CAV1 ELISA kit
- Known as:
- CAV1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CAV1-Hu
- 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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- Nanomedicines that perform well in conventional cell cultures often fail to translate into patients, in part due to the inability to reproduce the protein corona, and hence the biological identity, that nanoparticles acquire within the tumor microenvironment (TME). Here, we establish patient-derived colonic organoids (PDCOs) as a platform for profiling nano-bio interactions under physiologically tumor-relevant conditions using graphene quantum dots (GQD) and Silicon Quantum Dots (SiQD) as material-distinct probes. By combining spectral flow cytometry, confocal imaging, dynamic light scattering, and multi-spectral dimension-reduction analysis of single-cell uptake, we resolve how nanoparticle identity, uptake, and intracellular fate diverge between conventional culture and patient tissue. Conventional two-dimensional culture overestimated internalization by two-fold relative to ex vivo PDCOs, while TME-specific proteins directed nanoparticles to distinct organoid subpopulations. Exploiting this, we engineer the protein corona with tumor-specific proteins to redirect SiQDs to chemoresistant cells, from 3.8% to 70%, an 18-fold increase in targeted delivery to the cells that drive therapy resistance. Internalization was also model-dependent. PDCOs and fibroblasts favored clathrin/dynamin (DNM1)-mediated endocytosis into lysosomes, whereas cancer cells favored caveolae (CAV1)-mediated entry that bypasses lysosomal degradation. This distinction determines whether a nanocarrier is degraded or delivered intact. Collectively, these findings turn the protein corona into a programmable design tool and establish PDCOs as a next-generation platform for precision nano-oncology. - Source: PubMed
Publication date: 2026/09/07
Resmi Meenu PriyaChakrabarti JayatiPond Kelvin WGanesh Swarna - Arrhythmogenic cardiomyopathy (ACM) is an inherited disease characterized by fibrofatty remodeling and sudden cardiac death linked to desmosomal dysfunction. Yet, 40% of cases remain genetically unexplained, and non-desmosomal mutations offer insight into ACM pathophysiology. Myoferlin (MYOF), a calcium (Ca²⁺)-binding protein in cardiomyocytes, is linked to cardiomyopathy, but its mechanism remains unknown. Whole-exome sequencing identified a heterozygous missense variant (p.G1654S) in an ACM family; we subsequently found three unrelated p.G1654S cases. We hypothesized that MYOF deficiency promotes Ca²⁺ handling deficits and arrhythmogenesis in ACM. In patient iPSC-derived cardiomyocytes, MYOF p.G1654S protein dimerized with wild-type protein and underwent accelerated lysosomal degradation, showed disrupted Ca²⁺ handling, and displayed increased arrhythmia burden - all rescued by genomic correction. MYOF interacted with CaV1.2, and verapamil pharmacologically rescued arrhythmias. Heterozygous knockout mice showed systolic dysfunction and fibrosis. These findings establish MYOF as a causative ACM gene and therapeutic target that mediates arrhythmogenesis by disrupting MYOF-CaV1.2. - Source: PubMed
Publication date: 2026/09/22
Kirillova AnnaAytekin MetinChan IreneMina Amir IShao YuchengKirdar AlminaZhang David YKalepalli NishitaGirard William SAl Aaraj Yassmin YReuter ChloeAnnis Jeffery SYue YunshanJiang SiyiRao Rashmi JNouraie S MehdiPark JosephTang YingFlores ChristopherCreager Michael DKim Paul JBrittain Evan LScott Stuart AManning Janet ROkawa SatoshiSalama GuyWu HaodiZhang ManlingCamacho Carlos JGold Michael SParikh Victoria NChan Stephen Y - The myogenic response is the key autoregulatory mechanism that sets cerebral blood flow, and its mechanistic foundation is intimately tied to depolarization and the voltage gating of L-type Ca channels (Ca1.2). Although critical, this study argues for an additional mechanism. We hypothesize that increased intravascular pressure enhances Ca1.2 channel activity by promoting functional coupling and perimembrane trafficking, thereby increasing pressure-induced myogenic constriction. - Source: PubMed
Publication date: 2026/09/29
Mironova Galina YuMartín-Aragón Baudel MiguelLambride ChrysoKharche Sanjay RSteven David ALau JonathanMacDougall Keith WBoulton MelfortSchmid FrancaNavedo Manuel FWelsh Donald G - - Source: PubMed
Publication date: 2026/09/28
Tang ZhiyuanLi JieyingLu BingZhang XiaojingYang LeiQi YueJiang SutianWu QianqianWang YingjingCheng TongXu ManyuSun PingpingWang XudongMiao KaiWu HanHuang Jianfei - Functional dyspepsia (FD) is a disorder of gut-brain interaction involving heterogeneous motor, sensory, immune, and oxidative stress-related mechanisms. Simotang oral liquid (SMT), a traditional Chinese medicine formulation used for dyspeptic and gastrointestinal motility-related symptoms, has not been evaluated with an integrated clinical, functional, and molecular framework. This single-arm prospective pre-post study assessed gastric emptying by the 13C-octanoic acid breath test, gastric electrical activity by electrogastrography, postprandial tolerance by nutrient drink testing, symptom scores, serum biomarkers, and gastric antral tissue markers in patients with FD. FD-like mice were used for charcoal meal transit, smooth muscle strip tension, calcium channel blockade, and mucosal RNA sequencing. Public transcriptomic data from GSE169304 were analyzed to characterize FD-associated duodenal mucosal molecular features. SMT treatment was associated with reduced gastric emptying half-time, improved 3-cpm stability, lower gastric dysrhythmia, reduced Nepean Dyspepsia Index and Gastroparesis Cardinal Symptom Index scores, increased motilin and gastrin levels, lower malondialdehyde, higher superoxide dismutase activity, and lower tumor necrosis factor alpha and interleukin-6 levels. Paired gastric antral biopsy analyses showed increased α-smooth muscle actin and higher phosphorylation ratios of myosin light chain kinase and myosin light chain after SMT treatment. In mice, SMT increased intestinal transit, acetylcholine-induced smooth muscle tension, Cav1.2 abundance, calmodulin fluorescence, and p-MLCK/p-MLC signaling, while nifedipine reduced the SMT-associated phosphorylation changes. Transcriptomic analyses showed enrichment of smooth muscle contraction, calcium signaling, oxidative stress response, and Nrf2-related antioxidant pathways, while protein analyses showed reduced canonical NF-κB activation markers. The data are consistent with Ca-dependent smooth muscle contraction as the central motor pathway associated with SMT- related functional improvement in FD, with Nrf2/NF-κB modulation as a microenvironmental regulatory component. - Source: PubMed
Mao GuoHe ChunxiangLiu JiaqinWu DahuaZeng PuhuaMao Ye