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Structural studies have detailed its modular DNA‐binding domains, nuclear matrix–targeting sequences, and even a novel noncanonical nuclear localization signal that collectively underlie its ability to orchestrate large chromatin loops and regulate clusters of genes in parallel."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its architectural role, SATB1 modulates critical signal‐dependent gene programs in diverse lineages. In T lymphocytes, for example, it cooperates with β‐catenin during Wnt signaling to influence T helper cell differentiation, whereas in regulatory T cells SATB1 suppression—mediated directly by FOXP3 and associated microRNAs—ensures proper immune suppressive function. Moreover, SATB1 participates in dendritic cell development and even exerts a role in early erythroid differentiation by regulating globin gene expression. Posttranslational modifications such as phosphorylation further fine‐tune its interactions with chromatin regulators, ensuring context‐dependent recruitment of coactivators or corepressors."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nDeregulation of SATB1 is a recurrent theme in cancer, where its aberrant expression reprograms transcriptional profiles to favor tumor growth, epithelial–mesenchymal transition, invasion, and chemoresistance in a variety of malignancies including breast, gastric, lung, colorectal, esophageal, prostate, glioma, and even cutaneous T‐cell lymphomas. In different tumor models, SATB1 upregulates metastasis‐promoting genes while repressing tumor suppressors. Moreover, its expression is modulated by factors from the tumor microenvironment (for example, CAF‐secreted SDF-1 in pancreatic cancer) and is subject to regulation by oncogenic signaling networks. Additional studies have demonstrated that posttranslational modifications (such as phosphorylation and altered sumoylation) and chromatin context (influenced by modifications like N6-methyladenine) further impact SATB1 function in governing malignant phenotypes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "18", "end_ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nEmerging evidence also highlights regulatory circuits whereby noncoding RNAs modulate SATB1 expression—illustrated by long noncoding RNAs in renal cell carcinoma that bind microRNAs targeting SATB1—further adding layers to its functional versatility and demonstrating its potential as a biomarker and therapeutic target."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Hye-Jung Han, Jose Russo, Yoshinori Kohwi, et al. 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