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The aberrant upregulation of the transmembrane glycoprotein MUC1 has been demonstrated in TNBC
In X-ALD mice models, treatment with a high dosage of biotin removes excessive ROS by inducing the endogenous antioxidant response of NRF2 and normalizes redox in vivo via recovering mitochondrial biogenesis and energy supplement to improve symptoms of dyskinesia and axon injury consequently
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