ω-conotoxin GVIA, ω-conotoxin GVIA blocks Cav2.2
- Known as:
- ω-conotoxin GVIA, ω-conotoxin GVIA blocks Cav2.2
- Catalog number:
- 08CON003-01000
- Product Quantity:
- 1000 ug
- Category:
- -
- Supplier:
- Smartox
- Gene target:
- ω-conotoxin GVIA blocks Cav2.2
Related products to: ω-conotoxin GVIA, ω-conotoxin GVIA blocks Cav2.2
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- Topmouth culter () is one of the most economically important freshwater fish in China, but intensive aquaculture has caused germplasm degradation and reduced growth performance, while the genetic basis underlying growth variation in this species remains poorly understood. This study aimed to identify major-effect loci and candidate genes associated with growth-related traits to support molecular breeding. Whole-genome resequencing (average depth 11.44×) was performed on 300 individuals derived from random mating among three geographic populations (Danjiangkou, Taihu, and Poyang Lake); 239 individuals with complete phenotypic records were retained for a genome-wide association study (GWAS) of five growth-related traits, including body weight (BW), body weight without viscera (BWW), total length (TL), body length (BL), and body height (BH). After stringent filtering, 7,597,008 high-quality single-nucleotide polymorphisms (SNPs) were obtained, and association analysis was conducted using a linear mixed model, followed by Benjamini-Hochberg false discovery rate correction and 1000-permutation testing for BW and BL. Six genome-wide significant SNPs and 473 suggestive SNPs were identified, with individual significant SNPs explaining over 11% of phenotypic variance, indicating candidate loci of putatively moderate-to-large effect. Significant SNPs were predominantly clustered on chromosomes 16 and 19. Four candidate genes-, , , and -were identified, with functions related to lipid metabolism, muscle structure, and cell proliferation. This first population-level GWAS in topmouth culter provides valuable molecular markers for marker-assisted selection and lays a foundation for accelerated genetic improvement of this species. - Source: PubMed
Publication date: 2026/06/25
Jiang WenpingLuo JunzhiZheng JianboLiu ShiliChi MeiliCheng ShunZhu ChaoHang XiaoyingPeng MiaoLi Fei - N-type voltage-gated calcium channels (Ca2.2) are validated targets for chronic pain management. Although ziconotide is clinically effective, its use is hampered by a narrow therapeutic window and severe side effects. This review examines the subunit structure of Ca2.2 and its fundamental role in nociceptive signaling. We focus on emerging therapeutic strategies developed in recent years, including the optimization of direct blockade, the inhibition of channel trafficking, the modulation of signaling pathways, and targeted channel depletion. These advancements provide a deeper understanding of calcium channel regulation and identify promising targets for safer, more effective, and precision-based pain management. - Source: PubMed
Publication date: 2026/06/26
Luo FanglaSu JunweiKe XinlongChen YeruChen Gang - Autism spectrum disorder (ASD) may be a predisposing factor in the development of catatonia, which has been demonstrated to be effectively treated using electroconvulsive therapy (ECT). CACNA1 channelopathy mutations have been associated with autism spectrum disorder, intellectual disability, and epilepsy. The single published case report of ECT use in CACNA1 subunit mutations demonstrated a negative outcome, and no current case reports on CACNA1B, CACNA1C, CACNA1D, or CACNA1E mutations have been published. We present a case of an adolescent with a known CACNA1D mutation and symptoms of excited catatonia who experienced a reduction in the frequency and severity of self-injurious and violent behavior following treatment with ECT. Our case demonstrates the use of ECT for catatonia in an individual with a CACNA1 mutation without complication and with a positive therapeutic response. - Source: PubMed
Publication date: 2026/05/26
Mancine RyleyKuang JoannaRaghunandan ChristinaPalffy Alexander - Latrophilin 1 (LPHN1/ADGRL1), an adhesion G-protein-coupled receptor (GPCR), is the principal receptor for α-latrotoxin (αLTX), a toxin that triggers massive neurotransmitter release. However, its endogenous signaling mechanism remains elusive. Here, we dissect the LPHN1 signaling pathway at the vertebrate neuromuscular junction, using the pore-deficient αLTX mutant LTX as a selective agonist. Combining electrophysiological recordings from LPHN1 knockout mice with pharmacological inhibitors, calcium imaging, and biochemical assays, we delineate the cascade from receptor activation to spontaneous quantal acetylcholine release. We demonstrate that LPHN1 is specifically localized to the presynaptic membrane and mediates LTX-evoked release. Upon activation, LPHN1 engages the G-phospholipase C pathway to generate inositol 1,4,5-trisphosphate (IP), triggering Ca release from intracellular stores via IP receptors. This store depletion activates store-operated Ca entry (SOCE), providing sustained Ca required for LTX-induced burst-like exocytosis. We uncover distinct roles for Ca2.1 and Ca1 channels in initiating and sustaining this response. These findings establish LPHN1 as a GPCR that harnesses intracellular stores and SOCE to drive spontaneous neurotransmission, revealing a novel signaling paradigm for adhesion GPCRs in presynaptic function. - Source: PubMed
Publication date: 2026/04/30
Petitto EvelinaMeunier Frédéric AFidalgo SaraColasante CesareBlackburn Jennifer KRibchester Richard RUshkaryov Yuri A - Amyotrophic lateral sclerosis (ALS) is a late-onset, fatal neurodegenerative disease affecting upper and lower motor neurons in the central nervous system. Drugs like riluzole, edaravone, and tofersen treat disease symptoms or are designed for a specific pathological mutation (e.g., SOD1), but they cannot prevent or halt the disease. For this reason, the search for new therapeutic strategies continues. The voltage-gated calcium channel Ca2.2 might be a novel target in ALS treatment as the channel was shown to be overexpressed in murine SOD1*G93A cortical neurons, resulting in higher mortality. Further, murine SOD1*G93A motor neurons showed increased calcium currents mainly by an increased expression of the Ca2.2 channel. In addition, inhibition of the channel was hypothesized as mode of action for the all-d-enantiomeric peptide RD2RD2, a novel drug candidate for the treatment of ALS, which already demonstrated its efficacy in SOD1*G93A mice. To investigate the influence of the Ca2.2 channel on the progression of disease symptoms in the SOD1*G93A mouse model, a new double-transgenic line was created, combining the ALS phenotype with a knockout of the Ca2.2 channel. The study showed that the Ca2.2 knockout on the SOD1*G93A background led to reduced SHIRPA and splay scores, and a delayed disease onset. Additionally, differences were detected between wildtype and single-transgenic Ca2.2 knockout mice. However, survival was not affected. Post mortem analysis of human tissue found more Ca2.2 in ALS cases in comparison to healthy control subjects confirming involvement of the channel in human ALS. These results indicate that the Ca2.2 calcium channel may play an influential role in early disease progression of ALS. - Source: PubMed
Publication date: 2026/04/13
Wintz KatharinaLechtape Paul LucaKlenzendorf JannesSchemmert SarahDingley Andrew JWilluweit AntjeKutzsche Janine