Evidence map›Paper›PMID 20348446›Full record

ArticleRNA (New York, N.Y.)2010

Hypermutation induced by APOBEC-1 overexpression can be eliminated.

Zhigang Chen, Thomas L Eggerman, Alexander V Bocharov, Irina N Baranova, Tatyana G Vishnyakova, Gyorgy Csako, Amy P Patterson

Open access · bronzeAbstract read
In one paragraph

Article in RNA (New York, N.Y.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

12 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Curcumin modulates the apolipoprotein B mRNA editing by coordinating the expression of cytidine deamination to uridine editosome components in primary mouse hepatocytes.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2019
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. APOBEC-1 Complementation Factor: From RNA Binding to Cancer.Cancer control : journal of the Moffitt Cancer Center
    Review
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

7 authors at 2 institutions in 1 country.

Zhigang ChenDepartment of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland 20892, USA.
Thomas L Eggerman
Alexander V Bocharov
Irina N Baranova
Tatyana G Vishnyakova
Gyorgy Csako
Amy P Patterson
National Institutes of Health Clinical Center · USNational Institutes of Health · US

Funding

Analytical Performance/Clinical Utility Of Laboratory Tests For AtherothrombosisZIACL010306 · CLC · CLINICAL CENTER · PI CSAKO, GYORGY · 2009 to 2010
$0k
Intramural NIH HHS
6 · The paper itself

Abstract

APOBEC-1 overexpression in liver has been shown to effectively reduce apoB-100 levels. However, nonspecific hypermutation and liver tumor formation potentially related to hypermutation in transgenic animals compromise its potential use for gene therapy. In studying apoB mRNA editing regulation, we found that the core editing auxiliary factor ACF dose-dependently increases APOBEC-1 nonspecific hypermutation and specific editing with variable site sensitivity. Overexpression of APOBEC-1 together with ACF in human hepatic HepG2 cells hypermutated apoB mRNAs 20%-65% at sites 6639, 6648, 6655, 6762, 6802, and 6845, in addition to the normal 90% editing at 6666. The hypermutation activity of APOBEC-1 was decreased to background levels by a single point APOBEC-1 mutation of P29F or E181Q, while 50% of wild-type control editing at the normal site was retained. The hypermutations on both apoB and novel APOBEC-1 target 1 (NAT1) mRNA were also decreased to background levels with P29F and E181Q mutants in rat liver primary culture cells. The loss of hypermutation with the mutants was associated with significantly decreased APOBEC-1/ACF interaction. These data suggest that nonspecific hypermutation induced by overexpressing APOBEC-1 can be virtually eliminated by site-specific mutation, while maintaining specific editing activity at the normal site, reopening the potential use of APOBEC-1 gene therapy for hyperlipidemia.

Indexed as

MutationAmino Acid SubstitutionAnimalsAPOBEC-1 DeaminaseApolipoproteins BArylamine N-AcetyltransferaseBase SequenceCell LineCells, CulturedCytidine DeaminaseDNA PrimersGene ExpressionHepatocytesHumansIsoenzymesMutagenesis, Site-DirectedA1CF protein, humanAPOBEC-1 DeaminaseAPOBEC1 protein, humanApobec1 protein, ratApolipoproteins BArylamine N-AcetyltransferaseCytidine DeaminaseDNA PrimersIsoenzymesN-acetyltransferase 1Recombinant ProteinsRNA-Binding ProteinsRNA, Messenger

Identifiers

PMID20348446
PMCPMC2856876
OpenAlexW2113353956

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.