TRPV3, control peptide, goat, 50 ug.
- Known as:
- TRPV3, reference short protein sequence, caprine, 50 ug.
- Catalog number:
- P15180
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- TRPV3 control peptide goat 50 .
Related genes to: TRPV3, control peptide, goat, 50 ug.
- Gene:
- TRPV3 NIH gene
- Name:
- transient receptor potential cation channel subfamily V member 3
- Previous symbol:
- -
- Synonyms:
- VRL3
- Chromosome:
- 17p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-07-05
- Date modifiied:
- 2016-10-05
Related products to: TRPV3, control peptide, goat, 50 ug.
Related articles to: TRPV3, control peptide, goat, 50 ug.
- Transient receptor potential vanilloid 3 (TRPV3) is a non-selective cation channel highly expressed in the skin and intestine. While its roles in itch and skin inflammation are established, the physiological role of TRPV3 in the intestine remains relatively poorly understood. Topical application of a TRPV3 inhibitor, KM-001, has entered phase I clinical trials for the treatment of pruritus; however, its poor metabolic stability limits broader therapeutic application. Here, we show that the KM-001-derivative Colivin has comparable TRPV3-blocking activity, but enhanced metabolic stability and increased oral bioavailability. Cryo-EM and site-directed mutagenesis analyses established that Colivin binds to the vanilloid binding pocket of TRPV3, stabilizing one of two distinct non-conducting conformations. Oral administration of Colivin effectively suppressed DSS-induced ulcerative colitis (UC) in wild-type, but not Trpv3-deficient mice. Collectively, our findings establish TRPV3 inhibition as a novel therapeutic strategy for UC, offer key structural insights into the inhibition mechanism of TRPV3, and provide critical structural insights for the rational design of potent and selective TRPV3 inhibitors. - Source: PubMed
Publication date: 2026/08/13
Wang YujingChen JiahuiTang QinglianQin XuWang ShuxianXi ChuchuLu ZhaowenRen KeruiXue ChuShen JianhuaWang KaiZhu Michael XYu JieCao Zhengyu - In traditional Chinese medicine, frankincense is widely recognized for its anti-inflammatory and immunomodulatory capacities and has been conventionally applied to manage multiple chronic inflammatory skin disorders. Nevertheless, its therapeutic potency and molecular mechanisms against atopic dermatitis (AD) remain poorly clarified. This study aimed to explore the protective efficacy of frankincense oil extract (FOE) and its active constituents in AD mouse models, thereby clarifying underlying regulatory mechanisms. Two classic AD models induced by 2,4-dinitrochlorobenzene (DNCB) and carvacrol were established to evaluate the therapeutic performance of FOE and its bioactive components. Hematoxylin-eosin and toluidine blue staining were applied to characterize lesional histopathological alterations, immunohistochemistry was used to detect expression profiles of TRPV3, β-catenin, and COX-2 in skin lesions, and calcium fluorescence imaging was applied to monitor TRPV3-mediated intracellular calcium dynamics. The results showed that FOE markedly alleviated typical AD-like manifestations, reducing inflammatory injury, ear edema and splenomegaly in DNCB- and carvacrol-challenged mice. Histological evaluation confirmed that FOE improved pathological lesions, mitigated epidermal hyperplasia, and reduced mast cell infiltration. Meanwhile, FOE remodeled the abnormal expression patterns of TRPV3, β-catenin, and COX-2 triggered by AD stimulation. Additionally, FOE effectively regulated carvacrol-evoked calcium influx mediated by TRPV3 activation. Collectively, FOE and its active components exert anti-inflammatory effects, restraining epidermal over-proliferation and ameliorating epidermal structural disorders, thereby supporting the restoration of epidermal tissue morphology. Such benefits are attributed to modulating TRPV3 activity and remodeling the cutaneous inflammatory microenvironment. This work highlights FOE as a promising novel candidate for atopic dermatitis intervention. - Source: PubMed
Publication date: 2026/08/06
Tan Gang-NingZhang Wen-ShengLi Yu-SangTang He-Bin - Chemical irritants or ultraviolet exposure can lead to an imbalance in skin barrier homeostasis and trigger various inflammatory skin diseases. Daphnetin, a bioactive coumarin compound extracted from the traditional Chinese medicine Cortex Daphnes (Zushima), has been shown to suppress skin lesions induced by chemical irritants such as DNCB or DNFB in mice. However, the molecular mechanism underlying the action of daphnetin remains unclear. Here, we report that daphnetin alleviates skin inflammation by directly targeting the calcium-permeable and warmth-selective TRPV3 channel. Subcutaneous administration or topical application of daphnetin efficaciously suppresses DNFB- or UVB-induced dermatitis in wild-type mice but confers no additional benefit in Trpv3 knockout mice. In whole-cell patch-clamp recordings, daphnetin selectively inhibits human and mouse TRPV3 channel currents induced by 2-APB in a concentration-dependent manner, with IC values of 19.91 ± 2.83 μM (hTRPV3) and 24.10 ± 2.20 μM (mTRPV3), respectively. The single-channel patch-clamp results show that daphnetin significantly reduces the open probability and open frequency without significantly altering the unitary conductance of TRPV3 channel. Molecular docking and site-directed mutagenesis indicate that residue Q580 on the S4-S5 linker and residue T665 on the S6 segment of TRPV3 are critical for daphnetin binding to TRPV3. Taken together, our results demonstrate that daphnetin exerts its anti-inflammatory effects by selectively inhibiting TRPV3 channel via a novel dual-binding-site mechanism. Thus, daphnetin not only provides a valuable tool compound for understanding TRPV3 channel gating mechanisms but also serves as a lead compound for further modification of specific TRPV3 channel inhibitors. - Source: PubMed
