Turning up the volume on mutational pressure: is more of a good thing always better? (A case study of HIV-1 Vif and APOBEC3) - Wikidata - awgldk - TriplyDB

Turning up the volume on mutational pressure: is more of a good thing always better? (A case study of HIV-1 Vif and APOBEC3)

Turning up the volume on mutational pressure: is more of a good thing always better? (A case study of HIV-1 Vif and APOBEC3)

http://www.wikidata.org/entity/Q24645606

about

The restriction factors of human immunodeficiency virus Restriction of retroviral replication by APOBEC3G/F and TRIM5alpha HIV-1 Vif, APOBEC, and intrinsic immunity Biochemical characterization of enzyme fidelity of influenza A virus RNA polymerase complex Likely role of APOBEC3G-mediated G-to-A mutations in HIV-1 evolution and drug resistance Stochastic simulations suggest that HIV-1 survives close to its error threshold Differences in APOBEC3G expression in CD4+ T helper lymphocyte subtypes modulate HIV-1 infectivity.Quasispecies theory and the behavior of RNA viruses.The macrophage in HIV-1 infection: from activation to deactivation?Exploring the fitness landscape of an RNA virus by using a universal barcode microarray Interactions of host APOBEC3 restriction factors with HIV-1 in vivo: implications for therapeutics.APOBEC3G inhibits HIV-1 RNA elongation by inactivating the viral trans-activation response element.Remarkable lethal G-to-A mutations in vif-proficient HIV-1 provirus by individual APOBEC3 proteins in humanized mice APOBEC3D and APOBEC3F potently promote HIV-1 diversification and evolution in humanized mouse model.APOBEC3H haplotypes and HIV-1 pro-viral vif DNA sequence diversity in early untreated human immunodeficiency virus-1 infection.Intensity of deoxycytidine deamination of HIV-1 proviral DNA by the retroviral restriction factor APOBEC3G is mediated by the noncatalytic domain.APOBEC3G: a double agent in defense Multifaceted counter-APOBEC3G mechanisms employed by HIV-1 Vif.The HDAC6/APOBEC3G complex regulates HIV-1 infectiveness by inducing Vif autophagic degradation.Role of retroviral restriction factors in the interferon-α-mediated suppression of HIV-1 in vivo.Incomplete APOBEC3G/F Neutralization by HIV-1 Vif Mutants Facilitates the Genetic Evolution from CCR5 to CXCR4 Usage.Emerging complexities of APOBEC3G action on immunity and viral fitness during HIV infection and treatment.APOBEC3 Proteins in Viral Immunity.Running loose or getting lost: how HIV-1 counters and capitalizes on APOBEC3-induced mutagenesis through its Vif protein Host restriction factors in retroviral infection: promises in virus-host interaction.HIV-1 viral infectivity factor (Vif) alters processive single-stranded DNA scanning of the retroviral restriction factor APOBEC3G MDM2 is a novel E3 ligase for HIV-1 Vif.Stochastic properties of processive cytidine DNA deaminases AID and APOBEC3G.APOBEC3G mRNA expression in exposed seronegative and early stage HIV infected individuals decreases with removal of exposure and with disease progression Regulation of Vif mRNA splicing by human immunodeficiency virus type 1 requires 5' splice site D2 and an exonic splicing enhancer to counteract cellular restriction factor APOBEC3G The remarkable frequency of human immunodeficiency virus type 1 genetic recombination Tumultuous relationship between the human immunodeficiency virus type 1 viral infectivity factor (Vif) and the human APOBEC-3G and APOBEC-3F restriction factors.The curious chemical biology of cytosine: deamination, methylation, and oxidation as modulators of genomic potential.APOBECs and virus restriction.A functional conserved intronic G run in HIV-1 intron 3 is critical to counteract APOBEC3G-mediated host restriction.High level expression of the anti-retroviral protein APOBEC3G is induced by influenza A virus but does not confer antiviral activity.Hypermutation by intersegmental transfer of APOBEC3G cytidine deaminase.HIV-1 tolerates changes in A-count in a small segment of the pol gene.The role of cytidine deaminases on innate immune responses against human viral infections.Please comment, but with civility.

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Turning up the volume on mutational pressure: is more of a good thing always better? (A case study of HIV-1 Vif and APOBEC3)

http://www.wikidata.org/entity/Q24645606

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2008年の論文

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Turning up the volume on mutat ...... tudy of HIV-1 Vif and APOBEC3)

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Turning up the volume on mutat ...... tudy of HIV-1 Vif and APOBEC3)

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Turning up the volume on mutat ...... tudy of HIV-1 Vif and APOBEC3)

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Jason D Barbour

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Joseph K Wong

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P2860

Human APOBEC3F is another host factor that blocks human immunodeficiency virus type 1 replication

Natural variation in Vif: differential impact on APOBEC3G/3F and a potential role in HIV-1 diversification

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

Hypermutation of HIV-1 DNA in the absence of the Vif protein

HIV-1 Vif blocks the antiviral activity of APOBEC3G by impairing both its translation and intracellular stability

Selforganization of matter and the evolution of biological macromolecules

Stoichiometry of the antiviral protein APOBEC3G in HIV-1 virions

APOBEC3F properties and hypermutation preferences indicate activity against HIV-1 in vivo

Lethal mutagenesis of HIV with mutagenic nucleoside analogs

Newly synthesized APOBEC3G is incorporated into HIV virions, inhibited by HIV RNA, and subsequently activated by RNase H

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26

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10.1186/1742-4690-5-26

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1

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Satish K. Pillai

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5513544

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1000188895

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18339206

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infectious disease

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2323022

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