<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/GSE306nnn/GSE306200/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Other</omics_type><species>Homo sapiens</species><gds_type>Other</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE306200</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Modeling Stimulus-Induced Stress Responses in Microglia-like Cells Using a Commercial iPSC-dCas9-KRAB Line</name><description>This study investigates microglial responses to amyloid-beta (Aβ) and lipopolysaccharide (LPS) using human induced pluripotent stem cell (iPSC)-derived microglia-like cells (iMGLs). iMGLs were exposed to either Aβ or LPS and profiled by single-cell RNA sequencing (scRNA-seq) using the 10x Genomics platform. Transcriptomic analysis revealed both shared and stimulus-specific microglial activation states, characterized by inflammatory signaling, cell death pathways, and lipid metabolism. In parallel, a CRISPR-based pooled survival screen was performed to identify genes critical for microglial survival. Guide RNA representation was measured at multiple differentiation time points (days 12, 24, 36, and 45) to infer gene essentiality during iMGL development. Together, these datasets provide insights into the molecular programs driving microglial stress responses and survival under neuroinflammatory conditions.</description><dates><publication>2026/05/29</publication></dates><accession>GSE306200</accession><cross_references><GSM>GSM9194697</GSM><GSM>GSM9194694</GSM><GSM>GSM9194693</GSM><GSM>GSM9194696</GSM><GSM>GSM9194695</GSM><GPL>32242</GPL><GSE>306200</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>