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When IGF-1 (or an agonist analog such as IGF-1 LR3) binds the alpha subunits, the receptor undergoes a conformational change that activates the intrinsic tyrosine kinase domains of the beta subunits, triggering autophosphorylation and the recruitment of docking proteins

Homozygous null deletion of the Kat6a gene in mice causes foetal to perinatal death (depending on the genetic background), characterised by cleft palate, shortened jaws, cardiac septum defects, and interrupted aortic arch, as well as an anterior homeotic transformation of 19 body segments affecting the vertebral column and the nervous system (Voss et al, 2009, 2012

Melatonin mitigates PNMC-induced disruption of spindle assembly and mitochondrial function in mouse oocytes [J]

Glutathione defends mitochondria from oxidative damage