TRPV2 (Transient Receptor Potential Cation Channel Subfamily V Member 2)

Our data also provide the first evidence of heat-induced activation of human TRPV2. Considering previous evidence for TRPV2 and TRPC5 expression in the oral cavity and their roles in oral pain and cancer, our findings indicate that these polymodal channels may participate not only in detecting specific astringent compounds, but also in mediating their broader health-related and anesthetic actions.

Although the R-CHOP regimen has significantly improved the prognosis for most patients, a subset continues to experience poor therapeutic outcomes...The key gene TRPV2, associated with favorable prognosis, was found to promote M1-like polarization in monocytes/macrophages and enhance antigen presentation in B cells. This study establishes the NR risk score as a novel prognostic tool for DLBCL and underscores neuro-immune interactions as potential therapeutic targets.

Instead, tranilast seems to indirectly suppress channel activation by reducing reactive oxygen species (ROS). This refined understanding of how tranilast modulates TRPV2 has important implications for the interpretation of prior and future pharmacological studies targeting TRPV2.

Consequently, TRPV2 governs type I interferon production and natural killer cell-mediated cytotoxicity through the cGAS/STING pathway. The dual roles of TRPV2 provide an elegant mechanism for a balanced innate immune response.

However, 3 µM LPC induced a reversible potentiation of membrane currents induced by 2-APB, cannabidiol (CBD), probenecid (PBC) and weak acids, but not to heat...A disruption of the actin cytoskeleton with cytochalasin D, but also the depletion of cholesterol or sphingomyelin from the cell membrane diminished the potentiating effects of LPC on TRPV2. In conclusion, we present novel data describing that the PLA2 downstream signaling lipid LPC amplifies TRPV2-mediated responses via indirect mechanisms that seem to involve a destabilization of lipid rafts and the actin cytoskeleton.

Cells lacking TRPV2 fail to generate membrane currents induced by the nonselective TRPV-agonists 2-aminoethoxydiphenyl borate (2-APB) and probenecid (PBC), and they exhibit reduced proliferation, cell adhesion, migration and phagocytosis...Our data suggest that TRPV2 regulates actin-dependent mast cell-like properties of RBL2-2H3 cells. PBC can be used as a pharmacological tool to induce a TRPV2-dependent but IgE-independent degranulation, and it employs a novel molecular mechanism to activate TRPV2 in a proton-dependent manner.

This study identifies lipidome patterns as a risk factor for patient prognosis. Mechanistically, deficient PPARα-mediated lipophagy leads to the accumulation of ether-lipids within cancer cells, which in turn promotes cell mobility via calcium-dependent, TRPV2 channel-mediated cytoskeletal rearrangement.

Our data suggest that SET2 has high plasma bioavailability, limited tissue distribution, and is rapidly cleared. While acute cardiovascular effects were minimal, the troponin I elevation warrants further safety evaluation in chronic studies.

The study findings suggested that TRPV2 controls the proliferation, apoptosis, and migration of CC cells. Furthermore, the study identified high TRPV2 expression as a poor prognostic factor for patients with CC.

For both mTRPV2 and rTRPV2, we observed that the exchange of putative 2-APB binding residues within the vanilloid binding pocket alters overall channel sensitivity to 3 TRPV2 pharmacological activators that bind at different sites: 2-APB, cannabidiol, and probenecid...SIGNIFICANCE STATEMENT: This study resolves the conflict regarding how 2-aminoethoxydiphenyl borate binds to transient receptor potential vanilloid 2 (TRPV2), showing a shared mechanism despite sensitivity differences. These findings enhance TRPV2 modulation insights and highlight species considerations in drug design, aiding the development of selective TRPV2-targeted therapies.