<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/GSE311nnn/GSE311487/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE311487</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>The TENT5A–ATXN2 axis modulates cellular survival during heat stress.</name><description>Stress conditions elicit the formation of different kinds of stress granules. The assembly and composition of heat-induced stress granules remain poorly characterized. Here, we show that the cytoplasmic RNA polyadenylases TENT5A regulate the formation and function of ATXN2-positive heat-induced stress granules. Tent5a mRNA expression increases when somatic and germ cells are exposed to temperatures between 40°C and 42°C, but not upon exposure to other stressors. TENT5A decreases ATXN2 levels by reducing Atxn2 mRNA translation and accelerating ATXN2 protein decay. Upon heat exposure of the testis, ATXN2-positive stress granules are formed in pre-meiotic and meiotic cells independently of the presence of G3BP1 and the heat stress response protein DAZL. Depletion of TENT5A leads to increased cell-type-specific formation of ATXN2-positive stress granules and differentially regulates cell survival. In sum, TENT5A inhibits the formation of ATXN2-positive granules to modulate the heat shock response in vivo.</description><dates><publication>2026/07/10</publication></dates><accession>GSE311487</accession><cross_references><GSM>GSM9325936</GSM><GSM>GSM9325937</GSM><GPL>24973</GPL><GSE>311487</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>