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: EC 3.5.4.-; RNA processing; RNA-binding; Hydrolase
Chromosomal Location of Human Ortholog: 22q13.1-q13.2
Cellular Component: apolipoprotein B mRNA editing enzyme complex; cytoplasm; cytosol; ribonucleoprotein complex
Molecular Function: cytidine deaminase activity; dCTP deaminase activity; deoxycytidine deaminase activity; protein binding; RNA binding; zinc ion binding
Biological Process: base conversion or substitution editing; cytidine deamination; defense response to virus; innate immune response; negative regulation of retroviral genome replication; negative regulation of viral genome replication; negative regulation of viral reproduction; positive regulation of defense response to virus by host
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