The regulatory role of AP-2β in monoaminergic neurotransmitter systems: insights on its signalling pathway, linked disorders and theragnostic potential

Table 3 Summary of the mechanisms underlying AP-2β effects, and potential therapeutic interventions for specific monoamine neurotransmitter disorders (MNDs)

Monoamine Disorder	AP-2β effect	AP-2β target genes	Affected modulators	Possible pharmacological intervention	Possible therapeutics
Obesity and Type 2 diabetes	Induction	TH(+) [33, 82, 89] DBH (+) [33, 46, 82, 89, 90] PNMT (+) [46, 86,87,88] 5-HTT (−) [19, 20, 101] VMAT2 (?) [23] DRD1_A (-) [94] MAO (-) [28, 91,92,93] COMT (−) [21, 92] Adipokines-related genes (±) [34, 123, 131, 133,134,135] IRS-1(−) [134]	Norepinephrine (+) Epinephrine (+) Dopamine Serotonin (+) Adipocytokines (±) Insulin (−)	Inhibition of AP-2β	Peptide inhibitors
Neuroblastoma	Suppression	TH (+) [33, 82, 89] DBH (+) [33, 46, 82, 89, 90] PNMT (+) [46, 86,87,88]	Norepinephrine (+) Epinephrine (+) Dopamine	Activation of AP-2β	AP-2β analogue or activators Tetracycline [33]

TH tyrosine hydroxylase, PNMT: phenylethanolamine N-methyltransferase, MAO monoamine oxidase, 5-HTT serotonin transporter, DRD1_A: dopamine receptor D1A, VMAT2: Vesicular monoamine transporter 2, DBH dopamine-beta-hydroxylase, IRS-1: Insulin receptor substrate 1; COMT catechol-O-methyltransferase

ISSN: 2045-3701