APOBEC3G Localizes to Cytoplasmic Bodies
Subcellular localization images of living 293T cells transiently expressing APO3G-YFP (A), HeLa cells transiently expressing APO3G-YFP (B), HeLa-APO3G cells stably expressing APO3G-Myc (C), endogenous APOBEC3G in primary peripheral blood CD4+ T cells (D),
Michael J Wichroski (72634) +2 more
core +1 more source
Rapid evolution of primate antiviral enzyme APOBEC3G [PDF]
Human cytidine deaminase APOBEC3G and the virion infectivity factor (vif) of the human immunodeficiency virus (HIV) are a pair of antagonistic molecules. In the absence of vif, APOBEC3G induces a high rate of dC to dU mutations in the nascent reverse transcripts of HIV that leads to the degradation of the HIV genome.
Jianzhi, Zhang, David M, Webb
openaire +2 more sources
Vulnerability to APOBEC3G linked to the pathogenicity of deltaretroviruses
Human retroviruses are derived from simian ones through cross-species transmission. These retroviruses are associated with little pathogenicity in their natural hosts, but in humans, HIV causes AIDS, and human T-cell leukemia virus type 1 (HTLV-1) induces adult T-cell leukemia–lymphoma (ATL).
Takafumi Shichijo +15 more
openaire +6 more sources
The influence of APOBEC3G and deoxythymidylate kinase genetic diversity on HIV-1 hypermutation and response to treatment [PDF]
This thesis addresses two important topics in HIV-1 medicine; (i) the clinical relevance of pre-treatment G-A hypermutation and the contribution of host and viral genetics to its development and; (ii) the influence of genetic variation in host enzymes ...
Pace, Craig Stuart
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Intracellular interactions between APOBEC3G, RNA, and HIV-1 Gag: APOBEC3G multimerization is dependent on its association with RNA [PDF]
Abstract Background Host restriction factor APOBEC3G (A3G) blocks human immunodeficiency virus type 1 (HIV-1) replication by G-to-A hypermutation, and by inhibiting DNA synthesis and provirus formation. Previous reports have suggested that A3G is a dimer and its virion incorporation is mediated through interactions ...
Friew Yeshitila N +3 more
openaire +3 more sources
Lamin B1 safeguards the B cell genome and shapes lymphoma outcome
Abstract Lamin B1 is a structural component of the nuclear lamina that participates in genome organization and transcriptional control. During adaptive immune responses, B lymphocytes in germinal centers (GCs) undergo clonal expansion and programmed DNA damage at immunoglobulin loci, while simultaneously downregulating Lamin B1.
Filip Filipsky +12 more
wiley +1 more source
CCR6 ligands inhibit HIV by inducing APOBEC3G
AbstractWe have identified a postentry CCR6-dependent mechanism of inhibition of HIV occurring at an early stage of infection mediated by the induction of the host restriction factor apolipoprotein B mRNA-editing enzyme-catalytic polypeptide-like 3G (APOBEC3G).
M. K. Lafferty +4 more
openaire +4 more sources
APOBEC3G Genetic Variants and Their Influence on the Progression to AIDS [PDF]
ABSTRACT The cytosine deaminase APOBEC3G, in the absence of the human immunodeficiency virus type 1 (HIV-1) accessory gene HIV-1 viral infectivity factor ( vif ), inhibits viral replication by introducing G→A hypermutation in the newly synthesized HIV-1 DNA negative strand.
An, Ping +15 more
openaire +3 more sources
Beyond the Barrier: Epithelial Cells as Immune Sentinels in the Female Genital Tract
ABSTRACT Epithelial cells (ECs) of the female genital tract (FGT) serve as an essential barrier and the first line of defense against sexually transmitted pathogens. Beyond providing a physical barrier, these cells actively contribute to immune responses through pathogen recognition, cytokine release, and modulation of adaptive immune responses ...
Lauren Jirik +3 more
wiley +1 more source
Analysis of HIV-1 hypermutation and its relationship with APOBEC3G and vif genetic variation in vivo [PDF]
Background: Editing of HIV-1 DNA and RNA by APOBEC family cytidine deaminases to produce hypermutated sequences has emerged as a potent host antiviral response. This effect is modulated by the presence of vif that opposes APOBEC activity.
Carvalho, F. +8 more
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