ArticleScientific reports2018
Protein tyrosine kinase, PtkA, is required for Mycobacterium tuberculosis growth in macrophages.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 51 citations in OpenAlex.
- mTORC2 is crucial for regulating the recombinant Mycobacterium tuberculosis CFP-10 protein-induced phagocytosis in macrophages.BMC immunology · 2025Article
- Research progress on protein tyrosine phosphatase A from Mycobacterium tuberculosis.Frontiers in immunology · 2025Review
- Nanomaterial-mediated host directed therapy of tuberculosis by manipulating macrophage autophagy.Journal of nanobiotechnology · 2024Review
- Suppression of host gene expression is associated with latent TB infection: a possible diagnostic biomarker.Scientific reports · 2024Article
- Exploring host-pathogen interactions in the Dictyostelium discoideum-Mycobacterium marinum infection model of tuberculosis.Disease models & mechanisms · 2024Review
- Connection between protein-tyrosine kinase inhibition and coping with oxidative stress inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Large-scale Pan Genomic Analysis ofEvolutionary bioinformatics online · 2024Article
- Article
- Virulence-Associated Secretion inFrontiers in immunology · 2022Review
- Persistence ofFrontiers in cellular and infection microbiology · 2022Article
- Regulatory roles of extracellular vesicles in immune responses againstWorld journal of clinical cases · 2021Review
- Culture ofPathogens (Basel, Switzerland) · 2021Article
- From infection niche to therapeutic target: the intracellular lifestyle ofMicrobiology (Reading, England) · 2021Review
- Idiosyncratic Biogenesis of Intracellular Pathogens-Containing Vacuoles.Frontiers in cellular and infection microbiology · 2021Review
- Long-range replica exchange molecular dynamics guided drug repurposing against tyrosine kinase PtkA of Mycobacterium tuberculosis.Scientific reports · 2020Article
- Phosphoproteomic Approaches to Discover Novel Substrates of Mycobacterial Ser/Thr Protein Kinases.Molecular & cellular proteomics : MCP · 2020Review
- Host Cell Targets of Released Lipid and Secreted Protein Effectors ofFrontiers in cellular and infection microbiology · 2020Review
- Targeting redox heterogeneity to counteract drug tolerance in replicatingScience translational medicine · 2019Article
- Protein post-translational modifications in bacteria.Nature reviews. Microbiology · 2019Review
- Novel mechanistic insights into physiological signaling pathways mediated by mycobacterial Ser/Thr protein kinases.Genes and immunity · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Protein phosphorylation plays a key role in Mycobacterium tuberculosis (Mtb) physiology and pathogenesis. We have previously shown that a secreted protein tyrosine phosphatase, PtpA, is essential for Mtb inhibition of host macrophage acidification and maturation, and is a substrate of the protein tyrosine kinase, PtkA, encoded in the same operon. In this study, we constructed a ∆ptkA deletion mutant in Mtb and found that the mutant exhibited impaired intracellular survival in the THP-1 macrophage infection model, correlated with the strain's inability to inhibit macrophage phagosome acidification. By contrast, the mutant displayed increased resistance to oxidative stress in vitro. Proteomic and transcriptional analyses revealed upregulation of ptpA, and increased secretion of TrxB2, in the ΔptkA mutant. Kinase and protein-protein interaction studies demonstrated that TrxB2 is a substrate of PtkA phosphorylation. Taken together these studies establish a central role for the ptkA-ptpA operon in Mtb pathogenesis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.