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. 2023 Jun 15;18:31. doi: 10.1186/s13062-023-00381-x

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© The Author(s) 2023

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — Overexpression of lncRNA5251 disrupted spermatogenesis in F0 mice. (a) The protein staining of DDX4, PGK2 and SYCP3 in F0 mice testis after shRNA treatment detected by IHF. (b) The quantitative data for IHF in (a). (c) Gene ontology (GO) enrichment of up-regulated genes after knockdown of lncRNA5251. (d) GO enrichment of decreased genes after overexpression of lncRNA5251. (e) The protein levels of CADM2, CX43, CYP11A1 and BCL-XL detected by WB in F0 mouse testes. (f) The quantitative data for WB in (e). Data present as Average ± SEM. a, b indicate a significant difference among different treatments (p < 0.05)