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Additionally, we identify the FHA domain of SNIP1 as a reader of P-SF3B1, guiding the recruitment and assembly of the RES complex during spliceosome activation, and show that mutations in the FHA domain, including the neurodevelopmental disorder-linked E366G variant, impair this interaction, resulting in defects in splicing and cellular proliferation

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Therefore, future studies could focus on the role of synoviocytes and macrophages ferroptosis in OA synovial membrane, which may provide a new direction for future studies on OA

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