<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Le Minh G</submitter><funding>NCATS NIH HHS</funding><funding>NCI NIH HHS</funding><funding>NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>398</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11941746</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(6)</volume><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</pubmed_abstract><journal>Cells</journal><pubmed_title>GATAD2B O-GlcNAcylation Regulates Breast Cancer Stem-like Potential and Drug Resistance.</pubmed_title><pmcid>PMC11941746</pmcid><funding_grant_id>P30 CA138313</funding_grant_id><funding_grant_id>UL1 TR001450</funding_grant_id><funding_grant_id>S10 OD028692</funding_grant_id><funding_grant_id>1U01CA244303-24A5</funding_grant_id><funding_grant_id>P20 GM103542</funding_grant_id><funding_grant_id>U01 CA244303</funding_grant_id><funding_grant_id>1P30CA138313-24A5</funding_grant_id><funding_grant_id>1UL1TR001450-24A3</funding_grant_id><funding_grant_id>1T32CA193201-24A2</funding_grant_id><funding_grant_id>S10 OD025126</funding_grant_id><funding_grant_id>1P20GM103542-24A3</funding_grant_id><funding_grant_id>T32 CA193201</funding_grant_id><pubmed_authors>Lee MH</pubmed_authors><pubmed_authors>Comte-Walters S</pubmed_authors><pubmed_authors>Esquea EM</pubmed_authors><pubmed_authors>Sharp RJ</pubmed_authors><pubmed_authors>Ahmed NN</pubmed_authors><pubmed_authors>Le Minh G</pubmed_authors><pubmed_authors>Dhameliya TT</pubmed_authors><pubmed_authors>Agana B</pubmed_authors><pubmed_authors>Reginato MJ</pubmed_authors><pubmed_authors>Bethard JR</pubmed_authors><pubmed_authors>Merzy J</pubmed_authors><pubmed_authors>Young RG</pubmed_authors><pubmed_authors>Ball LE</pubmed_authors></additional><is_claimable>false</is_claimable><name>GATAD2B O-GlcNAcylation Regulates Breast Cancer Stem-like Potential and Drug Resistance.</name><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</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Mar</publication><modification>2026-04-15T03:28:28.707Z</modification><creation>2026-04-15T03:15:25.353Z</creation></dates><accession>S-EPMC11941746</accession><cross_references><pubmed>40136647</pubmed><doi>10.3390/cells14060398</doi></cross_references></HashMap>