Evidence map›Paper›PMID 26384561›Full record

ArticleNucleic acids research2015

Molecular basis of the attenuated phenotype of human APOBEC3B DNA mutator enzyme.

Vincent Caval, Mohamed S Bouzidi, Rodolphe Suspène, Hélène Laude, Marie-Charlotte Dumargne, Anu Bashamboo, Thomas Krey, Jean-Pierre Vartanian, Simon Wain-Hobson

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

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  6. APOBEC3A catalyzes mutation and drives carcinogenesis in vivo.The Journal of experimental medicine · 2020
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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

9 authors at 1 institution in 1 country.

Vincent CavalMolecular Retrovirology Unit, Institut Pasteur, 28 rue du Dr. Roux, 75724 Paris cedex 15, France.
Mohamed S BouzidiMolecular Retrovirology Unit, Institut Pasteur, 28 rue du Dr. Roux, 75724 Paris cedex 15, France.
Rodolphe SuspèneMolecular Retrovirology Unit, Institut Pasteur, 28 rue du Dr. Roux, 75724 Paris cedex 15, France.
Hélène LaudeMolecular Retrovirology Unit, Institut Pasteur, 28 rue du Dr. Roux, 75724 Paris cedex 15, France.
Marie-Charlotte DumargneHuman Developmental Genetics Unit, Institut Pasteur, 28 rue du Dr. Roux, 75724 Paris cedex 15, France.
Anu BashambooHuman Developmental Genetics Unit, Institut Pasteur, 28 rue du Dr. Roux, 75724 Paris cedex 15, France.
Thomas KreyStructural Virology Unit, Institut Pasteur, 28 rue du Dr. Roux, 75724 Paris cedex 15, France.
Jean-Pierre VartanianMolecular Retrovirology Unit, Institut Pasteur, 28 rue du Dr. Roux, 75724 Paris cedex 15, France.
Simon Wain-HobsonMolecular Retrovirology Unit, Institut Pasteur, 28 rue du Dr. Roux, 75724 Paris cedex 15, France simon.wain-hobson@pasteur.fr.
Institut Pasteur · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human APOBEC3A and APOBEC3B genes (A3A and A3B) encode DNA mutator enzymes that deaminate cytidine and 5-methylcytidine residues in single-stranded DNA (ssDNA). They are important sources of mutations in many cancer genomes which show a preponderance of CG->TA transitions. Although both enzymes can hypermutate chromosomal DNA in an experimental setting, only A3A can induce double strand DNA breaks, even though the catalytic domains of A3B and A3A differ by only 9% at the protein level. Accordingly we sought the molecular basis underlying A3B attenuation through the generation of A3A-A3B chimeras and mutants. It transpires that the N-terminal domain facilitates A3B activity while a handful of substitutions in the catalytic C-terminal domain impacting ssDNA binding serve to attenuate A3B compared to A3A. Interestingly, functional attenuation is also observed for the rhesus monkey rhA3B enzyme compared to rhA3A indicating that this genotoxic dichotomy has been selected for and maintained for some 38 million years. Expression of all human ssDNA cytidine deaminase genes is absent in mature sperm indicating they contribute to somatic mutation and cancer but not human diversity.

Indexed as

DNA Breaks, Double-StrandedAnimalsCell LineCytidine DeaminaseHeLa CellsHumansMacaca mulattaMinor Histocompatibility AntigensMutationPhenotypeProteinsProtein Structure, TertiaryQuailRNA EditingAPOBEC3A protein, humanAPOBEC3B protein, humanCytidine DeaminaseMinor Histocompatibility AntigensProteins

Identifiers

PMID26384561
PMCPMC4627089
OpenAlexW1447100581

What OpenQuestion holds

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LicenceCC BY
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.