SATB2, short for special AT-rich binding protein-2, is a member of the matrix attachment region-binding transcription factor family. It plays crucial roles in multiple biological processes, including craniofacial, neural, and osteoblastic differentiation. SATB2 modulates chromatin architecture to regulate gene expression and is involved in pathways related to cell pluripotency, self-renewal, and epithelial-mesenchymal transition (EMT) [2,3,4].

In mouse models, Satb2 loss in adult mice leads to the stable conversion of colonic stem cells into small intestine ileal-like stem cells, replacing the colonic mucosa with an ileum-like one. Conversely, SATB2 can confer colonic properties on the mouse ileum. This shows that SATB2 singularly preserves LGR5+ adult colonic stem cell and epithelial identity in mice and humans, mediating cross-tissue plasticity in mature intestines [1].

In conclusion, SATB2 is a versatile transcriptional regulator. Its functions span across development, from craniofacial and skeleton formation to neural development. In disease, it has implications in cancer, especially colorectal cancer where it may serve as a biomarker and potential therapeutic target. Mouse models, particularly those with Satb2 knockout or conditional knockout, have been instrumental in uncovering its role in maintaining colonic stem cell identity and understanding its implications in intestinal tissue plasticity and cancer-related processes [1,2].