ArticleBMC microbiology2009
Downregulation of protein kinase C-alpha enhances intracellular survival of Mycobacteria: role of PknG.
Article in BMC microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 54 citations in OpenAlex.
- Cloning, expression, purification, and characterization of glutamate decarboxylase (Rv3432c) from Mycobacterium tuberculosis.International microbiology : the official journal of the Spanish Society for Microbiology · 2025Article
- Characterization of the Biological Effect Mediated by Mycobacterial Kinase PknG on Protein Phosphorylation and Acetylation.ACS omega · 2025Article
- Protein kinase G-a key regulator of pathogenesis in Mycobacterium tuberculosis infection.Archives of microbiology · 2025Review
- Mycobacterial Rv1804c binds to the PEST domain of IκBα and activates macrophage-mediated proinflammatory responses.iScience · 2024Article
- Detection of microRNAs expression signatures in vitreous humor of intraocular tuberculosis.Molecular biology reports · 2023Article
- Host-Directed Therapies for Tuberculosis.Pathogens (Basel, Switzerland) · 2022Review
- Surface Glycans Regulate Salmonella Infection-Dependent Directional Switch in Macrophage Galvanotaxis Independent of NanH.Infection and immunity · 2022Article
- Coronin-1 is phosphorylated at Thr-412 by protein kinase Cα in human phagocytic cells.Biochemistry and biophysics reports · 2021Article
- Mycobacterium tuberculosis protein kinase G acts as an unusual ubiquitinating enzyme to impair host immunity.EMBO reports · 2021Article
- New insights into the evasion of host innate immunity by Mycobacterium tuberculosis.Cellular & molecular immunology · 2020Review
- "It Takes Two to Tango": Role of Neglected Macrophage Manipulators Coronin 1 and Protein Kinase G in Mycobacterial Pathogenesis.Frontiers in cellular and infection microbiology · 2020Review
- Infection-generated electric field in gut epithelium drives bidirectional migration of macrophages.PLoS biology · 2019Article
- PknG supports mycobacterial adaptation in acidic environment.Molecular and cellular biochemistry · 2018Article
- Protein kinase C-delta (PKCδ), a marker of inflammation and tuberculosis disease progression in humans, is important for optimal macrophage killing effector functions and survival in mice.Mucosal immunology · 2018Article
- Identification of Novel Mycobacterial Inhibitors Against Mycobacterial Protein Kinase G.Frontiers in microbiology · 2018Article
- Protein kinase G confers survival advantage toThe Journal of biological chemistry · 2017Article
- Epigenetic Phosphorylation Control of Mycobacterium tuberculosis Infection and Persistence.Microbiology spectrum · 2017Review
- Toxoplasma gondii GRA7-Targeted ASC and PLD1 Promote Antibacterial Host Defense via PKCα.PLoS pathogens · 2017Article
- Oxidative Unfolding of the Rubredoxin Domain and the Natively Disordered N-terminal Region Regulate the Catalytic Activity of Mycobacterium tuberculosis Protein Kinase G.The Journal of biological chemistry · 2016Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntracellular trafficking of mycobacteria is comprehensively dependent on the unusual regulation of host proteins. Recently, we have reported that infection of macrophages by Mycobacterium tuberculosis H37Rv (Rv) selectively downregulates the expression of PKCalpha while infection by Mycobacterium smegmatis (MS) does not.
resultsBased on our earlier study, we have extrapolated for the first time that knockdown of PKCalpha, impairs phagocytosis of mycobacteria by macrophages while their intracellular survival is drastically increased. Mycobacterium bovis BCG (BCG) and Mycobacterium tuberculosis H37Ra (Ra) have also been shown to downregulate the expression of PKCalpha during the infection. Since PknG is uniquely expressed in BCG, Ra, Rv but not in MS and has been reported to promote intracellular survival of mycobacteria, led us to believe that PknG may be involved in such downregulation of PKCalpha. THP-1 cells infected with recombinant MS expressing PknG (MS-G), showed significant reduction in PKCalpha expression. In normal THP-1 cells survival of MS-G was enhanced as compared to MS, while their behavior in PKCalpha deficient cells could not be distinguished. The results strongly demonstrate that pathogenic mycobacteria recognize and then inhibit PKCalpha to circumvent phagocytosis and the hostile environment of macrophages. We emphasize that, this inhibition is controlled by PknG.
conclusionsAll together, our data reveal a mechanism that shows substantial interdependence of PKCalpha with PknG, in sustaining mycobacterial infection.
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