<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sponchiado M</submitter><funding>NHLBI NIH HHS</funding><funding>NIH HHS</funding><pagination>1392443</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11070562</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15</volume><pubmed_abstract>&lt;b>Introduction:&lt;/b> Interleukin 13 (IL-13) is an important effector molecule in allergic asthma. IL-13-mediated mucin hypersecretion requires conversion of secretoglobin-positive club cells into goblet cells through suppression of &lt;i>forkhead box A2&lt;/i> (&lt;i>FOXA2&lt;/i>) and induction of &lt;i>SAM pointed domain containing ETS transcription factor&lt;/i> (&lt;i>SPDEF&lt;/i>). IL-13-mediated mucin hypersecretion may also include modulation of purinergic and muscarinic receptors that control basal and stimulated mucin secretion. We recently found that the transcription factor cAMP response element-binding protein (Creb1) inhibits &lt;i>FOXA2&lt;/i> and modulates mucus secretion in mice. &lt;b>Methods:&lt;/b> We tested the hypothesis that loss of club cell Creb1 mitigates the pro-mucin effects of IL-13. We challenged </pubmed_abstract><journal>Frontiers in physiology</journal><pubmed_title>Sex-dependent regulation of mucin gene transcription and airway secretion and mechanics following intra-airway IL-13 in mice with conditional loss of club cell Creb1.</pubmed_title><pmcid>PMC11070562</pmcid><funding_grant_id>R01 HL152101</funding_grant_id><funding_grant_id>OT2 OD026582</funding_grant_id><pubmed_authors>Trevizan-Bau P</pubmed_authors><pubmed_authors>Sponchiado M</pubmed_authors><pubmed_authors>Bonilla AL</pubmed_authors><pubmed_authors>Prabhakaran S</pubmed_authors><pubmed_authors>Reznikov LR</pubmed_authors><pubmed_authors>Fagan A</pubmed_authors><pubmed_authors>Mata L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Sex-dependent regulation of mucin gene transcription and airway secretion and mechanics following intra-airway IL-13 in mice with conditional loss of club cell Creb1.</name><description>&lt;b>Introduction:&lt;/b> Interleukin 13 (IL-13) is an important effector molecule in allergic asthma. IL-13-mediated mucin hypersecretion requires conversion of secretoglobin-positive club cells into goblet cells through suppression of &lt;i>forkhead box A2&lt;/i> (&lt;i>FOXA2&lt;/i>) and induction of &lt;i>SAM pointed domain containing ETS transcription factor&lt;/i> (&lt;i>SPDEF&lt;/i>). IL-13-mediated mucin hypersecretion may also include modulation of purinergic and muscarinic receptors that control basal and stimulated mucin secretion. We recently found that the transcription factor cAMP response element-binding protein (Creb1) inhibits &lt;i>FOXA2&lt;/i> and modulates mucus secretion in mice. &lt;b>Methods:&lt;/b> We tested the hypothesis that loss of club cell Creb1 mitigates the pro-mucin effects of IL-13. We challenged </description><dates><release>2024-01-01T00:00:00Z</release><publication>2024</publication><modification>2026-06-01T08:04:07.639Z</modification><creation>2026-04-08T10:48:26.911Z</creation></dates><accession>S-EPMC11070562</accession><cross_references><pubmed>38711951</pubmed><doi>10.3389/fphys.2024.1392443</doi></cross_references></HashMap>