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Several autistic models showed an increase in neuronal apoptosis resulting from the decrease in the expression of Bcl-2/Bcl-2-associated X protein (Bax) that increases activation of caspase-3, boosting uncontrolled apoptosis and eventually resulting in ASD

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[iv] Fleming, A., & Kato, S

Its structure and receptor-binding profile make it useful for exploring pigmentation pathways, receptor signalling, and peptidereceptor interactions in vitro

In addition, oxidation of substrates may alter their localization/binding partners and/or their cognate phosphatase activity, further exacerbating signal dysregulation