Rabbit Ryanodine receptor 1,RyR1 ELISA kit
- Known as:
- Rabbit Ryanodine receptor 1,RyR1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- E0068Rb
- Product Quantity:
- 48T
- Category:
- Elisa Kits
- Supplier:
- Btlab
- Gene target:
- Rabbit Ryanodine receptor 1 RyR1 ELISA kit
Related genes to: Rabbit Ryanodine receptor 1,RyR1 ELISA kit
- Gene:
- RYR1 NIH gene
- Name:
- ryanodine receptor 1
- Previous symbol:
- MHS, MHS1, CCO
- Synonyms:
- RYR, PPP1R137
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-12-01
- Date modifiied:
- 2019-04-23
Related products to: Rabbit Ryanodine receptor 1,RyR1 ELISA kit
Related articles to: Rabbit Ryanodine receptor 1,RyR1 ELISA kit
- Although acetylcholine (ACh) released by the vagus nerve can stimulate enterochromaffin cells (ECs) to secrete 5-hydroxytryptamine (5-HT), the precise regulatory mechanism underlying this process and its association with the pathogenesis of ulcerative colitis (UC) remain unclear. In this study, we aimed to investigate whether TRPV4-mediated calcium influx in ECs is involved the process of ACh promoting 5-HT secretion which leads to UC. In vitro experiments, western blotting, cellular calcium imaging, and patch clamp were applied to ECs, and dextran sulfate sodium (DSS)-induced UC of mouse model was used in vivo. Carbachol (CCh), a stable analog of ACh, activated mAChR/IP3/IP3R pathway to increase intracellular [Ca2+]ilevels in ECs, in which both TRPV4 channels and RyR were activated in response to CCh. The selective TRPV4 antagonist HC067047 inhibited the calcium signals and membrane currents induced by IP3/IP3R, as well as 5-HT secretion. In addition, selective blocker of RyR (Dantrolene) also significantly inhibited CCh-induced calcium signals and membrane currents. In vivo experiments, HC067047 significantly suppressed the synthesis and release of 5-HT from ECs and alleviated DSS-induced UC in mice. Taken together, this study reveals a novel mAChR/IP3/IP3R /TRPV4/5-HT pathway in ECs is likely involved in the pathogenesis of UC. Targeting this pathway holds a promise for the potential prevention and treatment of UC. - Source: PubMed
Publication date: 2026/08/13
Tong ShuoWang YujuanWang JianxinQu ChengxinPang ShudeZhao WenwenDong Hui - Natural products are important sources of bioactive fragments. Based on the scaffold-hopping strategy, 40 novel N-arylindole diamide derivatives with excellent insecticidal activity were synthesized by substituting the pyrazole moiety of chlorantraniliprole (CHL) with a natural indole substructure. Bioassay results demonstrated that compound I ai exhibited a slightly higher LC50 value (LC50 = 0.26 mg·L-1) compared to CHL (LC50 = 0.11 mg·L-1) against Mythimna separata. For Plutella xylostella, compounds I an (LC50 = 1.74 × 10-2 mg·L-1) and I ah (LC50 = 2.19 × 10-2 mg·L-1) showed the same level of biological activity as CHL (LC50 = 8.6 × 10-3 mg·L-1). Mechanism validation experiment revealed that compound I ai could activate the insect ryanodine receptor to induce calcium ion release. Molecular docking, density functional theory calculations, and toxicity assays against Danio rerio validated its biosafety profile. These results will provide important guidance for the discovery of indole-containing diamide insecticides. - Source: PubMed
Duan JiayingLi FengyuLu ChangxuLiu HongzhouXu YongzeDing YunqiXiong LixiaYang NaRen JinzhouFan Zhijin - Ryanodine receptor 1 (RyR1) is a key intracellular Ca release channel primarily expressed in skeletal muscle, but also in some immune cells. Gain-of-function RYR1 mutations are the most common cause of the pharmacogenetic disorder malignant hyperthermia susceptibility. Compatibly, mice knocked in for gain of function mutations develop malignant hyperthermia but also show subtle changes in their immune function, supporting a potential but yet to be explored effect of RyR1 mutations on the human immune system. Healthy controls and subjects classified as Malignant Hyperthermia Susceptible were enrolled in an anonymized allergy questionnaire study. PBMC and Epstein Barr virus immortalized B cells from the two cohorts were characterized for surface markers by flow cytometry and for calcium homeostasis using the intracellular calcium indicator Fluo-4. Serum samples were investigated for circulating cytokines by ELISA and Ig quantification was carried out by a clinical laboratory. Malignant hyperthermia susceptible