ArticleBiophysical journal2013
Sarcoplasmic reticulum K(+) (TRIC) channel does not carry essential countercurrent during Ca(2+) release.
Article in Biophysical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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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
19 citing papers in PubMed.
- Article
- Flecainide Specifically Targets the Monovalent Countercurrent Through the Cardiac Ryanodine Receptor, While a Dominant Opposing CaInternational journal of molecular sciences · 2024Article
- Flecainide induces a sustained countercurrent dependent effect on RyR2 in permeabilized WT ventricular myocytes but not in intact cells.Frontiers in pharmacology · 2023Article
- The roles of transmembrane family proteins in the regulation of store-operated CaCellular and molecular life sciences : CMLS · 2022Review
- TRIC-A regulates intracellular CaPflugers Archiv : European journal of physiology · 2021Review
- TRIC-A shapes oscillatory Ca2+ signals by interaction with STIM1/Orai1 complexes.PLoS biology · 2020Article
- Ion Channels of the Islets in Type 2 Diabetes.Journal of molecular biology · 2020Review
- TRIC-A Channel Maintains Store Calcium Handling by Interacting With Type 2 Ryanodine Receptor in Cardiac Muscle.Circulation research · 2020Article
- Tracking the sarcoplasmic reticulum membrane voltage in muscle with a FRET biosensor.The Journal of general physiology · 2018Article
- Sarcoplasmic Reticulum CaBiophysical journal · 2018Article
- TALK-1 channels control β cell endoplasmic reticulum CaScience signaling · 2017Article
- Structural basis for conductance through TRIC cation channels.Nature communications · 2017Article
- Ion- and water-binding sites inside an occluded hourglass pore of a trimeric intracellular cation (TRIC) channel.BMC biology · 2017Article
- Sarcoplasmic reticulum CaJournal of molecular and cellular cardiology · 2017Article
- Crystal structures of the TRIC trimeric intracellular cation channel orthologues.Cell research · 2016Article
- Absence of the ER Cation Channel TMEM38B/TRIC-B Disrupts Intracellular Calcium Homeostasis and Dysregulates Collagen Synthesis in Recessive Osteogenesis Imperfecta.PLoS genetics · 2016Article
- New and notable ion-channels in the sarcoplasmic/endoplasmic reticulum: do they support the process of intracellular Ca²⁺ release?The Journal of physiology · 2015Review
- Selecting ions by size in a calcium channel: the ryanodine receptor case study.Biophysical journal · 2014Article
- Trimeric intracellular cation channels and sarcoplasmic/endoplasmic reticulum calcium homeostasis.Circulation research · 2014Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
The charge translocation associated with sarcoplasmic reticulum (SR) Ca(2+) efflux is compensated for by a simultaneous SR K(+) influx. This influx is essential because, with no countercurrent, the SR membrane potential (Vm) would quickly (<1 ms) reach the Ca(2+) equilibrium potential and SR Ca(2+) release would cease. The SR K(+) trimeric intracellular cation (TRIC) channel has been proposed to carry the essential countercurrent. However, the ryanodine receptor (RyR) itself also carries a substantial K(+) countercurrent during release. To better define the physiological role of the SR K(+) channel, we compared SR Ca(2+) transport in saponin-permeabilized cardiomyocytes before and after limiting SR K(+) channel function. Specifically, we reduced SR K(+) channel conduction 35 and 88% by replacing cytosolic K(+) for Na(+) or Cs(+) (respectively), changes that have little effect on RyR function. Calcium sparks, SR Ca(2+) reloading, and caffeine-evoked Ca(2+) release amplitude (and rate) were unaffected by these ionic changes. Our results show that countercurrent carried by SR K(+) (TRIC) channels is not required to support SR Ca(2+) release (or uptake). Because K(+) enters the SR through RyRs during release, the SR K(+) (TRIC) channel most likely is needed to restore trans-SR K(+) balance after RyRs close, assuring SR Vm stays near 0 mV.
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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.