ArticleNature communications2015
Pharmaceutical screen identifies novel target processes for activation of autophagy with a broad translational potential.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
What it found
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Who cites it
77 citing papers in PubMed, 144 citations in OpenAlex.
- Respiratory syncytial virus-induced SIGLEC1 upregulation inhibits macrophage autophagy and facilitates inflammatory mediator secretion.BMJ open respiratory research · 2026Article
- Expansion of lysosomal capacity in early adult neurons driven by TFEB/HLH-30 protects dendrite maintenance during aging in Caenorhabditis elegans.PLoS biology · 2025Article
- Critical dysregulated signaling pathways in drug resistance: highlighting the repositioning of mebendazole for cancer therapy.Frontiers in pharmacology · 2025Review
- Design and validation of a reporter mouse to study the dynamic regulation of TFEB and TFE3 activity throughAutophagy · 2024Article
- A SPLICS reporter reveals [Formula: see text]-synuclein regulation of lysosome-mitochondria contacts which affects TFEB nuclear translocation.Nature communications · 2024Article
- The post-translational regulation of transcription factor EB (TFEB) in health and disease.EMBO reports · 2023Review
- A perspective on autophagy and transcription factor EB in Alcohol-Associated Alzheimer's disease.Biochemical pharmacology · 2023Review
- Novel Insight into Functions of Transcription Factor EB (TFEB) in Alzheimer's Disease and Parkinson's Disease.Aging and disease · 2023Review
- Functional TFEB activation characterizes multiple models of renal cystic disease and loss of polycystin-1.American journal of physiology. Renal physiology · 2023Article
- Beta-coronaviruses exploit cellular stress responses by modulating TFEB and TFE3 activity.iScience · 2023Article
- Euphejolkinolide A, a newHeliyon · 2023Article
- TRPML1 and TFEB, an Intimate Affair.Handbook of experimental pharmacology · 2023Article
- Transcription factor EB as a key molecular factor in human health and its implication in diseases.SAGE open medicine · 2023Review
- Review
- Designing of immunodiagnostic assay using polyclonal antibodies for detection of Shiga toxin producing pathogenic E. coli (STEC) strains.World journal of microbiology & biotechnology · 2022Article
- Flubendazole induces mitochondrial dysfunction and DRP1-mediated mitophagy by targeting EVA1A in breast cancer.Cell death & disease · 2022Article
- Impairment of the autophagy-lysosomal pathway in Alzheimer's diseases: Pathogenic mechanisms and therapeutic potential.Acta pharmaceutica Sinica. B · 2022Review
- Machine learning prediction and tau-based screening identifies potential Alzheimer's disease genes relevant to immunity.Communications biology · 2022Article
- Current Status of Autophagy Enhancers in Metabolic Disorders and Other Diseases.Frontiers in cell and developmental biology · 2022Review
- Interactions of Autophagy and the Immune System in Health and Diseases.Autophagy reports · 2022Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 2 countries.
Funding
Abstract
Autophagy is a conserved homeostatic process active in all human cells and affecting a spectrum of diseases. Here we use a pharmaceutical screen to discover new mechanisms for activation of autophagy. We identify a subset of pharmaceuticals inducing autophagic flux with effects in diverse cellular systems modelling specific stages of several human diseases such as HIV transmission and hyperphosphorylated tau accumulation in Alzheimer's disease. One drug, flubendazole, is a potent inducer of autophagy initiation and flux by affecting acetylated and dynamic microtubules in a reciprocal way. Disruption of dynamic microtubules by flubendazole results in mTOR deactivation and dissociation from lysosomes leading to TFEB (transcription factor EB) nuclear translocation and activation of autophagy. By inducing microtubule acetylation, flubendazole activates JNK1 leading to Bcl-2 phosphorylation, causing release of Beclin1 from Bcl-2-Beclin1 complexes for autophagy induction, thus uncovering a new approach to inducing autophagic flux that may be applicable in disease treatment.
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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.