<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/GSE310nnn/GSE310245/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Genomics</omics_type><species>Homo sapiens</species><gds_type>Genome binding/occupancy profiling by high throughput sequencing</gds_type><gds_type> Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE310245</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Retinoic acid regulates macular development in the human retina</name><description>The human retina possesses a region, the macula, specialized for high acuity vision, with a high density of cones and no rod photoreceptors. The mechanisms involved in macular formation are poorly understood. Increasing evidence suggests that retinoic acid (RA) may play a key role in its development. Specifically low RA levels in the macula, maintained by CYP26A1, leads to early cell cycle exit for macular progenitors, and a low rod to cone ratio. To test this model, we performed single cell RNA sequencing on Fetal D57 retina to examine the distribution of RA-associated genes across the central and peripheral retina.</description><dates><publication>2026/06/10</publication></dates><accession>GSE310245</accession><cross_references><GSM>GSM9292435</GSM><GSM>GSM9567288</GSM><GSM>GSM9292434</GSM><GSM>GSM9292437</GSM><GSM>GSM9567287</GSM><GSM>GSM9292436</GSM><GPL>18573</GPL><GPL>24676</GPL><GSE>310245</GSE><taxon>Homo sapiens</taxon><PMID>[42213783]</PMID></cross_references></HashMap>