<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/GSE301nnn/GSE301703/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Rattus norvegicus</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=GSE301703</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Investigation of the impact of Arylsulfatase L (ARSL) deletion in rat chondrosarcoma (RCS) cell lines</name><description>In this study, we identified arylsulfatase L (ARSL), which is mutated in X-linked chondrodysplasia punctata (CDPX), as a Golgi-localized enzyme responsible for glycosaminoglycan (GAG) desulfation. To elucidate the cellular and molecular consequences of ARSL deficiency, we performed trasncriptome profiling using RNA-sequencing (RNA-seq) in rat chondrosarcoma (RCS) wild-type (WT) and ARSL knockout (KO) cells.</description><dates><publication>2026/08/04</publication></dates><accession>GSE301703</accession><cross_references><GSM>GSM9087559</GSM><GSM>GSM9087558</GSM><GSM>GSM9087557</GSM><GSM>GSM9087563</GSM><GSM>GSM9087562</GSM><GSM>GSM9087561</GSM><GSM>GSM9087560</GSM><GSM>GSM9087556</GSM><GSM>GSM9087555</GSM><GSM>GSM9087564</GSM><GPL>25947</GPL><GSE>301703</GSE><taxon>Rattus norvegicus</taxon><PMID>[42103217]</PMID></cross_references></HashMap>