CAV1 ELISA kit
- Known as:
- CAV1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CAV1-Mu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CAV1 ELISA kit
Related genes to: CAV1 ELISA kit
- Gene:
- CAV1 NIH gene
- Name:
- caveolin 1
- Previous symbol:
- CAV
- Synonyms:
- -
- Chromosome:
- 7q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-02
- Date modifiied:
- 2016-10-05
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- Atrial fibrillation (AF) is the most prevalent clinical arrhythmia, yet current antiarrhythmic pharmacotherapies have limited efficacy and pose risks of off-target ventricular block. LY294002 was reported to inhibit the ultrarapid delayed-rectifier potassium current ( ) carried by Kv1.5 channels, a promising atrium-selective therapeutic target for AF. To determine whether LY294002 exhibits functional selectivity for , this study comprehensively examined its inhibitory effects on major counter-target cardiac ion currents. - Source: PubMed
Publication date: 2026/09/09
Niu RuiLi JiaweiFang HuanleZhao WeiDong ChaoHan NingjuanChen MengyuanMa LieLi LiangFan YunZhu BingBie BeibeiWu JieMatsuura HiroshiHorie Minoru - Benzo[a]pyrene (BaP) is a polycyclic fragrant hydrocarbon contaminant commonly establish throughout the surroundings. The International Agency for Research on Cancer has classified it as a Group 1 carcinogen; however, its exact contribution to the onset of prostate cancer (PCa) is still not well defined. This study systematically explores the mechanism underlying the association between BaP exposure and prostate cancer using approaches including network toxicology, machine learning, transcriptomic validation, immune infiltration assessment, single-cell analysis, molecular docking and external validation. The results showed that BaP and prostate cancer shared 975 overlapping targets, which were predominantly enriched in signaling pathways such as PI3K-Akt. Four core genes were screened out through differential analysis and machine learning, namely CAV1, TWIST1, PRKCA, and GDF15. Transcriptome verification showed that TWIST1 and GDF15 were up-regulated, CAV1 and PRKCA were down-regulated, and the AUC of the four-gene combined diagnosis reached 0.990. Core genes are associated with cellular growth and immune cell recruitment, and single-cell sequencing verified their specific cellular distribution and immunological shifts. Molecular docking showed that BaP binds well to the core target. External validation confirmed that BaP may promotes the progression of PCa, with upregulated expression of GDF15 and downregulated expression of PRKCA in PCa. In conclusion, BaP may promote the development of PCa by regulating pathways such as CAV1, TWIST1, GDF15 and PRKCA. - Source: PubMed
Publication date: 2026/09/23
Zhu SiqiLi ZhuangJiang KehuaSun FaZhu Jianguo - Evidence suggests dietary cholesterol intake associates with higher diabetes risk, but mechanisms need further study. Glucagon-like peptide-1 (GLP-1), a glucose-regulating hormone produced by intestinal L-cells, has served as the basis for widely used diabetes therapeutics. However, how dietary cholesterol and intracellular cholesterol in L-cells affects GLP-1 and glucose regulation remains unclear. We studied ABCA1 (a cholesterol efflux protein) in L-cells using L cell specific gene null nice ( ) mice and ABCA1-targeted interventions in STC-1 and GLUTag cells. A high-cholesterol diet induced mouse glucose intolerance and reduced GLP-1. mice showed worse hyperglycemia and GLP-1 impairment disrupted caveolin-1--catenin signaling. overexpression and cholesterol depletion in STC-1 and GLUTag cells enhanced the CAV1--catenin pathway and GLP-1 secretion, whereas cholesterol loading, siRNA knockdown, and treatment with probucol (an ABCA1 inhibitor) produced opposite effects. The findings of this study confirm that ABCA1 is a key regulator in maintaining cholesterol homeostasis in intestinal L cells and in the synthesis and secretion of GLP-1. Moreover, the regulatory effect of ABCA1 on GLP-1 is mediated through the CAV1--catenin signaling pathway. These observations further uncover promising therapeutic targets for metabolic disorders linked to diabetes. - Source: PubMed
Publication date: 2026/07/16
Gao LuyangLin YubiYe QianqianZhao YuhangHe WenxinLv ShijieYang KeChen JiaZhang ZhenXiang XinxinXu Geyang - Globally, hypercholesterolemia affects over 20% of the population; and while many studies have examined its impact on cardiovascular health, little is known about its effects on the lymphatic system. In mice, hypercholesterolemia has been linked to multiple aspects of lymphatic dysfunction; and a recent study demonstrated that cholesterol depletion by cyclodextrins promoted lymphatic vessel regeneration and restored lymphatic drainage in mouse models of lymphedema. Collecting lymphatic vessels rely on the spontaneous and highly entrained contractions of lymphatic muscle cells (LMCs) and competent unidirectional on-way valves to propel lymph forward. Critical to lymphatic pacemaking and contractility is the proper functioning of ion channels, which are known to be modulated by the cholesterol content in the plasma membrane. Therefore, we sought to understand the role cholesterol plays in regulating lymphatic contractility. The effects of cholesterol depletion by the cyclodextrins MβCD and HPβCD were assessed in cannulated and pressurized inguinal-axillary collecting lymphatic vessels (CLVs) from C57BL6/J (WT) mice. Noteworthy, studies have shown that HPβCD is safe for human use, and in fact, it is commonly used as a drug excipient. Acute treatment with both cyclodextrins significantly increased the pumping capacity of CLVs, as demonstrated by the increased contraction amplitudes by ~50±12% and calculated fluid volume displacement by each contraction by ~35±11%. Calcium imaging demonstrated that HPβCD increased the amplitude and duration of the large Cav1.2-mediated calcium events (termed calcium flashes. In contrast, cholesterol supplementation by incubation with BODIPY-cholesterol, which presumably incorporates cholesterol into the cell membrane, significantly impaired the contractile activity of CLVs compared to controls by decreasing contraction amplitude (control: 42±2 µm versus BODIPY-cholesterol: 20±7 µm) and calculated fluid volume displacement (control: 9.2±3.9 nL versus BODIPY cholesterol: 3.3±1.2 nL) which were significantly restored with subsequent cholesterol depletion using HPβCD (amplitude: 36±11 µm, volume displacement: 5.5±2.4 nL). Similarly, treatment with HPβCD significantly improved the contractile capacity of dysfunctional CLVs isolated from hypercholesterolemic ApoEKO mice. In conclusion, changes to cell membrane cholesterol content acutely and significantly altered CLV contractility with depletion improving contractility associated with recruitment of voltage-gated Cav1.2 channels in lymphatic muscle cells (LMCs). Future studies from our lab will determine whether pharmacological depletion of membrane cholesterol can be therapeutic strategy to improve and/or restore lymphatic contractile function in secondary lymphedema, including obesity/hypercholesterolemia-induced and cancer-related lymphedemas. - Source: PubMed
Publication date: 2026/09/15
Keane KeithCastorena-Gonzalez Jorge A - Patients with ST-segment elevation myocardial infarction (STEMI) frequently experience no-reflow (NRF) during percutaneous coronary intervention (PCI). Nevertheless, the pathogenesis of NRF involves multiple factors and has not been fully elucidated to date. Given that endothelial dysfunction, inflammation, and oxidative stress are jointly implicated in both MP-related processes and NRF occurrence, this study was performed to explore the potential role of circulating microparticles (MPs) in the development of NRF. - Source: PubMed
Li Wen-BoZhang WeiChang Feng-JunLi ZheYang Yu-JuanCheng GongJiang Xin