TRPA1, antiserum, rabbit, 100 ul.
- Known as:
- TRPA1, antibodies, host: rabbit, 100 ul.
- Catalog number:
- RA14135-100
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- TRPA1 antiserum rabbit 100 .
Related genes to: TRPA1, antiserum, rabbit, 100 ul.
- 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, antiserum, rabbit, 100 ul.
#10 Rubber Bands, 1Lb Box Pale Crepe Gold#10 Rubber Bands, 1Lb Box Pale Crepe Gold#10 Rubber Bands, 1Lb Box Pale Crepe Gold(-)-Epigallocatechin gallate(-)-Epigallocatechin gallate (EGCG)(-)-JQ1(-)-Scopolamine Perchlorate (Hyoscine perchlorate)(Alpha)_ 1 _ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_1_ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2 Related articles to: TRPA1, antiserum, rabbit, 100 ul.
- This study investigated the chemical composition, anti-inflammatory and antinociceptive activities of murici leaf (ELM) and bark (EBM) extracts using adult zebrafish (Danio rerio). HPLC analysis identified rutin, isoquercitrin, and kaempferol-3-O-rutinoside as the major phenolic compounds. Both extracts exhibited low toxicity and no sedative effects at the lowest tested doses. ELM showed abdominal antinociceptive activity mediated by TRPA1 and significantly reduced carrageenan-induced abdominal edema. EBM inhibited both corneal (TRPV1) and abdominal (TRPA1) nociception, producing effects similar to morphine. Molecular docking corroborated the in vivo findings, revealing favorable interactions with TRPA1, COX-2, and TRPV1, supported by stable hydrogen-bond formation. The combined chemical, biological, and computational evidence highlights murici as a promising natural source of multifunctional phytotherapeutic agents with antinociceptive activity and potential anti-inflammatory properties. - Source: PubMed
Frota Lucas SBarbosa Sara I C Gde Oiveira Maria R Cdo Nascimento Gabriela ASantos Sacha A A RIshiki Hamilton MMagalhães Francisco E ACampos Adriana Rde Morais Selene M - Temperature variability is a critical environmental trigger for airway hyperresponsiveness (AHR); however, the specific neuroimmune mechanisms linking thermal stress to respiratory inflammation remain underexplored. - Source: PubMed
Publication date: 2026/09/14
Wang YanjieZhao QianruZhang HaoxiangWang LuyaoFu SiruiCheng FengliQi XuepingZhu XiaojiaZhang QiXu DanniLiu MuzeZhao Changqing - The airway epithelium must constantly adapt to maintain function, as disrupted epithelial homeostasis contributes to asthma and other respiratory diseases. Toxic electrophilic aldehydes, quinones, and substituted phenols are transient receptor potential ankyrin-1 (TRPA1) channel agonists found in common air pollutants, including wood and biomass smoke, cigarette smoke, and vehicle exhaust. TRPA1 agonists damage airway epithelial cells in part by disrupting calcium homeostasis and triggering endoplasmic reticulum stress. A detailed understanding of how inhaled toxicants affect epithelial homeostasis is critical for understanding their effects and managing adverse effects. We integrated results from kinase-targeted phenotypic screening, unbiased mass spectrometry-based global proteomics and phosphoproteomics, live-cell imaging, calcium flux assays, gene expression assays, and Western blot analyses to decipher systematic changes in kinase signaling that control TRPA1 agonist-induced injury. We show that injury coincides with changes in cell structure and motility overlaid with epidermal growth factor receptor (EGFR) transactivation, and that inhibiting kinase pathways known to favor survival and wound repair, including EGFR, extracellular signal-regulated kinase 1/2, phosphoinositide 3-kinase/protein kinase B, and c-Jun N-terminal kinases, exacerbated injury, while inhibiting protein kinase C and p38 mitogen-activated kinase, and others, reduced injury. We attributed the protective effects of protein kinase C and p38 mitogen-activated kinase inhibition to an attenuation of TRPA1 activity, balanced by enhanced transient receptor potential vanilloid-3 expression, resulting in a net shift toward proadaptive kinase-driven signaling downstream of EGFR. Our results support a model in which repair depends on kinase-regulated transitions through a transient injury state that could potentially be targeted prophylactically to reduce injury caused by selected inhaled toxicants. SIGNIFICANCE STATEMENT: This study shows that inhibiting protein kinase C and p38 mitogen-activated kinase reduces transient receptor potential ankyrin-1 activity and enhances transient receptor potential vanilloid-3 expression and prosurvival kinase signaling, favoring cell adaptation and repair following acute injury, offering insight into potential therapeutic approaches to limit transient receptor potential ankyrin-1 agonist-induced injury through a vital network of transient receptor potential channels. - Source: PubMed
Publication date: 2026/09/18
Serna Samantha NRomero Erin GOng Shao-EnGolkowski MartinSun LiliReilly Christopher A - Transient receptor potential (TRP) cation channel subfamily V member 1 (TRPV1) is predominantly expressed in sensory neurons and activated by nociceptive stimuli, including capsaicin, heat, and acidic conditions. Recent research has highlighted the role of TRPV1 in the pathophysiology of dry eye disease (DED). This study evaluated the antagonistic activity and TRP channel selectivity of motugivatrep, a novel TRPV1 antagonist. The inhibitory effects of motugivatrep were assessed in cells expressing various TRP channels as well as in rat dorsal root ganglion (DRG) cells, with agonist-induced intracellular Ca influx used as an indicator. Off-target effects were evaluated using comprehensive Cerep pharmacology profiling, which included radiolabeled ligand-binding assays for major ion channels, receptors, and enzyme assays. Motugivatrep exhibited pronounced inhibition of capsaicin-stimulated TRPV1 across multiple species, with IC values ranging from 0.46 to 2.1 nM. Furthermore, although motugivatrep exhibited weak inhibition of human TRPV4, it had no significant effects on TRPV3, TRPA1, or TRPM8. Additionally, motugivatrep suppressed capsaicin-induced intracellular Ca influx in DRG cells (IC = 2.8 nM). Off-target profiling revealed minimal binding to 5-HT and 5-HT receptors. Overall, these findings indicate that motugivatrep is a potent and highly selective TRPV1 antagonist, supporting its potential as a therapeutic candidate for disorders associated with TRPV1 activation, such as DED. - Source: PubMed
Uemura TomokaUchida HideharuHigashi ChikaAmano Ken-IchiKanda Atsuhiro - Transforming growth factor-β1 (TGF-β1) is a pleiotropic cytokine implicated in the pathogenesis of inflammatory airway diseases such as asthma. Airway hypersensitivity (AHS), arising from sensitization of capsaicin-sensitive lung vagal (CSLV) afferents, is a hallmark of these airway diseases. Although the immunoregulatory roles of TGF-β1 in airway diseases are well documented, its effects on pulmonary sensory neurons remain unexplored. Since TGF-β1 sensitizes dorsal root ganglion neurons, a somatic counterpart of CSLV neurons, we investigated whether TGF-β1 could sensitize CSLV afferents, thereby promoting AHS. - Source: PubMed
Chen Yueh-YinChan Nai-JuHsu Chun-Chun