Deaminase-independent inhibition of HIV-1 reverse transcription by APOBEC3G. - Wikidata - wikimedia - TriplyDB

Deaminase-independent inhibition of HIV-1 reverse transcription by APOBEC3G.

Deaminase-independent inhibition of HIV-1 reverse transcription by APOBEC3G.

http://www.wikidata.org/entity/Q36328929

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Deaminase-independent inhibition of parvoviruses by the APOBEC3A cytidine deaminase HIV-1 replication and APOBEC3 antiviral activity are not regulated by P bodies APOBEC3A, APOBEC3B, and APOBEC3H haplotype 2 restrict human T-lymphotropic virus type 1 Structure-function analyses point to a polynucleotide-accommodating groove essential for APOBEC3A restriction activities HIV-1 Vif versus the APOBEC3 cytidine deaminases: an intracellular duel between pathogen and host restriction factors Restriction of retroviral replication by APOBEC3G/F and TRIM5alpha HIV-1 Vif, APOBEC, and intrinsic immunity Human cytidine deaminase APOBEC3H restricts HIV-1 replication Human APOBEC3G can restrict retroviral infection in avian cells and acts independently of both UNG and SMUG1 Cytidine deamination induced HIV-1 drug resistance Multiple APOBEC3 restriction factors for HIV-1 and one Vif to rule them all The APOBEC3 family of retroelement restriction factors Suppression of APOBEC3-mediated restriction of HIV-1 by Vif Structural Insights into HIV-1 Vif-APOBEC3F Interaction NMR structure of human restriction factor APOBEC3A reveals substrate binding and enzyme specificity Restriction of HIV-1 replication in monocytes is abolished by Vpx of SIVsmmPBj RNA-dependent oligomerization of APOBEC3G is required for restriction of HIV-1 Multi-scale modeling of HIV infection in vitro and APOBEC3G-based anti-retroviral therapy Studies on the restriction of murine leukemia viruses by mouse APOBEC3 Multiple ways of targeting APOBEC3-virion infectivity factor interactions for anti-HIV-1 drug development.AID and Apobec3G haphazard deamination and mutational diversity Mov10 suppresses retroelements and regulates neuronal development and function in the developing brain.APOBEC3G and APOBEC3F require an endogenous cofactor to block HIV-1 replication.APOBEC3G inhibits elongation of HIV-1 reverse transcripts.Differences in APOBEC3G expression in CD4+ T helper lymphocyte subtypes modulate HIV-1 infectivity.Inducible APOBEC3G-Vif double stable cell line as a high-throughput screening platform to identify antiviral compounds.Quantification of deaminase activity-dependent and -independent restriction of HIV-1 replication mediated by APOBEC3F and APOBEC3G through experimental-mathematical investigation.Different modes of retrovirus restriction by human APOBEC3A and APOBEC3G in vivo.Leveraging APOBEC3 proteins to alter the HIV mutation rate and combat AIDS.Interactions of host APOBEC3 restriction factors with HIV-1 in vivo: implications for therapeutics.Identification of dominant negative human immunodeficiency virus type 1 Vif mutants that interfere with the functional inactivation of APOBEC3G by virus-encoded Vif Vif of feline immunodeficiency virus from domestic cats protects against APOBEC3 restriction factors from many felids APOBEC3G inhibits HIV-1 RNA elongation by inactivating the viral trans-activation response element.Biophysical characterization of DNA binding from single molecule force measurements Innate immune signaling induces high levels of TC-specific deaminase activity in primary monocyte-derived cells through expression of APOBEC3A isoforms Long-term restriction by APOBEC3F selects human immunodeficiency virus type 1 variants with restored Vif function Two genetic determinants acquired late in Mus evolution regulate the inclusion of exon 5, which alters mouse APOBEC3 translation efficiency N-terminal hemagglutinin tag renders lysine-deficient APOBEC3G resistant to HIV-1 Vif-induced degradation by reduced polyubiquitination.Fundamental differences between the nucleic acid chaperone activities of HIV-1 nucleocapsid protein and Gag or Gag-derived proteins: biological implications Random mutagenesis MAPPIT analysis identifies binding sites for Vif and Gag in both cytidine deaminase domains of Apobec3G.

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Deaminase-independent inhibition of HIV-1 reverse transcription by APOBEC3G.

http://www.wikidata.org/entity/Q36328929

description

2007 nî lūn-bûn

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2007年學術文章

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name

Deaminase-independent inhibition of HIV-1 reverse transcription by APOBEC3G.

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Deaminase-independent inhibition of HIV-1 reverse transcription by APOBEC3G.

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type

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Deaminase-independent inhibition of HIV-1 reverse transcription by APOBEC3G.

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Deaminase-independent inhibition of HIV-1 reverse transcription by APOBEC3G.

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Deaminase-independent inhibition of HIV-1 reverse transcription by APOBEC3G.

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Deaminase-independent inhibition of HIV-1 reverse transcription by APOBEC3G.

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Nucleic Acids Research

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Deaminase-independent inhibition of HIV-1 reverse transcription by APOBEC3G.

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Denise S B Chan

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F Wang

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Ioulia Rouzina

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Judith G Levin

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Kristen Stewart Maynard

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Wataru Sugiura

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P2860

An anthropoid-specific locus of orphan C to U RNA-editing enzymes on chromosome 22

APOBEC3A is a potent inhibitor of adeno-associated virus and retrotransposons

APOBEC3F can inhibit the accumulation of HIV-1 reverse transcription products in the absence of hypermutation. Comparisons with APOBEC3G

APOBEC3A and APOBEC3B are potent inhibitors of LTR-retrotransposon function in human cells

Complex interactions of HIV-1 nucleocapsid protein with oligonucleotides

Inhibition of tRNA₃(Lys)-primed reverse transcription by human APOBEC3G during human immunodeficiency virus type 1 replication

Human immunodeficiency virus type 1 cDNAs produced in the presence of APOBEC3G exhibit defects in plus-strand DNA transfer and integration

Nucleic acid binding and chaperone properties of HIV-1 Gag and nucleocapsid proteins

Isolation of a human gene that inhibits HIV-1 infection and is suppressed by the viral Vif protein

Broad antiretroviral defence by human APOBEC3G through lethal editing of nascent reverse transcripts

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10.1093/NAR/GKM750

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21

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35

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Angela M Gronenborn

Karin Musier-Forsyth

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Yasumasa Iwatani

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2007-10-16T00:00:00Z

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17942420

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