ArticleThe Journal of physiology2006
Ca2+-calmodulin-dependent myosin light chain kinase is essential for activation of TRPC5 channels expressed in HEK293 cells.
Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 71 citations in OpenAlex.
- Analysis of genome and methylation changes in Chinese indigenous chickens over time provides insight into species conservation.Communications biology · 2022Article
- How filopodia respond to calcium in the absence of a calcium-binding structural protein: non-channel functions of TRP.Cell communication and signaling : CCS · 2022Article
- Purinoreceptors and ectonucleotidases control ATP-induced calcium waveforms and calcium-dependent responses in microglia: Roles of P2 receptors and CD39 in ATP-stimulated microglia.Frontiers in physiology · 2022Article
- α1-Adrenergic receptor regulates papillary muscle and aortic segment contractile function via modulation of store-operated CaJournal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2021Article
- Development of Store-Operated Calcium Entry-Targeted Compounds in Cancer.Frontiers in pharmacology · 2021Review
- Integration of TRPC6 and NADPH oxidase activation in lysophosphatidylcholine-induced TRPC5 externalization.American journal of physiology. Cell physiology · 2017Article
- Calcium permeability of transient receptor potential canonical (TRPC) 4 channels measured by TRPC4-GCaMP6s.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2017Article
- TRP channels in oxygen physiology: distinctive functional properties and roles of TRPA1 in OProceedings of the Japan Academy. Series B, Physical and biological sciences · 2017Review
- Functional interplay between ganglioside GM1 and cross-linking galectin-1 induces axon-like neuritogenesis via integrin-based signaling and TRPC5-dependent Ca²⁺ influx.Journal of neurochemistry · 2016Article
- Myosin light chain kinase controls voltage-dependent calcium channels in vascular smooth muscle.Pflugers Archiv : European journal of physiology · 2014Article
- Regulation of calcium channels in smooth muscle: new insights into the role of myosin light chain kinase.Channels (Austin, Tex.) · 2014Review
- Selective Gαi subunits as novel direct activators of transient receptor potential canonical (TRPC)4 and TRPC5 channels.The Journal of biological chemistry · 2012Article
- Properties and therapeutic potential of transient receptor potential channels with putative roles in adversity: focus on TRPC5, TRPM2 and TRPA1.Current drug targets · 2011Review
- TRP Channels as Sensors and Signal Integrators of Redox Status Changes.Frontiers in pharmacology · 2011Article
- Article
- Activation and regulation of store-operated calcium entry.Journal of cellular and molecular medicine · 2010Review
- TRPC channels function independently of STIM1 and Orai1.The Journal of physiology · 2009Article
- Intracellular calcium strongly potentiates agonist-activated TRPC5 channels.The Journal of general physiology · 2009Article
- STIM and Orai: the long-awaited constituents of store-operated calcium entry.Trends in pharmacological sciences · 2009Review
- Elucidation of a TRPC6-TRPC5 channel cascade that restricts endothelial cell movement.Molecular biology of the cell · 2008Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mammalian homologues of Drosophila transient receptor potential (TRP) proteins are responsible for receptor-activated Ca(2+) influx in vertebrate cells. We previously reported the involvement of intracellular Ca(2+) in the receptor-mediated activation of mammalian canonical transient receptor potential 5 (TRPC5) channels. Here we investigated the role of calmodulin, an important sensor of changes in intracellular Ca(2+), and its downstream cascades in the activation of recombinant TRPC5 channels in human embryonic kidney (HEK) 293 cells. Ca(2+) entry through TRPC5 channels, induced upon stimulation of the G-protein-coupled ATP receptor, was abolished by treatment with W-13, an inhibitor of calmodulin. ML-9 and wortmannin, inhibitors of Ca(2+)-calmodulin-dependent myosin light chain kinase (MLCK), and the expression of a dominant-negative mutant of MLCK inhibited the TRPC5 channel activity, revealing an essential role of MLCK in maintaining TRPC5 channel activity. It is important to note that ML-9 impaired the plasma membrane localization of TRPC5 channels. Furthermore, TRPC5 channel activity measured using the whole-cell patch-clamp technique was inhibited by ML-9, whereas TRPC5 channel activity observed in the cell-excised, inside-out patch was unaffected by ML-9. An antibody that recognizes phosphorylated myosin light chain (MLC) revealed that the basal level of phosphorylated MLC under unstimulated conditions was reduced by ML-9 in HEK293 cells. These findings strongly suggest that intracellular Ca(2+)-calmodulin constitutively activates MLCK, thereby maintaining TRPC5 channel activity through the promotion of plasma membrane TRPC5 channel distribution under the control of phosphorylation/dephosphorylation equilibrium of MLC.
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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.