ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2009
Modulation of ileal apical Na+-dependent bile acid transporter ASBT by protein kinase C.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Contribution of organic anion transporting polypeptides to bile acid uptake in the Caco-2 cell monolayer and gastrointestinal tract.The Journal of biological chemistry · 2026Article
- Article
- Article
- Intestinal Absorption of Bile Acids in Health and Disease.Comprehensive Physiology · 2019Review
- Tyrosine Phosphorylation Regulates Plasma Membrane Expression and Stability of the Human Bile Acid Transporter ASBT (Molecular pharmaceutics · 2019Article
- A novel bioluminescence-based method to investigate uptake of bile acids in living cells.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
- Protein Kinases C-Mediated Regulations of Drug Transporter Activity, Localization and Expression.International journal of molecular sciences · 2017Review
- N-glycosylation is essential for ileal ASBT function and protection against proteases.American journal of physiology. Cell physiology · 2015Article
- 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
- Sodium-dependent bile salt transporters of the SLC10A transporter family: more than solute transporters.Pflugers Archiv : European journal of physiology · 2014Review
- Human Organic Solute Transporter (hOST): protein interaction and membrane sorting process.International journal of biochemistry and molecular biology · 2012Article
- Hu antigen R and tristetraprolin: counter-regulators of rat apical sodium-dependent bile acid transporter by way of effects on messenger RNA stability.Hepatology (Baltimore, Md.) · 2011Article
- Ileal apical Na+-dependent bile acid transporter ASBT is upregulated in rats with diabetes mellitus induced by low doses of streptozotocin.American journal of physiology. Gastrointestinal and liver physiology · 2010Article
- Green tea catechin EGCG inhibits ileal apical sodium bile acid transporter ASBT.American journal of physiology. Gastrointestinal and liver physiology · 2010Article
- The solute carrier family 10 (SLC10): beyond bile acid transport.Molecular aspects of medicineReview
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Ileal apical Na(+)-dependent bile acid transporter (ASBT) is responsible for reabsorbing the majority of bile acids from the intestinal lumen. Rapid adaptation of ASBT function in response to physiological and pathophysiological stimuli is essential for the maintenance of bile acid homeostasis. However, not much is known about molecular mechanisms responsible for acute posttranscriptional regulation of ileal ASBT. The protein kinase C (PKC)-dependent pathway represents a major cell signaling mechanism influencing intestinal epithelial functions. The present studies were, therefore, undertaken to investigate ASBT regulation in intestinal Caco-2 monolayers by the well-known PKC activator phorbol 12-myristate 13-acetate (PMA). Our results showed that Na(+)-dependent [(3)H]taurocholic acid uptake in Caco-2 cells was significantly inhibited in response to 2 h incubation with 100 nM PMA compared with incubation with 4alpha-PMA (inactive form). The inhibitory effect of PMA was blocked in the presence of 5 microM bisindolylmaleimide I (PKC inhibitor) but not 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-AM (Ca(2+) chelator) or LY-294002 (phosphatidylinositol 3-kinase inhibitor). PMA inhibition of ASBT function was also abrogated in the presence of myristoylated PKCzeta pseudosubstrate peptide, indicating involvement of the atypical PKCzeta isoform. The inhibition by PMA was associated with a significant decrease in the maximal velocity of the transporter and a reduction in ASBT plasma membrane content, suggesting a modulation by vesicular recycling. Our novel findings demonstrate a posttranscriptional modulation of ileal ASBT function and membrane expression by phorbol ester via a PKCzeta-dependent pathway.
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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.