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Taken together, our data indicate that the loss of GSH triggered by Gclc deletion induces a defective mitochondrial accumulation in FoB, which may lead to compensation through upregulation of glycolytic metabolism
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Il10, 5- TTG AAT TCC CTG GGT GAG AAG-3 (forward) and 5- TCC ACT GCC TTG CTC TTA TTT-3 (reverse)
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