{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe REL gene – which encodes the NF‑κB family member c‑Rel – plays a central role in the regulation of immune‐related processes. It is critical for modulating the transcription of cytokines and other immune mediators that drive inflammatory responses and lymphocyte differentiation. For instance, c‑Rel activity has been implicated in proper T‑cell receptor–mediated responses, the induction of cytokines such as interleukin‑2, interferon‑γ, and granulocyte‑macrophage colony‐stimulating factor, and in the development of regulatory T‑cell progenitors. Moreover, genetic studies have linked REL variants to autoimmune and inflammatory disorders – including psoriasis, non‑Hodgkin lymphoma–associated inflammatory conditions, and primary sclerosing cholangitis – and even to altered cytokine responses following fungal recognition."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nREL also functions as an oncogene in hematolymphoid malignancies. Genomic gains and amplification at the REL locus are frequently observed in classical Hodgkin lymphoma, primary mediastinal B‑cell lymphoma, and other lymphoid tumors. Mutant and deletion‐analysis studies have demonstrated that an optimal level of c‑Rel–mediated transactivation is required for transformation. In this context, altered subcellular localization – often with increased nuclear accumulation – and post‑translational modifications (such as O‑GlcNAcylation) further modulate its oncogenic potential. Collectively, these genetic and functional studies associate REL with aberrant NF‑κB signals that favor lymphomagenesis and influence disease prognosis in diffuse large B‑cell lymphoma and related neoplasms."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn solid tumors and other cellular contexts, c‑Rel influences cancer cell behavior by interfacing with other signal transduction pathways. In prostate cancer cells, for example, c‑Rel interacts with the androgen receptor to modulate target gene expression. In breast and head and neck cancers, dysregulation of c‑Rel (often through its derepression via altered estrogen receptor or PKCθ–Akt signaling) correlates with enhanced invasiveness, survival, and resistance to apoptosis. Such findings underscore the role of c‑Rel in controlling epithelial–mesenchymal transition processes and chemoresistance—as illustrated by studies demonstrating its impact on pro‑inflammatory and pro‑survival gene expression in pancreatic ductal adenocarcinoma and chemoresistant ovarian cancer cells."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in immunity and oncogenesis, REL is also involved in diverse biological processes such as the regulation of metabolic and stress‐response pathways, epigenetic modulation, and neuroprotection. For example, in neuronal cells, c‑Rel enhances the expression of mitochondrial uncoupling proteins to mitigate oxidative stress, while in immune effector cells its activity influences neutrophil mobilization and inflammatory resolution. Moreover, recent evidence indicates that altered m^6A RNA methylation can target c‑Rel (in conjunction with RelA) to modulate the tumor microenvironment, and that NF‑κB c‑Rel signaling may intersect with chromatin‐modifying machinery in both normal and transformed cells."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "37"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Ashish Jain, Chi A Ma, Eduardo Lopez-Granados, et al. 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