections is not determined by known karyophilic viral elements.
about
tRNAs promote nuclear import of HIV-1 intracellular reverse transcription complexesHIV-1 capsid-cyclophilin interactions determine nuclear import pathway, integration targeting and replication efficiencySAMHD1 restricts the replication of human immunodeficiency virus type 1 by depleting the intracellular pool of deoxynucleoside triphosphatesVirus strategies for passing the nuclear envelope barrierHIV-1 protease and reverse transcriptase control the architecture of their nucleocapsid partnerThe structural biology of HIV assembly.Differential effects of human immunodeficiency virus type 1 capsid and cellular factors nucleoporin 153 and LEDGF/p75 on the efficiency and specificity of viral DNA integrationRetroviral DNA integration: viral and cellular determinants of target-site selectionHigh-throughput, library-based selection of a murine leukemia virus variant to infect nondividing cellsCentrosomal latency of incoming foamy viruses in resting cells.Evidence for direct involvement of the capsid protein in HIV infection of nondividing cells.Positive selection and increased antiviral activity associated with the PARP-containing isoform of human zinc-finger antiviral protein.The requirement for cellular transportin 3 (TNPO3 or TRN-SR2) during infection maps to human immunodeficiency virus type 1 capsid and not integrase.Flexible use of nuclear import pathways by HIV-1.Deciphering the code for retroviral integration target site selectionPerturbation of host nuclear membrane component RanBP2 impairs the nuclear import of human immunodeficiency virus -1 preintegration complex (DNA)Host hindrance to HIV-1 replication in monocytes and macrophages.The functions of the HIV1 protein Vpr and its action through the DCAF1.DDB1.Cullin4 ubiquitin ligase.Mouse mammary tumor virus-based vector transduces non-dividing cells, enters the nucleus via a TNPO3-independent pathway and integrates in a less biased fashion than other retroviruses.Methods for integration site distribution analyses in animal cell genomesExposed hydrophobic residues in human immunodeficiency virus type 1 Vpr helix-1 are important for cell cycle arrest and cell deathAdaptive evolution of a tagged chimeric gammaretrovirus: identification of novel cis-acting elements that modulate splicing.The HIV-1 integrase mutant R263A/K264A is 2-fold defective for TRN-SR2 binding and viral nuclear import.Gammaretroviral vectors: biology, technology and applicationDifferential effects of Vpr on single-cycle and spreading HIV-1 infections in CD4+ T-cells and dendritic cells.The HIV-1 central polypurine tract functions as a second line of defense against APOBEC3G/F.Evidence for a functional link between uncoating of the human immunodeficiency virus type 1 core and nuclear import of the viral preintegration complex.A perspective of the dynamic structure of the nucleus explored at the single-molecule levelInterplay between HIV entry and transportin-SR2 dependencyHow TRIM5alpha defends against retroviral invasionsRole of HIV-1 nucleocapsid protein in HIV-1 reverse transcription.Compensatory substitutions in the HIV-1 capsid reduce the fitness cost associated with resistance to a capsid-targeting small-molecule inhibitor.Nucleoporin NUP153 phenylalanine-glycine motifs engage a common binding pocket within the HIV-1 capsid protein to mediate lentiviral infectivity.Human immunodeficiency virus type 1 modified to package Simian immunodeficiency virus Vpx efficiently infects macrophages and dendritic cells.Vpx rescues HIV-1 transduction of dendritic cells from the antiviral state established by type 1 interferon.A cyclophilin homology domain-independent role for Nup358 in HIV-1 infection.HIV infection of non-dividing cells: a divisive problem.The requirement for nucleoporin NUP153 during human immunodeficiency virus type 1 infection is determined by the viral capsid.Residual HIV-1 DNA Flap-independent nuclear import of cPPT/CTS double mutant viruses does not support spreading infectionSJP-L-5, a novel small-molecule compound, inhibits HIV-1 infection by blocking viral DNA nuclear entry.
P2860
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P2860
The cell cycle independence of HIV infections is not determined by known karyophilic viral elements.
description
2005 nî lūn-bûn
@nan
2005 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
2005 թվականի նոյեմբերին հրատարակված գիտական հոդված
@hy
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
name
The cell cycle independence of ...... own karyophilic viral elements
@nl
The cell cycle independence of ...... wn karyophilic viral elements.
@ast
The cell cycle independence of ...... wn karyophilic viral elements.
@en
type
label
The cell cycle independence of ...... own karyophilic viral elements
@nl
The cell cycle independence of ...... wn karyophilic viral elements.
@ast
The cell cycle independence of ...... wn karyophilic viral elements.
@en
prefLabel
The cell cycle independence of ...... own karyophilic viral elements
@nl
The cell cycle independence of ...... wn karyophilic viral elements.
@ast
The cell cycle independence of ...... wn karyophilic viral elements.
@en
P2860
P1433
P1476
The cell cycle independence of ...... wn karyophilic viral elements.
@en
P2093
Masahiro Yamashita
P2860
P356
10.1371/JOURNAL.PPAT.0010018
P407
P577
2005-11-11T00:00:00Z