<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/GSE308337/</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><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE308337</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>The C16orf87 protein is a subunit of the MIER corepressor complex controlling embryonic development and cell migration</name><description>Histone modifications by histone deacetylases (HDACs) are essential for controlling chromatin structure and regulating gene expression. Functionally, HDACs act as enzymatic subunits within diverse multisubunit corepressor complexes, thereby targeting distinct sets of genes. Here, we identify C16orf87 as a previously uncharacterized functional subunit of the MIER corepressor complex that mediates HDAC1 and MIER1 protein interactions. Using CRISPR/Cas9 genome editing, we demonstrate that loss of C16orf87 in human cells alters chromatin accessibility, reduces cell migration, and impairs healthy embryonic development of zebrafish. Based on these findings, we propose renaming C16orf87 as HDAC Interacting Protein (HDIP), to reflect its newly revealed function.</description><dates><publication>2026/04/17</publication></dates><accession>GSE308337</accession><cross_references><GSM>GSM9242505</GSM><GSM>GSM9242506</GSM><GSM>GSM9242503</GSM><GSM>GSM9242504</GSM><GSM>GSM9242507</GSM><GSM>GSM9242502</GSM><GPL>30173</GPL><GSE>308337</GSE><taxon>Homo sapiens</taxon><PMID>[42062449]</PMID></cross_references></HashMap>