Ap2b1, also known as adaptor-related protein complex 2 subunit beta 1, is involved in endocytosis, a process crucial for cells to take in substances from their environment. It is part of the AP-2 complex, which plays a role in clathrin-mediated endocytosis, a major pathway for internalizing extracellular materials. This gene is important in maintaining normal cellular function and has implications in various biological processes [5].

In the context of high-altitude cerebral edema (HACE), NRF1 up-regulates Ap2B1 in activated microglia under hypoxia. This enhances the phagocytic function of microglia, which is part of the mechanism leading to HACE [1]. In a male mouse model of noise-induced sensorineural hearing loss (SNHL), miR-145b negatively regulates Ap2b1, and depletion of miR-145b can alleviate auditory threshold shifts and outer hair cell loss, suggesting Ap2b1's role in SNHL [2]. For influenza A virus entry, SLC35B4 affects the expression level of Ap2B1 through HS modification-mediated AGRN protein homeostasis, influencing virus internalization [3]. The G protein-coupled receptor FFAR2 promotes influenza A virus entry via the FFAR2-β-arrestin1-AP2B1 signaling cascade, with knockdown of AP2B1 impairing virus replication [5]. In the Zika virus infection, LINC08148 knockout down-regulates the transcription level of Ap2B1, and among other genes, loss of Src (which is up-regulated by LINC08148) significantly decreases the uptake of Zika virus, indicating Ap2B1's role in the virus entry process [4].

In Parkinson's disease and related disorders, lower levels of AP2B1 were observed in multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) compared to healthy controls, suggesting its potential as a biomarker for synaptic dysfunction [6]. In triple-negative breast cancer, overexpression of AP2B1 (a downstream target of ZHX2 and HIF1α) could partially rescue the cell growth defect caused by ZHX2 depletion, highlighting its role in cancer cell growth [7]. In major depressive disorder, AP2B1 was identified as a hub gene in the protein-protein interaction network of differentially expressed genes, potentially serving as a therapeutic target [8]. In the study of human umbilical cord mesenchymal stem cell (hUC-MSC) extracellular vesicles for treating Alzheimer's disease, AP2B1 in hUC-MSC-derived EVs may play a role in regulating the synaptic vesicle cycle signalling pathway [9].

In summary, Ap2b1 is mainly involved in endocytosis-related processes and has been shown to play important roles in various disease conditions such as HACE, SNHL, viral infections, neurodegenerative diseases, cancer, and mental disorders. The use of mouse models in these studies has helped to uncover the functions of Ap2b1 in different biological processes and disease mechanisms, providing potential targets for treatment and new insights into disease pathogenesis.