ArticleJournal of lipid research2012
Intestine-specific expression of Apobec-1 rescues apolipoprotein B RNA editing and alters chylomicron production in Apobec1 -/- mice.
Article in Journal of lipid research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
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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.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- The N-terminus of apolipoprotein B mediates the interaction of atherogenic lipoproteins with endothelial cells.The Journal of clinical investigation · 2026Article
- RNA editing in cardiovascular health and disease.Communications biology · 2026Review
- APOBEC1-Dependent RNA Eiting of TNF Signaling Orchestrates Ileal Villus Morphogenesis in Pigs: Integrative Transcriptomic and Editomic Insights.Animals : an open access journal from MDPI · 2025Article
- Identification of RBM46 as a novel APOBEC1 cofactor for C-to-U RNA-editing activity.Journal of molecular biology · 2023Article
- From worms to humans: Understanding intestinal lipid metabolism via model organisms.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2023Review
- The Remnant Lipoprotein Hypothesis of Diabetes-Associated Cardiovascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2022Review
- Epithelial Indoleamine 2,3-Dioxygenase 1 Modulates Aryl Hydrocarbon Receptor and Notch Signaling to Increase Differentiation of Secretory Cells and Alter Mucus-Associated Microbiota.Gastroenterology · 2019Article
- Thioesterase Superfamily Member 2 Promotes Hepatic VLDL Secretion by Channeling Fatty Acids Into Triglyceride Biosynthesis.Hepatology (Baltimore, Md.) · 2019Article
- PCSK9 deficiency reduces atherosclerosis, apolipoprotein B secretion, and endothelial dysfunction.Journal of lipid research · 2018Article
- Epitranscriptomic profiling across cell types reveals associations between APOBEC1-mediated RNA editing, gene expression outcomes, and cellular function.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
- Incorporating alternative splicing and mRNA editing into the genetic analysis of complex traits.BioEssays : news and reviews in molecular, cellular and developmental biology · 2014Article
- High-resolution genetic mapping in the diversity outbred mouse population identifies Apobec1 as a candidate gene for atherosclerosis.G3 (Bethesda, Md.) · 2014Article
- Genome-wide identification and functional analysis of Apobec-1-mediated C-to-U RNA editing in mouse small intestine and liver.Genome biology · 2014Article
- Induction of body weight loss through RNAi-knockdown of APOBEC1 gene expression in transgenic rabbits.PloS one · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Intestinal apolipoprotein B (apoB) mRNA undergoes C-to-U editing, mediated by the catalytic deaminase apobec-1, which results in translation of apoB48. Apobec1(-/-) mice produce only apoB100 and secrete larger chylomicron particles than those observed in wild-type (WT) mice. Here we show that transgenic rescue of intestinal apobec-1 expression (Apobec1(Int/O)) restores C-to-U RNA editing of apoB mRNA in vivo, including the canonical site at position 6666 and also at approximately 20 other newly identified downstream sites present in WT mice. The small intestine of Apobec1(Int/O) mice produces only apoB48, and the liver produces only apoB100. Serum chylomicron particles were smaller in Apobec1(Int/O) mice compared with those from Apobec1(-/-) mice, and the predominant fraction of serum apoB48 in Apobec1(Int/O) mice migrated in lipoproteins smaller than chylomicrons, even when these mice were fed a high-fat diet. Because apoB48 arises exclusively from the intestine in Apobec1(Int/O) mice and intestinal apoB48 synthesis and secretion rates were comparable to WT mice, we were able to infer the major sites of origin of serum apoB48 in WT mice. Our findings imply that less than 25% of serum apoB48 in WT mice arises from the intestine, with the majority originating from the liver.
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Registered trials
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.