ArticleHepatology (Baltimore, Md.)2011
Hu antigen R and tristetraprolin: counter-regulators of rat apical sodium-dependent bile acid transporter by way of effects on messenger RNA stability.
Article in Hepatology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
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.
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
11 citing papers in PubMed, 17 citations in OpenAlex.
- ASBT governs neonatal bile acid homeostasis early in life despite its strong ileal repression.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Metabolic immaturity and breastmilk bile acid metabolites are central determinants of heightened newborn vulnerability to norovirus diarrhea.Cell host & microbe · 2024Article
- Intestinal Absorption of Bile Acids in Health and Disease.Comprehensive Physiology · 2019Review
- Organic Solute Transporter α-β Protects Ileal Enterocytes From Bile Acid-Induced Injury.Cellular and molecular gastroenterology and hepatology · 2018Article
- RNA binding protein, tristetraprolin in a murine model of recurrent pregnancy loss.Oncotarget · 2016Article
- Intestinal epithelial HuR modulates distinct pathways of proliferation and apoptosis and attenuates small intestinal and colonic tumor development.Cancer research · 2014Article
- A single element in the 3'UTR of the apical sodium-dependent bile acid transporter controls both stabilization and destabilization of mRNA.The Biochemical journal · 2014Article
- c-Fos mediates repression of the apical sodium-dependent bile acid transporter by fibroblast growth factor-19 in mice.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- A role for RNA post-transcriptional regulation in satellite cell activation.Skeletal muscle · 2012Article
- The solute carrier family 10 (SLC10): beyond bile acid transport.Molecular aspects of medicineReview
- Tristetraprolin (TTP): interactions with mRNA and proteins, and current thoughts on mechanisms of action.Biochimica et biophysica actaReview
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledThe apical sodium-dependent bile acid transporter (ASBT, SLC10A2) mediates intestinal, renal, and cholangiocyte bile acid reclamation. Transcriptional regulation of ASBT is well described, whereas information on posttranscriptional regulation is limited. Prior studies suggested that ontogeny of ASBT is controlled in part by changes in messenger RNA (mRNA) stability. We studied the role that Hu antigen R (HuR) and tristetraprolin (TTP) play in regulating the expression of mRNA that contains the 3' untranslated region (UTR) of rat ASBT. The 3'UTR was incorporated into an SV-40 driven luciferase reporter (rASBT3-luciferase) for rapid screening of regulatory effects. Silencing HuR reduced luciferase reporter activity, whereas silencing TTP enhanced luciferase activity. Conversely, overexpression of HuR enhanced rASBT3-luciferase reporter activity. The same 3'UTR fragments of rat ASBT were incorporated into a beta-globin coding mRNA construct for analysis of mRNA stability (rASBT3-βglobin). mRNA half-life was progressively shortened by the incorporation of increasing sized fragments of the 3'UTR. Silencing HuR shortened the half-life of rASBT3-βglobin containing 0.3 kb of the rat ASBT 3'UTR. Gel shift assays revealed binding of HuR and TTP to rat ASBT 3'UTR. Endogenously expressed human ASBT mRNA half-lives and steady-state protein levels in Caco-2 cells were repressed when HuR was silenced but was enhanced when TTP was silenced. Developmental changes in HuR and TTP protein abundance correlated with previously characterized ontogenic changes in rat ileal and renal ASBT expression.
conclusionThese studies not only show that ASBT expression is controlled at the level of mRNA stability by way of its 3'UTR, but also identify HuR and TTP as two key transacting factors that are involved in exerting counterregulatory effects on ASBT mRNA stability.
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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.