ArticleNature chemical biology2020
Functional dissection of the retrograde Shiga toxin trafficking inhibitor Retro-2.
Article in Nature chemical biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- Retrograde trafficking inhibitors allosterically trap Get3 to block tail-anchored protein biogenesis.bioRxiv : the preprint server for biology · 2026Article
- Repurposing screens reveal a role for PKCη and NF1 in SARS-CoV-2 infection.PLoS pathogens · 2026Article
- Shiga toxin-centered pathophysiology defines the therapeutic limits of enterohemorrhagic Escherichia coli infection.Archives of microbiology · 2026Review
- Stress-induced proteome remodeling at the Golgi-endosome interface.Journal of cell science · 2026Article
- Towards a unified framework for the function of endoplasmic reticulum exit sites.Nature reviews. Molecular cell biology · 2025Review
- Diabetes mellitus and the key role of endoplasmic reticulum stress in pancreatic β cells.Nature reviews. Endocrinology · 2025Review
- Inhibition of OSBP blocks retrograde trafficking by inducing partial Golgi degradation.Nature chemical biology · 2025Article
- Development of Effective Medical Countermeasures Against the Main Biowarfare Agents: The Importance of Antibodies.Microorganisms · 2024Review
- Fragment Screening to Identify Inhibitors Targeting Ribosome Binding of Shiga Toxin 2.ACS infectious diseases · 2024Article
- TANGO1 inhibitors reduce collagen secretion and limit tissue scarring.Nature communications · 2024Article
- Spatiotemporal proteomic profiling of cellular responses to NLRP3 agonists.bioRxiv : the preprint server for biology · 2024Article
- Kennedy Epitope (KE)-dependent Retrograde Transport of Efficiently Cleaved HIV-1 Envelopes (Envs) and its Effect on Env Cell Surface Expression and Viral Particle Formation.The protein journal · 2024Article
- ER exit in physiology and disease.Frontiers in molecular biosciences · 2024Review
- A New Derivative of Retro-2 Displays Antiviral Activity against Respiratory Syncytial Virus.International journal of molecular sciences · 2023Article
- Syntaxin-5's flexibility in SNARE pairing supports Golgi functions.Traffic (Copenhagen, Denmark) · 2023Article
- Medical Countermeasures against Ricin Intoxication.Toxins · 2023Review
- Sec22b is a critical and nonredundant regulator of plasma cell maintenance.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Common Markers and Small Molecule Inhibitors in Golgi Studies.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Diagnosis and Treatment for Shiga Toxin-ProducingToxins · 2022Review
- In Vivo Sustained Release of the Retrograde Transport Inhibitor Retro-2.1 Formulated in a Thermosensitive Hydrogel.International journal of molecular sciences · 2022Article
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Authors and funding
20 authors at 4 institutions in 2 countries.
Funding
Abstract
The retrograde transport inhibitor Retro-2 has a protective effect on cells and in mice against Shiga-like toxins and ricin. Retro-2 causes toxin accumulation in early endosomes and relocalization of the Golgi SNARE protein syntaxin-5 to the endoplasmic reticulum. The molecular mechanisms by which this is achieved remain unknown. Here, we show that Retro-2 targets the endoplasmic reticulum exit site component Sec16A, affecting anterograde transport of syntaxin-5 from the endoplasmic reticulum to the Golgi. The formation of canonical SNARE complexes involving syntaxin-5 is not affected in Retro-2-treated cells. By contrast, the interaction of syntaxin-5 with a newly discovered binding partner, the retrograde trafficking chaperone GPP130, is abolished, and we show that GPP130 must indeed bind to syntaxin-5 to drive Shiga toxin transport from the endosomes to the Golgi. We therefore identify Sec16A as a druggable target and provide evidence for a non-SNARE function for syntaxin-5 in interaction with GPP130.
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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.