APOBEC3G: 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. May also prevent the transposition of a subset of retroelements. Binds a variety of RNAs, but does not display detectable APOB, NF1 and NAT1 mRNA editing. Belongs to the cytidine and deoxycytidylate deaminase family. 2 isoforms of the human protein are produced by alternative splicing.
Protein type: RNA processing; EC 3.5.4.-; RNA-binding; Hydrolase
Chromosomal Location of Human Ortholog: 22q13.1-q13.2
Cellular Component: cytoplasm; apolipoprotein B mRNA editing enzyme complex; cytosol; ribonucleoprotein complex
Molecular Function: protein binding; protein homodimerization activity; deoxycytidine deaminase activity; zinc ion binding; RNA binding; cytidine deaminase activity
Biological Process: negative regulation of retroviral genome replication; base conversion or substitution editing; negative regulation of viral genome replication; viral reproduction; innate immune response; cytidine deamination; positive regulation of defense response to virus by host; negative regulation of viral reproduction; defense response to virus
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