ArticleMolecular biology of the cell2008
Cholecystokinin activates pancreatic calcineurin-NFAT signaling in vitro and in vivo.
Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Integrative single-cell characterization of a frugivorous and an insectivorous bat kidney and pancreas.Nature communications · 2024Article
- Our Mental Health Is Determined by an Intrinsic Interplay between the Central Nervous System, Enteric Nerves, and Gut Microbiota.International journal of molecular sciences · 2023Review
- Gut Bacteria and Neurotransmitters.Microorganisms · 2022Review
- Gut Bacteria and Neuropsychiatric Disorders.Microorganisms · 2021Review
- The Orai CaThe Journal of physiology · 2019Article
- SOCE induced calcium overload regulates autophagy in acute pancreatitis via calcineurin activation.Cell death & disease · 2018Article
- Transcriptional Maintenance of Pancreatic Acinar Identity, Differentiation, and Homeostasis by PTF1A.Molecular and cellular biology · 2016Article
- Nuclear Factor of Activated T Cells-dependent Down-regulation of the Transcription Factor Glioma-associated Protein 1 (GLI1) Underlies the Growth Inhibitory Properties of Arachidonic Acid.The Journal of biological chemistry · 2016Article
- NFATc4 Regulates Sox9 Gene Expression in Acinar Cell Plasticity and Pancreatic Cancer Initiation.Stem cells international · 2016Article
- Exposure to Radiocontrast Agents Induces Pancreatic Inflammation by Activation of Nuclear Factor-κB, Calcium Signaling, and Calcineurin.Gastroenterology · 2015Article
- The gastrin and cholecystokinin receptors mediated signaling network: a scaffold for data analysis and new hypotheses on regulatory mechanisms.BMC systems biology · 2015Article
- NFATc1 Links EGFR Signaling to Induction of Sox9 Transcription and Acinar-Ductal Transdifferentiation in the Pancreas.Gastroenterology · 2015Article
- ERK activation is required for CCK-mediated pancreatic adaptive growth in mice.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Adenylyl cyclases in the digestive system.Cellular signalling · 2014Review
- The prelude on novel receptor and ligand targets involved in the treatment of diabetes mellitus.Advanced pharmaceutical bulletin · 2014Review
- Adenylyl cyclase 6 mediates the action of cyclic AMP-dependent secretagogues in mouse pancreatic exocrine cells via protein kinase A pathway activation.The Journal of physiology · 2013Article
- Preparation of pancreatic acinar cells for the purpose of calcium imaging, cell injury measurements, and adenoviral infection.Journal of visualized experiments : JoVE · 2013Article
- Parsing good versus bad signaling pathways in the heart: role of calcineurin-nuclear factor of activated T-cells.Circulation research · 2013Article
- Bile acids induce pancreatic acinar cell injury and pancreatitis by activating calcineurin.The Journal of biological chemistry · 2013Article
- c-Jun/AP-1 is required for CCK-induced pancreatic acinar cell dedifferentiation and DNA synthesis in vitro.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
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Authors and funding
5 authors.
Funding
Abstract
Elevated endogenous cholecystokinin (CCK) release induced by protease inhibitors leads to pancreatic growth. This response has been shown to be mediated by the phosphatase calcineurin, but its downstream effectors are unknown. Here we examined activation of calcineurin-regulated nuclear factor of activated T-cells (NFATs) in isolated acinar cells, as well as in an in vivo model of pancreatic growth. Western blotting of endogenous NFATs and confocal imaging of NFATc1-GFP in pancreatic acini showed that CCK dose-dependently stimulated NFAT translocation from the cytoplasm to the nucleus within 0.5-1 h. This shift in localization correlated with CCK-induced activation of NFAT-driven luciferase reporter and was similar to that induced by a calcium ionophore and constitutively active calcineurin. The effect of CCK was dependent on calcineurin, as these changes were blocked by immunosuppressants FK506 and CsA and by overexpression of the endogenous protein inhibitor CAIN. Parallel NFAT activation took place in vivo. Pancreatic growth was accompanied by an increase in nuclear NFATs and subsequent elevation in expression of NFAT-luciferase in the pancreas, but not in organs unresponsive to CCK. The changes also required calcineurin, as they were blocked by FK506. We conclude that CCK activates NFATs in a calcineurin-dependent manner, both in vitro and in vivo.
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