Evidence map›Paper›PMID 25403660›Full record

ArticleAntimicrobial agents and chemotherapy2015

Novel strategy for biofilm inhibition by using small molecules targeting molecular chaperone DnaK.

Ken-ichi Arita-Morioka, Kunitoshi Yamanaka, Yoshimitsu Mizunoe, Teru Ogura, Shinya Sugimoto

Open access · bronzeAbstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
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

40 citing papers in PubMed, 82 citations in OpenAlex.

  1. A Small Molecule Substrate Mimic to Inhibit Bacterial Hsp70 Chaperone Function.Chembiochem : a European journal of chemical biology · 2026
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  4. The Role ofInternational journal of molecular sciences · 2025
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  6. SMR peptide antagonizesMicrobiology spectrum · 2024
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  9. Frontiers in cellular and infection microbiology · 2022
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  10. Review
  11. Pathogens (Basel, Switzerland) · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
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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

5 authors at 2 institutions in 1 country.

Ken-ichi Arita-MoriokaDepartment of Molecular Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan.
Kunitoshi YamanakaDepartment of Molecular Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan.
Yoshimitsu MizunoeDepartment of Bacteriology, The Jikei University School of Medicine, Tokyo, Japan.
Teru OguraDepartment of Molecular Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Kumamoto, Japan.
Shinya SugimotoDepartment of Bacteriology, The Jikei University School of Medicine, Tokyo, Japan ssugimoto@jikei.ac.jp.
Kumamoto University · JPJikei University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Biofilms are complex communities of microorganisms that attach to surfaces and are embedded in a self-produced extracellular matrix. Since these cells acquire increased tolerance against antimicrobial agents and host immune systems, biofilm-associated infectious diseases tend to become chronic. We show here that the molecular chaperone DnaK is important for biofilm formation and that chemical inhibition of DnaK cellular functions is effective in preventing biofilm development. Genetic, microbial, and microscopic analyses revealed that deletion of the dnaK gene markedly reduced the production of the extracellular functional amyloid curli, which contributes to the robustness of Escherichia coli biofilms. We tested the ability of DnaK inhibitors myricetin (Myr), telmisartan, pancuronium bromide, and zafirlukast to prevent biofilm formation of E. coli. Only Myr, a flavonol widely distributed in plants, inhibited biofilm formation in a concentration-dependent manner (50% inhibitory concentration [IC50] = 46.2 μM); however, it did not affect growth. Transmission electron microscopy demonstrated that Myr inhibited the production of curli. Phenotypic analyses of thermosensitivity, cell division, intracellular level of RNA polymerase sigma factor RpoH, and vulnerability to vancomycin revealed that Myr altered the phenotype of E. coli wild-type cells to make them resemble those of the isogenic dnaK deletion mutant, indicating that Myr inhibits cellular functions of DnaK. These findings provide insights into the significance of DnaK in curli-dependent biofilm formation and indicate that DnaK is an ideal target for antibiofilm drugs.

Indexed as

BenzimidazolesBenzoatesBiofilmsDose-Response Relationship, DrugEscherichia coliEscherichia coli ProteinsFlavonoidsHSP70 Heat-Shock ProteinsIndolesInhibitory Concentration 50Methicillin-Resistant Staphylococcus aureusMolecular ChaperonesMolecular Targeted TherapyPancuroniumPhenylcarbamatesStaphylococcus aureusBenzimidazolesBenzoatesdnaK protein, E coliEscherichia coli ProteinsFlavonoidsHSP70 Heat-Shock ProteinsIndolesMolecular ChaperonesmyricetinPancuroniumPhenylcarbamatesSulfonamidesTelmisartanTosyl CompoundsVancomycinzafirlukast

Identifiers

PMID25403660
PMCPMC4291377
OpenAlexW2142791469

What OpenQuestion 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 OpenQuestion graph.