Introduction Human APOBEC3G is a host defense factor that potently inhibits HIV replication. We hypothesize that HIV-infected children with a genetic variant of APOBEC3G will have a more rapid disease progression.
Bunupuradah Torsak +12 more
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Dissecting APOBEC3G Substrate Specificity by Nucleoside Analog Interference [PDF]
The apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like (APOBEC) cytidine deaminase genes encode a set of enzymes including APOBEC1 (A1), APOBEC2 (A2), APOBEC4 (A4), and APOBEC3A-H (A3A-H). Although each possesses one or more zinc binding motifs conserved among enzymes catalyzing C-->U conversion, the functions and substrate specificities ...
Jason W, Rausch +3 more
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APOBEC3G expression and HIV-1 infection in Burkina Faso
APOBEC3G is a potent inhibitor of HIV-1 replication, and act by deaminating cytidines in uracil on the negative strand of the viral cDNA. In this case-control study, APOBEC3G expression in subjects’ naïve to HAART infected by HIV-1 and the effect of ...
Tegwinde Rebeca Compaore +11 more
doaj +1 more source
Dysregulated APOBEC3G causes DNA damage and promotes genomic instability in multiple myeloma
Multiple myeloma (MM) is a heterogeneous disease characterized by significant genomic instability. Recently, a causal role for the AID/APOBEC deaminases in inducing somatic mutations in myeloma has been reported.
Srikanth Talluri +8 more
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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
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Human retroviral host restriction factors APOBEC3G and APOBEC3F localize to mRNA processing bodies.
APOBEC3G is an antiviral host factor capable of inhibiting the replication of both exogenous and endogenous retroviruses as well as hepatitis B, a DNA virus that replicates through an RNA intermediate.
Michael J Wichroski +2 more
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HIV-1 adaptation studies reveal a novel Env-mediated homeostasis mechanism for evading lethal hypermutation by APOBEC3G. [PDF]
HIV-1 replication normally requires Vif-mediated neutralization of APOBEC3 antiviral enzymes. Viruses lacking Vif succumb to deamination-dependent and -independent restriction processes.
Terumasa Ikeda +5 more
doaj +1 more source
High-molecular-mass APOBEC3G complexes restrict Alu retrotransposition [PDF]
APOBEC3G (A3G) and related deoxycytidine deaminases are potent intrinsic antiretroviral factors. A3G is expressed either as an enzymatically active low-molecular-mass (LMM) form or as an enzymatically inactive high-molecular-mass (HMM) ribonucleoprotein complex. Resting CD4 T cells exclusively express LMM A3G, where it functions as a powerful postentry
Ya-Lin, Chiu +7 more
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Single-stranded RNA facilitates nucleocapsid: APOBEC3G complex formation [PDF]
Binding of APOBEC3G to the nucleocapsid (NC) domain of the human immunodeficiency virus (HIV) Gag polyprotein may represent a critical early step in the selective packaging of this antiretroviral factor into HIV virions. Previously, we and others have reported that this interaction is mediated by RNA.
Hal P, Bogerd, Bryan R, Cullen
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Endogenous origins of HIV-1 G-to-A hypermutation and restriction in the nonpermissive T cell line CEM2n. [PDF]
The DNA deaminase APOBEC3G converts cytosines to uracils in retroviral cDNA, which are immortalized as genomic strand G-to-A hypermutations by reverse transcription.
Eric W Refsland +2 more
doaj +1 more source

