Zusammenfassung
Advances in genetics and molecular biology have provided an extensive
body of information on the structure and function of the elementary
building blocks of living systems. Genetic defects in membrane ion
channels can disrupt the delicate balance of dynamic interactions
between the ion channels and the cellular environment, leading to
altered cell function. As ion-channel defects are typically studied
in isolated expression systems, away from the cellular environment
where they function physiologically, a connection between molecular
findings and the physiology and pathophysiology of the cell is rarely
established. Here we describe a single-channel-based Markovian modelling
approach that bridges this gap. We achieve this by determining the
cellular arrhythmogenic consequences of a mutation in the cardiac
sodium channel that can lead to a clinical arrhythmogenic disorder
(the long-QT syndrome) and sudden cardiac death.
- 10448858
- action
- cardiovascular,
- chains,
- channel
- channels,
- gating,
- genetic,
- gov't,
- humans,
- ion
- long
- markov
- models,
- mutation,
- myocardium,
- non-u.s.
- p.h.s.,
- phenotype,
- potentials,
- qt
- research
- sodium
- support,
- syndrome,
- u.s.
Nutzer