Evidence map›Paper›PMID 16055734›Full record

ArticleMolecular and cellular biology2005

Targeted deletion of the murine apobec-1 complementation factor (acf) gene results in embryonic lethality.

Valerie Blanc, Jeffrey O Henderson, Elizabeth P Newberry, Susan Kennedy, Jianyang Luo, Nicholas O Davidson

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

33 citing papers in PubMed, 55 citations in OpenAlex.

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  13. Parent-of-origin effects of A1CF and AGO2 on testicular germ-cell tumors, testicular abnormalities, and fertilization bias.Proceedings of the National Academy of Sciences of the United States of America · 2016
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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

6 authors at 1 institution in 1 country.

Valerie BlancDivision of Gastroenterology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Jeffrey O Henderson
Elizabeth P Newberry
Susan Kennedy
Jianyang Luo
Nicholas O Davidson
Washington University in St. Louis · US

Funding

Washington University DDRCC Supplemental Equipment RequestP30DK052574 · NIDDK · WASHINGTON UNIVERSITY · PI Jeffrey Wade Brown · 2000 to 2026
$30.8M
HEPATIC SYNTHESIS AND SECRETION OF APOLIPOPROTEIN (A)R01DK056260 · NIDDK · WASHINGTON UNIVERSITY · PI DAVIDSON, NICHOLAS O. · 1999 to 2017
$5.9M
ENTEROHEPATIC LIPID FLUX AND APOPROTEIN BIOSYNTHESIS.R37HL038180 · NHLBI · WASHINGTON UNIVERSITY · PI DAVIDSON, NICHOLAS O. · 2000 to 2009
$5.1M
ENTEROHEPATIC LIPID FLUX AND APOPROTEIN BIOSYNTHESISR01HL038180 · NHLBI · WASHINGTON UNIVERSITY · PI DAVIDSON, NICHOLAS O. · 1986 to 2018
$3.8M
NHLBI NIH HHS HL-38180NHLBI NIH HHS R01 HL038180NHLBI NIH HHS R37 HL038180NIDDK NIH HHS DK-52574NIDDK NIH HHS DK-56260NIDDK NIH HHS P30 DK052574NIDDK NIH HHS R01 DK056260
6 · The paper itself

Abstract

apobec-1 complementation factor (ACF) is an hnRNP family member which functions as the obligate RNA binding subunit of the core enzyme mediating C-to-U editing of the nuclear apolipoprotein B (apoB) transcript. ACF binds to both apoB RNA and apobec-1, the catalytic cytidine deaminase, which then results in site-specific posttranscriptional editing of apoB mRNA. Targeted deletion of apobec1 eliminates C-to-U editing of apoB mRNA but is otherwise well tolerated. However, the functions and potential targets of ACF beyond apoB mRNA editing are unknown. Here we report the results of generating acf knockout mice using homologous recombination. While heterozygous acf(+/)(-) mice were apparently healthy and fertile, no viable acf(-)(/)(-) mice were identified. Mutant acf(-)(/)(-) embryos were detectable only until the blastocyst (embryonic day 3.5 [E3.5]) stage. No acf(-)(/)(-) blastocysts were detectable following implantation at E4.5, and isolated acf(-)(/)(-) blastocysts failed to proliferate in vitro. Small interfering RNA knockdown of ACF in either rat (apobec-1-expressing) or human (apobec-1-deficient) hepatoma cells decreased ACF protein expression and induced a commensurate increase in apoptosis. Taken together, these data suggest that ACF plays a crucial role, which is independent of apobec-1 expression, in cell survival, particularly during early embryonic development.

Indexed as

Gene Expression Regulation, DevelopmentalGenetic Complementation TestAnimalsApolipoproteins BApoptosisCrosses, GeneticCytidine DeaminaseEmbryo ImplantationExonsGene DeletionGenetic VectorsGenotypeHeterogeneous-Nuclear RibonucleoproteinsHeterozygoteHomozygoteHumansA1CF protein, humanapobec-1 complementation factor, mouseApolipoproteins BCytidine DeaminaseHeterogeneous-Nuclear RibonucleoproteinsRNARNA-Binding ProteinsRNA, MessengerRNA, Small Interfering

Identifiers

PMID16055734
PMCPMC1190267
OpenAlexW1984705730

What Socratic 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 Socratic graph.