ArticlemSphere2021
Collateral Sensitivity to β-Lactam Drugs in Drug-Resistant Tuberculosis Is Driven by the Transcriptional Wiring of BlaI Operon Genes.
Article in mSphere, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Evolutionary trajectories determine feasibility of collateral sensitivity-based antibiotic treatment strategies in critical bacterial pathogens.Communications biology · 2025Article
- Navigating collateral sensitivity: insights into the mechanisms and applications of antibiotic resistance trade-offs.Frontiers in microbiology · 2024Review
- Article
- Transcriptional regulation and drug resistance inFrontiers in cellular and infection microbiology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The evolution of resistance to one antimicrobial can result in enhanced sensitivity to another, known as "collateral sensitivity." This underexplored phenomenon opens new therapeutic possibilities for patients infected with pathogens unresponsive to classical treatments. Intrinsic resistance to β-lactams in Mycobacterium tuberculosis (the causative agent of tuberculosis) has traditionally curtailed the use of these low-cost and easy-to-administer drugs for tuberculosis treatment. Recently, β-lactam sensitivity has been reported in strains resistant to classical tuberculosis therapy, resurging the interest in β-lactams for tuberculosis. However, a lack of understanding of the molecular underpinnings of this sensitivity has delayed exploration in the clinic. We performed gene expression and network analyses and
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