ArticleVirology2018
Mouse APOBEC3 expression in NIH 3T3 cells mediates hypermutation of AKV murine leukemia virus.
Article in Virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Apobec-mediated retroviral hypermutation in vivo is dependent on mouse strain.PLoS pathogens · 2024Article
- The Role of APOBECs in Viral Replication.Microorganisms · 2020Review
- Mouse APOBEC3 Restriction of Retroviruses.Viruses · 2020Review
- Friend retrovirus studies reveal complex interactions between intrinsic, innate and adaptive immunity.FEMS microbiology reviews · 2019Review
- A Protein Antagonist of Activation-Induced Cytidine Deaminase Encoded by a Complex Mouse Retrovirus.mBio · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Mouse APOBEC3 (mA3) is a cytidine deaminase that can act on the single-stranded DNA reverse transcripts of retroviruses resulting in G→A hypermutation of proviral DNA. Many mA3 studies have used NIH 3T3 cells assuming that endogenous mA3 production was negligible. We developed a monoclonal antibody specific for mA3 that reveals detectable mA3 in NIH 3T3 cells and we demonstrate that AKV released from the cells undergoes G→A hypermutation. Inactivation of the mA3 gene abolished the deamination confirming that AKV hypermutation was mediated by mA3. The G→A mutations in AKV viral transcripts deviated from a normal distribution with all the mutations contained within only 20% of the transcripts. Single cell analyses revealed that the expression of mA3 in NIH 3T3 cells was limited to 20% of the cells, which likely accounted for the abnormal distribution of mutations. Endogenous NIH 3T3 mA3 was found to restrict AKV replication.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.