ReviewAmerican journal of physiology. Cell physiology2016
Orai1 and STIM1 in ER/PM junctions: roles in pancreatic cell function and dysfunction.
Review in American journal of physiology. Cell physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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Who cites it
11 citing papers in PubMed.
- CRAC and SK Channels: Their Molecular Mechanisms Associated with Cancer Cell Development.Cancers · 2022Review
- The Role of Lipids in CRAC Channel Function.Biomolecules · 2022Review
- Orai1 Channel Regulates Human-Activated Pancreatic Stellate Cell Proliferation and TGFCancers · 2021Article
- Molecular Choreography and Structure of CaMembranes · 2020Review
- The odorant receptor OR2W3 on airway smooth muscle evokes bronchodilation via a cooperative chemosensory tradeoff between TMEM16A and CFTR.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Sticking With It: ER-PM Membrane Contact Sites as a Coordinating Nexus for Regulating Lipids and Proteins at the Cell Cortex.Frontiers in cell and developmental biology · 2020Review
- STIM1 holds a STING in its (N-terminal) tail.Cell calcium · 2019Article
- Recent Insights Into the Pathogenic Mechanism of Pancreatitis: Role of Acinar Cell Organelle Disorders.Pancreas · 2019Review
- Review
- Synergy of cAMP and calcium signaling pathways in CFTR regulation.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- New insights into the pathways initiating and driving pancreatitis.Current opinion in gastroenterology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Membrane contact sites (MCS) are critical junctions that form between the endoplasmic reticulum (ER) and membranes of various organelles, including the plasma membrane (PM). Signaling complexes, including mediators of Ca(2+) signaling, are assembled within MCS, such as the ER/PM junction. This is most evident in polarized epithelial cells, such as pancreatic cells. Core Ca(2+) signaling proteins cluster at the apical pole, the site of inositol 1,4,5-trisphosphate-mediated Ca(2+) release and Orai1/transient receptor potential canonical-mediated store-dependent Ca(2+) entry. Recent advances have characterized the proteins that tether the membranes at MCS and the role of these proteins in modulating physiological and pathological intracellular signaling. This review discusses recent advances in the characterization of Ca(2+) signaling at ER/PM junctions and the relation of these junctions to physiological and pathological Ca(2+) signaling in pancreatic acini.
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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.