ArticleCells2019
Niclosamide Triggers Non-Canonical LC3 Lipidation.
Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 33 citations in OpenAlex.
- Broad-spectrum host-targeting antivirals for rhinovirus infections: mechanisms and future perspectives.Frontiers in immunology · 2026Review
- CARMIL1-AA selectively inhibits macropinocytosis while sparing autophagy.Molecular biology of the cell · 2025Article
- Non-autophagic Golgi-LC3 lipidation facilitates TFE3 stress response against Golgi dysfunction.The EMBO journal · 2024Article
- Missing WD40 Repeats in ATG16L1 Delays Canonical Autophagy and Inhibits Noncanonical Autophagy.International journal of molecular sciences · 2024Article
- New Salicylanilide Derivatives and Their Peptide Conjugates as Anticancer Compounds: Synthesis, Characterization, andACS omega · 2024Article
- Anti-influenza A (H1N1) virus effect of gallic acid through inhibition of virulent protein production and association with autophagy.Food science & nutrition · 2024Article
- Noncanonical autophagy is a new strategy to inhibit HSV-1 through STING1 activation.Autophagy · 2023Article
- Niclosamide as a chemical probe for analyzing SARS-CoV-2 modulation of host cell lipid metabolism.Frontiers in microbiology · 2023Article
- Toosendanin Induces Hepatocyte Damage by Inhibiting Autophagic Flux via TFEB-Mediated Lysosomal Dysfunction.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Many roads lead to CASM: Diverse stimuli of noncanonical autophagy share a unifying molecular mechanism.Science advances · 2022Review
- Discovery of an autophagy inducer J3 to lower mutant huntingtin and alleviate Huntington's disease-related phenotype.Cell & bioscience · 2022Article
- Identification of a novel compound that simultaneously impairs the ubiquitin-proteasome system and autophagy.Autophagy · 2022Article
- Article
- Targeting S100A4 with niclosamide attenuates inflammatory and profibrotic pathways in models of amyotrophic lateral sclerosis.Journal of neuroinflammation · 2021Article
- Coronavirus Interplay With Lipid Rafts and Autophagy Unveils Promising Therapeutic Targets.Frontiers in microbiology · 2020Review
- Maternal-to-zygotic transition as a potential target for niclosamide during early embryogenesis.Toxicology and applied pharmacology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is a highly- evolutionarily-conserved catabolic pathway activated by various cellular stresses. Recently, non-canonical autophagy (NCA), which does not require all of the ATG proteins to form autophagosome or autophagosome-like structures, has been found in various conditions. Moreover, mounting evidence has indicated that non-canonical LC3 lipidation (NCLL) may reflect NCA. We and others have reported that niclosamide (Nic), an anti-helminthic drug approved by the Food and Drug Administration, could induce canonical autophagy via a feedback downregulation of mTOR complex 1. In this study, we found that Nic could also induce NCLL, which is independent of the ULK1 complex and Beclin 1 complex, but dependent on ubiquitin-like conjugation systems. Although bafilomycin A1 and concanamycin A, two known V-ATPase inhibitors, significantly inhibited Nic-induced NCLL, Nic-induced NCLL was demonstrated to be independent of V-ATPase. In addition, the Golgi complex and vimentin were involved in Nic-induced NCLL, which might be a platform or membrane source for Nic-induced LC3-positive structures. These results would be helpful to broaden our understanding of the working mechanisms of Nic and evaluate its pharmacological activities in diseases.
Indexed as
Identifiers
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.