Mitochondria from a mouse model of the human infantile neuroaxonal dystrophy (INAD) with genetic defects in VIA iPLA 2 have disturbed Ca 2+ regulation with reduction in Ca 2+ capacity
Mitochondria from a mouse model of the human infantile neuroaxonal dystrophy (INAD) with genetic defects in VIA iPLA 2 have disturbed Ca 2+ regulation with reduction in Ca 2+ capacity
作者
关键词
Infantile neuroaxonal dystrophy (INAD), Mitochondrial disorder, Ca, signaling, Neuron, Mouse models of INAD, Phospholipase A, 2
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