<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/GSE299nnn/GSE299622/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</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=GSE299622</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Transcriptome regulation in iPSC and astrocyte derived from CLN3 deficient patient</name><description>CLN3 Batten disease is a severe pediatric neurodegenerative disorder caused by mutations in the CLN3 gene, most commonly a 1 kb deletion affecting exons 7 and 8. While research has focused on neuronal dysfunction, glial cells are increasingly recognized as key contributors to disease pathology. Here, we establish the iPSC and astrocyte model derived from a CLN3 patient fibrpblast cells with the 1 kb deletion and analyse the transcriptome regulation in both iPSC and astrocyte stages.</description><dates><publication>2026/09/09</publication></dates><accession>GSE299622</accession><cross_references><GSM>GSM9042130</GSM><GSM>GSM9042131</GSM><GSM>GSM9042120</GSM><GSM>GSM9042121</GSM><GSM>GSM9042122</GSM><GSM>GSM9042123</GSM><GSM>GSM9042124</GSM><GSM>GSM9042125</GSM><GSM>GSM9042126</GSM><GSM>GSM9042127</GSM><GSM>GSM9042128</GSM><GSM>GSM9042129</GSM><GPL>23227</GPL><GSE>299622</GSE><taxon>Homo sapiens</taxon><PMID>[42129767]</PMID></cross_references></HashMap>