Zzz3, also known as zinc finger ZZ-type containing 3, is involved in multiple biological processes. It is a subunit of the Ada-two-A-containing (ATAC) histone acetyltransferase complex, and its ZZ-type zinc finger domain can specifically recognize histone H3. This recognition is crucial for the ATAC complex-mediated maintenance of histone acetylation and gene activation [3]. It also has connections to pathways related to cell proliferation, ribosome biogenesis, and translation, and may be involved in processes relevant to human embryonic stem cell homeostasis, diffuse large B-cell lymphoma, and non-union skeletal fractures [1,2,4].

In human embryonic stem cells, knockdown of Zzz3 negatively impacts ribosome biogenesis, translation, and mTOR signaling, leading to a significant reduction in cell proliferation without affecting pluripotency, suggesting Zzz3-depleted cells enter a "dormant-like" state [1]. In diffuse large B-cell lymphoma, Zzz3 upregulates the transcription of CD70 by binding to its super-enhancer, and the Zzz3/CD70 axis regulates the interactions between lymphoma cells and natural killer cells. Silencing CD70 promotes the proliferation of co-cultured NK cells and LDH release from lymphoma cells, an effect counteracted by Zzz3 overexpression [2]. In non-union skeletal fractures, bioinformatics analysis suggests that Zzz3 may be related to cell proliferation [4].

In conclusion, Zzz3 is essential for processes such as histone acetylation, gene activation, and cell proliferation. Its role in models of human embryonic stem cell homeostasis, diffuse large B-cell lymphoma, and non-union skeletal fractures provides insights into potential mechanisms in these biological and disease-related contexts. Understanding Zzz3 through these model-based studies could offer new perspectives on disease mechanisms and potential therapeutic targets in relevant diseases.