<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Patzelt T</submitter><funding>Helmholtz-Gemeinschaft</funding><funding>Deutsche Forschungsgemeinschaft</funding><funding>European Research Council</funding><funding>Deutsche Krebshilfe</funding><pagination>3120-3125</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5866538</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>115(12)</volume><pubmed_abstract>The transcription factor Foxp1 is critical for early B cell development. Despite frequent deregulation of Foxp1 in B cell lymphoma, the physiological functions of Foxp1 in mature B cells remain unknown. Here, we used conditional gene targeting in the B cell lineage and report that Foxp1 disruption in developing and mature B cells results in reduced numbers and frequencies of follicular and B-1 B cells and in impaired antibody production upon T cell-independent immunization in vivo. Moreover, &lt;i>Foxp1&lt;/i>-deficient B cells are impaired in survival even though they exhibit an increased capacity to proliferate. Transcriptional analysis identified defective expression of the prosurvival Bcl-2 family gene &lt;i>Bcl2l1&lt;/i> encoding Bcl-xl in Foxp1-deficient B cells, and we identified Foxp1 binding </pubmed_abstract><journal>Proceedings of the National Academy of Sciences of the United States of America</journal><pubmed_title>Foxp1 controls mature B cell survival and the development of follicular and B-1 B cells.</pubmed_title><pmcid>PMC5866538</pmcid><funding_grant_id>SFB746</funding_grant_id><funding_grant_id>111026</funding_grant_id><funding_grant_id>ImmunoSensation</funding_grant_id><funding_grant_id>PCCC/WP8</funding_grant_id><funding_grant_id>EXC294</funding_grant_id><funding_grant_id>SFB1054/B01</funding_grant_id><funding_grant_id>70112036</funding_grant_id><funding_grant_id>RU 695/6-1</funding_grant_id><funding_grant_id>TRR130</funding_grant_id><funding_grant_id>322865</funding_grant_id><funding_grant_id>322972</funding_grant_id><pubmed_authors>Patzelt T</pubmed_authors><pubmed_authors>Gorka O</pubmed_authors><pubmed_authors>Thoene S</pubmed_authors><pubmed_authors>Wartewig T</pubmed_authors><pubmed_authors>Reth M</pubmed_authors><pubmed_authors>Ruland J</pubmed_authors><pubmed_authors>Keppler SJ</pubmed_authors><pubmed_authors>Lang R</pubmed_authors><pubmed_authors>Buchner M</pubmed_authors><pubmed_authors>Forster I</pubmed_authors></additional><is_claimable>false</is_claimable><name>Foxp1 controls mature B cell survival and the development of follicular and B-1 B cells.</name><description>The transcription factor Foxp1 is critical for early B cell development. Despite frequent deregulation of Foxp1 in B cell lymphoma, the physiological functions of Foxp1 in mature B cells remain unknown. Here, we used conditional gene targeting in the B cell lineage and report that Foxp1 disruption in developing and mature B cells results in reduced numbers and frequencies of follicular and B-1 B cells and in impaired antibody production upon T cell-independent immunization in vivo. Moreover, &lt;i>Foxp1&lt;/i>-deficient B cells are impaired in survival even though they exhibit an increased capacity to proliferate. Transcriptional analysis identified defective expression of the prosurvival Bcl-2 family gene &lt;i>Bcl2l1&lt;/i> encoding Bcl-xl in Foxp1-deficient B cells, and we identified Foxp1 binding </description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Mar</publication><modification>2026-05-01T20:11:27.283Z</modification><creation>2019-03-26T23:47:20Z</creation></dates><accession>S-EPMC5866538</accession><cross_references><pubmed>29507226</pubmed><doi>10.1073/pnas.1711335115</doi></cross_references></HashMap>