Triadin Overexpression Stimulates Excitation-Contraction Coupling and Increases Predisposition to Cellular Arrhythmia in Cardiac Myocytes

No abstract is available for this paper.

• Publication year

  2005

• Venue

  Circulation Research

• Publication date

  2005-04-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1161/01.RES.0000160609.98948.25PMID 15731460
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• IL-13受体α2降低血吸虫病肉芽肿的炎症反应并延长宿主存活时间[英]/Mentink-Kane MM,Cheever AW，Thompson RW，et al//Proc Natl Acad Sci U S A

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• Macromolecular complexes regulating cardiac ryanodine receptor function.

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• Negatively Charged Amino Acids within the Intraluminal Loop of Ryanodine Receptor Are Involved in the Interaction with Triadin*

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• RyR 2 mutations linked to ventricular tachycardia and sudden death reduce the threshold for store-overload-induced Ca 2 release ( SOICR )

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• The role of calsequestrin, triadin, and junctin in conferring cardiac ryanodine receptor responsiveness to luminal calcium.

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• Cardiac Hypertrophy and Impaired Relaxation in Transgenic Mice Overexpressing Triadin 1*

  2001cited by this paper
• A missense mutation in a highly conserved region of CASQ2 is associated with autosomal recessive catecholamine-induced polymorphic ventricular tachycardia in Bedouin families from Israel.

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• Mutations in the Cardiac Ryanodine Receptor Gene (hRyR2) Underlie Catecholaminergic Polymorphic Ventricular Tachycardia

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• Early and delayed afterdepolarizations in rabbit heart Purkinje cells viewed by confocal microscopy.

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• Cardiac-specific overexpression of calsequestrin results in left ventricular hypertrophy, depressed force-frequency relation and pulsus alternans in vivo.

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• KEKE motifs

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• Spontaneous Myocardial Calcium Oscillations:

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