ArticleThe Journal of biological chemistry2009
Transient receptor potential canonical type 1 (TRPC1) operates as a sarcoplasmic reticulum calcium leak channel in skeletal muscle.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 59 citations in OpenAlex.
- Editorial: Stretch and the heart: mechanoelectrical coupling and arrhythmias.Frontiers in physiology · 2023Article
- Editorial: The evolving picture of CaFrontiers in physiology · 2023Article
- TRPC1 channels underlie stretch-modulated sarcoplasmic reticulum calcium leak in cardiomyocytes.Frontiers in physiology · 2022Article
- Effects of Sarcolemmal Background CaFrontiers in physiology · 2022Article
- TRPC3, but not TRPC1, as a good therapeutic target for standalone or complementary treatment of DMD.Journal of translational medicine · 2021Article
- Distribution and Assembly of TRP Ion Channels.Advances in experimental medicine and biology · 2021Article
- Transcriptomic Profiling of Ca2+ Transport Systems During the Formation of the Cerebral Cortex in Mice.Cells · 2020Article
- Location and function of transient receptor potential canonical channel 1 in ventricular myocytes.Journal of molecular and cellular cardiology · 2020Article
- TRPC channels in exercise-mimetic therapy.Pflugers Archiv : European journal of physiology · 2019Review
- Identification of Inhibitory CaiScience · 2019Article
- Glycogen Synthase Kinase 3 Beta Controls Presenilin-1-Mediated Endoplasmic Reticulum Ca²⁺ Leak Directed to Mitochondria in Pancreatic Islets and β-Cells.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2019Article
- An Update on Sec61 Channel Functions, Mechanisms, and Related Diseases.Frontiers in physiology · 2017Review
- Functional role of TRP channels in modulating ER stress and Autophagy.Cell calcium · 2016Review
- Article
- Both Orai1 and TRPC1 are Involved in Excessive Store-Operated Calcium Entry in Striatal Neurons Expressing Mutant Huntingtin Exon 1.Frontiers in physiology · 2015Article
- Review
- IL-1α reversibly inhibits skeletal muscle ryanodine receptor. a novel mechanism for critical illness myopathy?American journal of respiratory cell and molecular biology · 2014Article
- Characterization of functional TRPV1 channels in the sarcoplasmic reticulum of mouse skeletal muscle.PloS one · 2013Article
- Altered store operated calcium entry increases cyclic 3',5'-adenosine monophosphate production and extracellular signal-regulated kinases 1 and 2 phosphorylation in polycystin-2-defective cholangiocytes.Hepatology (Baltimore, Md.) · 2012Article
- Sarcoplasmic reticulum Ca2+ permeation explored from the lumen side in mdx muscle fibers under voltage control.The Journal of general physiology · 2012Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extensive studies performed in nonexcitable cells and expression systems have shown that type 1 transient receptor potential canonical (TRPC1) channels operate mainly in plasma membranes and open through phospholipase C-dependent processes, membrane stretch, or depletion of Ca(2+) stores. In skeletal muscle, it is proposed that TRPC1 channels are involved in plasmalemmal Ca(2+) influx and stimulated by store depletion or membrane stretch, but direct evidence for TRPC1 sarcolemmal channel activity is not available. We investigated here the functional role of TRPC1 using an overexpressing strategy in adult mouse muscle fibers. Immunostaining for endogenous TRPC1 revealed a striated expression pattern that matched sarcoplasmic reticulum (SR) Ca(2+) pump immunolabeling. In cells expressing TRPC1-yellow fluorescent protein (YFP), the same pattern of expression was observed, compatible with a longitudinal SR localization. Resting electric properties, action potentials, and resting divalent cation influx were not altered in TRPC1-YFP-positive cells. Poisoning with the SR Ca(2+) pump blocker cyclopiazonic acid elicited a contracture of the fiber at the level of the overexpression site in presence and absence of external Ca(2+) which was not observed in control cells. Ca(2+) measurements indicated that resting Ca(2+) and the rate of Ca(2+) increase induced by cyclopiazonic acid were higher in the TRPC1-YFP-positive zone than in the TRPC1-YFP-negative zone and control cells. Ca(2+) transients evoked by 200-ms voltage clamp pulses decayed slower in TRPC1-YFP-positive cells. In contrast to previous hypotheses, these data demonstrate that TRPC1 operates as a SR Ca(2+) leak channel in skeletal muscle.
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