<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Tagoh H</submitter><funding>Medical Research Council</funding><pagination>1070-80</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC1409732</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>25(5)</volume><pubmed_abstract>The transcription factor Pax5 (BSAP) is required for the expression of a B-cell-specific genetic program and for B-cell differentiation, and also to suppress genes of alternative lineages. The molecular mechanism by which repression of myeloid genes occurs during early B-lineage restriction is unknown and in this study we addressed this question. One of the genes repressed by Pax5 in B cells is the colony-stimulating factor receptor 1 gene (csf1r or c-fms). We examined the changes in chromatin caused by Pax5 activity, and we show that Pax5 is directly recruited to c-fms resulting in the rapid loss of RNA polymerase II binding, followed by loss of transcription factor binding and DNaseI hypersensitivity at all cis-regulatory elements. We also show that Pax5 targets the basal transcription m</pubmed_abstract><journal>The EMBO journal</journal><pubmed_title>The mechanism of repression of the myeloid-specific c-fms gene by Pax5 during B lineage restriction.</pubmed_title><pmcid>PMC1409732</pmcid><funding_grant_id>MC_U105161083</funding_grant_id><pubmed_authors>Bonifer C</pubmed_authors><pubmed_authors>Warren AJ</pubmed_authors><pubmed_authors>Ingram R</pubmed_authors><pubmed_authors>Clarke D</pubmed_authors><pubmed_authors>Busslinger M</pubmed_authors><pubmed_authors>Salvagiotto G</pubmed_authors><pubmed_authors>Tagoh H</pubmed_authors><pubmed_authors>Wilson N</pubmed_authors></additional><is_claimable>false</is_claimable><name>The mechanism of repression of the myeloid-specific c-fms gene by Pax5 during B lineage restriction.</name><description>The transcription factor Pax5 (BSAP) is required for the expression of a B-cell-specific genetic program and for B-cell differentiation, and also to suppress genes of alternative lineages. The molecular mechanism by which repression of myeloid genes occurs during early B-lineage restriction is unknown and in this study we addressed this question. One of the genes repressed by Pax5 in B cells is the colony-stimulating factor receptor 1 gene (csf1r or c-fms). We examined the changes in chromatin caused by Pax5 activity, and we show that Pax5 is directly recruited to c-fms resulting in the rapid loss of RNA polymerase II binding, followed by loss of transcription factor binding and DNaseI hypersensitivity at all cis-regulatory elements. We also show that Pax5 targets the basal transcription m</description><dates><release>2006-01-01T00:00:00Z</release><publication>2006 Mar</publication><modification>2026-05-02T09:06:13.126Z</modification><creation>2026-04-07T17:46:50.647Z</creation></dates><accession>S-EPMC1409732</accession><cross_references><pubmed>16482219</pubmed><doi>10.1038/sj.emboj.7600997</doi></cross_references></HashMap>