ArticleBiochimica et biophysica acta2007
Functional characterization of APOBEC-1 complementation factor phosphorylation sites.
Article in Biochimica et biophysica acta, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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.
Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Article
- Review
- Functions and regulation of the APOBEC family of proteins.Seminars in cell & developmental biology · 2012Review
- Metabolic regulation of APOBEC-1 complementation factor trafficking in mouse models of obesity and its positive correlation with the expression of ApoB protein in hepatocytes.Biochimica et biophysica acta · 2010Article
- APOBEC-1 complementation factor (ACF) forms RNA-dependent multimers.Biochemical and biophysical research communications · 2010Article
- The expression of apoB mRNA editing factors is not the sole determinant for the induction of editing in differentiating Caco-2 cells.Biochemical and biophysical research communications · 2010Article
- Towards Inhibition of Vif-APOBEC3G Interaction: Which Protein to Target?Advances in virology · 2010Article
- The multifaceted roles of RNA binding in APOBEC cytidine deaminase functions.Wiley interdisciplinary reviews. RNAReview
- APOBEC-1 Complementation Factor: From RNA Binding to Cancer.Cancer control : journal of the Moffitt Cancer CenterReview
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
ApoB mRNA editing involves site-specific deamination of cytidine 6666 producing an in-frame translation stop codon. Editing minimally requires APOBEC-1 and APOBEC-1 complementation factor (ACF). Metabolic stimulation of apoB mRNA editing in hepatocytes is associated with serine phosphorylation of ACF localized to editing competent, nuclear 27S editosomes. We demonstrate that activation of protein kinase C (PKC) stimulated editing and enhanced ACF phosphorylation in rat primary hepatocytes. Conversely, activation of protein kinase A (PKA) had no effect on editing. Recombinant PKC efficiently phosphorylated purified ACF64 protein in vitro, whereas PKA did not. Mutagenesis of predicted PKC phosphorylation sites S154 and S368 to alanine inhibited ethanol-stimulated induction of editing suggesting that these sites function in the metabolic regulation of editing. Consistent with this interpretation, substitution of S154 and S368 with aspartic acid stimulated editing to levels comparable to ethanol treatment in control McArdle RH7777 cells. These data suggest that phosphorylation of ACF by PKC may be a key regulatory mechanism of apoB mRNA editing in rat hepatocytes.
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What OpenQuestion holds
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 OpenQuestion graph.