Sun Hee Yim

Abstract Skeletal muscle aging is characterized by the loss of muscle mass, strength and function, mainly attributed to the atrophy of glycolytic fibers. Underlying mechanisms driving the skeletal muscle functional impairment are yet to be elucidated. To unbiasedly uncover its molecular mechanisms, we recurred to gene expression and metabolite profiling in a glycolytic muscle, Extensor digitorum longus (EDL), from young and aged C57BL/6JRj mice.

Highlights • Se deficiency reduces selenoprotein expression but does not affect lifespan of mice • Se deficiency reduces amino acid levels and elevates mononucleotides • Se deficiency activates pathways linked to nutrient sensing • Se deficiency is associated with pro-longevity mechanisms Summary Selenium (Se) is an essential trace element because of its presence in selenoproteins in the form of selenocysteine residue.

Systemic Selenof Deficiency in Mice Leads to Elevated Ig Levels without Altering Immune Functions Selenof Deficiency Leads to Elevated Secretion of IgM during Plasma B Cell Differentiation Increased Ig Levels in Selenof KO Mice Are Not Associated with Increased Phagocytosis and Bacterial Killing Potential Selenof-Deficient Cells Are Not More Vulnerable to ER Stress but Show Changes Associated with ER-to-Golgi Transport Since protein synthesis and secretion are linked to ER function (the...