From systems biology to drug targets: ATP synthase subunit upregulation causes mitochondrial dysfunction in Shank3Δ4-22 mouse model of autism
Wajeha Hamoudi, Manish Tripathi, Maryam Kartawy, Haitham Amal · FENS Forum 2024
A strong link between the SHANK3 gene mutations and autism spectrum disorder (ASD) has been established but its molecular mechanisms remain unknown. Here we hypothesize that a mutation in the Shank3 gene leads to alterations in the global proteome, and consequently, these alterations converge into cellular and behavioral deficits of ASD. To test this hypothesis, we comprehensively mapped the global proteome within the cortex of the Shank3Δ4-22 mice. Our preliminary results revealed a significant increase in one of the ATP synthase subunits (ATP-S) expression levels in the cortex of Shank3Δ4-22
ePoster · Neuroscience