Ryanodine receptor mutations in arrhythmia: The continuing mystery of channel dysfunction

Mutations in RyR2 are causative of an inherited disorder which often results in sudden cardiac death. Dysfunctional channel behaviour has been the subject of many investigations varying from single channel analysis through to complex animal models. This review discusses recent advances in the field,...

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Published inFEBS letters Vol. 584; no. 10; pp. 2153 - 2160
Main Authors Thomas, N. Lowri, Maxwell, Chloé, Mukherjee, Saptarshi, Williams, Alan J.
Format Journal Article
LanguageEnglish
Published England Elsevier B.V 17.05.2010
Subjects
12.6 kDa FK506 binding protein
Animals
Arrhythmia
Arrhythmias, Cardiac - drug therapy
Arrhythmias, Cardiac - genetics
Arrhythmias, Cardiac - metabolism
atrial fibrillation
Ca 2+ release channel
Ca2+ release channel
Ca2+-calmodulin dependent protein kinase
calsequestrin
CaMKII
cAMP
Catecholaminergic polymorphic ventricular tachycardia
CCD
central core disease
CPVT
CSQ
cyclic adenosine monophosphate
DAD
delayed-after depolarisation
Epac
exchange protein activated by cAMP
excitation–contraction
FKBP12.6
H-89
heart failure
HEK 293
human embryonic kidney 293
Humans
I-1
ICD
implantable cardioverter defibrillator
malignant hyperthermia
Mutation
N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide dihydrochloride
open probability
P o
phosphatase inhibitor 1
Phosphorylation
PKA
Polymorphism, Genetic
PP1
protein kinase A
protein phosphatase 1
reactive oxygen species
ROS
Ryanodine receptor
Ryanodine Receptor Calcium Release Channel - chemistry
Ryanodine Receptor Calcium Release Channel - genetics
Ryanodine Receptor Calcium Release Channel - metabolism
RyR
sarcoplasmic reticulum
SCD
sudden cardiac death
Tachycardia, Ventricular - drug therapy
ventricular tachycardia
wild type
β-adrenergic receptor
β-AR
β-AR
Arrhythmia
H-89
Ryanodine receptor
RyR
cAMP
Epac
MH
WT
EC
P o
FKBP12.6
SR
CSQ
AF
CCD
DAD
PKA
ICD
I-1
PP1
CaMKII
CPVT
HEK 293
SCD
ROS
Ca 2+ release channel
Catecholaminergic polymorphic ventricular tachycardia
Mutation
HF
VT
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Abstract Mutations in RyR2 are causative of an inherited disorder which often results in sudden cardiac death. Dysfunctional channel behaviour has been the subject of many investigations varying from single channel analysis through to complex animal models. This review discusses recent advances in the field, describes the controversy surrounding the exact consequences of RyR2 mutation and how the disparate data may be reconciled. This heterogeneity of function with respect to the effects of polymorphisms, phosphorylation, cytosolic and luminal Ca 2+ as well as inter-domain interactions may have important implications for the recent pharmaceutical therapies which have been put forward. We surmise that a comprehensive characterisation of mutations on a case-by-case basis may be beneficial for the development of specifically targeted therapies.
AbstractList Mutations in RyR2 are causative of an inherited disorder which often results in sudden cardiac death. Dysfunctional channel behaviour has been the subject of many investigations varying from single channel analysis through to complex animal models. This review discusses recent advances in the field, describes the controversy surrounding the exact consequences of RyR2 mutation and how the disparate data may be reconciled. This heterogeneity of function with respect to the effects of polymorphisms, phosphorylation, cytosolic and luminal Ca(2+) as well as inter-domain interactions may have important implications for the recent pharmaceutical therapies which have been put forward. We surmise that a comprehensive characterisation of mutations on a case-by-case basis may be beneficial for the development of specifically targeted therapies.
Mutations in RyR2 are causative of an inherited disorder which often results in sudden cardiac death. Dysfunctional channel behaviour has been the subject of many investigations varying from single channel analysis through to complex animal models. This review discusses recent advances in the field, describes the controversy surrounding the exact consequences of RyR2 mutation and how the disparate data may be reconciled. This heterogeneity of function with respect to the effects of polymorphisms, phosphorylation, cytosolic and luminal Ca2+ as well as inter‐domain interactions may have important implications for the recent pharmaceutical therapies which have been put forward. We surmise that a comprehensive characterisation of mutations on a case‐by‐case basis may be beneficial for the development of specifically targeted therapies.
