Regulation of A-to-I RNA editing and stop codon recoding to control selenoprotein expression during skeletal myogenesis.

ABSTRACT: Selenoprotein N (SELENON), a selenocysteine (Sec)-containing protein with high reductive activity, maintains redox homeostasis, thereby contributing to skeletal muscle differentiation and function. Loss-of-function mutations in SELENON cause severe neuromuscular disorders. In the early-to-middle stage of myoblast differentiation, SELENON maintains redox homeostasis and modulates endoplasmic reticulum (ER) Ca²⁺ concentration, resulting in a gradual reduction from the middle-to-late stages due to unknown mechanisms. The present study describes post-transcriptional mechanisms that regulate SELENON expression during myoblast differentiation. Part of an Alu element in the second intron of SELENON pre-mRNA is frequently exonized during splicing, resulting in an aberrant mRNA that is d

SUBMITTER: Noda Y 

PROVIDER: S-EPMC9076623 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature