Zfp536, also known as Zinc Finger Protein 536, is likely involved in multiple biological processes. It has been associated with cell lineage differentiation, potentially playing a role in regulating the development of specific cell types. It may participate in gene regulatory networks and could be involved in pathways related to tissue development and homeostasis [1,2,3,4]. Genetic models, such as mouse models, can be valuable for further exploring its functions.

In the development of perinatal mouse skin, Zfp536 was detected as a putative key driver gene for the papillary fibroblast trajectory, indicating its role in dermal fibroblast lineage differentiation [1]. In the developing cerebral cortex, a sense lncRNA, SenZfp536, which is transcribed downstream of and partially overlaps with Zfp536, cis-regulates Zfp536. Knocking down SenZfp536 increased the proliferation of cortical neural progenitor cells (NPCs), and overexpressing Zfp536 in cortical NPCs reversed this enhanced proliferation, suggesting Zfp536's role in suppressing NPC self-renewal [2]. In tooth initiation, Zfp536 was found near the Sox2:Tfap2a/Tfap2b interface in the mandibular epithelium, and disruption of domain-specific transcription factors led to changes in the expression of genes like Zfp536, affecting tooth initiation site patterning [3]. Computational analysis identified Zfp536 as potentially part of the core transcriptional regulatory networks of Sox2+ dental epithelial stem cells in both embryonic and postnatal stages [4].

In summary, Zfp536 is involved in cell lineage differentiation processes in skin, cerebral cortex, and tooth development. Mouse models have been crucial in uncovering its role in these biological processes, providing insights into the molecular mechanisms underlying tissue development and potentially related disease conditions such as abnormal skin or tooth development, as well as neural development-related disorders [1,2,3,4].