Mutations in RyR2 are causative of an inherited disorder which often results in sudden cardiac death. Dysfunctional channel behaviour has been the subject of many investigations varying from single channel analysis through to complex animal models. This review discusses recent advances in the field, describes the controversy surrounding the exact consequences of RyR2 mutation and how the disparate data may be reconciled. This heterogeneity of function with respect to the effects of polymorphisms, phosphorylation, cytosolic and luminal Ca(2+) as well as inter-domain interactions may have important implications for the recent pharmaceutical therapies which have been put forward. We surmise that a comprehensive characterisation of mutations on a case-by-case basis may be beneficial for the development of specifically targeted therapies.Mutations in RyR2 are causative of an inherited disorder which often results in sudden cardiac death. Dysfunctional channel behaviour has been the subject of many investigations varying from single channel analysis through to complex animal models. This review discusses recent advances in the field, describes the controversy surrounding the exact consequences of RyR2 mutation and how the disparate data may be reconciled. This heterogeneity of function with respect to the effects of polymorphisms, phosphorylation, cytosolic and luminal Ca(2+) as well as inter-domain interactions may have important implications for the recent pharmaceutical therapies which have been put forward. We surmise that a comprehensive characterisation of mutations on a case-by-case basis may be beneficial for the development of specifically targeted therapies.
Mutations in RyR2 are causative of an inherited disorder which often results in sudden cardiac death. Dysfunctional channel behaviour has been the subject of many investigations varying from single channel analysis through to complex animal models. This review discusses recent advances in the field, describes the controversy surrounding the exact consequences of RyR2 mutation and how the disparate data may be reconciled. This heterogeneity of function with respect to the effects of polymorphisms, phosphorylation, cytosolic and luminal Ca 2+ as well as inter‐domain interactions may have important implications for the recent pharmaceutical therapies which have been put forward. We surmise that a comprehensive characterisation of mutations on a case‐by‐case basis may be beneficial for the development of specifically targeted therapies.
Mutations in RyR2 are causative of an inherited disorder which often results in sudden cardiac death. Dysfunctional channel behaviour has been the subject of many investigations varying from single channel analysis through to complex animal models. This review discusses recent advances in the field, describes the controversy surrounding the exact consequences of RyR2 mutation and how the disparate data may be reconciled. This heterogeneity of function with respect to the effects of polymorphisms, phosphorylation, cytosolic and luminal Ca 2+ as well as inter-domain interactions may have important implications for the recent pharmaceutical therapies which have been put forward. We surmise that a comprehensive characterisation of mutations on a case-by-case basis may be beneficial for the development of specifically targeted therapies.
Author Mukherjee, Saptarshi
Thomas, N. Lowri
Williams, Alan J.
Maxwell, Chloé
Author_xml – sequence: 1
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  surname: Thomas
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  givenname: Alan J.
  surname: Williams
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  email: williamsaj9@cardiff.ac.uk
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FEBS Letters 584 (2010) 1873-3468 © 2015 Federation of European Biochemical Societies
Copyright 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Copyright 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Copyright_xml – notice: 2010 Federation of European Biochemical Societies
– notice: FEBS Letters 584 (2010) 1873-3468 © 2015 Federation of European Biochemical Societies
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– notice: Copyright 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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Issue 10
Keywords β-AR
Arrhythmia
H-89
Ryanodine receptor
RyR
cAMP
Epac
MH
WT
EC
P o
FKBP12.6
SR
CSQ
AF
CCD
DAD
PKA
ICD
I-1
PP1
CaMKII
CPVT
HEK 293
SCD
ROS
Ca 2+ release channel
Catecholaminergic polymorphic ventricular tachycardia
Mutation
HF
VT
Language English
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Snippet Mutations in RyR2 are causative of an inherited disorder which often results in sudden cardiac death. Dysfunctional channel behaviour has been the subject of...
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SubjectTerms 12.6 kDa FK506 binding protein
Animals
Arrhythmia
Arrhythmias, Cardiac - drug therapy
Arrhythmias, Cardiac - genetics
Arrhythmias, Cardiac - metabolism
atrial fibrillation
Ca 2+ release channel
Ca2+ release channel
Ca2+-calmodulin dependent protein kinase
calsequestrin
CaMKII
cAMP
Catecholaminergic polymorphic ventricular tachycardia
CCD
central core disease
CPVT
CSQ
cyclic adenosine monophosphate
DAD
delayed-after depolarisation
Epac
exchange protein activated by cAMP
excitation–contraction
FKBP12.6
H-89
heart failure
HEK 293
human embryonic kidney 293
Humans
I-1
ICD
implantable cardioverter defibrillator
malignant hyperthermia
Mutation
N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide dihydrochloride
open probability
P o
phosphatase inhibitor 1
Phosphorylation
PKA
Polymorphism, Genetic
PP1
protein kinase A
protein phosphatase 1
reactive oxygen species
ROS
Ryanodine receptor
Ryanodine Receptor Calcium Release Channel - chemistry
Ryanodine Receptor Calcium Release Channel - genetics
Ryanodine Receptor Calcium Release Channel - metabolism
RyR
sarcoplasmic reticulum
SCD
sudden cardiac death
Tachycardia, Ventricular - drug therapy
ventricular tachycardia
wild type
β-adrenergic receptor
β-AR
Title Ryanodine receptor mutations in arrhythmia: The continuing mystery of channel dysfunction
URI https://dx.doi.org/10.1016/j.febslet.2010.01.057
https://onlinelibrary.wiley.com/doi/abs/10.1016%2Fj.febslet.2010.01.057
https://www.ncbi.nlm.nih.gov/pubmed/20132818
https://www.proquest.com/docview/733088371
https://www.proquest.com/docview/762267480
Volume 584
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