Effect of depletion of FAM129B on gene expression during skeletal muscle differentiation of C2C12 cells

Muscle atrophy, a decline in muscle mass and quantity caused by a variety of factors such as cancer, aging, and long-term use of glucocorticoids, manifested at the molecular level as excessive protein catabolism. Muscle atrophy severely affects the quality of life and the treatment remains an unresolved challenge. FAM129B is an antioxidant protein that plays a key role in signal transduction.FAM129B has previously been reported to be involved in muscle growth and development in cattle. The current study aims to describe the role of FAM129B in muscle atrophy, which is expected to be a potential therapeutic target for skeletal muscle atrophy. Overall design: To investigate the function of FAM129B in the regulation of skeletal muscle atrophy, we established C2C12 cells in which FAM129B has been knocked down by siRNA