Specifications
Immunogen
Synthetic peptide conjugated to KLH derived from within residues 150 - 250 of Human APOBEC3G.
Applications
Application Notes
WB: 0.5 μg/ml;
Target
Alternative Names
APOBEC3F; apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3F; DNA dC->dU-editing enzyme APOBEC-3F; ARP8; BK150C2.4.MRNA; KA6; DNA dC-> dU-editing enzyme APOBEC-3F; induced upon T-cell activation; apolipoprotein B mRNA editing enzyme
Product Background
Antigen Description
DNA deaminase (cytidine deaminase) that mediates a form of innate resistance to retroviral infections (at least to HIV-1 infection) by triggering G-to-A hypermutation in the newly synthesized viral DNA. The replacements C-to-U in the minus strand DNA of HIV-1 during reverse transcription, leads to G-to-A transitions in the plus strand. The inhibition of viral replication is either due to the degradation of the minus strand before its integration or to the lethality of the hypermutations. Modification of both DNA strands is not excluded. This antiviral activity is neutralized by the virion infectivity factor (VIF), that prevents the incorporation of APOBEC3G into progeny HIV-1 virions by both inhibiting its translation and/or by inducing its ubiquitination and subsequent degradation by the 26S proteasome. APOBEC3G binds a variety of RNAs, but does not display detectable APOB, NF1 and NAT1 mRNA editing.
Pathway
APOBEC3G mediated resistance to HIV-1 infection, organism-specific biosystem; Disease, organism-specific biosystem; HIV Infection, organism-specific biosystem; Host Interactions of HIV factors, organism-specific biosystem; Vif-mediated degradation of APOBEC3G, organism-specific biosystem.
Citations
Publication ()
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