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注意:仅列出部分参考文献,下载原文获取全部文献信息。Human and Rhesus APOBEC3D, APOBEC3F, APOBEC3G, and APOBEC3H Demonstrate a Conserved Capacity To Restrict Vif-Deficient HIV-1
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Human T-cell leukemia virus type 1 p8 protein increases cellular conduits and virus transmission
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Antiretroelement activity of APOBEC3H was lost twice in recent human evolution
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CELL HOST & MICROBE (2008)
Human cytidine deaminase APOBEC3H restricts HIV-1 replication
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Evidence for editing of human papillomavirus DNA by APOBEC3 in benign and precancerous lesions
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Inhibition of Alpharetrovirus replication by a range of human APOBEC3 proteins
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Deaminase-independent inhibition of HIV-1 reverse transcription by APOBEC3G
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NUCLEIC ACIDS RESEARCH (2007)
Targeting APOBEC3A to the viral nucleoprotein complex confers antiviral activity
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The intrinsic antiretroviral factor APOBEC3B contains two enzymatically active cytidine deaminase domains
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Human immunodeficiency virus type 1 cDNAs produced in the presence of APOBEC3G exhibit defects in plus-strand DNA transfer and integration
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Human T cell leukemia virus type I is resistant to the antiviral effects of APOBEC3
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Antiviral potency of APOBEC proteins does not correlate with cytidine deamination
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APOBEC3 proteins inhibit human LINE-1 retrotransposition
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ONCOGENE (2005)
Extensive editing of a small fraction of human T-cell leukemia virus type 1 genomes by four APOBEC3 cytidine deaminases
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Human APOBEC3B is a potent inhibitor of HIV-1 infectivity and is resistant to HIV-1 Vif
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JOURNAL OF INFECTIOUS DISEASES (2005)
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JOURNAL OF GENERAL VIROLOGY (2005)
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JOURNAL OF BIOLOGICAL CHEMISTRY (2004)
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SCIENCE (2003)
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CELL (2003)
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Spread of HTLV-I between lymphocytes by virus-induced polarization of the cytoskeleton
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SCIENCE (2003)
The antiretroviral enzyme APOBEC3G is degraded by the proteasome in response to HIV-1 Vif
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HIV-1 Vif protein binds the editing enzyme APOBEC3G and induces its degradation
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NATURE MEDICINE (2003)
Isolation of a human gene that inhibits HIV-1 infection and is suppressed by the viral Vif protein
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Human immunodeficiency virus type 1 DNA sequences genetically damaged by hypermutation are often abundant in patient peripheral blood mononuclear cells and may be generated during near-simultaneous infection and activation of CD4+ T cells
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MOLECULAR BIOLOGY AND EVOLUTION (2001)
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