{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRBPJ—also known as CSL, CBF‐1, or Suppressor of Hairless—is the pivotal nuclear effector of canonical Notch signaling. In unstimulated cells, RBPJ binds DNA and recruits corepressor complexes (including histone deacetylases and other factors) to maintain target genes in a repressed state. Upon Notch receptor activation, the liberated intracellular domain (NICD) engages RBPJ via a highly conserved RAM motif and nearby determinants, displacing repressors and assembling a coactivator complex that includes Mastermind‐like proteins. Structural and biophysical studies have defined the critical interactions between NICD and the beta‐trefoil domain of RBPJ, establishing the molecular basis for the switch from transcriptional repression to activation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn developmental and homeostatic contexts, RBPJ‐mediated transcription regulates cell fate decisions in diverse tissues. For example, genetic association studies have implicated loci near RBPJ in autoimmune disorders, while in cellular models RBPJ governs differentiation in pancreatic progenitors, endothelial cells, and intestinal epithelium—where its loss can cause senescence, barrier defects, or aberrant fibroblast activation. In lymphoid cells, RBPJ is central to Notch‐driven programs that modulate T‐cell progenitor fate and autoimmune gene networks, and Notch2–RBPJ interactions have been shown to control the expression of extracellular matrix genes such as Tenascin‑C. Moreover, interplay between RBPJ and factors such as p53 and estrogen receptor further underlies its multifaceted role in maintaining tissue integrity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nRBPJ’s functions extend into oncogenic and infectious contexts where its normal regulatory activity is subverted. In several cancers—including glioblastoma, breast, and laryngeal carcinomas—loss or misregulation of RBPJ leads to de‐repression of target genes, enhanced cell proliferation, cancer stem cell traits, and even altered responses to hypoxia. Viral pathogens such as Kaposi’s sarcoma–associated herpesvirus and Epstein–Barr virus hijack RBPJ to redirect transcriptional programs; viral proteins either engage RBPJ directly to promote lytic reactivation or displace its corepressors to deregulate cellular genes. In addition, microRNAs (for example, miR‑375) can target RBPJ to modulate the tumor microenvironment by inducing fibroblast polarization toward a cancer‐associated state. These studies underscore how disruption of RBPJ–mediated transcriptional control, whether via genetic, viral, or epigenetic mechanisms, contributes to tumorigenesis and disease progression."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yunsun Nam, Piotr Sliz, Luyan Song, et al. 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