ArticlePLoS biology2020
TRIC-A shapes oscillatory Ca2+ signals by interaction with STIM1/Orai1 complexes.
Article in PLoS biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- The ion channels of endomembranes.Physiological reviews · 2024Review
- The role of calcium channels in osteoporosis and their therapeutic potential.Frontiers in endocrinology · 2024Review
- Novel insights into STIM1's role in store-operated calcium entry and its implications for T-cell mediated inflammation in trigeminal neuralgia.Frontiers in molecular neuroscience · 2024Article
- The roles of transmembrane family proteins in the regulation of store-operated CaCellular and molecular life sciences : CMLS · 2022Review
- Spatiotemporal regulation of store-operated calcium entry in cancer metastasis.Biochemical Society transactions · 2021Review
- The Diverse Cellular Functions of Inner Nuclear Membrane Proteins.Cold Spring Harbor perspectives in biology · 2021Review
- TRIC-A regulates intracellular CaPflugers Archiv : European journal of physiology · 2021Review
- SOCE in the cardiomyocyte: the secret is in the chambers.Pflugers Archiv : European journal of physiology · 2021Review
- Knockout ofInternational journal of molecular sciences · 2020Article
- Transcriptomic Profiling of Ca2+ Transport Systems During the Formation of the Cerebral Cortex in Mice.Cells · 2020Article
- Decreased cardiac pacemaking and attenuated β-adrenergic response in TRIC-A knockout mice.PloS one · 2020Article
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8 authors at 2 institutions in 2 countries.
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Abstract
Trimeric intracellular cation (TRIC) channels have been proposed to modulate Ca2+ release from the endoplasmic reticulum (ER) and determine oscillatory Ca2+ signals. Here, we report that TRIC-A-mediated amplitude and frequency modulation of ryanodine receptor 2 (RyR2)-mediated Ca2+ oscillations and inositol 1,4,5-triphosphate receptor (IP3R)-induced cytosolic signals is based on attenuating store-operated Ca2+ entry (SOCE). Further, TRIC-A-dependent delay in ER Ca2+ store refilling contributes to shaping the pattern of Ca2+ oscillations. Upon ER Ca2+ depletion, TRIC-A clusters with stromal interaction molecule 1 (STIM1) and Ca2+-release-activated Ca2+ channel 1 (Orai1) within ER-plasma membrane (PM) junctions and impairs assembly of the STIM1/Orai1 complex, causing a decrease in Orai1-mediated Ca2+ current and SOCE. Together, our findings demonstrate that TRIC-A is a negative regulator of STIM1/Orai1 function. Thus, aberrant SOCE could contribute to muscle disorders associated with loss of TRIC-A.
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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.