<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE308nnn/GSE308359/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species> Mus musculus</species><species>Homo sapiens</species><gds_type> Other</gds_type><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE308359</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>RPL41 stabilizes ribosome dynamics and supports long-protein homeostasis in mammals</name><description>Ribosomal protein L41 (RPL41 or eL41) is the smallest ribosomal protein and forms the eukaryote-specific bridge, eB14, near the decoding center; however, its role in mammalian translation remains unclear. In this study, we established RPL41-deficient models of human HEK293T cells and mice to define its function. Cryo-electron microscopy revealed that RPL41 constrains intersubunit conformational dynamics without inducing major local static rearrangements. Loss of RPL41 altered A-site dynamics, slowed elongation, modestly increased amino acid misincorporation, and modestly enhanced readthrough of collision-inducing reporter sequences. Quantitative proteomic analysis suggested that these translational defects compromise long-protein homeostasis, as evidenced by increased insolubility and reduced abundance of long proteins. In vivo, Rpl41−/− mice were viable but exhibited growth retardation and decreased abundance of long proteins in tissues. Our findings reveal a conserved role for RPL41 in maintaining ribosome dynamics and translational fidelity, indicating that RPL41 supports ribosome function and long-protein homeostasis in mammals.</description><dates><publication>2026/07/27</publication></dates><accession>GSE308359</accession><cross_references><GSM>GSM9244012</GSM><GSM>GSM9244011</GSM><GSM>GSM9244010</GSM><GSM>GSM9244016</GSM><GSM>GSM9244015</GSM><GSM>GSM9244014</GSM><GSM>GSM9244013</GSM><GSM>GSM9244019</GSM><GSM>GSM9244018</GSM><GSM>GSM9244017</GSM><GSM>GSM9243999</GSM><GSM>GSM9244023</GSM><GSM>GSM9244022</GSM><GSM>GSM9244021</GSM><GSM>GSM9244020</GSM><GSM>GSM9244027</GSM><GSM>GSM9243972</GSM><GSM>GSM9243971</GSM><GSM>GSM9244026</GSM><GSM>GSM9243970</GSM><GSM>GSM9244025</GSM><GSM>GSM9244024</GSM><GSM>GSM9243976</GSM><GSM>GSM9243975</GSM><GSM>GSM9244029</GSM><GSM>GSM9243974</GSM><GSM>GSM9243973</GSM><GSM>GSM9244028</GSM><GSM>GSM9243969</GSM><GSM>GSM9243968</GSM><GSM>GSM9244030</GSM><GSM>GSM9244034</GSM><GSM>GSM9244033</GSM><GSM>GSM9244032</GSM><GSM>GSM9244031</GSM><GSM>GSM9243983</GSM><GSM>GSM9244038</GSM><GSM>GSM9243982</GSM><GSM>GSM9244037</GSM><GSM>GSM9244036</GSM><GSM>GSM9243981</GSM><GSM>GSM9243980</GSM><GSM>GSM9244035</GSM><GSM>GSM9243987</GSM><GSM>GSM9243986</GSM><GSM>GSM9243985</GSM><GSM>GSM9244039</GSM><GSM>GSM9243984</GSM><GSM>GSM9243979</GSM><GSM>GSM9243978</GSM><GSM>GSM9243977</GSM><GSM>GSM9244041</GSM><GSM>GSM9244040</GSM><GSM>GSM9243990</GSM><GSM>GSM9244001</GSM><GSM>GSM9244000</GSM><GSM>GSM9243994</GSM><GSM>GSM9244005</GSM><GSM>GSM9243993</GSM><GSM>GSM9244004</GSM><GSM>GSM9244003</GSM><GSM>GSM9243992</GSM><GSM>GSM9243991</GSM><GSM>GSM9244002</GSM><GSM>GSM9244009</GSM><GSM>GSM9243998</GSM><GSM>GSM9244008</GSM><GSM>GSM9243997</GSM><GSM>GSM9243996</GSM><GSM>GSM9244007</GSM><GSM>GSM9244006</GSM><GSM>GSM9243995</GSM><GSM>GSM9243989</GSM><GSM>GSM9243988</GSM><GPL>24676</GPL><GPL>24247</GPL><GSE>308359</GSE><taxon> Mus musculus</taxon><taxon>Homo sapiens</taxon><PMID>[42613035]</PMID></cross_references></HashMap>