<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/GSE132nnn/GSE132520/</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><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE132520</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>RNA sequencing of poly(A+) transcriptome of quadriceps muscles from wildtype and CaMK2gVV/CaMK2gVV mice under sedentary and post-acute exercise conditions</name><description>Reactive oxygen species (ROS) contribute to health and disease. CaMKII is a widely expressed enzyme whose activation by oxidation of regulatory domain methionines (ox-CaMKII) contributes to cardiovascular disease, asthma, and cancer. Here we integrate comparative genomic and experimental data to show that CaMKII activation by ROS arose more than half-a-billion years ago on the vertebrate stem lineage where it constituted a bridge between ROS and increased intracellular Ca2+ release, exercise responsive gene transcription, and improved performance in skeletal muscle.  These enhancements to fight-or-flight physiology were likely key in facilitating a well-evidenced shift in the behavioural ecology of our immediate chordate ancestors, and, in turn, the evolutionary success of vertebrates. Still, the ox-CaMKII innovation must be considered a critical evolutionary trade-off, as it rendered us more susceptible to common and often fatal diseases by providing ROS an expanded role in those processes. This poly(A+) transcriptome profiling study examined the actue transcriptional response of mouse skeletal muscles three hours after a single bout of submaximal exericse in wildtype and mutant mice whose CaMKIIg cannot be activated by reactive oxygen species.</description><dates><publication>2021/05/01</publication></dates><accession>GSE132520</accession><cross_references><GSM>GSM3872555</GSM><GSM>GSM3872556</GSM><GSM>GSM3872557</GSM><GSM>GSM3872558</GSM><GSM>GSM3872562</GSM><GSM>GSM3872551</GSM><GSM>GSM3872563</GSM><GSM>GSM3872552</GSM><GSM>GSM3872553</GSM><GSM>GSM3872554</GSM><GSM>GSM3872559</GSM><GSM>GSM3872548</GSM><GSM>GSM3872549</GSM><GSM>GSM3872560</GSM><GSM>GSM3872561</GSM><GSM>GSM3872550</GSM><GPL>24247</GPL><SRA>SRP201066</SRA><GSE>132520</GSE><taxon>Mus musculus</taxon><PMID>[34039988]</PMID></cross_references></HashMap>