Abstract
Duchenne muscular dystrophy (DMD) is caused by lack of dystrophin. Characteristic signs of dystrophic muscles are membrane fragility and abnormally elevated levels of intracellular calcium, detrimental to the cells. Increased activity of store-operated calcium channels (SOC) has been proposed as a possible mechanism for the enhanced calcium concentration. Studies of SOC have indicated the enzyme calcium-independent phospholipase A2β (iPLA2β) as an important mediator of calcium influx. We have previously shown that SOC entry in FDB fibres isolated from mdx mice is reduced in the presence of bromoenol lactone (BEL), a suicide inhibitor of iPLA2.
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