Evidence map›Paper›PMID 42586984›Full record

ArticleNature communications2026

A systematic identification of resistance determinants to antisense antibiotics suggests adaptation strategies dependent on the delivery peptide.

Adam J Mulkern, Thu-Hien Vu, Linda Popella, Tobias Kerrinnes, Svetlana Ðurica-Mitić, Manuel Halte, Kylee Dresbach-Hill, Anne-Catrin Uhlemann, Stephan Uphoff, Lars Barquist and 2 more

Abstract read
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Adam J MulkernInstitute for Molecular Bacteriology, TWINCORE Centre for Experimental and Clinical Infection Research, a joint venture between the Hannover Medical School (MHH) and the Helmholtz Centre for Infection Research (HZI), Hannover, Germany.ORCID http://orcid.org/0000-0002-5246-6617
Thu-Hien VuInstitute for Molecular Bacteriology, TWINCORE Centre for Experimental and Clinical Infection Research, a joint venture between the Hannover Medical School (MHH) and the Helmholtz Centre for Infection Research (HZI), Hannover, Germany.
Linda PopellaInstitute of Molecular Infection Biology, University of Würzburg, Würzburg, Germany.ORCID http://orcid.org/0000-0002-5309-5838
Tobias KerrinnesHelmholtz Institute for RNA-based Infection Research (HIRI), Helmholtz Centre for Infection Research (HZI), Würzburg, Germany.
Svetlana Ðurica-MitićInstitute of Molecular Infection Biology, University of Würzburg, Würzburg, Germany.
Manuel HalteDepartment of Biochemistry, University of Oxford, Oxford, UK.
Kylee Dresbach-HillDepartment of Nutritional and Metabolic Biology, Columbia University Irving Medical Center, New York, NY, USA.
Anne-Catrin UhlemannDivision of Infectious Diseases, Columbia University Irving Medical Center, New York, NY, USA.ORCID http://orcid.org/0000-0002-9798-4768
Stephan UphoffDepartment of Biochemistry, University of Oxford, Oxford, UK.ORCID http://orcid.org/0000-0002-3579-0888
Lars BarquistHelmholtz Institute for RNA-based Infection Research (HIRI), Helmholtz Centre for Infection Research (HZI), Würzburg, Germany.ORCID http://orcid.org/0000-0003-4732-2667
Jörg VogelInstitute of Molecular Infection Biology, University of Würzburg, Würzburg, Germany.ORCID http://orcid.org/0000-0003-2220-1404
Marco GalardiniInstitute for Molecular Bacteriology, TWINCORE Centre for Experimental and Clinical Infection Research, a joint venture between the Hannover Medical School (MHH) and the Helmholtz Centre for Infection Research (HZI), Hannover, Germany. galardini.marco@mh-hannover.de.ORCID http://orcid.org/0000-0003-2018-8242

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) 390874280Deutsche Forschungsgemeinschaft (German Research Foundation) Vo875-18
6 · The paper itself

Abstract

The rise of antimicrobial resistance (AMR) among human pathogens is a serious threat to global health, demanding novel treatment strategies. Antibiotics based on programmable antisense oligomers (asobiotics) offer an attractive solution, as their specificity can be quickly updated to target resistant bacteria. To understand the genetic architecture of resistance to asobiotics, we used laboratory evolution assays to identify mutations that decrease susceptibility to antisense peptide nucleic acids (PNAs) in four major gram-negative pathogens: Escherichia coli, Klebsiella pneumoniae, Salmonella enterica, and Pseudomonas aeruginosa. Reduced susceptibility depended on the cell-penetrating peptide (CPP) conjugated to the PNA, with reduced uptake emerging as a common adaptation only against the (KFF)

Indexed as

Anti-Bacterial AgentsCell-Penetrating PeptidesDrug Resistance, BacterialOligonucleotides, AntisensePeptide Nucleic AcidsAdaptation, PhysiologicalBacterial ProteinsEscherichia coliEscherichia coli ProteinsKlebsiella pneumoniaeMembrane Transport ProteinsMicrobial Sensitivity TestsMutationPseudomonas aeruginosaSalmonella entericaAnti-Bacterial AgentsBacterial ProteinsCell-Penetrating PeptidesEscherichia coli ProteinsMembrane Transport ProteinsOligonucleotides, AntisensePeptide Nucleic AcidsSbmA protein, E coli

Identifiers

PMID42586984
PMCPMC13469510

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.