# APOBEC3B

Source: https://onco.cc/targets/apobec3b/  
OnCo record `apobec3b` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

APOBEC3B (DNA dC->dU-editing enzyme APOBEC-3B) is an enzyme. In the public catalogues the evidence so far is association rather than a proven role. Tied to Skin cancer.

## Summary

DNA deaminase (cytidine deaminase) which acts as an inhibitor of retrovirus replication and retrotransposon mobility via deaminase-dependent and -independent mechanisms. After the penetration of retroviral nucleocapsids into target cells of infection and the initiation of reverse transcription, it can induce the conversion of cytosine to uracil in the minus-sense single-strand viral DNA, leading to G-to-A hypermutations in the subsequent plus-strand viral DNA. The resultant detrimental levels of mutations in the proviral genome, along with a deamination-independent mechanism that works prior to the proviral integration, together exert efficient antiretroviral effects in infected target cells.

Open Targets scores its association with cancer at 0.63 (direct and indirect evidence; datatypes literature 0.99, genetic association 0.24, somatic mutation 0.95).

## Fields

- Kind: Target
- Last checked: 2026-09-23
- Also known as: apolipoprotein B mRNA editing enzyme catalytic subunit 3B; DNA dC->dU-editing enzyme APOBEC-3B; PHRBNL; FLJ21201
- Tags: cancer-genes-wave
- Symbol: APOBEC3B
- Class: enzyme
- Biology: DNA deaminase (cytidine deaminase) which acts as an inhibitor of retrovirus replication and retrotransposon mobility via deaminase-dependent and -independent mechanisms. After the penetration of retroviral nucleocapsids into target cells of infection and the initiation of reverse transcription, it can induce the conversion of cytosine to uracil in the minus-sense single-strand viral DNA, leading to G-to-A hypermutations in the subsequent plus-strand viral DNA. The resultant detrimental levels of mutations in the proviral genome, along with a deamination-independent mechanism that works prior to the proviral integration, together exert efficient antiretroviral effects in infected target cells. Selectively targets single-stranded DNA and does not deaminate double-stranded DNA or single- or double-stranded RNA. Exhibits antiviral activity against simian immunodeficiency virus (SIV), hepatitis B virus (HBV) and human T-cell leukaemia virus type 1 (HTLV-1) and may inhibit the mobility of LTR and non-LTR retrotransposons. Location: Nucleus (UniProt). Locus 22q13.1 (HGNC).
- Where found: Skin cancer: Open Targets association 0.50 with skin cancer (MONDO_0002898)

## Notes

- Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: none stated by the sources. Evidence tier "association-only" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.

## Sources

- HGNC HGNC:17352: https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:17352
- UniProt Q9UH17: https://www.uniprot.org/uniprotkb/Q9UH17/entry
- NCBI Gene 9582: https://www.ncbi.nlm.nih.gov/gene/9582
- Ensembl ENSG00000179750: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000179750

## Connected records

- collections: [Open Targets Platform](https://onco.cc/collections/open-targets/)
- cancers: [Skin cancer (all types)](https://onco.cc/cancers/skin-cancer/)

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JSON: https://onco.cc/api/v1/entities/apobec3b.json