Key result
Primary myocytes lacking ankyrin-B display defects in Kir6.2 protein expression, membrane expression, and function, demonstrating its role in regulating cardiac K(ATP) channels.
Population
Primary cardiac myocytes
Design
Preclinical
Authors
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Ankyrin-B loss impairs K(ATP) channels in animal myocytes; leaves open human relevance and therapeutic targeting.
Ankyrin-B plays a critical role in regulating the membrane expression and function of cardiac K(ATP) channels via Kir6.2.
Li et al. (2010) studied Cardiac cell biology. Ankyrin-B deficiency vs. Normal ankyrin-B expression was evaluated on Kir6.2 protein expression, membrane expression, and function. Primary myocytes lacking ankyrin-B display defects in Kir6.2 protein expression, membrane expression, and function, demonstrating its role in regulating cardiac K(ATP) channels.
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