{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSP1 is a ubiquitous transcription factor central to the regulation of many constitutively expressed (“housekeeping”) genes as well as genes involved in neurodegenerative and vascular functions. For example, in Huntington’s disease, SP1 interacts with huntingtin and its coactivators to overcome mutant huntingtin–induced transcriptional inhibition and neuronal toxicity, while in endothelial cells SP1 maintains basal endoglin and eNOS gene transcription through its binding to GC-rich promoter elements. In addition, SP1 is essential for the transcriptional control of genes lacking canonical TATA boxes including BACE1—whose SP1‐dependent expression affects APP processing in Alzheimer’s disease—and hTERT, where SP1/Sp3 binding mediates both repression and activation in a context‐dependent manner; SP1 also exerts a similar role in the regulation of SOD2 expression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn cancer cells, SP1 has emerged as a multifaceted regulator whose aberrant expression and posttranslational modifications can drive oncogenesis and tumor progression. SP1 has been implicated in both the activation and suppression of key oncogenes and tumor suppressors as well as in the regulation of genes involved in angiogenesis and cell cycle control. For instance, SP1 was shown to induce the expression of oncogenic long noncoding RNAs, such as TINCR in gastric carcinoma, and to contribute to HIV‐1 latency by forming complexes with c-Myc and HDAC1. SP1 binding to GC-rich elements is also critical for Akt-induced VEGF transcription and for the regulation of genes like cyclin D1 and p21 by agents such as DIM and curcumin. Moreover, the SP1-regulated promoters of genes including EGFR, CD147, u-PAR, and others underpin SP1’s central role in modulating pathways that govern proliferation, apoptosis, and invasion. MicroRNAs, including miR-335, miR-29b, miR-22, and miR-149, further fine-tune these processes by targeting SP1 itself, thereby affecting cancer cell behavior and clinical outcomes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in transcriptional activation in healthy and neoplastic cells, SP1 is also instrumental in mediating inflammatory, metabolic, and viral gene responses. SP1 contributes to cytokine regulation by influencing IL-10 expression via microRNA networks and participates in the transcriptional control of monoamine oxidase A in response to steroid receptor signaling. Furthermore, SP1 is involved in the regulation of cyclin D1 through interactions with galectin-3 and modulates death receptor expression in response to bile acids via JNK-mediated phosphorylation. In addition, SP1 is recruited into multiprotein complexes that integrate TGF-β signals (through TβRII activation) and inflammatory cues (through COX-2 up-regulation in gliomas), while also playing roles in the regulation of the calcium-sensing receptor and tenascin-C expression. Viral gene expression is not spared either, with SP1 directly interacting with viral proteins such as HTLV-1 HBZ to up-regulate telomerase and support proliferation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "39"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFinally, recent evidence implicates SP1 in the modulation of innate immune responses. Notably, SP1 facilitates the binding of repair proteins such as OGG1 to oxidatively damaged promoter regions, thereby enabling a rapid transcriptional response to inflammatory stimuli and contributing to host defense mechanisms."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "40"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Anthone W Dunah, Hyunkyung Jeong, April Griffin, et al. 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