CACNa1H ELISA kit
- Known as:
- CACNa1H Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CACNa1H-Mu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CACNa1H ELISA kit
Related genes to: CACNa1H ELISA kit
- Gene:
- CACNA1H NIH gene
- Name:
- calcium voltage-gated channel subunit alpha1 H
- Previous symbol:
- -
- Synonyms:
- Cav3.2
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-08
- Date modifiied:
- 2016-02-04
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- As a primary substitute for bisphenol A (BPA), the potential threats of environmental exposure to bisphenol F (BPF) on intestinal health have raised significant concerns. However, the underlying regulatory mechanisms involving circular RNA (circRNA) remain unclear. Utilizing whole-transcriptome sequencing, this study discovered that hsa_circ_0003655 was significantly upregulated in response to BPF toxicity in both human colonic epithelial cells (NCM460) and mouse models, exhibiting high cross-species conservation. Mechanistically, BPF disrupted cellular calcium homeostasis through a hsa_circ_0003655-mediated "dual-axis" pathway. This dual-axis comprises a CACNA1H-driven extracellular calcium influx and a SND1-driven intracellular calcium redistribution. Specifically, BPF not only promoted extracellular calcium influx by increasing the methylation level of CACNA1H via hsa_circ_0003655, but also, with hsa_circ_0003655 acting as a competing endogenous RNA (ceRNA), facilitated the transfer of cytosolic calcium into mitochondria and the endoplasmic reticulum through the hsa-miR-212-5p/SND1 axis. Furthermore, we revealed that this SND1-mediated process drives organelle calcium overload by specifically upregulating SERCA3 and MICU1. This dual-axis disruption ultimately led to organelle calcium overload and subsequent cellular injury. In summary, this study elucidates the critical role of hsa_circ_0003655 in mediating BPF-induced intestinal toxicity, providing novel biomarkers for the risk assessment of environmental pollutants and offering potential strategies for targeted interventions against intestinal damage. - Source: PubMed
Publication date: 2026/09/27
Niu GuoleiWang JingZhu JiahaoMai HuanzhuoGao YushuangHuang TengkaiCao LeleMeng QingtaoChen Rui - Lung cancer recurrence and therapeutic resistance are driven by cancer stem cells (CSCs), yet clinically available CSC-targeted therapies remain lacking. To identify actionable anti-CSC agents, we screened 1018 FDA-approved drugs using a 3D sphere culture system enriching lung CSC-like cells. Trimebutine, a gastrointestinal motility regulator targeting G-protein-coupled receptors (GPCRs), was identified as a potent agent with over 49.5-fold higher selectivity toward lung CSC-like cells (SI > 49.55) compared with standard therapies such as cisplatin (SI = 1.39) and gefitinib (SI = 1.00). In H460-SP spheres, trimebutine markedly impaired sphere-forming capacity, reduced cell viability, and downregulated key CSC surface markers (CD133, CD44) alongside stemness regulators (c-MYC, EpCAM, BMI1, OCT3/4, NANOG, SOX2, SMAD3). Mechanistically, trimebutine suppressed overexpressed calcium and potassium channels (, , , , ), attenuating downstream YAP/TAZ-TEAD signaling within the Hippo pathway to trigger apoptosis. In combination with cisplatin, trimebutine exhibited strong synergistic efficacy (Chou-Talalay combination index, CI = 0.015-0.228) in H460-SP spheres and patient-derived lung tumor organoids, suppressing cell viability, stemness marker suppression, and apoptotic cleavage of caspase-3 and PARP compared to monotherapies. Overall, trimebutine targets lung CSC populations by disrupting GPCR-ion channel-Hippo signaling crosstalk, providing a strong preclinical rationale for trimebutine-cisplatin combination strategies to overcome drug resistance and recurrence in lung cancer. - Source: PubMed
Publication date: 2026/09/15
