{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRCOR1, the core component of the CoREST multiprotein corepressor complex, plays a pivotal structural role by tethering enzymatic activities—including the histone demethylase LSD1 and histone deacetylases—to chromatin. High‐resolution structural and biophysical studies have revealed that the LSD1–CoREST complex adopts an elongated, bivalent conformation that enables multivalent interactions with nucleosomes. Detailed analyses demonstrate that RCOR1 (as CoREST) forms a “nanoscale clamp” with LSD1, engaging both the histone H3 tail and extranucleosomal DNA, and undergoing conformational switching (e.g., open versus closed states modulated by ligands such as tetrahydrofolate) to facilitate efficient demethylation and chromatin remodeling. These insights from crystallography, electron microscopy, and thermodynamic measurements establish that RCOR1 is essential for the assembly and proper regulation of enzymatic activities targeting chromatin modifications."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its structural role, RCOR1 is a crucial mediator of transcriptional repression in neuronal and related cell types. Through its partnership with the repressor protein REST, RCOR1 helps silence neuronal gene expression in nonneuronal tissues, with its activity fine‐tuned by posttranslational modifications such as SUMOylation. RCOR1‐dependent complexes modulate the epigenetic landscape during neurodevelopment, stress responses (for example, in heat shock attenuation), and even in diseases such as Rett syndrome and tinnitus. These studies underscore how RCOR1, via its interactions with factors like PC4 and SUMO‐modified proteins, orchestrates chromatin modifications to control gene expression programs that determine cellular identity and responsiveness."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond developmental and neuroepigenetic regulation, RCOR1 is instrumental in diverse cellular contexts—including hematopoiesis, immune modulation, viral gene expression, and cancer. Disruption of RCOR1 function (or deletions in its gene) has been linked to severe defects in blood cell maturation, aberrant expression of key transcription factors during erythroid differentiation, and to adverse outcomes in malignancies such as diffuse large B‐cell lymphoma and breast cancer. Moreover, RCOR1‐containing complexes participate in the regulation of viral genome silencing and the maintenance of HIV latency in microglia, while also interfacing with DNA–repair machineries to influence the cellular response to genomic stress and inflammation. These findings, bolstered by studies in T‐regulatory cells and by the design of hybrid epigenetic inhibitors, highlight RCOR1 as a multifaceted regulator whose altered activity can impact immunity, oncogenesis, and cellular responses to both pathogen and DNA damage."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "20", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Maojun Yang, Christian B Gocke, Xuelian Luo, et al. 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