ReviewCurrent protein & peptide science2012
Rational identification of enoxacin as a novel V-ATPase-directed osteoclast inhibitor.
Review in Current protein & peptide science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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.
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
21 citing papers in PubMed, 25 citations in OpenAlex.
- Canonical microRNA loss drives tumor development, implicating therapeutic efficacy of enoxacin in angiosarcoma.RNA (New York, N.Y.) · 2026Article
- Meta-analysis of functional genomics studies reveals conserved cellular pathways required by viruses of pandemic concern.Access microbiology · 2026Article
- Canonical microRNA loss drives tumor development implicating therapeutic efficacy of enoxacin in angiosarcoma.bioRxiv : the preprint server for biology · 2025Article
- Schisandrol A protects AGEs-induced neuronal cells death by allosterically targeting ATP6V0d1 subunit of V-ATPase.Acta pharmaceutica Sinica. B · 2022Article
- The New Face of a Well-Known Antibiotic: A Review of the Anticancer Activity of Enoxacin and Its Derivatives.Cancers · 2022Review
- Bisphosphonate-enoxacin inhibit osteoclast formation and function by abrogating RANKL-induced JNK signalling pathways during osteoporosis treatment.Journal of cellular and molecular medicine · 2021Article
- Selective toxicity of antibacterial agents-still a valid concept or do we miss chances and ignore risks?Infection · 2021Review
- Actin and Actin-Associated Proteins in Extracellular Vesicles Shed by Osteoclasts.International journal of molecular sciences · 2019Review
- Specialized Roles for Actin in Osteoclasts: Unanswered Questions and Therapeutic Opportunities.Biomolecules · 2019Review
- The proteome of extracellular vesicles released by clastic cells differs based on their substrate.PloS one · 2019Article
- Enoxacin and bis-enoxacin stimulate 4T1 murine breast cancer cells to release extracellular vesicles that inhibit osteoclastogenesis.Scientific reports · 2018Article
- L-plastin phosphorylation regulates the early phase of sealing ring formation by actin bundling process in mouse osteoclasts.Experimental cell research · 2018Article
- V-ATPases and osteoclasts: ambiguous future of V-ATPases inhibitors in osteoporosis.Theranostics · 2018Review
- Vacuolar HBiotarget · 2017Article
- Direct interaction of the Golgi V-ATPase a-subunit isoform with PI(4)P drives localization of Golgi V-ATPases in yeast.Molecular biology of the cell · 2017Article
- Bovine parathyroid hormone enhances osteoclast bone resorption by modulating V-ATPase through PTH1R.International journal of molecular medicine · 2016Article
- A New Tool for in vivo Manipulation of Brain microRNA Levels: The Work of Smalheiser et al. (2014).Frontiers in psychiatry · 2015Article
- Article
- Bis-enoxacin inhibits bone resorption and orthodontic tooth movement.Journal of dental research · 2013Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Binding between vacuolar H+-ATPases (V-ATPases) and microfilaments is mediated by an actin binding domain in the B-subunit. Both isoforms of mammalian B-subunit bind microfilaments with high affinity. A similar actinbinding activity has been demonstrated in the B-subunit of yeast. A conserved "profilin-like" domain in the B-subunit mediates this actin-binding activity, named due to its sequence and structural similarity to an actin-binding surface of the canonical actin binding protein profilin. Subtle mutations in the "profilin-like" domain eliminate actin binding activity without disrupting the ability of the altered protein to associate with the other subunits of V-ATPase to form a functional proton pump. Analysis of these mutated B-subunits suggests that the actin-binding activity is not required for the "housekeeping" functions of V-ATPases, but is important for certain specialized roles. In osteoclasts, the actin-binding activity is required for transport of V-ATPases to the plasma membrane, a prerequisite for bone resorption. A virtual screen led to the identification of enoxacin as a small molecule that bound to the actin-binding surface of the B2-subunit and competitively inhibited B2-subunit and actin interaction. Enoxacin disrupted osteoclastic bone resorption in vitro, but did not affect osteoblast formation or mineralization. Recently, enoxacin was identified as an inhibitor of the virulence of Candida albicans and more importantly of cancer growth and metastasis. Efforts are underway to determine the mechanisms by which enoxacin and other small molecule inhibitors of B2 and microfilament binding interaction selectively block bone resorption, the virulence of Candida, cancer growth, and metastasis.
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What OpenQuestion holds
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.