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. 2024 May 27;52(14):8534–8551. doi: 10.1093/nar/gkae431

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© The Author(s) 2024. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 6. — U-poor py tract of GOLGA2 exon 8 dictates its dependency on DDX39B expression. (A) Top panel shows the change in alternative splicing of GOLGA2 exon 8 and CELF1 exon 2 upon DDX39B and DDX39A depletion, respectively. (Bottom panel) Construction of GOLGA2 exon 8 reporters with wild-type GOLGA2 intron 7 py tract and CELF1 intron 1 py tract. RT-PCR analysis of GOLGA2 exon 8 reporters splicing changes with (B) wild-type GOLGA2 intron 7 and (C) CELF1intron 1 py tracts in DDX39A (siD09) and DDX39B (siD13) knockdown and control cells. The top panel shows the RT-PCR amplicons on 6% TBE gels and the bottom panel shows the bar graphs depicting the percent exon 8 skipping based on quantification of these gels. Statistical significance was calculated using the Student's t test (**P ≤ 0.01)