Fig. 5

Possible sites and targets that can be potentially exploited to modulate AP-2β activities and/or levels. One proposal for modulating AP-2β is through protein–protein interactions whereby co-activators/suppressors bind to the transactivation domain and modify AP-2β transcription activity and DNA-binding activities, as indicated within the yellow square. Inducing degradation of AP-2β could be achieved through designing peptide inhibitors binding selectively to its transactivation domain to form a non-functional complex or by enhancing PKD phosphorylation of AP-2β [71] or by developing specific monoclonal antibodies that can bind and inactivate AP-2β. By contrast, enhancing AP-2β activity could be feasible by designing artificial transcription factor analogues (TFA) that can act as AP-2β agonists. Some monoaminergic drugs, such as phenelzine and citalopram, also have been shown to alter the brain levels of AP-2β [38, 39]] while tetracycline induces its gene expression[33]. KCTD1 & KCTD15: potassium channel tetramerization domain 1 & 15; UBC9: ubiquitin carrier protein 9; HIF-2α: hypoxia-inducible factor-2alpha; YEATS4: YEATS domain-containing protein 4; CITED2 & 4: Cpb/p300-interacting transactivator 2 & 4; PKD: the protein kinase D; DAG: diacylglycerol. The Figure was created with BioRender.com