<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Belhart K</submitter><funding>Consejo Nacional de Investigaciones Científicas y Técnicas</funding><funding>International Union of Biochemestry and Molecular Biology</funding><funding>LSU Health Shreveport</funding><funding>Center of Excellence for Arthritis and Rheumatology</funding><funding>Universidad Nacional de La Plata</funding><funding>Universidad Nacional de La Plata,Argentina</funding><funding>Agencia Nacional de Promoción Científica y Tecnológica</funding><funding>Louisiana Board of Regents</funding><funding>National Institutes of Health</funding><funding>NIH HHS</funding><pagination>7157</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10154355</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(1)</volume><pubmed_abstract>Bordetella bronchiseptica is a gram-negative bacterium that causes respiratory diseases in different animals, including mice, making B. bronchiseptica the gold-standard model to investigate host-pathogen interaction at the molecular level. B. bronchiseptica utilizes many different mechanisms to precisely regulate the expression of virulence factors. Cyclic di-GMP is a second messenger synthesized by diguanylate cyclases and degraded by phosphodiesterases that regulates the expression of multiple virulence factors including biofilm formation. As in other bacteria, we have previously shown that c-di-GMP regulates motility and biofilm formation in B. bronchiseptica. This work describes the diguanylate cyclase BdcB (Bordetella diguanylate cyclase B) as an active diguanylate cyclase that promot</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>Bordetella bronchiseptica diguanylate cyclase BdcB inhibits the type three secretion system and impacts the immune response.</pubmed_title><pmcid>PMC10154355</pmcid><funding_grant_id>NIH COBRE award 1P20-GM134974-0181</funding_grant_id><funding_grant_id>PID-UNLP-X819</funding_grant_id><funding_grant_id>Research Career</funding_grant_id><funding_grant_id>IUBMB Wood-Whelan Research Fellowship</funding_grant_id><funding_grant_id>LEQSF(2022-25)-RD-A-33</funding_grant_id><funding_grant_id>Research Fellowship</funding_grant_id><funding_grant_id>PICT-2019-00680</funding_grant_id><funding_grant_id>Intramural Research Council Seed package support</funding_grant_id><funding_grant_id>intramural award</funding_grant_id><pubmed_authors>Sisti F</pubmed_authors><pubmed_authors>Gestal MC</pubmed_authors><pubmed_authors>Fernandez J</pubmed_authors><pubmed_authors>Belhart K</pubmed_authors></additional><is_claimable>false</is_claimable><name>Bordetella bronchiseptica diguanylate cyclase BdcB inhibits the type three secretion system and impacts the immune response.</name><description>Bordetella bronchiseptica is a gram-negative bacterium that causes respiratory diseases in different animals, including mice, making B. bronchiseptica the gold-standard model to investigate host-pathogen interaction at the molecular level. B. bronchiseptica utilizes many different mechanisms to precisely regulate the expression of virulence factors. Cyclic di-GMP is a second messenger synthesized by diguanylate cyclases and degraded by phosphodiesterases that regulates the expression of multiple virulence factors including biofilm formation. As in other bacteria, we have previously shown that c-di-GMP regulates motility and biofilm formation in B. bronchiseptica. This work describes the diguanylate cyclase BdcB (Bordetella diguanylate cyclase B) as an active diguanylate cyclase that promot</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 May</publication><modification>2025-04-05T00:11:49.561Z</modification><creation>2025-04-05T00:11:49.561Z</creation></dates><accession>S-EPMC10154355</accession><cross_references><pubmed>37130958</pubmed><doi>10.1038/s41598-023-34106-x</doi></cross_references></HashMap>