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Last update 08 May 2025

RYR3

Last update 08 May 2025

Basic Info

Synonyms

Brain ryanodine receptor-calcium release channel, Brain-type ryanodine receptor, HBRR

+ [4]

Introduction

Cytosolic calcium-activated calcium channel that mediates the release of Ca(2+) from the sarcoplasmic reticulum into the cytoplasm in muscle and thereby plays a role in triggering muscle contraction (PubMed:12354756, PubMed:9395096). May regulate Ca(2+) release by other calcium channels. Calcium channel that mediates Ca(2+)-induced Ca(2+) release from the endoplasmic reticulum in non-muscle cells. Contributes to cellular calcium ion homeostasis (By similarity). Plays a role in cellular calcium signaling.

Drugs associated with RYR3

M-201

Target

RYR1 x RYR2 x RYR3

Mechanism

RYR1 modulators [+2]

Active Org.

AETAS Pharma Co., Ltd.

Originator Org.

AETAS Pharma Co., Ltd.

Active Indication

Heart Failure

Inactive Indication

Atrial Fibrillation

Drug Highest PhasePhase 2

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Alzheimer's disease (Miramoon Pharma)

Target

RYR1 x RYR2 x RYR3

Mechanism

RYR1 modulators [+2]

Active Org.

Miramoon Pharma SL

Originator Org.

Miramoon Pharma SL

Active Indication

Alzheimer Disease

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with RYR3

NCT04464681

/ CompletedPhase 1IIT

A Randomized, Double-Blind, Placebo-Controlled, Multiple Continuous Intravenous Injection, Dose Escalation, Phase I Study to Evaluate the Safety, Tolerability and Pharmacokinetics of M201-A in Healthy Japanese Subjects

This Phase I is designed to evaluate the safety, tolerability and pharmacokinetics of multiple ascending doses of M201-A administered by multiple continuous intravenous injection in Healthy Japanese subjects.

Start Date30 Mar 2020

Sponsor / Collaborator

Kitasato University

[+1]

NCT04609059

/ Unknown statusPhase 2IIT

First-in-Patient Study for Sing le Dose of M201-A Hydrochloride Injection in Japanese Patients With Paroxysmal Atrial Fibrillation

First-in-Patient Study for sing le dose of M201-A hydrochloride injection in Japanese patients with paroxysmal atrial fibrillation.

Start Date07 May 2019

Sponsor / Collaborator

Kitasato University

[+1]

NCT03055403

/ CompletedPhase 1IIT

A Randomized, Double-Blind, Placebo-Controlled, Single Continuous Intravenous Injection, Dose Escalation, Phase I Study to Evaluate the Safety, Tolerability and Pharmacokinetics of M201-A in Healthy Japanese Subjects

This Phase I first-in-human is designed to evaluate the safety, tolerability and pharmacokinetics of single ascending doses of M201-A administered by single continuous intravenous injection in Healthy Japanese subjects.

Start Date17 Feb 2017

Sponsor / Collaborator

Kitasato University

[+1]

100 Clinical Results associated with RYR3

100 Translational Medicine associated with RYR3

0 Patents (Medical) associated with RYR3

471

Literatures (Medical) associated with RYR3

01 Apr 2025·Stroke

Spatial Transcriptomics and Proteomics Profiling After Ischemic Stroke Reperfusion: Insights Into Vascular Alterations

Article

Author: Postnov, Dmitry D. ; Staehr, Christian ; Hansen, Line Mathilde Brostrup ; Pedersen, Tina Myhre ; Dam, Vibeke Secher ; Lin, Lin ; Kalucka, Joanna Maria ; Matchkov, Vladimir V. ; Guldbrandsen, Halvor Østerby ; Beck, Hans Christian

BACKGROUND:More than half of patients with ischemic stroke experience futile reperfusion, increasing the risk of death and disabilities despite a successful recanalization. The reason behind this is debated, and we aim to investigate cerebrovascular changes toward a broader understanding of these conditions. We hypothesize that ischemic stroke reperfusion modifies the expression profile in the microvasculature in a spatial manner toward peri-infarct brain edema and circulatory failure.METHODS:We investigated the early (24-hour) changes in spatial gene expression in the brain parenchymal endothelial cells and mural cells following ischemia stroke reperfusion in 13- to 14-week-old C57BL/6JRj male mice (n=5). Ischemia was induced by occlusion of the middle cerebral artery for 60 minutes, and Nissl staining was used to validate infarct size. Spatial transcriptomics complemented by bulk proteomics was conducted in the peri-infarct cortex region and validated with immunohistochemical semiquantification of proteins of interest. To avoid individual biological variations, changes in the peri-infarct cortex region were expressed relatively to the matching contralateral hemisphere region.RESULTS: Ischemic stroke reperfusion impaired the blood-brain barrier integrity through junctional Cldn5 (claudin-5) downregulation, changes of the actin cytoskeleton adhesion, and high expression of the proinflammatory Il-6 (interleukin-6). Molecules important for extracellular Ca 2+ influx and intracellular Ca 2+ release, Cacna1e (R-type Ca 2+channels ), Orai2 , Ryr3 , Itpr1 , and Itpka (inositol-trisphosphate 3-kinase A), were markedly reduced. Furthermore, reduced Grm5 (glutamate receptor 5) associated with upregulated Nfatc3 and Stat3 implicates suppression of the contractile phenotype, suggesting reduced poststroke vascular resistance due to loss of mural cell tone. The complete spatial transcriptomics map over the ipsilateral and contralateral hemispheres is available online as a Web tool. CONCLUSIONS:Emphasizing the spatial molecular pattern behind blood-brain barrier disruption and loss of the vascular tone in the acute phase following ischemic stroke reperfusion suggests the gene expression contribution for a therapeutic target in ischemia-reperfusion abnormalities.

01 Feb 2025·Neurological Sciences

Whole exome sequencing revealed ultra-rare genetic variations in juvenile myoclonic epilepsy

Article

Author: Al-Mistarehi, Abdel-Hameed ; Yacoub, Ansam M ; Almomani, Rowida F ; Aqaileh, Suha ; Mahasneh, Amjad A ; Yassin, Ahmed

OBJECTIVESJuvenile Myoclonic Epilepsy (JME) is the most common adolescent and adult-onset genetic generalized epilepsy. In this study, we aimed to identify all rare variants present in exons and exon-intron junctions in patients who met the criteria of JME, determine potentially pathogenic variants, and find the assumed genotype/phenotype correlation between the identified variants and the JME clinical features.METHODSWhole Exome Sequencing (WES) was performed for ten JME patients from different families. Validation, co-segregation and mode of inheritance were determined using Sanger DNA sequencing.RESULTSPredictable damaging variants were found in six families with positive co-segregation. Eight variants in eight genes (SCN1B, KCNQ2, CACNA1I, GABRA3, BSN, RYR3, SEZ6, and RYR2) and one novel variant in (TNR) gene were found to be associated with JME. All these genes play key roles in the interactions between neurons, neurotransmitter release, and maintenance of the balance between neuronal excitation and inhibition.SIGNIFICANCESince the identified genes are involved in the molecular mechanisms underlying seizures, such variants can potentially be epileptogenic. In conclusion, the identified variants that co-segregate with JME symptoms and likely contribute in creating the adequate genetic background for the JME phenotype.

01 Feb 2025·Biochemical and Biophysical Research Communications

Exercise-induced cytosolic calcium oscillations: mechanisms and modulation of T-cell function

Article

Author: Liu, Renyi ; Ye, Xing

This study investigated time-dependent changes in intracellular Ca²⁺ levels in T cells, regulatory mechanisms, and functional effects after acute exercise. Male C57BL/6 mice were assigned to control and exercise groups, with the latter sacrificed at different intervals post-exercise. Murine splenic lymphocytes were isolated, and cytosolic Ca²⁺ levels were measured using Fluo-3/AM. T-cell proliferation was assessed by flow cytometry and CFSE labeling, apoptosis by Annexin V/PI staining, and cytokine levels by CBA. RNA sequencing results were validated by qRT-PCR. The findings revealed that exercise significantly altered intracellular calcium oscillations in CD3⁺ cells, leading to reduced mitogen-stimulated proliferation, increased IL-6, IL-5, and IL-13 production, and decreased IL-2 secretion. Additionally, there was an increase in the apoptotic fraction of CD3⁺ cells, with upregulated expression of Cav1.1, Cav3.2, Cav3.3, SERCA2B, PKCθ, Bcl-xL, and FADD, and downregulated Ryr3 (p < 0.05). Transcriptomic analysis identified 607 differentially expressed genes involved in calcium ion binding and related pathways, including calcium signaling and cytokine-cytokine receptor interactions. Thus, acute exercise induces specific calcium oscillation patterns in T cells, mediated by PKCθ, affecting proliferation, apoptosis, and cytokine production. These changes are attributed to increased calcium influx through Cav1.1, Cav3.2, and Cav3.3 channels, decreased calcium reuptake via SERCA2B, and reduced calcium release through Ryr3. This research provides novel insights into how exercise modulates immune cell function by altering calcium levels, potential implications for enhancing immune responses or reducing inflammation.

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RYR3

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