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Grant: Project Grant

University of British Columbia

$993,851.00

Cardiac Excitation-Contraction Coupling: The Dynamic Dyad

FY 2015-16

Summary
My lab has discovered that a protein that regulates the strength of cardiac contraction, the ryanodine receptor (RyR2), can be quickly re-positioned by physiological and pathological factors. The redistribution seems to be a fundamental mechanism by which the protein's function is changed; the goal of this project is to prove that. This unexpected discovery was made possible by years of basic research, by the acquisition of new hardware and by the development of new imaging visualization and analysis algorithms in my lab. The discovery is important because dysfunctional RyR2 cause arrhythmia and death in many acquired (e.g. heart failure) and genetic (catecholaminergic polymorphic ventricular tachycardia) heart diseases. Some existing therapies are being re-purposed in an attempt to control these 'leaky' RyR2, while there are efforts to develop new therapies. Discovering a new, fundamental, mechanism that regulates RyR2 and cardiac contractility will open new avenues for translational research.
Program
Project Grant
Location
British Columbia, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database

As published

Id
343887
Name
Moore Edwin D
Region
British Columbia
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Circulatory and Respiratory Health
Theme2
Biomedical
Prcname2
Project Grant Competition
Projecttitle
Cardiac Excitation-Contraction Coupling: The Dynamic Dyad
Programtype2
Operating Grants
Orgnameinp2
University of British Columbia
Cihramount2
$993,851
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Cardiomyocytes; Cellular Imaging; Electron Microscopy; Electron Tomography; Excitation-Contraction Coupling; Heart Muscle; Immunofluorescence; Structure; Suiperresolution Immunofluorescence Microscopy; Type 2 Ryanodine Receptors
Abstract
My lab has discovered that a protein that regulates the strength of cardiac contraction, the ryanodine receptor (RyR2), can be quickly re-positioned by physiological and pathological factors. The redistribution seems to be a fundamental mechanism by which the protein's function is changed; the goal of this project is to prove that. This unexpected discovery was made possible by years of basic research, by the acquisition of new hardware and by the development of new imaging visualization and analysis algorithms in my lab. The discovery is important because dysfunctional RyR2 cause arrhythmia and death in many acquired (e.g. heart failure) and genetic (catecholaminergic polymorphic ventricular tachycardia) heart diseases. Some existing therapies are being re-purposed in an attempt to control these 'leaky' RyR2, while there are efforts to develop new therapies. Discovering a new, fundamental, mechanism that regulates RyR2 and cardiac contractility will open new avenues for translational research.
Competitiondate
201603
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Moore, Edwin D
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $993,851~ $0~