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http://purl.uniprot.org/citations/29537866http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29537866http://www.w3.org/2000/01/rdf-schema#comment"Physiological functions of type 3 ryanodine receptors (RyR3) in smooth muscle (SM) tissues are not well understood, in spite of their wide expression. However, the short isoform of RyR3 is known to be a dominant-negative variant (DN-RyR3), which may negatively regulate functions of both RyR2 and full-length (FL) RyR3 by forming hetero-tetramers. Here, functional roles of RyR3 in the regulation of Ca2+ signaling in mesenteric artery SM cells (MASMCs) were examined using RyR3 homozygous knockout mice (RyR3-/-). Quantitative PCR analyses suggested that the predominant RyR3 subtype in MASMs from wild-type mice (RyR3+/+) was DN-RyR3. In single MASMCs freshly isolated from RyR3-/-, the EC50 of caffeine to induce Ca2+ release was lower than that in RyR3+/+ myocytes. The amplitude and frequency of Ca2+ sparks and spontaneous transient outward currents in MASMCs from RyR3-/- were all larger than those from RyR3+/+. Importantly, mRNA and functional expressions of voltage-dependent Ca2+ channel and large-conductance Ca2+-activated K+ (BK) channel in MASMCs from RyR3-/- were identical to those from RyR3+/+. However, in the presence of BK channel inhibitor, paxilline, the pressure rises induced by BayK8644 in MA vascular beds of RyR3-/- were significantly larger than in those of RyR3+/+. This indicates that the negative feedback effects of BK channel activity on intracellular Ca2+ signaling was enhanced in RyR3-/-. Thus, RyR3, and, in fact, mainly DN-RyR3, via a complex with RyR2 suppresses Ca2+ release and indirectly regulated membrane potential by reducing BK channel activity in MASMCs and presumably can affect the regulation of intrinsic vascular tone."xsd:string
http://purl.uniprot.org/citations/29537866http://purl.org/dc/terms/identifier"doi:10.1152/ajpcell.00006.2018"xsd:string
http://purl.uniprot.org/citations/29537866http://purl.uniprot.org/core/author"Suzuki Y."xsd:string
http://purl.uniprot.org/citations/29537866http://purl.uniprot.org/core/author"Takemoto M."xsd:string
http://purl.uniprot.org/citations/29537866http://purl.uniprot.org/core/author"Yamamura H."xsd:string
http://purl.uniprot.org/citations/29537866http://purl.uniprot.org/core/author"Takeshima H."xsd:string
http://purl.uniprot.org/citations/29537866http://purl.uniprot.org/core/author"Imaizumi Y."xsd:string
http://purl.uniprot.org/citations/29537866http://purl.uniprot.org/core/author"Ohya S."xsd:string
http://purl.uniprot.org/citations/29537866http://purl.uniprot.org/core/author"Kato D."xsd:string
http://purl.uniprot.org/citations/29537866http://purl.uniprot.org/core/author"Matsuki K."xsd:string
http://purl.uniprot.org/citations/29537866http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/29537866http://purl.uniprot.org/core/name"Am J Physiol Cell Physiol"xsd:string
http://purl.uniprot.org/citations/29537866http://purl.uniprot.org/core/pages"C1-C9"xsd:string
http://purl.uniprot.org/citations/29537866http://purl.uniprot.org/core/title"Negative regulation of cellular Ca2+ mobilization by ryanodine receptor type 3 in mouse mesenteric artery smooth muscle."xsd:string
http://purl.uniprot.org/citations/29537866http://purl.uniprot.org/core/volume"315"xsd:string
http://purl.uniprot.org/citations/29537866http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/29537866
http://purl.uniprot.org/citations/29537866http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/29537866
http://purl.uniprot.org/uniprot/#_A0A140LI87-mappedCitation-29537866http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29537866
http://purl.uniprot.org/uniprot/#_A0A140LJF7-mappedCitation-29537866http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29537866
http://purl.uniprot.org/uniprot/#_A0A140LJK7-mappedCitation-29537866http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29537866
http://purl.uniprot.org/uniprot/#_A2AGL3-mappedCitation-29537866http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29537866
http://purl.uniprot.org/uniprot/#_B7ZMP2-mappedCitation-29537866http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29537866
http://purl.uniprot.org/uniprot/#_E9PW34-mappedCitation-29537866http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29537866
http://purl.uniprot.org/uniprot/#_Q14AQ9-mappedCitation-29537866http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29537866