{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nYTHDC1 is a key nuclear reader of N⁶-methyladenosine (m6A) modifications that exerts multifaceted control over RNA metabolism. Structural and biochemical studies reveal that its YTH domain specifically recognizes m6A‐modified RNA—including single‐stranded RNAs and even m6A-modified DNA—with a distinct aromatic cage that stabilizes these interactions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": " By engaging m6A-modified sites, YTHDC1 regulates pre-mRNA processing through modulation of splicing outcomes—for example, promoting exon inclusion by recruiting splicing factor SRSF3 and excluding SRSF10, as well as affecting alternative splicing events in viral transcripts—and facilitates the nuclear export of methylated mRNAs via interactions with factors such as SRSF3 and NXF1."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "9"}]}, {"type": "t", "text": " Moreover, YTHDC1 contributes to noncanonical RNA processing such as back-splicing in circular RNA biogenesis, participates in the DNA damage response via recruitment to damage sites, and forms liquid-like condensates at enhancers, thereby facilitating gene transcription."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn diverse disease contexts, aberrant regulation or altered expression of YTHDC1 has notable functional consequences. In cancer, for example, YTHDC1 modulates leukemogenesis by sustaining m6A-dependent stabilization of oncogenic transcripts in acute myeloid leukemia, influences human papillomavirus (HPV) RNA splicing to favor viral oncogene expression, and, in bladder, ovarian, colorectal, and lung cancers, its m6A-dependent regulation of key tumor suppressors or oncogenes (such as PTEN, PIK3R1, MCM4, GLUT3, and FSP1) affects proliferation, survival, and therapy sensitivity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "20"}]}, {"type": "t", "text": " Outside of oncogenesis, YTHDC1 is essential for maintaining beta-cell function in type 2 diabetes, modulating hepatoblastoma susceptibility, and controlling placental gene expression by promoting the degradation of circular RNAs (e.g. circMPP1), thereby ensuring proper trophoblast function. Its role also extends to the regulation of oxidative stress responses in vascular endothelium—implicating it in conditions such as aortic dissection—and to the integration of m6A signals in glucose metabolism (and hence overall energy homeostasis), while YTHDC1-mediated interactions with long noncoding RNAs like HOXB-AS3 further contribute to the self-renewal of leukemic stem cells."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Fiona L Wilkinson, James M Holaska, Zhayi Zhang, et al. 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