Ontology highlight
ABSTRACT: Background
Sexually dimorphic growth has been attributed to the growth hormone (GH)/insulin-like growth factor 1 (IGF1) axis, particularly GH-induced activation of the intracellular signal transducer and activator of transcription 5B (STAT5B), because deletion of STAT5B reduces body mass and the mass of skeletal muscles in male mice to that in female mice. However, it remains unclear why these effects are sex- and species-specific, because the loss of STAT5B retards growth in girls, but not in male mice. Our objectives were to determine whether sexually dimorphic growth of skeletal muscle persisted in STAT5B-/- mice and investigate the mechanisms by which STAT5B regulates sexually dimorphic growth.Methods
Blood and skeletal muscle were harvested from male and fem
SUBMITTER: Paul RG
PROVIDER: S-EPMC6589877 | biostudies-literature | 2019 Jun
REPOSITORIES: biostudies-literature