Last update 01 Nov 2024

RYR3

Last update 01 Nov 2024

Basic Info

Synonyms

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

+ [4]

Introduction

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. 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

524

Literatures (Medical) associated with RYR3

01 Sep 2024·American Journal of Physiology-Cell Physiology

Purinergic agonists increase [Ca²⁺]_i in rat conjunctival goblet cells through ryanodine receptor type 3

Article

Author: Yang, Menglu ; Utheim, Tor P. ; Lee, Changrim ; Bair, Jeffrey ; Dartt, Darlene ; Reiten, Ole K. ; Fjaervoll, Haakon K. ; Fjaervoll, Ketil A.

ATP and benzoylbenzoyl-ATP (BzATP) induce mucin secretion through an increase in free cytosolic calcium concentration ([Ca2+]i) in conjunctival goblet cells (CGCs). The mechanisms through which ATP and BzATP increase [Ca2+]i in CGCs are unclear. Ryanodine receptors (RyRs) are fundamental in [Ca2+]i regulation in excitable cells. Herein, we find that ATP and BzATP increase [Ca2+]i through the activation of protein kinase A, voltage-gated calcium channels, and RyRs, and that RyRs are crucial for nonexcitable CGCs’ Ca2+i homeostasis.

01 Aug 2024·British Journal of Pharmacology

Differential contributions of G protein‐ or arrestin subtype‐mediated signalling underlie urocortin 3‐induced somatostatin secretion in pancreatic δ cells

Article

Author: Xiao, Peng ; Ning, Shang-Lei ; Wang, Jin ; Lin, Jing-Yu ; Fang, Le ; Pan, Wei ; Cheng, Jie ; Yang, Fan ; Yu, Xiao ; Wang, Kai-Yu ; Qi, Hai-Bo ; Cheng, Qiu-Xia ; Gao, Ming-Xin ; Sun, Jin-Peng ; An, Wen-Tao

AbstractBackground and PurposePancreatic islets are modulated by cross‐talk among different cell types and paracrine signalling plays important roles in maintaining glucose homeostasis. Urocortin 3 (UCN3) secreted by pancreatic β cells activates the CRF2 receptor (CRF2R) and downstream pathways mediated by different G protein or arrestin subtypes in δ cells to cause somatostatin (SST) secretion, and constitutes an important feedback circuit for glucose homeostasis.Experimental ApproachHere, we used Arrb1−/−, Arrb2−/−, Gsfl/fl and Gqfl/fl knockout mice, the G11‐shRNA‐GFPfl/fl lentivirus, as well as functional assays and pharmacological characterization to study how the coupling of Gs, G11 and β‐arrestin1 to CRF2R contributed to UCN3‐induced SST secretion in pancreatic δ cells.Key ResultsOur study showed that CRF2R coupled to a panel of G protein and arrestin subtypes in response to UCN3 engagement. While RyR3 phosphorylation by PKA at the S156, S2706 and S4697 sites may underlie the Gs‐mediated UCN3‐ CRF2R axis for SST secretion, the interaction of SYT1 with β‐arrestin1 is also essential for efficient SST secretion downstream of CRF2R. The specific expression of the transcription factor Stat6 may contribute to G11 expression in pancreatic δ cells. Furthermore, we found that different UCN3 concentrations may have distinct effects on glucose homeostasis, and these effects may depend on different CRF2R downstream effectors.Conclusions and ImplicationsCollectively, our results provide a landscape view of signalling mediated by different G protein or arrestin subtypes downstream of paracrine UCN3‐ CRF2R signalling in pancreatic β‐δ‐cell circuits, which may facilitate the understanding of fine‐tuned glucose homeostasis networks.

01 Jun 2024·The Pharmacogenomics Journal

Polygenic scores for cardiovascular risk factors improve estimation of clinical outcomes in CCB treatment compared to pharmacogenetic variants alone

Article

Author: Pilling, Luke C ; Bowden, Jack ; Masoli, Jane A H ; Melzer, David ; Türkmen, Deniz ; Kuo, Chia-Ling ; Delgado, João

AbstractPharmacogenetic variants are associated with clinical outcomes during Calcium Channel Blocker (CCB) treatment, yet whether the effects are modified by genetically predicted clinical risk factors is unknown. We analyzed 32,000 UK Biobank participants treated with dihydropiridine CCBs (mean 5.9 years), including 23 pharmacogenetic variants, and calculated polygenic scores for systolic and diastolic blood pressures, body fat mass, and other patient characteristics. Outcomes included treatment discontinuation and heart failure. Pharmacogenetic variant rs10898815-A (NUMA1) increased discontinuation rates, highest in those with high polygenic scores for fat mass. The RYR3 variant rs877087 T-allele alone modestly increased heart failure risks versus non-carriers (HR:1.13, p = 0.02); in patients with high polygenic scores for fat mass, lean mass, and lipoprotein A, risks were substantially elevated (HR:1.55, p = 4 × 10−5). Incorporating polygenic scores for adiposity and lipoprotein A may improve risk estimates of key clinical outcomes in CCB treatment such as treatment discontinuation and heart failure, compared to pharmacogenetic variants alone.

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RYR3

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