<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhou H</submitter><funding>the China Postdoctoral Science Foundation</funding><funding>the Basic Research Plan of Jinling Hospital affiliated to Nanjing University</funding><pagination>58</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11786355</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>23(1)</volume><pubmed_abstract>&lt;h4>Introduction&lt;/h4>Ionizing radiation (IR) poses a significant threat to male fertility by inducing substantial changes in the testis, yet the mechanisms underlying IR-induced spermatogenesis disorders remain poorly understood, necessitating the development of more effective radioprotective agents.&lt;h4>Methods&lt;/h4>We employed Bulk RNA-seq and single-cell RNA-seq (scRNA-seq) on Balb/c mice testes models following IR exposure to assess cellular and transcriptional alterations. Histological examination, sperm concentration and motility analysis, Western blotting (WB), and reverse transcription quantitative PCR (RT-qPCR) were used to evaluate testicular injury. The therapeutic potential of NF-κB agonists was investigated in an IR-induced spermatogenesis disorder model.&lt;h4>Results&lt;/h4>A 6 Gy I</pubmed_abstract><journal>Cell communication and signaling : CCS</journal><pubmed_title>Ionizing radiation-induced disruption of Rela-Bclaf1-spliceosome regulatory axis in primary spermatocytes causing spermatogenesis dysfunction.</pubmed_title><pmcid>PMC11786355</pmcid><funding_grant_id>No. 22JCYYZD9</funding_grant_id><funding_grant_id>No. 2023M734291</funding_grant_id><funding_grant_id>No. 2023JCYJYB104</funding_grant_id><funding_grant_id>No. 2023JCYJYB103</funding_grant_id><pubmed_authors>Pan W</pubmed_authors><pubmed_authors>Xia X</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Wu Q</pubmed_authors><pubmed_authors>Chen M</pubmed_authors><pubmed_authors>Pang Y</pubmed_authors><pubmed_authors>Li W</pubmed_authors><pubmed_authors>Liu Z</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Jiang C</pubmed_authors><pubmed_authors>Zhang C</pubmed_authors><pubmed_authors>Zhou H</pubmed_authors><pubmed_authors>Xu Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>Ionizing radiation-induced disruption of Rela-Bclaf1-spliceosome regulatory axis in primary spermatocytes causing spermatogenesis dysfunction.</name><description>&lt;h4>Introduction&lt;/h4>Ionizing radiation (IR) poses a significant threat to male fertility by inducing substantial changes in the testis, yet the mechanisms underlying IR-induced spermatogenesis disorders remain poorly understood, necessitating the development of more effective radioprotective agents.&lt;h4>Methods&lt;/h4>We employed Bulk RNA-seq and single-cell RNA-seq (scRNA-seq) on Balb/c mice testes models following IR exposure to assess cellular and transcriptional alterations. Histological examination, sperm concentration and motility analysis, Western blotting (WB), and reverse transcription quantitative PCR (RT-qPCR) were used to evaluate testicular injury. The therapeutic potential of NF-κB agonists was investigated in an IR-induced spermatogenesis disorder model.&lt;h4>Results&lt;/h4>A 6 Gy I</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Jan</publication><modification>2025-04-03T23:58:21.841Z</modification><creation>2025-04-03T23:58:21.841Z</creation></dates><accession>S-EPMC11786355</accession><cross_references><pubmed>39891142</pubmed><doi>10.1186/s12964-025-02067-5</doi></cross_references></HashMap>