Congenital long-QT syndrome caused by a novel mutation in a conserved acidic domain of the cardiac Na+ channel. [electronic resource]
Producer: 19990708Description: 3165-71 p. digitalISSN:- 1524-4539
- Adolescent
- Animals
- Base Sequence
- Cloning, Molecular
- Conserved Sequence
- DNA Primers
- Death, Sudden
- Electrocardiography
- Electrophysiology
- Female
- Humans
- Long QT Syndrome -- congenital
- Male
- Membrane Potentials -- drug effects
- Molecular Sequence Data
- Mutagenesis, Site-Directed
- Myocardium -- chemistry
- NAV1.5 Voltage-Gated Sodium Channel
- Oocytes -- physiology
- Pedigree
- Point Mutation
- Polymorphism, Single-Stranded Conformational
- Protein Structure, Tertiary
- Sequence Homology, Amino Acid
- Sodium Channels -- chemistry
- Structure-Activity Relationship
- Tetrodotoxin -- pharmacology
- Xenopus
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Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
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