Trafficking defects and gating abnormalities of a novel SCN5A mutation question gene-specific therapy in long QT syndrome type 3.
about
Multiple arrhythmic syndromes in a newborn, owing to a novel mutation in SCN5ATherapeutic Approaches to Genetic Ion Channelopathies and Perspectives in Drug DiscoveryCardiac sodium channel Nav1.5 mutations and cardiac arrhythmiaRecent advances in genetic testing and counseling for inherited arrhythmiasThe role of the SCN5A-encoded channelopathy in irritable bowel syndrome and other gastrointestinal disordersRecent developments in the management of patients at risk for sudden cardiac death.Genetic testing of inherited arrhythmias.Inherited long QT syndrome: clinical manifestation, genetic diagnostics, and therapy.The role of ion channelopathies in sudden cardiac death: implications for clinical practice.Pharmacology and Toxicology of Nav1.5-Class 1 anti-arrhythmic drugs.Difference of sodium currents between pediatric and adult human atrial myocytes: evidence for developmental changes of sodium channels.Functional characterization of a novel frameshift mutation in the C-terminus of the Nav1.5 channel underlying a Brugada syndrome with variable expression in a Spanish family.Cardiac Safety Implications of hNav1.5 Blockade and a Framework for Pre-Clinical Evaluation.Genetics of sudden death: focus on inherited channelopathies.An introduction to murine models of atrial fibrillationNeurological perspectives on voltage-gated sodium channels.Reduced Penetrance and Variable Expression of SCN5A Mutations and the Importance of Co-inherited Genetic Variants: Case Report and Review of the Literature.Pharmacotherapy for inherited arrhythmia syndromes: mechanistic basis, clinical trial evidence and practical application.Advances in the pharmacologic treatment of ventricular arrhythmias.Therapeutic Strategies Targeting Inherited Cardiomyopathies.Depolarization of the conductance-voltage relationship in the NaV1.5 mutant, E1784K, is due to altered fast inactivation.The human Nav1.5 F1486 deletion associated with long QT syndrome leads to impaired sodium channel inactivation and reduced lidocaine sensitivity.Sodium Channel Trafficking.The congenital long QT syndrome Type 3: An update.Kinetic modeling of Nav1.7 provides insight into erythromelalgia-associated F1449V mutation.Sinus Bradycardia in Carriers of the SCN5A-1795insD Mutation: Unraveling the Mechanism through Computer Simulations.Complex interactions in a novel SCN5A compound mutation associated with long QT and Brugada syndrome: Implications for Na+ channel blocking pharmacotherapy for de novo conduction disease.Variants: Association With Cardiac DisordersMexiletine rescues a mixed biophysical phenotype of the cardiac sodium channel arising from the SCN5A mutation, N406K, found in LQT3 patients
P2860
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P2860
Trafficking defects and gating abnormalities of a novel SCN5A mutation question gene-specific therapy in long QT syndrome type 3.
description
2010 nî lūn-bûn
@nan
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
2010年论文
@zh
2010年论文
@zh-cn
name
Trafficking defects and gating ...... py in long QT syndrome type 3.
@en
Trafficking defects and gating ...... py in long QT syndrome type 3.
@nl
type
label
Trafficking defects and gating ...... py in long QT syndrome type 3.
@en
Trafficking defects and gating ...... py in long QT syndrome type 3.
@nl
prefLabel
Trafficking defects and gating ...... py in long QT syndrome type 3.
@en
Trafficking defects and gating ...... py in long QT syndrome type 3.
@nl
P2093
P1433
P1476
Trafficking defects and gating ...... py in long QT syndrome type 3.
@en
P2093
Carlo Napolitano
Marco Denegri
Morena Seregni
Silvia G Priori
Stefano Morotti
Stefano Severi
Tiziana Bachetti
Yanfei Ruan
P304
P356
10.1161/CIRCRESAHA.110.218891
P577
2010-03-25T00:00:00Z