individuals report a higher frequency of allergies, show changes in circulating immunoglobulin and cytokine levels and their circulating B cells exhibit a pre-activated state, with increased surface expression of the co-stimulatory molecules CD86 and CD40. Stimulation of EBV-immortalized B lymphocytes with the RyR1 agonist caffeine results in a tetracaine-sensitive increased surface expression of CD86, which was more pronounced in cells from malignant hyperthermia susceptible individuals. Our results support a functional role of RyR1 in B-lymphocyte Ca signaling and show that in humans the presence of gain of function mutations leads to the pre-activation of B cells. - Source: PubMed
Publication date: 2026/07/27
Li HuiyingAndrade Pamela VCeren Irem HuriyeRuiz AlexisSilva Aline IFarias Murilo FZorzeto Thalles SVainzof MarizZorzato FrancescoSilva Helga C ATreves Susan - Type 2 ryanodine receptor (RyR2), a Ca release channel located in the endoplasmic reticulum (ER) membrane, expresses catecholamine-induced polymorphic ventricular tachycardia (CPVT), and is a potential risk factor of autism spectrum disorder (ASD). However, the pathological relationship between RyR2 mutation-induced Ca dysregulation and ASD pathology remains unclear. This study examined the association between CPVT-related RyR2 mutations and ASD pathology to determine its dopaminergic pathological role in ASD. Patient-derived stem cells from human exfoliated deciduous teeth were obtained from a boy with comorbid CPVT and ASD, and differentiated to dopaminergic neurons (RyR2-DNs). Two heterozygous missense mutations were identified in RyR2: c.9910C > G, p.Q3304E in exon 69 and c.14222C > T, p.A4741V in exon 99 (RyR2). RyR2-DNs showed cytosolic and mitochondrial Ca accumulation, and impaired neurite outgrowth, suggesting that RyR2 is a gain-of-function mutation that promotes Ca release from the ER and attenuates neurite development. RyR2-DNs also exhibited increased mitochondrial reactive oxygen species along with impaired mitochondrial oxidative phosphorylation. These mitochondrial abnormalities and neurite outgrowth were managed by pharmacological intervention of mitochondrial Ca accumulation. Thus, RyR2 hyper-activation-induced mitochondrial Ca overload may cause oxidative stress-related mitochondrial dysfunction, impairing DN development and dopaminergic dysregulation in ASD. - Source: PubMed
Publication date: 2026/08/08
Ito YosukeDong ShuangshanKato HirokiZhou ZhiyanWang LuHirofuji YutaSato HiroshiChong Pin FeeHirata YuichiroYamamura KenichiroKato Takahiro ASakai YasunariFukumoto SatoshiMasuda Keiji - Skeletal muscle excitation-contraction coupling (ECC) is a highly specialized process that converts membrane depolarization into contraction through tightly regulated intracellular Ca²⁺ dynamics. Recent advances in molecular genetics have expanded the spectrum of skeletal muscle disorders associated with ECC-related proteins, including congenital myopathies, malignant hyperthermia susceptibility, exertional rhabdomyolysis, exertional heat illness, and related episodic disorders. Although these disorders have traditionally been classified according to clinical manifestations, pathological findings, and causative genes, accumulating evidence suggests that genetically and clinically heterogeneous disorders converge on overlapping abnormalities in intracellular Ca²⁺ handling and ECC function. This review provides an integrative overview of ECC-related skeletal muscle disorders from the perspective of shared abnormalities in intracellular Ca²⁺ handling and the molecular mechanisms that underlie them. We discuss how pathogenic variants affecting the voltage-sensing skeletal muscle L-type calcium channel (CaV1.1), the ryanodine receptor type 1 (RyR1), and other triad-associated proteins disrupt Ca²⁺ release from the sarcoplasmic reticulum (SR), luminal Ca²⁺ regulation, and SR Ca²⁺ reuptake, leading to diverse but partially convergent phenotypes. We also discuss secondary pathological changes associated with chronic intracellular Ca²⁺ dysregulation, including mitochondrial dysfunction, oxidative stress, and skeletal muscle remodeling. Finally, we present a functional perspective centered on intracellular Ca²⁺ handling that complements conventional genetic and clinicopathological classifications of ECC-related skeletal muscle disorders. - Source: PubMed
Publication date: 2026/08/10
Endo Yukari