Seo JiHyeLee HeejinChoi Dong KyuKim Young-KyuWoo SominLee ChangkyuChoi Jeong InJiang GeOh Bae JunLee Dong-SeokMin Sang-Hyun - Chronic psychological stress is an environmental factor associated with chronic disease risk and health disparities. Since environmental stressors alter gene expression and physiologic responses through epigenetic mechanisms, perceived discrimination (PD), or the subjective experience of receiving negative treatment related to personal characteristics may influence DNA methylation (DNAm) of CpGs within genes linked to chronic disease. Using the Illumina 850K EPIC chip and psychosocial stress-associated discrimination scales, including the lifetime, racial, and everyday discrimination scales, we identified novel CpGs and differentially methylated positions (DMPs) associated with PD in the context of age, sex, and poverty status among African American and White adults and ones that overlap previous findings of differentially methylated sites (or genes) with discrimination, inflammation, and chronic disease. Ingenuity Pathway Analysis identified several pathways associated with the DNAm patterns and PD with age, sex, and/or poverty status. With age, the white adipose tissue browning pathway was activated among African American participants. This was related to the differential methylation found in the , and genes. Among White participants, the opioid signaling pathway was activated and significantly enriched for the genes , and . Additionally, CpG sites associated with PD among White participants with poverty status revealed that the netrin signaling, opioid signaling, and calcium signaling pathways were activated and significantly enriched for differentially methylated genes, including . The identified novel DNAm genes associated with PD transduce effects through biological pathways related to inflammation and immune response, white adipose tissue browning, and calcium signaling. - Source: PubMed
Publication date: 2026/08/14
Chitrala Kumaraswamy NaiduMoody Danielle L BeattyMode Nicolle AShen BotongHooten Nicole NorenZonderman Alan BEzike NgoziEvans Michele K - Mutations in the CACNA1H and PPP2R5D genes have been associated with functional abnormalities affecting both the endocrine and nervous systems. The CACNA1H gene encodes the T-type calcium channel CaV3.2, and pathogenic variants may alter channel activation and inactivation, resulting in increased intracellular calcium influx. Elevated intracellular calcium in adrenal zona glomerulosa cells acts as a key signal for aldosterone biosynthesis, thereby promoting excessive aldosterone secretion and contributing to the development of hypertension. The PPP2R5D gene encodes a regulatory subunit of protein phosphatase 2A (PP2A). Mutations in this gene may disrupt the regulatory function of PP2A, impairing the dephosphorylation of key neuroproteins and consequently affecting neural signal transduction and brain function. Cases of early-onset hypertension accompanied by intellectual disability associated with concurrent CACNA1H and PPP2R5D mutations remain rare. We report the case of an 18-year-old female presenting with early-onset hypertension and intellectual disability. Hypertension was first diagnosed at the age of 10 years and was accompanied by recurrent dizziness and headache. Physical examination revealed central obesity and signs of hyperandrogenism. Laboratory evaluation demonstrated elevated aldosterone levels with suppressed plasma renin activity, suggesting primary aldosteronism. Genetic analysis identified heterozygous variants in CACNA1H (c.6866C>T) and PPP2R5D (c.985A>G). Based on the clinical features and genetic findings, the patient was diagnosed with familial hyperaldosteronism type IV complicated by intellectual disability. This case highlights the importance of considering genetic forms of primary aldosteronism in young patients with early-onset hypertension and atypical clinical manifestations. Genetic testing may facilitate accurate diagnosis and guide individualized management. - Source: PubMed
Publication date: 2026/08/26
Zhang WennanZhang YiwenWang YangyangXue YuXu LiliYan Hui - Sex differences in major depressive disorder (MDD) are well documented, but it remains unclear whether sex-related variation in peripheral endocannabinoid system (ECS)-related biomarkers is detectable in MDD. - Source: PubMed
Publication date: 2026/08/25
Sorkhou MaryamKim Helena KFarzan FaranakFoster Jane AFrey Benicio NHusain Muhammad IKennedy Sidney HLam Raymond WMilev RoumenMulsant Benoit HMüller Daniel JQuilty Lena CSoares Claudio NTaylor Valerie HTurecki GustavoKloiber Stefan