<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Baros-Steyl SS</submitter><funding>University of Capetown</funding><funding>South African Medical Research Council</funding><funding>National Research Foundation</funding><pagination>5585-5603</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12604046</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>24(11)</volume><pubmed_abstract>Pathogenic mycobacteria, such as &lt;i>Mycobacterium tuberculosis&lt;/i>, modulate the host immune system to evade clearance and promote long-term persistence, leading to disease progression or latent infection. Understanding how these mycobacteria evade elimination is key to uncovering the molecular mechanisms of infection. Protein kinase G (PknG) in pathogenic mycobacteria plays a critical role in avoiding macrophage clearance by inhibiting phagosome-lysosome fusion; however, the exact mechanism is not completely understood. To investigate the role of PknG during early events of macrophage infection, RAW 264.7 macrophages were infected with &lt;i>Mycobacterium bovis&lt;/i> BCG wild-type and PknG knockout mutant strains. Phosphoproteomic analysis, including TiO&lt;sub>2&lt;/sub>-based phosphopeptide enrich</pubmed_abstract><journal>Journal of proteome research</journal><pubmed_title>A Phosphoproteomic Analysis of Mycobacterial PknG-Mediated Host Immune Evasion.</pubmed_title><pmcid>PMC12604046</pmcid><funding_grant_id>95984</funding_grant_id><funding_grant_id>467126</funding_grant_id><pubmed_authors>Soares NC</pubmed_authors><pubmed_authors>Ganief TA</pubmed_authors><pubmed_authors>Blackburn JM</pubmed_authors><pubmed_authors>Nakedi KC</pubmed_authors><pubmed_authors>Baros-Steyl SS</pubmed_authors></additional><is_claimable>false</is_claimable><name>A Phosphoproteomic Analysis of Mycobacterial PknG-Mediated Host Immune Evasion.</name><description>Pathogenic mycobacteria, such as &lt;i>Mycobacterium tuberculosis&lt;/i>, modulate the host immune system to evade clearance and promote long-term persistence, leading to disease progression or latent infection. Understanding how these mycobacteria evade elimination is key to uncovering the molecular mechanisms of infection. Protein kinase G (PknG) in pathogenic mycobacteria plays a critical role in avoiding macrophage clearance by inhibiting phagosome-lysosome fusion; however, the exact mechanism is not completely understood. To investigate the role of PknG during early events of macrophage infection, RAW 264.7 macrophages were infected with &lt;i>Mycobacterium bovis&lt;/i> BCG wild-type and PknG knockout mutant strains. Phosphoproteomic analysis, including TiO&lt;sub>2&lt;/sub>-based phosphopeptide enrich</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Nov</publication><modification>2026-06-05T12:49:57.127Z</modification><creation>2026-05-17T03:07:51.949Z</creation></dates><accession>S-EPMC12604046</accession><cross_references><pubmed>41064949</pubmed><doi>10.1021/acs.jproteome.5c00416</doi></cross_references></HashMap>