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Since many pathologic and toxic conditions result in sustained increase in cytosolic free Ca 2+ , which can lead to activation of CMK and phosphorylation of GCLC, theoretically, inhibition of GCL may further contribute to toxicity under these conditions
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ER stress contributes via IRE1α-mediated JNK activation, enhancing FAS ligand transcription and Bax translocation, while JNK inhibition of Bcl-2 reinforces apoptosis [53]
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