ArticleThe Journal of physiology2009
Obligatory role for phosphatidylinositol 4,5-bisphosphate in activation of native TRPC1 store-operated channels in vascular myocytes.
Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 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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Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
- Impact of C-Terminal PKC Phosphorylation on TRPC6 Current Kinetics.International journal of molecular sciences · 2025Article
- Role for the PIPJournal of cell communication and signaling · 2024Review
- TRP Channels in Stroke.Neuroscience bulletin · 2024Review
- Cholesterol Stimulates the Transient Receptor Potential Melastatin 4 Channel in mpkCCDFrontiers in pharmacology · 2021Article
- Obligatory role for PKCδ in PIPThe Journal of physiology · 2020Article
- PIPProceedings of the National Academy of Sciences of the United States of America · 2020Review
- Insights into Activation Mechanisms of Store-Operated TRPC1 Channels in Vascular Smooth Muscle.Cells · 2020Review
- Review
- Phosphoinositide Signaling and Mechanotransduction in Cardiovascular Biology and Disease.Frontiers in cell and developmental biology · 2020Review
- Contrasting effects of phosphatidylinositol 4,5-bisphosphate on cloned TMEM16A and TMEM16B channels.British journal of pharmacology · 2017Article
- Evidence that Orai1 does not contribute to store-operated TRPC1 channels in vascular smooth muscle cells.Channels (Austin, Tex.) · 2017Article
- Store-operated interactions between plasmalemmal STIM1 and TRPC1 proteins stimulate PLCβ1 to induce TRPC1 channel activation in vascular smooth muscle cells.The Journal of physiology · 2017Article
- Store depletion induces Gαq-mediated PLCβ1 activity to stimulate TRPC1 channels in vascular smooth muscle cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Transient receptor potential channels in the vasculature.Physiological reviews · 2015Review
- Inhibitory role of phosphatidylinositol 4,5-bisphosphate on TMEM16A-encoded calcium-activated chloride channels in rat pulmonary artery.British journal of pharmacology · 2014Article
- Phosphoinositide regulation of TRP channels.Handbook of experimental pharmacology · 2014Review
- Myristoylated alanine-rich C kinase substrate coordinates native TRPC1 channel activation by phosphatidylinositol 4,5-bisphosphate and protein kinase C in vascular smooth muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Phosphoinositides: tiny lipids with giant impact on cell regulation.Physiological reviews · 2013Review
- Pharmacological profile of phosphatidylinositol 3-kinases and related phosphatidylinositols mediating endothelin(A) receptor-operated native TRPC channels in rabbit coronary artery myocytes.British journal of pharmacology · 2012Article
- Role of protein kinase C in the activation of store-operated Ca(2+) entry in airway smooth muscle cells.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2012Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In the present study the effect of phosphatidylinositol 4,5-bisphosphate (PIP(2)) was studied on a native TRPC1 store-operated channel (SOC) in freshly dispersed rabbit portal vein myocytes. Application of diC8-PIP(2), a water soluble form of PIP(2), to quiescent inside-out patches evoked single channel currents with a unitary conductance of 1.9 pS. DiC8-PIP(2)-evoked channel currents were inhibited by anti-TRPC1 antibodies and these characteristics are identical to SOCs evoked by cyclopiazonic acid (CPA) and BAPTA-AM. SOCs stimulated by CPA, BAPTA-AM and the phorbol ester phorbol 12,13-dibutyrate (PDBu) were reduced by anti-PIP(2) antibodies and by depletion of tissue PIP(2) levels by pre-treatment of preparations with wortmannin and LY294002. However, these reagents did not alter the ability of PIP(2) to activate SOCs in inside-out patches. Co-immunoprecipitation techniques demonstrated association between TRPC1 and PIP(2) at rest, which was greatly decreased by wortmannin and LY294002. Pre-treatment of cells with PDBu, which activates protein kinase C (PKC), augmented SOC activation by PIP(2) whereas the PKC inhibitor chelerythrine decreased SOC stimulation by PIP(2). Co-immunoprecipitation experiments provide evidence that PKC-dependent phosphorylation of TRPC1 occurs constitutively and was increased by CPA and PDBu but decreased by chelerythrine. These novel results show that PIP(2) can activate TRPC1 SOCs in native vascular myocytes and plays an important role in SOC activation by CPA, BAPTA-AM and PDBu. Moreover, the permissive role of PIP(2) in SOC activation requires PKC-dependent phosphorylation of TRPC1.
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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.