ArticleProceedings of the National Academy of Sciences of the United States of America2004
Regulation of canonical transient receptor potential isoform 3 (TRPC3) channel by protein kinase G.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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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
58 citing papers in PubMed, 160 citations in OpenAlex.
- Pathophysiological significance and modulation of the transient receptor potential canonical 3 ion channel.Medicinal research reviews · 2024Review
- Orai1 and Orai3 act through distinct signalling axes to promote stemness and tumorigenicity of breast cancer stem cells.Stem cell research & therapy · 2024Article
- Pathogen recognition by sensory neurons: hypotheses on the specificity of sensory neuron signaling.Frontiers in immunology · 2023Article
- Review
- Article
- Article
- Canonical Transient Receptor Potential Channels and Their Link with Cardio/Cerebro-Vascular Diseases.Biomolecules & therapeutics · 2017Review
- The regulation of transient receptor potential canonical 4 (TRPC4) channel by phosphodiesterase 5 inhibitor via the cyclic guanosine 3'5'-monophosphate.Pflugers Archiv : European journal of physiology · 2017Article
- Pathophysiological Significance of Store-Operated Calcium Entry in Megakaryocyte Function: Opening New Paths for Understanding the Role of Calcium in Thrombopoiesis.International journal of molecular sciences · 2016Review
- Translocation of PKG1α acts on TRPV4-C1 heteromeric channels to inhibit endothelial Ca(2+) entry.Acta pharmacologica Sinica · 2016Article
- Tadalafil Treatment Delays the Onset of Cardiomyopathy in Dystrophin-Deficient Hearts.Journal of the American Heart Association · 2016Article
- Old dog, new tricks: novel cardiac targets and stress regulation by protein kinase G.Cardiovascular research · 2016Review
- TRPC5 channels participate in pressure-sensing in aortic baroreceptors.Nature communications · 2016Article
- Axial stretch-dependent cation entry in dystrophic cardiomyopathy: Involvement of several TRPs channels.Cell calcium · 2016Article
- Orai1 forms a signal complex with BKCa channel in mesenteric artery smooth muscle cells.Physiological reports · 2016Article
- Permeation, regulation and control of expression of TRP channels by trace metal ions.Pflugers Archiv : European journal of physiology · 2015Review
- Ca(2+) signaling initiated by canonical transient receptor potential channels in dendritic development.Neuroscience bulletin · 2015Review
- Transient receptor potential channels in the vasculature.Physiological reviews · 2015Review
- Role of TRP channels in the cardiovascular system.American journal of physiology. Heart and circulatory physiology · 2015Review
- Adenosine modulates light responses of rat retinal ganglion cell photoreceptors througha cAMP-mediated pathway.The Journal of physiology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Canonical transient receptor potential (TRPC) channels are Ca2+-permeable nonselective cation channels that are widely expressed in numerous cell types. Seven different members of TRPC channels have been isolated. The activity of these channels is regulated by the filling state of intracellular Ca2+ stores and/or diacylglycerol and/or Ca2+/calmodulin. However, no evidence is available as to whether TRPC channels are regulated by direct phosphorylation on the channels. In the present study, TRPC isoform 3 (TRPC3) gene was overexpressed in HEK293 cells that were stably transfected with protein kinase G (PKG). We found that the overexpressed TRPC3 mediated store-operated Ca2+ influx and that this type of Ca2+ influx was inhibited by cGMP. The inhibitory effect of cGMP was abolished by KT5823 or H8. Point mutations at two consensus PKG phosphorylation sites (T11A and S263Q) of TRPC3 channel markedly reduced the inhibitory effect of cGMP. In addition, TRPC3 proteins were purified from HEK293 cells that were transfected with either wild-type or mutant TRPC3 constructs, and in vitro PKG phosphorylation assay was carried out. It was found that wild-type TRPC3 could be directly phosphorylated by PKG in vitro and that the phosphorylation was abolished in the presence of KT5823. The phosphorylation signal was greatly reduced in mutant protein T11A or S263Q. Taken together, TRPC3 channels could be directly phosphorylated by PKG at position T11 and S263, and this phosphorylation abolished the store-operated Ca2+ influx mediated by TRPC3 channels in HEK293 cells.
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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.