UHRF2, also known as NIRF, is an E3 ubiquitin ligase that plays crucial roles in multiple biological processes. It is involved in cell cycle regulation, epigenetics, and DNA repair pathways. UHRF2 interacts with various proteins such as cyclins, CDKs, p53, and proteins related to DNA methylation and histone modifications, highlighting its importance in coordinating different cellular functions [4].

In mice, Uhrf2 -/- mice show no differences in complete blood counts, BM findings, and spleen weights, but their hematopoietic progenitor cells have impaired repopulating ability, suggesting UHRF2's role in hematopoiesis [1]. In the retina, conditional deletion of Uhrf2 from mouse retinal progenitor cells reduces 5hmC, alters gene expressions, and disrupts retinal cell proliferation and differentiation [3]. In the intestine, loss of Uhrf2 in ApcMin mice inhibits tumor initiation and progression, prolonging their lifespan [2]. Uhrf2 knockout mice are viable but develop spontaneous seizures with decreased 5mC levels at certain genomic loci in the brain [5].

In conclusion, UHRF2 is essential for regulating multiple biological processes including hematopoiesis, retinal development, intestinal tumorigenesis, and maintaining local 5mC levels in the brain. The gene knockout mouse models have significantly contributed to understanding UHRF2's role in these specific biological processes and disease-related conditions, providing insights into potential therapeutic targets for related diseases.