ArticlemLife2026
Mechanistic insights into HipA-mediated bacterial persistence: Role of initial cellular states and toxin expression kinetics.
Article in mLife, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Persistent bacteria subpopulations showing multidrug tolerance pose significant challenges to antibiotic therapy. While the HipBA toxin-antitoxin (TA) system is known to play a role in persister formation, existing studies predominantly focus on its kinase activity and intracellular regulatory pathways, with limited attention to the environmental or conditional factors. In this study, we administered controlled induction of HipA across varied growth conditions in
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Registered trials
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.