Evidence map›Paper›PMID 23620282›Full record

ArticleNucleic acids research2013

APOBEC3G cytosine deamination hotspots are defined by both sequence context and single-stranded DNA secondary structure.

Colleen M Holtz, Holly A Sadler, Louis M Mansky

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Vulnerability to APOBEC3G linked to the pathogenicity of deltaretroviruses.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Article
  7. Review
  8. Review
  9. APOBECs: Our fickle friends?PLoS pathogens · 2023
    Article
  10. Review
  11. Review
  12. Article
  13. Molecular Biology and Diversification of Human Retroviruses.Frontiers in virology (Lausanne, Switzerland) · 2022
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Colleen M HoltzInstitute for Molecular Virology, University of Minnesota, Minneapolis, MN 55455, USA.
Holly A Sadler
Louis M Mansky
University of Minnesota System · USUniversity of Minnesota · US

Funding

MINNESOTA PAIN RESEARCH TRAINING PROGRAMT32DE007288 · NIDCR · UNIVERSITY OF MINNESOTA TWIN CITIES · PI HERZBERG, MARK C · 1996 to 2011
$8.8M
Minnesota Craniofacial Research Training ProgramT90DE022732 · NIDCR · UNIVERSITY OF MINNESOTA · PI MANSKY, KIM CARPENTER · 2012 to 2023
$4.9M
Mechanisms of HIV-1 VariationR01GM056615 · NIGMS · UNIVERSITY OF MINNESOTA TWIN CITIES · PI MANSKY, LOUIS M. · 2003 to 2011
$2.6M
NIDCR NIH HHS T32 DE007288NIDCR NIH HHS T90 DE022732NIGMS NIH HHS R01 GM56615
6 · The paper itself

Abstract

Apolipoprotein B mRNA-editing, enzyme-catalytic, polypeptide-like 3G (i.e., APOBEC3G or A3G) is an evolutionarily conserved cytosine deaminase that potently restricts human immunodeficiency virus type 1 (HIV-1), retrotransposons and other viruses. A3G has a nucleotide target site specificity for cytosine dinucleotides, though only certain cytosine dinucleotides are 'hotspots' for cytosine deamination, and others experience little or no editing by A3G. The factors that define these critical A3G hotspots are not fully understood. To investigate how A3G hotspots are defined, we used an in vitro fluorescence resonance energy transfer-based oligonucleotide assay to probe the site specificity of A3G. Our findings strongly suggest that the target single-stranded DNA (ssDNA) secondary structure as well as the bases directly 3' and 5' of the cytosine dinucleotide are critically important A3G recognition. For instance, A3G cannot readily deaminate a cytosine dinucleotide in ssDNA stem structures or in nucleotide base loops composed of three bases. Single-stranded nucleotide loops up to seven bases in length were poor targets for A3G activity unless cytosine residues flanked the cytosine dinucleotide. Furthermore, we observed that A3G favors adenines, cytosines and thymines flanking the cytosine dinucleotide target in unstructured regions of ssDNA. Low cytosine deaminase activity was detected when guanines flanked the cytosine dinucleotide. Taken together, our findings provide the first demonstration that A3G cytosine deamination hotspots are defined by both the sequence context of the cytosine dinucleotide target as well as the ssDNA secondary structure. This knowledge can be used to better trace the origins of mutations to A3G activity, and illuminate its impact on processes such as HIV-1 genetic variation.

Indexed as

Base SequenceCell LineCytidine DeaminaseCytosineDeaminationDNA, Single-StrandedHumansNucleic Acid ConformationCytidine DeaminaseCytosineDNA, Single-Stranded

Identifiers

PMID23620282
PMCPMC3695494
OpenAlexW2081938725

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.