<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Peng Y</submitter><funding>Natural Science Foundation of Hubei Province</funding><funding>National Natural Science Foundation of China</funding><funding>the Special Fund for Chinese Agricultural Research System (Beef/yaks)</funding><pagination>1019</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11201411</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(12)</volume><pubmed_abstract>&lt;i>Mycobacterium tuberculosis&lt;/i> causes 6.4 million cases of tuberculosis and claims 1.6 million lives annually. Mycobacterial adhesion, invasion of host cells, and subsequent intracellular survival are crucial for the infection and dissemination process, yet the cellular mechanisms underlying these phenomena remain poorly understood. This study created a &lt;i>Bacillus Calmette-Guérin&lt;/i> (BCG) transposon library using a MycomarT7 phage carrying a Himar1 Mariner transposon to identify genes related to mycobacteria adhesion and invasion. Using adhesion and invasion model screening, we found that the mutant strain B2909 lacked adhesion and invasion abilities because of an inactive &lt;i>fadD18&lt;/i> gene, which encodes a fatty-acyl CoA ligase, although the specific function of this gene remains un</pubmed_abstract><journal>Cells</journal><pubmed_title>&lt;i>Mycobacterium tuberculosis&lt;/i> FadD18 Promotes Proinflammatory Cytokine Secretion to Inhibit the Intracellular Survival of &lt;i>Bacillus Calmette-Guerin&lt;/i>.</pubmed_title><pmcid>PMC11201411</pmcid><funding_grant_id>2021CFA016</funding_grant_id><funding_grant_id>U22A20525</funding_grant_id><funding_grant_id>CARS-37</funding_grant_id><pubmed_authors>Liu H</pubmed_authors><pubmed_authors>Peng Y</pubmed_authors><pubmed_authors>Zhu Y</pubmed_authors><pubmed_authors>Zhou S</pubmed_authors><pubmed_authors>Wang C</pubmed_authors><pubmed_authors>Li Q</pubmed_authors><pubmed_authors>Chen H</pubmed_authors><pubmed_authors>Zhou X</pubmed_authors><pubmed_authors>Sun Q</pubmed_authors><pubmed_authors>Bermudez LE</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Tang T</pubmed_authors><pubmed_authors>Guo A</pubmed_authors></additional><is_claimable>false</is_claimable><name>&lt;i>Mycobacterium tuberculosis&lt;/i> FadD18 Promotes Proinflammatory Cytokine Secretion to Inhibit the Intracellular Survival of &lt;i>Bacillus Calmette-Guerin&lt;/i>.</name><description>&lt;i>Mycobacterium tuberculosis&lt;/i> causes 6.4 million cases of tuberculosis and claims 1.6 million lives annually. Mycobacterial adhesion, invasion of host cells, and subsequent intracellular survival are crucial for the infection and dissemination process, yet the cellular mechanisms underlying these phenomena remain poorly understood. This study created a &lt;i>Bacillus Calmette-Guérin&lt;/i> (BCG) transposon library using a MycomarT7 phage carrying a Himar1 Mariner transposon to identify genes related to mycobacteria adhesion and invasion. Using adhesion and invasion model screening, we found that the mutant strain B2909 lacked adhesion and invasion abilities because of an inactive &lt;i>fadD18&lt;/i> gene, which encodes a fatty-acyl CoA ligase, although the specific function of this gene remains un</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jun</publication><modification>2026-04-08T19:05:17.573Z</modification><creation>2025-04-05T17:54:47.236Z</creation></dates><accession>S-EPMC11201411</accession><cross_references><pubmed>38920649</pubmed><doi>10.3390/cells13121019</doi></cross_references></HashMap>