ArticleThe Journal of biological chemistry2015
Post-translational regulation of the type III inositol 1,4,5-trisphosphate receptor by miRNA-506.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 82 citations in OpenAlex.
- Primary Biliary Cholangitis Pathogenesis: A Pathophysiology-Based Narrative Review.International journal of molecular sciences · 2026Review
- Autoantibodies in Primary Biliary Cholangitis: From Classical Markers to Emerging Targets.Journal of clinical medicine · 2025Review
- Research progress and perspectives of non-coding RNAs in primary biliary cholangitis: from mechanisms to therapeutics.Frontiers in medicine · 2025Review
- Molecular Mechanisms of Fibrosis in Cholestatic Liver Diseases and Regenerative Medicine-Based Therapies.Cells · 2024Review
- Exploring the Pathogenesis of Autoimmune Liver Diseases from the Heterogeneity of Target Cells.Journal of clinical and translational hepatology · 2024Review
- Review
- Steady-state regulation of COPII-dependent secretory cargo sorting by inositol trisphosphate receptors, calcium, and penta EF hand proteins.The Journal of biological chemistry · 2023Article
- New insights into the pathogenesis of primary biliary cholangitis asymptomatic stage.World journal of gastroenterology · 2023Review
- Primary biliary cholangitis: molecular pathogenesis perspectives and therapeutic potential of natural products.Frontiers in immunology · 2023Review
- Neuronal microRNAs safeguard ER CaCellular and molecular life sciences : CMLS · 2022Article
- Involvement of oxidative species in cyclosporine-mediated cholestasis.Frontiers in pharmacology · 2022Review
- Roles of Non-Coding RNAs in Primary Biliary Cholangitis.Frontiers in molecular biosciences · 2022Review
- CREB regulates the expression of type 1 inositol 1,4,5-trisphosphate receptors.Journal of cell science · 2021Article
- Role of miR-506 in ulcerative colitis associated with primary sclerosing cholangitis.Scientific reports · 2021Article
- ITPR3 facilitates tumor growth, metastasis and stemness by inducing the NF-ĸB/CD44 pathway in urinary bladder carcinoma.Journal of experimental & clinical cancer research : CR · 2021Article
- Neutrophils interact with cholangiocytes to cause cholestatic changes in alcoholic hepatitis.Gut · 2021Article
- Melatonin Protects Cholangiocytes from Oxidative Stress-Induced Proapoptotic and Proinflammatory Stimuli via miR-132 and miR-34.International journal of molecular sciences · 2020Article
- Inositol 1,4,5-trisphosphate receptor type 3 plays a protective role in hepatocytes during hepatic ischemia-reperfusion injury.Cell calcium · 2020Article
- Type 3 Inositol 1,4,5-Trisphosphate Receptor Is Increased and Enhances Malignant Properties in Cholangiocarcinoma.Hepatology (Baltimore, Md.) · 2020Article
- Primary biliary cholangitis: pathogenesis and therapeutic opportunities.Nature reviews. Gastroenterology & hepatology · 2020Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The type III isoform of the inositol 1,4,5-trisphosphate receptor (InsP3R3) is apically localized and triggers Ca(2+) waves and secretion in a number of polarized epithelia. However, nothing is known about epigenetic regulation of this InsP3R isoform. We investigated miRNA regulation of InsP3R3 in primary bile duct epithelia (cholangiocytes) and in the H69 cholangiocyte cell line, because the role of InsP3R3 in cholangiocyte Ca(2+) signaling and secretion is well established and because loss of InsP3R3 from cholangiocytes is responsible for the impairment in bile secretion that occurs in a number of liver diseases. Analysis of the 3'-UTR of human InsP3R3 mRNA revealed two highly conserved binding sites for miR-506. Transfection of miR-506 mimics into cell lines expressing InsP3R3-3'UTR-luciferase led to decreased reporter activity, whereas co-transfection with miR-506 inhibitors led to enhanced activity. Reporter activity was abrogated in isolated mutant proximal or distal miR-506 constructs in miR-506-transfected HEK293 cells. InsP3R3 protein levels were decreased by miR-506 mimics and increased by inhibitors, and InsP3R3 expression was markedly decreased in H69 cells stably transfected with miR-506 relative to control cells. miR-506-H69 cells exhibited a fibrotic signature. In situ hybridization revealed elevated miR-506 expression in vivo in human-diseased cholangiocytes. Histamine-induced, InsP3-mediated Ca(2+) signals were decreased by 50% in stable miR-506 cells compared with controls. Finally, InsP3R3-mediated fluid secretion was significantly decreased in isolated bile duct units transfected with miR-506, relative to control IBDU. Together, these data identify miR-506 as a regulator of InsP3R3 expression and InsP3R3-mediated Ca(2+) signaling and secretion.
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Registered trials
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