<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/GSE308549/</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=GSE308549</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>RNA-seq of primary murine liver sinusoidal endothelial cells (LSECs) with constitutive Notch activation and MASH-like liver fibrosis diet</name><description>Liver sinusoidal endothelial cells (LSECs) form discontinuous, permeable microvessels, with a unique gene expression program that differs significantly from that of continuous microvascular endothelial cells in other organs such as the lungs. Unbalanced hepatic endothelial Notch signaling leads either to vascular malformations or MASH-like liver fibrosis. Here, we investigated the elusive duality of these reaction patterns in a model with constitutively active Notch signaling in LSECs under physiologic conditions as well as under a dietary model of MASH-like liver fibrosis.</description><dates><publication>2026/09/29</publication></dates><accession>GSE308549</accession><cross_references><GSM>GSM9247892</GSM><GSM>GSM9247893</GSM><GSM>GSM9247894</GSM><GSM>GSM9247895</GSM><GSM>GSM9247890</GSM><GSM>GSM9247891</GSM><GSM>GSM9247889</GSM><GSM>GSM9247900</GSM><GSM>GSM9247901</GSM><GSM>GSM9247902</GSM><GSM>GSM9247896</GSM><GSM>GSM9247897</GSM><GSM>GSM9247887</GSM><GSM>GSM9247898</GSM><GSM>GSM9247899</GSM><GSM>GSM9247888</GSM><GPL>21626</GPL><GSE>308549</GSE><taxon>Mus musculus</taxon><PMID>[42785433]</PMID></cross_references></HashMap>