BAZ2B, the bromodomain adjacent to zinc finger 2B, is a regulatory subunit of the ISWI (Imitation Switch) remodeling complex, engaging in nucleosome remodeling. It contains multiple domains such as the PHD, BRD, and TAM domains. BAZ2B is crucial in various biological processes and its malfunction is associated with different diseases [1].

Loss-of-function and haploinsufficiency of BAZ2B are linked to an autosomal dominant neurodevelopmental syndrome. Phenotypes associated with BAZ2B deficiency include developmental delay, intellectual disability, autism spectrum disorder, speech delay, behavioral abnormalities, seizures, vision-related issues, congenital heart defects, poor fetal growth, and dysmorphic features [2,5]. Ablation of Baz2b, the mouse orthologue of BAZ-2 in C. elegans, attenuates age-dependent body-weight gain and prevents cognitive decline in ageing mice, suggesting its role in healthy ageing [3]. In vivo CRISPR screening identified Baz2b as a regulator of mammalian liver regeneration, and specific inhibitors can accelerate liver healing [4].

In summary, BAZ2B plays essential roles in neurodevelopment, healthy ageing, and liver regeneration. Studies on BAZ2B knockout mouse models have significantly contributed to understanding its functions in these processes and the associated diseases, providing potential therapeutic targets for related disorders.