<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sevinc K</submitter><funding>Cancer Research UK</funding><funding>Versus Arthritis</funding><funding>Medical Research Council</funding><funding>Academy of Medical Sciences</funding><pagination>2629-2642</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9768578</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>17(12)</volume><pubmed_abstract>Epigenetic reprogramming to pluripotency requires extensive remodeling of chromatin landscapes to silence existing cell-type-specific genes and activate pluripotency genes. ATP-dependent chromatin remodeling complexes are important regulators of chromatin structure and gene expression; however, the role of recently identified Bromodomain-containing protein 9 (BRD9) and the associated non-canonical BRG1-associated factors (ncBAF) complex in reprogramming remains unknown. Here, we show that genetic or chemical inhibition of BRD9, as well as ncBAF complex subunit GLTSCR1, but not the closely related BRD7, increase human somatic cell reprogramming efficiency and can replace KLF4 and c-MYC. We find that BRD9 is dispensable for human induced pluripotent stem cells under primed but not under naiv</pubmed_abstract><journal>Stem cell reports</journal><pubmed_title>BRD9-containing non-canonical BAF complex maintains somatic cell transcriptome and acts as a barrier to human reprogramming.</pubmed_title><pmcid>PMC9768578</pmcid><funding_grant_id>20522</funding_grant_id><funding_grant_id>MR/V010182/1</funding_grant_id><funding_grant_id>NAF004\1004</funding_grant_id><pubmed_authors>Kelekci S</pubmed_authors><pubmed_authors>Cribbs AP</pubmed_authors><pubmed_authors>Qi J</pubmed_authors><pubmed_authors>Can H</pubmed_authors><pubmed_authors>Dunford JE</pubmed_authors><pubmed_authors>Sevinc K</pubmed_authors><pubmed_authors>Sevinc GG</pubmed_authors><pubmed_authors>Oppermann U</pubmed_authors><pubmed_authors>Philpott M</pubmed_authors><pubmed_authors>Cavga AD</pubmed_authors><pubmed_authors>Sigua LH</pubmed_authors><pubmed_authors>Yıldız AB</pubmed_authors><pubmed_authors>Ata D</pubmed_authors><pubmed_authors>Onder TT</pubmed_authors><pubmed_authors>Yılmaz A</pubmed_authors><pubmed_authors>Ayar ES</pubmed_authors><pubmed_authors>Arabacı DH</pubmed_authors></additional><is_claimable>false</is_claimable><name>BRD9-containing non-canonical BAF complex maintains somatic cell transcriptome and acts as a barrier to human reprogramming.</name><description>Epigenetic reprogramming to pluripotency requires extensive remodeling of chromatin landscapes to silence existing cell-type-specific genes and activate pluripotency genes. ATP-dependent chromatin remodeling complexes are important regulators of chromatin structure and gene expression; however, the role of recently identified Bromodomain-containing protein 9 (BRD9) and the associated non-canonical BRG1-associated factors (ncBAF) complex in reprogramming remains unknown. Here, we show that genetic or chemical inhibition of BRD9, as well as ncBAF complex subunit GLTSCR1, but not the closely related BRD7, increase human somatic cell reprogramming efficiency and can replace KLF4 and c-MYC. We find that BRD9 is dispensable for human induced pluripotent stem cells under primed but not under naiv</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2026-05-28T21:31:07.503Z</modification><creation>2024-10-18T13:12:47.661Z</creation></dates><accession>S-EPMC9768578</accession><cross_references><pubmed>36332631</pubmed><doi>10.1016/j.stemcr.2022.10.005</doi></cross_references></HashMap>