{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nDLX5 is a homeobox transcription factor that plays a pivotal role during embryogenesis. It is essential for proper craniofacial and limb patterning, as well as inner‐ear morphogenesis, acting in concert with other homeoproteins (for example, the MSX family) and transcriptional regulators such as p63. Disruption of these regulatory networks—whether by mutations in the DLX5 coding region, by deletions or duplications that affect its cis‐regulatory elements, or by altered enhancer binding—has been linked to congenital malformations, most notably split‐hand/foot malformation type 1 and other limb defects. In several studies, coordinated expression of DLX5 with its homolog DLX6 in embryonic tissues has been demonstrated, and alterations in its dosage or promoter/enhancer structure have been implicated in such developmental disorders."}, {"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": "\nIn mesenchymal contexts, DLX5 functions as a master regulator of osteogenesis and related differentiation processes. It is critical for bone development, fracture healing, and mineralization through promoting osteoblast-specific gene expression and by interfacing with key signaling pathways—including those mediated by bone morphogenetic proteins (BMPs), STAT5A, and epigenetic regulators such as KDM4B. Studies in diverse mesenchymal stem cell populations (from bone marrow, dental follicle cells, and periodontal ligament fibroblasts) have shown that DLX5 enhances the expression of osteogenic markers, regulates cell hypertrophy and apoptotic processes, and can be modulated by small molecules or microRNAs to influence matrix formation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its developmental and osteogenic functions, aberrant DLX5 expression is implicated in tumorigenesis and other pathological conditions. In various cancers—including lung, ovarian, T-cell lymphoma, breast, and oral squamous cell carcinoma—DLX5 overexpression can drive cell proliferation by directly transactivating oncogenes such as MYC and CCND1, thereby promoting cell cycle progression. Epigenetic modifications, such as altered DNA methylation patterns and loss of imprinting, as well as regulatory loops involving microRNAs and chromatin remodeling factors, modulate its function. Moreover, studies have highlighted associations between dysregulated DLX5 expression and neurological conditions such as autism spectrum disorders and Rett syndrome, underlining the gene’s broader role in maintaining normal tissue homeostasis and its sensitivity to epigenetic control."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "H Zhang, G Hu, H Wang, et al. 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