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Kalaria & Harik, 1987)

NMDA-Rs also allow influx of Ca 2+ and have thereby a regulatory role in synaptic plasticity by connecting synaptic activity with Ca 2+ -mediated biochemical signaling [31]

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after acting on the tumor cell surface System X C - [112], it directly binds to mitochondrial voltage-dependent anion channel 2 (VDAC2) and induces mitochondrial damage that produces ROS in an NADH-dependent manner to inhibit GSH synthesis

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