TRPV1 _ Vanilloid receptor 1
- Known as:
- TRPV1 _ Vanilloid receptor 1
- Catalog number:
- VR11-A
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- TRPV1 _ Vanilloid receptor 1
Ask about this productRelated genes to: TRPV1 _ Vanilloid receptor 1
- Gene:
- TRPV1 NIH gene
- Name:
- transient receptor potential cation channel subfamily V member 1
- Previous symbol:
- VR1
- Synonyms:
- -
- Chromosome:
- 17p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-12-05
- Date modifiied:
- 2016-01-28
Related products to: TRPV1 _ Vanilloid receptor 1
"Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP"(Ala1)-PAR-4 (1-6) (mouse)
(Ala1)-Thrombin Receptor-Like 3 (1-6) (mouse), (Ala1)-Proteinase Activated Receptor 4 (1-6) (mouse), (Ala1)-Coagulation Factor II Receptor-Like 3 (1-6) (mouse), AYPGKF 98%(Ala1)-PAR-4 (1-6) amide (mouse)
AYPGKFamide, (Ala1)-Thrombin Receptor-Like 3 (1-6) amide (mouse), (Ala1)-Coagulation Factor II Receptor-Like 3 (1-6) amide (mouse), (Ala1)-Proteinase Activated Recepto(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II Related articles to: TRPV1 _ Vanilloid receptor 1
- Excessive dietary salt intake poses significant health risks and is closely associated with the pathogenesis of hypertension and cardiovascular diseases. Developing strategies that achieve salt reduction without compromising saltiness perception has become a major focus in food science and public health research. The study and application of kokumi peptides provide a novel approach to achieving "salt reduction without loss of saltiness." Although kokumi substances themselves are usually tasteless or only weakly flavored, they can markedly enhance the intensity and persistence of other taste modalities within complex food systems, thereby improving overall flavor perception. Kokumi peptides are widely derived from natural food sources and can effectively reduce sodium intake without sacrificing palatability, showing remarkable potential for food applications. This review systematically summarizes the primary preparation methods, sensory evaluation techniques, and molecular mechanisms underlying the salt-enhancing properties of kokumi peptides. Particular emphasis is placed on calcium-sensing receptor (CaSR)-mediated taste sensation and its potential crosstalk with key salt-taste transduction pathways, including the epithelial sodium channel (ENaC), transient receptor potential vanilloid 1 (TRPV1), and transmembrane channel-like protein 4 (TMC4). Moreover, the review discusses the potential applications of kokumi peptides in salt-reduced foods and seasonings, as well as their roles in flavor enhancement, physiological activity, and multisensory synergy. Finally, the current challenges in kokumi peptide research are identified, and promising prospects for health-oriented food innovation and salt-reduction strategy optimization are proposed. - Source: PubMed
Sun TingtingFeng TaoJiang TaoKhan Mati UllahWang HuatianYao LingyunSong ShiqingSun MinYu Chuang - Ovarian cancer remains among the most lethal gynecological malignancies, primarily due to the persistent challenges of chemotherapy resistance and limited effectiveness of existing therapeutic strategies. - Source: PubMed
Publication date: 2026/07/10
Kim Tae Woo - Autonomic dysreflexia (AD) is a severe and potentially life-threatening complication of a spinal cord injury (SCI), particularly in patients with lesions at or above the sixth thoracic level. Neurogenic detrusor overactivity (NDO) is one of the main triggering factors. The impact of NDO treatment on AD remains insufficiently clarified. - Source: PubMed
Publication date: 2026/07/08
