ArticleTranslational research : the journal of laboratory and clinical medicine2021
The von Hippel-Lindau Cullin-RING E3 ubiquitin ligase regulates APOBEC3 cytidine deaminases.
Article in Translational research : the journal of laboratory and clinical medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Hypoxia Independently Induces AID Expression in CH12 B Cells.European journal of immunology · 2026Article
- APOBEC3B regulates HPV replication by inducing R-loop formation and DNA damage.PLoS pathogens · 2026Article
- RNase H-sensitive accumulation of APOBEC3B in a nucleolus after DNA damage.Bioscience reports · 2025Article
- HIV proviral transcription and infectivity are enhanced by neddylation.Journal of virology · 2025Article
- Design and Characterization of Inhibitors of Cell-Mediated Degradation of APOBEC3G That Decrease HIV-1 Infectivity.Viruses · 2025Article
- An overview of the functions and mechanisms of APOBEC3A in tumorigenesis.Acta pharmaceutica Sinica. B · 2024Review
- Article
- The APOBEC3B cytidine deaminase is an adenovirus restriction factor.PLoS pathogens · 2023Article
- APOBEC3: Friend or Foe in Human Papillomavirus Infection and Oncogenesis?Annual review of virology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The 7 members of the A3 family of cytidine deaminases (A3A to A3H) share a conserved catalytic activity that converts cytidines in single-stranded (ss) DNA into uridines, thereby inducing mutations. After their initial identification as cell-intrinsic defenses against HIV and other retroviruses, A3s were also found to impair many additional viruses. Moreover, some of the A3 proteins (A3A, A3B, and A3H haplotype I) are dysregulated in cancer cells, thereby causing chromosomal mutations that can be selected to fuel progression of malignancy. Viral mechanisms that increase transcription of A3 genes or induce proteasomal degradation of A3 proteins have been characterized. However, only a few underlying biological mechanisms regulating levels of A3s in uninfected cells have been described. Here, we characterize that the von Hippel-Lindau tumor suppressor (pVHL), via its CRL
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