Publication date: 2026/07/27
Yue XinyingLiu YuningMo ShilunTang XiaowenSun Xiaoying - Inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), is characterized by chronic relapsing intestinal inflammation driven by complex interactions among immune dysregulation, epithelial barrier disruption, vascular dysfunction, oxidative stress, and gut microbiota imbalance. Despite advances in biologic and small-molecule therapies, a substantial proportion of patients remain refractory to treatment or experience significant adverse effects, underscoring the need for novel mechanistic insights and therapeutic targets. Emerging evidence suggests that the Transient Receptor Potential Vanilloid (TRPV) channel family may represent one of several potential integrative nodes of neurogenic inflammation, immune activation, microvascular dysfunction, epithelial injury, and redox imbalance in IBD. Transient Receptor Potential Vanilloid (TRPV) channels are broadly expressed in intestinal epithelial cells, immune cells, sensory neurons, and vascular endothelial cells, where they regulate Ca-dependent signaling pathways and reactive oxygen species (ROS)-mediated responses. Functionally, TRPV1 promotes neurogenic inflammation and visceral hypersensitivity through neuropeptide release and inflammatory sensitization; TRPV2 regulates macrophage phagocytosis, chemotaxis, and inflammasome-associated signaling; TRPV3 contributes to epithelial ATP release and barrier-associated purinergic signaling; TRPV4 regulates vascular permeability, VEGF signaling, mechanotransduction, and oxidative stress responses; whereas TRPV5/6 participate in calcium homeostasis, epithelial regeneration, and mucosal repair. Importantly, TRPV-mediated Ca influx and ROS signaling form a self-amplifying inflammation-angiogenesis-oxidative stress network that may sustain chronic intestinal injury and therapeutic resistance. This Review systematically summarizes the structural characteristics, cell-specific functions, and pathological roles of TRPV channels in IBD, with particular emphasis on the neuro-immune-vascular-epithelial regulatory axis and the emerging interplay between TRPV signaling, oxidative stress, and pathological angiogenesis. We further discuss current progress and major challenges in TRPV-targeted therapies, including small-molecule modulators, natural compounds, combination strategies, and tissue-specific drug delivery systems. Collectively, these findings raise the possibility that targeting TRPV channels might offer potential avenues for precision medicine and translational intervention in IBD. However, the transition from molecular mechanisms to viable clinical therapeutics remains constrained by current pharmacological limitations. - Source: PubMed
Publication date: 2026/07/27
Li PeihongZhang YikunGuo SiqingHu HongyiCheng TingJunZeng KexinZhang TingtingZhong LindaLin JiangSun Boyun - Hair yield is the main economic value of Zhexi Angora rabbit, and it is an important index to measure its productive traits. The TRPV3 gene has been found to be associated with wool yield. This study aims to investigate the correlation between TRPV3 and wool production traits in rabbits, with the goal of improving wool yield. In the current study, flow cytometry and CCK-8 assays were used to investigate the effect of the TRPV3 gene on the proliferation and apoptosis of dermal papilla cells (DPCs) in rabbit hair follicles (HFs). Results showed that the TRPV3 gene regulates the mRNA expression of genes involved in HF development (BMP4, SFRP2, TGF-β1, WNT5a, and STAT1), as detected by qRT-PCR analysis. The core promoter region of TRPV3 was identified through dual luciferase activity tests, and Sanger sequencing was used to detect polymorphisms in both the exonic and promoter regions of TRPV3. The analysis showed a single SNP in the exon region, which had no significant association with wool production. However, five SNPs were detected in the promoter region, with the g.48897415G> A site showing a significant association with wool production in Zhexi Angora rabbits. Moreover, rabbits carrying the AA genotype also showed higher transcriptional activity. The mutation at g.48897415G> A in the promoter region introduced seven extra transcription factors (TFs) (RFX4, RFX3, RFX2, ZNF45, RFX1, Zfp668, and ZNF655). In conclusion, the g.48897415G > A mutation in TRPV3 is significantly associated with wool yield, and the TRPV3 gene inhibits the proliferation of DPCs. This locus can be used as a molecular marker for wool traits in rabbits, allowing early selection and precise breeding of high-wool-yield strains to shorten the breeding cycle and improve efficiency to enhance both the yield and quality of rabbit wool. - Source: PubMed
Publication date: 2026/07/22
Li RongrongZhao BohaoShen NingLiu YanChen YangWu Xinsheng