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Description

RHEB was tethered to the LUVs by means of a thiolmaleimide reaction between the functionalized lipid PE MCC and its only cysteine residue, C181, which is the farnesylation site of endogenous RHEB (Fig

Kim, S., Park, D

10.1089/ars.2011.4501 Antioxid Redox Signal

doi: 10.1111/j.1365-2036.2005.02658.x 16

Skeletal muscle atrophy results from mitochondrial toxicity in denervated skeletal muscle, which can impair the scavenging of reactive oxygen species (ROS), leading to oxidative injury and the apoptosis of skeletal muscle cells [9, 10]