ReviewGenes and immunity2019
Novel mechanistic insights into physiological signaling pathways mediated by mycobacterial Ser/Thr protein kinases.
Review in Genes and immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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.
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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.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Protein kinase G-a key regulator of pathogenesis in Mycobacterium tuberculosis infection.Archives of microbiology · 2025Review
- Identification and Design of Novel Potential Antimicrobial Peptides Targeting Mycobacterial Protein Kinase PknB.The protein journal · 2024Article
- The Role of Phosphorylation and Acylation in the Regulation of Drug Resistance inBiomedicines · 2022Review
- Stringent Response in Mycobacteria: From Biology to Therapeutic Potential.Pathogens (Basel, Switzerland) · 2021Review
- β-Lactams against the Fortress of the Gram-PositiveChemical reviews · 2021Review
- Probing the Highly Disparate Dual Inhibitory Mechanisms of Novel Quinazoline Derivatives againstMolecules (Basel, Switzerland) · 2020Article
- Potential therapeutic approaches for a sleeping pathogen: tuberculosis a case for bioinorganic chemistry.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2020Review
- Cell Surface Biosynthesis and Remodeling Pathways in Mycobacteria Reveal New Drug Targets.Frontiers in cellular and infection microbiology · 2020Review
- Protein kinase B controls Mycobacterium tuberculosis growth via phosphorylation of the transcriptional regulator Lsr2 at threonine 112.Molecular microbiology · 2019Article
- Predictive Binding Affinity of Plant-Derived Natural Products Towards the Protein Kinase G Enzyme ofPlants (Basel, Switzerland) · 2019Article
- In Vivo Methods to Study Protein-Protein Interactions as Key Players inPathogens (Basel, Switzerland) · 2019Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein phosphorylation is known to be one of the keystones of signal sensing and transduction in all living organisms. Once thought to be essentially confined to the eukaryotic kingdoms, reversible phosphorylation on serine, threonine, and tyrosine residues, has now been shown to play a major role in many prokaryotes, where the number of Ser/Thr protein kinases (STPKs) equals or even exceeds that of two-component systems. Mycobacterium tuberculosis, the etiological agent of tuberculosis, is one of the most studied organisms for the role of STPK-mediated signaling in bacteria. Driven by the interest and tractability of these enzymes as potential therapeutic targets, extensive studies revealed the remarkable conservation of protein kinases and their cognate phosphatases across evolution, and their involvement in bacterial physiology and virulence. Here, we present an overview of the current knowledge of mycobacterial STPK structures and kinase activation mechanisms, and we then focus on PknB and PknG, two well-characterized STPKs that are essential for the intracellular survival of the bacillus. We summarize the mechanistic evidence that links PknB to the regulation of peptidoglycan synthesis in cell division and morphogenesis, and the major findings that establish PknG as a master regulator of central carbon and nitrogen metabolism. Two decades after the discovery of STPKs in M. tuberculosis, the emerging landscape of O-phosphosignaling is starting to unveil how eukaryotic-like kinases can be engaged in unique, non-eukaryotic-like, signaling mechanisms in mycobacteria.
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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.