Tfap2b, also known as transcription factor AP-2 beta, is a pivotal transcription factor. It plays critical roles within neural crest cells and their derived lineages, and is involved in various biological processes such as development, cell differentiation, and gene regulation [4].

In mice, heterozygous deletion of Tfap2b reduces sleep [1]. Specific deletion of Tfap2b in GABAergic neurons leads to shortened NREM and REM sleep time, and reduced delta and theta power, indicating its essential role in normal sleep regulation through GABAergic neurons [1].

In zebrafish, disruption of tfap2b leads to decreased enteric neuronal numbers, delayed transit time, and decreased levels of ednrbb mRNA, suggesting its involvement in gastrointestinal development and function [2].

Overexpression of TFAP2B in cultured primary neurons can improve cell survival and autophagy, and reduce apoptosis during oxygen-glucose deprivation/reperfusion (OGD/R) by enhancing BNIP3-mediated mitophagy, protecting against OGD/R injury of neurons, and alleviating middle cerebral artery occlusion and reperfusion (MCAO/R) damage in vivo [3].

In conclusion, Tfap2b is crucial for normal sleep regulation, gastrointestinal development and function, and protection against cerebral ischemia-reperfusion injury. The gene knockout and conditional knockout mouse models, as well as zebrafish models, have significantly contributed to revealing the roles of Tfap2b in these biological processes and disease-related conditions, providing insights into the underlying mechanisms and potential therapeutic targets.