ArticleJournal of the American Chemical Society2015
Catalytic spectrum of the penicillin-binding protein 4 of Pseudomonas aeruginosa, a nexus for the induction of β-lactam antibiotic resistance.
Article in Journal of the American Chemical Society, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Non canonical perspectives on AmpR mediated ampC expression in Gram negative bacteria, with particular emphasis on the potential regulatory purview of FtsZ.World journal of microbiology & biotechnology · 2026Review
- Genomic and structural analysis of dacB variants associated with cephalosporin resistance in Pseudomonas aeruginosa.Scientific reports · 2026Article
- Article
- Characterization of VldE (Spr1875), a Pneumococcal Two-State l,d-Endopeptidase with a Four-Zinc Cluster in the Active Site.ACS catalysis · 2024Article
- Multidrug resistance in Pseudomonas aeruginosa: genetic control mechanisms and therapeutic advances.Molecular biomedicine · 2024Review
- Article
- Success stories of natural product-derived compounds from plants as multidrug resistance modulators in microorganisms.RSC advances · 2023Review
- Express Yourself: Quantitative Real-Time PCR Assays for Rapid Chromosomal Antimicrobial Resistance Detection in Pseudomonas aeruginosa.Antimicrobial agents and chemotherapy · 2022Article
- Infectious disease: how to manage Gram-positive and Gram-negative pathogen conundrums with dual beta-lactam therapy.Drugs in context · 2022Review
- Article
- β-lactam Resistance inPathogens (Basel, Switzerland) · 2021Review
- Detection of Carbapenem-Resistance Genes inAntibiotics (Basel, Switzerland) · 2020Article
- Fluorescence Assessment of the AmpR-Signaling Network ofACS chemical biology · 2020Article
- Constructing and deconstructing the bacterial cell wall.Protein science : a publication of the Protein Society · 2020Review
- Regulation of AmpC-Driven β-Lactam Resistance in Pseudomonas aeruginosa: Different Pathways, Different Signaling.mSystems · 2019Article
- Cell-Wall Recycling of the Gram-Negative Bacteria and the Nexus to Antibiotic Resistance.Chemical reviews · 2018Review
- Article
- Review
- Article
- In vivo functional and molecular characterization of the Penicillin-Binding Protein 4 (DacB) of Pseudomonas aeruginosa.BMC microbiology · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Pseudomonas aeruginosa is an opportunistic Gram-negative bacterial pathogen. A primary contributor to its ability to resist β-lactam antibiotics is the expression, following detection of the β-lactam, of the AmpC β-lactamase. As AmpC expression is directly linked to the recycling of the peptidoglycan of the bacterial cell wall, an important question is the identity of the signaling molecule(s) in this relationship. One mechanism used by clinical strains to elevate AmpC expression is loss of function of penicillin-binding protein 4 (PBP4). As the mechanism of the β-lactams is PBP inactivation, this result implies that the loss of the catalytic function of PBP4 ultimately leads to induction of antibiotic resistance. PBP4 is a bifunctional enzyme having both dd-carboxypeptidase and endopeptidase activities. Substrates for both the dd-carboxypeptidase and the 4,3-endopeptidase activities were prepared by multistep synthesis, and their turnover competence with respect to PBP4 was evaluated. The endopeptidase activity is specific to hydrolysis of 4,3-cross-linked peptidoglycan. PBP4 catalyzes both reactions equally well. When P. aeruginosa is grown in the presence of a strong inducer of AmpC, the quantities of both the stem pentapeptide (the substrate for the dd-carboxypeptidase activity) and the 4,3-cross-linked peptidoglycan (the substrate for the 4,3-endopeptidase activity) increase. In the presence of β-lactam antibiotics these altered cell-wall segments enter into the muropeptide recycling pathway, the conduit connecting the sensing event in the periplasm and the unleashing of resistance mechanisms in the cytoplasm.
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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.