Evidence map›Paper›PMID 22157092›Full record

ArticleCell cycle (Georgetown, Tex.)2012

APOBEC3 proteins and genomic stability: the high cost of a good defense.

Iñigo Narvaiza, Sébastien Landry, Matthew D Weitzman

Abstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

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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

3 authors.

Iñigo NarvaizaLaboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, CA, USA.
Sébastien Landry
Matthew D Weitzman

Funding

Mechanisms of APOBEC3A InhibitionR01AI074967 · NIAID · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI WEITZMAN, MATTHEW D. · 2009 to 2013
$2.3M
AAV and the DNA Damage MachineryR01AI067952 · NIAID · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI WEITZMAN, MATTHEW D. · 2006 to 2010
$2.1M
NIAID NIH HHS AI067952NIAID NIH HHS AI074967NIAID NIH HHS R01 AI067952NIAID NIH HHS R01 AI074967
6 · The paper itself

Abstract

The human APOBEC3 family of cytidine deaminases constitutes a cellular intrinsic defense mechanism that is effective against a range of viruses and retro-elements. While it is well established that these enzymes are powerful mutators of viral DNA, the possibility that their activity could threaten the integrity of the host genome has only recently begun to be investigated. Here, we discuss the implications of new evidence suggesting that APOBEC3 proteins can mediate the deamination of cellular DNA. The maintenance of genomic integrity in the face of this potential off-target activity must require high fidelity DNA repair and strict regulation of APOBEC3 gene expression and enzyme activity. Conversely, the ability of specific members of the APOBEC3 family to activate DNA damage signaling pathways might also reflect another way that these proteins contribute to the host immune response.

Indexed as

Genomic InstabilityAPOBEC DeaminasesCytidine DeaminaseCytosine DeaminaseDeaminationDNADNA DamageDNA RepairHumansImmunity, InnateSignal TransductionUracil-DNA GlycosidaseAPOBEC3 proteins, humanAPOBEC DeaminasesCytidine DeaminaseCytosine DeaminaseDNAUracil-DNA Glycosidase

Identifiers

PMID22157092
PMCPMC3272230

What OpenQuestion holds

Textmetadata
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.