{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Le Minh G"],"funding":["NCATS NIH HHS","NCI NIH HHS","NIH HHS","NIGMS NIH HHS"],"pagination":["398"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11941746"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(6)"],"pubmed_abstract":["The growth of breast tumors is driven and controlled by a subpopulation of cancer cells resembling adult stem cells, which are called cancer stem-like cells (CSCs). In breast cancer, the function and maintenance of CSCs are influenced by protein O-GlcNAcylation and the enzyme responsible for this post-translational modification, O-GlcNAc transferase (OGT). However, the mechanism of CSCs regulation by OGT and O-GlcNAc cycling in breast cancer is still unclear. Analysis of the proteome and O-GlcNAcome, revealed GATAD2B, a component of the Nucleosome Remodeling and Deacetylase (NuRD) complex, as a substrate regulated by OGT. Reducing GATAD2B genetically impairs mammosphere formation, decreases expression of self-renewal factors and CSCs population. O-GlcNAcylation of GATAD2B at the C-terminus"],"journal":["Cells"],"pubmed_title":["GATAD2B O-GlcNAcylation Regulates Breast Cancer Stem-like Potential and Drug Resistance."],"pmcid":["PMC11941746"],"funding_grant_id":["P30 CA138313","UL1 TR001450","S10 OD028692","1U01CA244303-24A5","P20 GM103542","U01 CA244303","1P30CA138313-24A5","1UL1TR001450-24A3","1T32CA193201-24A2","S10 OD025126","1P20GM103542-24A3","T32 CA193201"],"pubmed_authors":["Lee MH","Comte-Walters S","Esquea EM","Sharp RJ","Ahmed NN","Le Minh G","Dhameliya TT","Agana B","Reginato MJ","Bethard JR","Merzy J","Young RG","Ball LE"],"additional_accession":[]},"is_claimable":false,"name":"GATAD2B O-GlcNAcylation Regulates Breast Cancer Stem-like Potential and Drug Resistance.","description":"The growth of breast tumors is driven and controlled by a subpopulation of cancer cells resembling adult stem cells, which are called cancer stem-like cells (CSCs). In breast cancer, the function and maintenance of CSCs are influenced by protein O-GlcNAcylation and the enzyme responsible for this post-translational modification, O-GlcNAc transferase (OGT). However, the mechanism of CSCs regulation by OGT and O-GlcNAc cycling in breast cancer is still unclear. Analysis of the proteome and O-GlcNAcome, revealed GATAD2B, a component of the Nucleosome Remodeling and Deacetylase (NuRD) complex, as a substrate regulated by OGT. Reducing GATAD2B genetically impairs mammosphere formation, decreases expression of self-renewal factors and CSCs population. O-GlcNAcylation of GATAD2B at the C-terminus","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2026-04-15T03:28:28.707Z","creation":"2026-04-15T03:15:25.353Z"},"accession":"S-EPMC11941746","cross_references":{"pubmed":["40136647"],"doi":["10.3390/cells14060398"]}}