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. 2022 Jul 11;13(7):597. doi: 10.1038/s41419-022-05040-z

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — A RIP assays detected the combination between DKC1 and SNORA50C in NB cells. (Student’s t-test) B, C RIP assays detected the combination between DKC1 and SNORA50C in NB cells with SNHG25 silence or overexpression. (Two-way ANOVA, Tukey) D ActD assay detected the stability of SNORA50C mRNA in SK-N-AS and SK-N-SH cells with SNHG25 silence. (Two-way ANOVA, Tukey) E ActD assay detected the stability of SNORA50C mRNA in SK-N-AS and SK-N-SH cells transfected with vector, SNHG25 and SNHG25 + sh-DKC1#1. (One-way ANOVA, Dunnett) F Co-IP assay detected the binding of DKC1 and other snoRNP-related proteins (NAF1, NOP10, NHP2, and GAR1) in the presence of SNHG25 and RNase R. G Co-IP assay detected the binding of DKC1 with NAF1, NOP10, NHP2, and GAR1 in SK-N-AS and SK-N-SH cells with SNHG25 deficiency. ^*P < 0.05, ^**P < 0.01^. Error bars indicate mean ± SD. (N = 3).