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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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We also wish to extend our gratitude to the research team of the Medical Institute of Developmental Disabilities Research at Showa University for their assistance in data acquisition

Graft-versus-host disease Nat Rev Immunol

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