Ask about this productRelated genes to: TRPA1 Blocking Peptide
- Gene:
- TRPA1 NIH gene
- Name:
- transient receptor potential cation channel subfamily A member 1
- Previous symbol:
- ANKTM1
- Synonyms:
- -
- Chromosome:
- 8q21.11
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-15
- Date modifiied:
- 2016-10-05
Related products to: TRPA1 Blocking Peptide
Related articles to: TRPA1 Blocking Peptide
- Potassium superoxide (KO), a superoxide anion donor, can be applied to induce reactive oxygen species (ROS) triggered pain and inflammation. -Chalcone (TC) is an atypical flavonoid because its molecular structure does not possess intrinsic antioxidant properties. This characteristic allows investigating the mechanisms of action of flavonoids excluding inherent chemical antioxidant effect. In the present study, we investigated the activity and mechanisms of TC in a model of inflammation and pain triggered by a superoxide anion donor, which to our knowledge have not been assessed yet. - Source: PubMed
Publication date: 2026/04/25
Piva MaiaraManchope Marília FBarbosa-Costa FernandaBianchini Beatriz H SAndrade Ketlem CSilva Letícia CoelhoCalixto-Campos CássiaRasquel-Oliveira Fernanda SFattori VictorZarpelon-Schutz Ana CarlaCamilios-Neto DoumitBorghi Sergio MCasagrande RubiaVerri Waldiceu A - Following spinal cord injury (SCI), mechanical trauma and an inflammatory microenvironment activate the PKCδ-TRPA1 pathway, resulting in calcium overload within neurons and subsequently inducing endoplasmic reticulum (ER) stress-mediated neuronal apoptosis. The mechanisms and therapeutic potential of electroacupuncture (EA) in the treatment of SCI have yet to be fully elucidated. This study aimed to explore the causes of neuronal Ca overload post-SCI and to investigate the neuroprotective and regenerative mechanisms of EA in an SCI mouse model. - Source: PubMed
Publication date: 2025/10/24
Zhang YihuiLiang ChenheHuang ZhiyangHu YusiMo YujunNing ShaoxiaLi ZiyiWu YungangZhang JiaxinLi XiaokunWang Zhouguang - Allergic contact dermatitis (ACD) is a frequent inflammatory skin disease with limited therapeutic options. While neuronal Transient Receptor Potential Ankyrin 1 (TRPA1) has been implicated in ACD, the role of keratinocyte TRPA1 remains unclear. We investigated whether allergen binding to keratinocyte TRPA1 drives cytotoxicity, cytokine release and inflammatory amplification. - Source: PubMed
Publication date: 2026/04/30
Jaber AreejHorváth SzabinaZsidó Balázs ZoltánKormos ViktóriaKonkoly JánosHetényi CsabaPintér ErikaKemény ÁgnesGyulai Rolland - Chemotherapy-induced peripheral neuropathy (CIPN) is a common and serious clinical condition that results when a chemotherapeutic agent damages the peripheral nervous system and is usually characterized by abnormal pain in the distal limbs and increased sensitivity to hot and cold stimuli. However, few clinical treatments for CIPN are available, so it is critical to identify effective treatment modalities. Transient receptor potential ankyrin 1 (TRPA1), an injury receptor, can be activated by oxidative stress, inflammatory mediators, and hypothermic conditions during the pathogenesis and progression of CIPN. TRPA1 modulates the downstream inflammatory pathway and promotes the release of inflammatory factors and neuropeptides, resulting in abnormal immune regulation, which in turn leads to a neurogenic inflammatory response and pain signaling. In this study, the role of TRPA1 in the pathogenesis of CIPN is examined, the possibility of targeting TRPA1 to treat CIPN by inhibiting neuroinflammation is verified, and the prospects of using TRPA1 antagonists and natural herbs for the clinical treatment of CIPN are explored. - Source: PubMed
Publication date: 2026/04/10
Yao HuiniLi MingzhuJin ShengboYu JunJiang YuxinPiao HaozheLi NingxinLiu QianShen YueYan Sizuo - Transient Receptor Potential Ankyrin 1 (TRPA1) channels are multi-modal receptors in animals for sensing noxious physical and chemical factors. They are considered promising biochemical targets for developing repellents of arthropod disease vectors and drugs to treat a variety of medical conditions including pain, inflammation, and itch. Recently, we discovered that cinnamodial (CDIAL), a natural drimane sesquiterpene produced by the medicinal plant Cinnamosma fragrans, activates mosquito TRPA1 channels and is antifeedant and repellent to Aedes aegypti. However, the selectivity of CDIAL for mosquito vs. human TRPA1 and the mechanism(s) of how CDIAL binds to TRPA1 channels are unknown. The first goal of this study was to characterize the activation of Aedes aegypti (Aa) and Homo sapiens (Hs) TRPA1 channels by CDIAL and compare the activation to that of two known TRPA1 agonists, nepetalactone and JT010. Electrophysiological measurements of AaTRPA1 and HsTRPA1 activation (when expressed heterologously in Xenopus laevis oocytes) revealed that CDIAL activated both channels in a similar concentration-dependent manner. Compared to CDIAL, nepetalactone was a less potent agonist of both AaTRPA1 and HsTRPA1, but showed stronger selectivity for AaTRPA1. JT010 did not detectably activate AaTRPA1, but potently activated HsTRPA1. The second goal of this study was to generate insights into a putative binding site of CDIAL on AaTRPA1. We mutated six Lys residues (656, 678, 681, 728, 738, 744) and/or a Cys residue (684) in the coupling domain previously hypothesized to be involved. Simultaneous mutation of the six Lys residues to Ala dampened the electrophysiological activation of AaTRPA1 by CDIAL, whereas changing Cys684 to Ser had no detectable impact. Protein modeling and molecular docking simulations predicted that CDIAL interacts with distinct binding pockets in AaTRPA1 and HsTRPA1 that nonetheless promote similar channel activation, contrasting with JT010, which engages a pocket centered on Cys621 (aligned to Cys684 in AaTRPA1) only in HsTRPA1. These findings illuminate potential species-dependent binding determinants for TRPA1 activation that may lead to the design of novel mosquito-selective repellents and/or TRPA1-targeted therapeutics. - Source: PubMed
Publication date: 2026/04/09
Lee TaeLiu JaycePark YeaeunRakotondraibe Harinantenaina LCheng XiaolinPiermarini Peter M