Le Ba ThienDenys PierreJoussain Charles - The excitability of afferents involved in nociceptive signaling reflects the interaction of several co-expressed membrane receptors. Current studies have shown that Toll-like receptor-4 (TLR-4) signaling can exacerbate excitation evoked by transient receptor potential vanilloid type 1 (TRPV1) activity, and this interaction plays a key role in driving and sustaining facilitated pain states. The mechanism by which this potentiated TRPV1 activity secondary to TLR-4 agonism occurs in sensory neurons remains unknown, although intracellular kinase activity is a strong candidate. To address this hypothesized linkage, neuronal cell cultures prepared from dorsal root ganglia (DRG) of male wildtype (WT) and mice were used to evaluate calcium transients of neurons after capsaicin administration in culture, pre-treated for 30 minutes with the TLR-4 agonist, lipopolysaccharide (LPS). TRPV1 protein expression at the neuron surface in cultured DRG cells with or without LPS treatment was quantified by flow cytometry assay. The roles of protein kinase A (PKA) and C were assessed using selective inhibitors (KT5720 for PKA and Chelerythrine chloride for PKC) applied to WT-DRG neurons or administered in vivo by intraplantar or intrathecal injection, prior to LPS and capsaicin administration. Behavioral effects of in vivo TRPV1 activation were assessed through paw flinch responses evoked by intraplantar capsaicin injection and by hind paw tactile thresholds measured by von Frey filaments. LPS incubation in cultured DRG neurons enhances the intensity of calcium influx following TRPV1 activation in WT but not cells. The augmented calcium influx evoked by capsaicin was prevented by the inhibition of PKA but not PKC. Similarly, mice treated with LPS in the hind paw displayed greater nociceptive responding after capsaicin and increased tactile allodynia. The facilitated component was prevented by the local pre-treatment with the PKA inhibitor. Correspondingly, lumbar spinal blockade of PKA resulted in temporary reversal of hyperalgesia induced by intrathecal LPS injection in mice. Together, these results demonstrate the relevance of TLR-4 in modulating the excitability of nociceptor signaling by regulating TRPV1, thereby influencing pain transmission through PKA signaling. - Source: PubMed
Publication date: 2026/06/29
Borges Paes Lemes JuliaFranco Malange KauêPanichkina AlisaNavia-Pelaez JulianaChoi Soo-HoDolmat MaksimGonçalves Dos Santos GilsonDochnal SaraCorr MaripatMiller Yury IYaksh Tony - Epilepsy affects approximately 50 million people worldwide, with nearly 30% of patients exhibiting drug-resistant seizures despite treatment with multiple antiepileptic drugs (AEDs). In this context, cannabidiol (CBD) has emerged as a promising therapeutic candidate. This review examines the mechanistic basis of CBD's antiepileptic effects, focusing on its modulation of neurotransmitter systems, ion channels, and neuroinflammatory pathways, alongside its relevance in current clinical practice. By integrating mechanistic neuropharmacology with a critical appraisal of clinical trial data, this review identifies key translational gaps that may limit the optimization of CBD-based therapeutic strategies. The pharmacokinetic profile of CBD varies across routes of administration and is associated with clinically significant drug-drug interactions, particularly via inhibition of CYP2C19 and CYP3A4, thereby influencing the plasma levels and safety of concomitant AEDs. While emerging evidence supports the efficacy of CBD in certain refractory epilepsies, comprehensive and standardized evaluations across broader epilepsy subtypes remain limited. Safety concerns, including long-term outcomes and interaction profiles, necessitate careful patient monitoring and dose individualization. Furthermore, the evolving regulatory landscape and increasing consumer-driven use underscore the need for robust evidence generation, interdisciplinary collaboration, and standardized clinical protocols. Overall, this review aims to delineate the therapeutic potential of CBD in epilepsy management, positioning it as a valuable adjunct in the antiepileptic armamentarium. Notably, it uniquely integrates a critical mechanistic comparison of GPR55 and TRPV1 pathways-including conflicting evidence-with a structured critique of clinical trials and explicit evidence-level grading to support clinical recommendations. - Source: PubMed
Publication date: 2026/06/26
Gupta NishaMaan PreetiShrivastava JyotiAnsari Mohd Hafizur Rehman