ArticleThe Journal of physiology2004
A role for SNAP-25 but not VAMPs in store-mediated Ca2+ entry in human platelets.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 41 citations in OpenAlex.
- Syntaxin-1a and SNAP-25 expression level is increased in the blood samples of ischemic stroke patients.Scientific reports · 2022Article
- Influence of atherosclerosis on the molecular expression of the TRPC1/BK signal complex in the aortic smooth muscles of mice.Experimental and therapeutic medicine · 2022Article
- Advances in Intracellular Calcium Signaling Reveal Untapped Targets for Cancer Therapy.Biomedicines · 2021Review
- Identification of a Mutation in FGF23 Involved in Mandibular Prognathism.Scientific reports · 2015Article
- G protein-coupled receptor signalling potentiates the osmo-mechanical activation of TRPC5 channels.Pflugers Archiv : European journal of physiology · 2014Article
- Endothelial transient receptor potential conical channel (TRPC)-3 activation induces vasogenic edema formation in the rat piriform cortex following status epilepticus.Cellular and molecular neurobiology · 2013Article
- The reverse roles of transient receptor potential canonical channel-3 and -6 in neuronal death following pilocarpine-induced status epilepticus.Cellular and molecular neurobiology · 2013Article
- Bacterial toxins and the nervous system: neurotoxins and multipotential toxins interacting with neuronal cells.Toxins · 2010Review
- PAR-1-stimulated factor IXa binding to a small platelet subpopulation requires a pronounced and sustained increase of cytoplasmic calcium.Biochemistry · 2006Article
- Localization of TRPC1 channel in the sinus endothelial cells of rat spleen.Histochemistry and cell biology · 2005Article
- Structure-function analysis of TRPV channels.Naunyn-Schmiedeberg's archives of pharmacology · 2005Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Store-mediated Ca2+ entry (SMCE) is a major mechanism for Ca2+ influx in non-excitable cells. Recently, a conformational coupling mechanism allowing coupling between transient receptor potential channels (TRPCs) and IP3 receptors has been proposed to activate SMCE. Here we have investigated the role of two soluble N-ethylmaleimide-sensitive-factor attachment protein receptors (SNAREs), which are involved in membrane trafficking and docking, in SMCE in human platelets. We found that the synaptosome-associated protein (SNAP-25) and the vesicle-associated membrane proteins (VAMP) coimmunoprecipitate with hTRPC1 in platelets. Treatment with botulinum toxin (BoNT) E or with tetanus toxin (TeTx), induced cleavage and inactivation of SNAP-25 and VAMPs, respectively. BoNTs significantly reduced thapsigargin- (TG) and agonist-evoked SMCE. Treatment with BoNTs once SMCE had been activated decreased Ca2+ entry, indicating that SNAP-25 is required for the activation and maintenance of SMCE. In contrast, treatment with TeTx had no effect on either the activation or the maintenance of SMCE in platelets. Finally, treatment with BoNT E impaired the coupling between naturally expressed hTRPC1 and IP3 receptor type II in platelets. From these findings we suggest SNAP-25 has a role in SMCE in human platelets.
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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.