{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["42(11)"],"submitter":["Calderon MR"],"funding":["Canadian Institutes of Health Research"],"pubmed_abstract":["We identified a novel interaction between ligand-dependent corepressor (LCoR) and the corepressor KRAB-associated protein-1 (KAP-1). The two form a complex with C2H2 zinc-finger transcription factor ZBRK1 on an intronic binding site in the growth arrest and DNA-damage-inducible α (GADD45A) gene and a novel site in the fibroblast growth factor 2 (FGF2) gene. Chromatin at both sites is enriched for histone methyltransferase SETDB1 and histone 3 lysine 9 trimethylation, a repressive epigenetic mark. Depletion of ZBRK1, KAP-1 or LCoR led to elevated GADD45A and FGF2 expression in malignant and non-malignant breast epithelial cells, and caused apoptotic death. Loss of viability could be rescued by simultaneous knockdowns of FGF2 and transcriptional coregulators or by blocking FGF2 function. FGF"],"journal":["Nucleic acids research"],"pagination":["7012-27"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4066800"],"repository":["biostudies-literature"],"pubmed_title":["Ligand-dependent corepressor contributes to transcriptional repression by C2H2 zinc-finger transcription factor ZBRK1 through association with KRAB-associated protein-1."],"pmcid":["PMC4066800"],"pubmed_authors":["Dimitrov V","Verway M","Mader S","White JH","Bouttier M","Calderon MR","Benslama RO","Birlea M"],"additional_accession":[]},"is_claimable":false,"name":"Ligand-dependent corepressor contributes to transcriptional repression by C2H2 zinc-finger transcription factor ZBRK1 through association with KRAB-associated protein-1.","description":"We identified a novel interaction between ligand-dependent corepressor (LCoR) and the corepressor KRAB-associated protein-1 (KAP-1). The two form a complex with C2H2 zinc-finger transcription factor ZBRK1 on an intronic binding site in the growth arrest and DNA-damage-inducible α (GADD45A) gene and a novel site in the fibroblast growth factor 2 (FGF2) gene. Chromatin at both sites is enriched for histone methyltransferase SETDB1 and histone 3 lysine 9 trimethylation, a repressive epigenetic mark. Depletion of ZBRK1, KAP-1 or LCoR led to elevated GADD45A and FGF2 expression in malignant and non-malignant breast epithelial cells, and caused apoptotic death. Loss of viability could be rescued by simultaneous knockdowns of FGF2 and transcriptional coregulators or by blocking FGF2 function. FGF","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Jun","modification":"2025-04-21T20:09:36.575Z","creation":"2019-03-27T01:30:40Z"},"accession":"S-EPMC4066800","cross_references":{"pubmed":["24829459"],"doi":["10.1093/nar/gku413"]}}