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In dendritic cells, for instance, it suppresses durable neoantigen‐specific T cell responses by facilitating the translation of lysosomal proteases, thereby impairing tumor antigen cross‐presentation (1:."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In ovarian cancer, YTHDF1 binds m⁶A‐modified EIF3C transcripts to augment overall translation and promote tumorigenesis (2:"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": ", whereas in non–small cell lung cancer (NSCLC) its amplification orchestrates cell cycle progression via enhanced translation of CDK2, CDK4 and cyclin D1 (3:."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": " In the context of viral infection, YTHDF1 binds HIV‐1 transcripts to inhibit reverse transcription (4:"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": ", and in hepatocellular carcinoma (HCC) it promotes autophagy through translation of ATG2A and ATG14 under hypoxic conditions (5:"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": "; 6:."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": " Similar m⁶A‐dependent translational control mechanisms of YTHDF1 have been implicated in cervical cancer by stabilizing hexokinase 2 mRNA (7:"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": "; in gastric cancer by promoting synthesis of the Wnt receptor FZD7 (8:"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": "; in chemoresistant ovarian cancer by enhancing TRIM29 translation and cancer stem cell features (9:"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": "; and in NSCLC where high YTHDF1/2 expression correlates with increased tumor‐infiltrating lymphocytes and favorable outcome (10:."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "10"}]}, {"type": "t", "text": " Moreover, YTHDF1 facilitates S‐phase entry and DNA repair in breast cancer cells via stabilization of E2F8 (11:"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": ", promotes cyclin E2 translation in acute myelogenous leukemia (12:"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": ", enhances NOTCH1 expression to drive HCC stemness and drug resistance (13:"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "13"}]}, {"type": "t", "text": ", and supports cyclin B1 translation in KRAS/TP53‐mutated lung adenocarcinoma (14:."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": " In prostate cancer and its immune evasion, YTHDF1 is upregulated and correlates with aggressive progression by stabilizing PD‐L1 mRNA (15:"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "15"}]}, {"type": "t", "text": "; 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High‐resolution structural and biophysical studies have elucidated its m⁶A recognition via a conserved aromatic cage and revealed its ability to enter phase‐separated states that facilitate mRNA degradation (28:"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "28"}]}, {"type": "t", "text": "; 29:"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "29"}]}, {"type": "t", "text": "; 30:."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "30"}]}, {"type": "t", "text": " In neurons, YTHDF1’s activity is modulated by phosphorylation events that impact its interaction with FMRP, thereby fine‐tuning stimulus‐dependent translation (31:."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "31"}]}, {"type": "t", "text": " Moreover, YTHDF1 directs the translation of Traf6 mRNA to boost intestinal innate immune responses (32:"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "32"}]}, {"type": "t", "text": ", and its regulatory circuit in alveolar epithelial cells contributes to the pathogenesis of arsenite‐induced pulmonary fibrosis by affecting TGF‐β₁ secretion (33:."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "33"}]}, {"type": "t", "text": " Its ability to protect cells from ferroptosis has been demonstrated in nucleus pulposus cells, delaying intervertebral disc degeneration (34:"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "34"}]}, {"type": "t", "text": ", and it further modulates osteoclast differentiation and inflammatory bone resorption via regulation of key mRNAs (35:."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "35"}]}, {"type": "t", "text": " In the intestine, YTHDF1 sustains stem cell renewal through enhancing TEAD1 translation in a m⁶A‐dependent manner (36:."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, YTHDF1 binds m⁶A‐modified transcripts to enhance their translation and stability, a function further refined by its low‐complexity domains and regulated by post‐translational modifications such as O‐GlcNAcylation that dictate its nucleocytoplasmic shuttling and interaction with the export machinery. 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