ArticleNature structural & molecular biology2025
Structural insights into TRPV2 modulation by probenecid.
Article in Nature structural & molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Large-Pore Channels at the Maternal-Fetal Interface: Progress and Open Research Avenues.Biology · 2026Review
- Inactivation Switch for Run-up in TRPV2.Research square · 2026Article
- Thermodynamic coupling between cold and heat activations of TRPV2.Scientific reports · 2026Article
- Visualizing insecticide control of insect TRP channel function and assembly.Nature communications · 2025Article
- Visualization of lysosomal membrane proteins by cryo electron tomography.Nature communications · 2025Article
- Determinants for Activation of the Ion Channel TRPV3 by Weak Acids.International journal of molecular sciences · 2025Article
- Molecular determinants of 2-aminoethoxydiphenyl borate sensitivity of transient receptor potential vanilloid 2-unexpected differences between 2 rodent orthologs.Molecular pharmacology · 2025Article
- Current status, hotspots and frontiers of ion channel-related research in glioblastoma: a bibliometric analysis from 2005 to 2024.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transient receptor potential vanilloid 2 (TRPV2) cation channel is a key player in cardiovascular physiology and pathophysiology. Probenecid (PBC), an FDA-approved uricosuric agent thought to activate TRPV2, has shown promise in enhancing cardiovascular function in both preclinical and clinical studies. Here our electrophysiological data reveal that PBC significantly potentiates rat TRPV2 to known stimuli, and cryo electron microscopy structures show that PBC directly interacts with rat TRPV2 in a previously unidentified intracellular binding pocket. PBC binding at a conserved TRPV2-specific histidine prevents the channel from taking on the inactivated carboxyl-terminal conformation. This effect extends to TRPV1 and TRPV3 channels when glutamine is substituted with histidine at the corresponding position, increasing their sensitivity to PBC. While PBC alone does not induce TRPV2 opening, its combination with 2-aminoethoxydiphenyl borate enables the channel to adopt an intermediate, potentiated state. Our results offer insights into potential therapeutic advancements for TRPV2 through this pocket.
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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.