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                <identifier>oai:data.mendeley.com/rtmx74k5s8.1</identifier>
                <datestamp>2026-07-15T12:25:18Z</datestamp>
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    <dc:creator>meng, weiying</dc:creator>
    <dc:title>A study of SMD2 reads pseudouridines to regulate mRNA splicing and promote tumorigenesis</dc:title>
    <dc:publisher>Mendeley Data</dc:publisher>
    <dc:description>Pseudouridines (Ψ) in mRNA are linked to alternative splicing, but their regulatory mechanisms remain unclear due to the lack of identified reader proteins. Here, we identify SMD2, a core spliceosomal component, as a direct Ψ reader. Using in vitro and ex vivo assays, we show that SMD2 preferentially binds Ψ over unmodified uridines. SMD2 collaborates with PUS family enzymes to regulate alternative splicing by binding Ψ near exon-intron boundaries, modulating the splicing of numerous pre-mRNAs. Notably, the gene encoding SMD2, SNRPD2, is overexpressed across multiple cancers and is essential for tumor cell proliferation through the maturation of key transcripts. These findings uncover a direct mechanistic link between Ψ and spliceosomal function, establishing SMD2 as a critical regulator of Ψ-mediated splicing and a potential cancer therapeutic target.The original images have been uploaded according to their corresponding figure numbers.</dc:description>
    <dc:subject>Molecular Biology</dc:subject>
    <dc:subject>RNA</dc:subject>
    <dc:subject>Epigenetics</dc:subject>
    <dc:type>Dataset</dc:type>
    <dc:identifier>doi:10.17632/rtmx74k5s8.1</dc:identifier>
    <dc:identifier>oai:data.mendeley.com/rtmx74k5s8.1</dc:identifier>
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    <dc:date>2026-07-15T12:25:18Z</dc:date>
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