CAV1 antibody - N-terminal region (P100998_P050)
- Known as:
- CAV1 (anti-) - N-terminal region (P100998_P050)
- Catalog number:
- p100998_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CAV1 antibody - N-terminal region (P100998_P050)
Related genes to: CAV1 antibody - N-terminal region (P100998_P050)
- 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
Related products to: CAV1 antibody - N-terminal region (P100998_P050)
Related articles to: CAV1 antibody - N-terminal region (P100998_P050)
- To date, no study has focused on the combined effects of arsenic and lipid exposure on vascular disorders. Substantial evidence indicates that vascular endothelial dysfunction is a primary driver of vascular diseases. EPCs exert pivotal roles in repairing dysfunctional vascular endothelial cells. Therefore, elucidating the role of EPCs in endothelial dysfunction induced by combined exposure to arsenic and lipid is of great significance. Our results revealed that 25 mg/L sodium arsenite combined with high-fat diet had the most detrimental effect on vascular endothelial function. Exposure to 30 μmol/L NaAsO + 10 μg/mL Ox-LDL, it significantly reduces the cell viability, intracellular NO content, and NOS activity in both MAECs and EPCs. Both in vivo and in vitro, a certain number of EPCs could both repair the damaged endothelial function caused by the combined exposure to arsenic and high-fat diet, or Ox-LDL. Proteomic analysis identified Caveolin-1 (Cav-1) as a candidate molecule whose expression was remarkably altered in EPCs under combined exposure, and under 5 μg/mL Cav-1 recombinant protein intervention, the repair ability of EPCs on the dysfunctional MAECs was significantly improved. Moreover, 5 μg/mL Cav-1 recombinant protein has comparable repairing effects on endothelial function as intravenous injection of EPCs. Collectively, our systematic studies provide novel promising measures on the prevention and treatment of vascular diseases induced by chronic arsenic exposure and high lipid. - Source: PubMed
Publication date: 2026/04/23
Li JinyuHe JingCheng JinDong YishanWang ShuoLiu QiaolingYang ZhihanCui JingZhang Wei - Lipotoxicity caused β-cell mass decrease and impaired β-cell function in type 2 diabetes mellitus (T2DM). We previously reported that caveolin-1 (Cav-1) deficiency protected pancreatic β cells against palmitate (PA)-induced apoptosis and dysfunction in both NIT-1 cells and isolated islets. In this study, we firstly established inducible β-cell-specific Cav-1 knockout (iβ-Cav1 KO) mice model. Next, we investigated whether Cav-1 depletion in vitro or in vivo affected β-cell function and survival through the regulation of autophagy under lipotoxicity. Our results showed that Cav-1 depletion exhibited increased islets size, improved insulin resistance and glucose tolerance in lipid stressing conditions. In addition, knockout of Cav-1 also increased β-cell viability through suppression of gene expression of proapopototic molecules (BIM, BID, SMAC, Apaf, Caspase9, Caspase3, AIF and Endo G). Mechanism studies revealed that Cav-1 depletion protected β cells from PA-induced apoptosis through p38 MAPK signaling pathway. Meanwhile, we also found that Cav-1 depletion enhanced autophagy through elevated expression of Beclin-1 and Lc3b, and increased degradation of p62 protein. Further investigation indicated that mTOR signaling pathway was participated in the regulation of PA-induced autophagy. Taking together, our data suggested that Cav-1 depletion ameliorated PA-induced glucose metabolism abnormality, increased cell viability, and improved β-cell apoptosis through the enhancement of autophagy. Our findings would provide valuable clues for developing novel treatments based on Cav-1 inhibition against diabetes under lipotoxicity. - Source: PubMed
Publication date: 2026/04/22
Zeng WenCai NanLiu JiaLiu KunyingLin ShuoYang XubinZeng Longyi - Calmodulinopathies are caused by mutations in calmodulin (CaM) and result in debilitating cardiac arrythmias such as long-QT syndrome (LQTS) and catecholaminergic polymorphic ventricular tachycardia (CPVT). In addition, many patients exhibit neurological comorbidities, including developmental delay and autism spectrum disorder. Prior studies have identified the impairment of Ca2+/CaM-dependent inactivation (CDI) of CaV1.2 channels as a major pathogenic mechanism leading to the LQTS phenotype in these patients. However, the impact of these mutations on other voltage-gated calcium channels (VGCCs) has yet to be fully explored. Here, we examine the potential for pathological CaM variants to impair the Ca2+/CaM-dependent regulation of CaV1.3 and CaV2.1, both essential for neuronal function. We find that pathogenic mutations in CaM can impair the CDI of CaV1.3, with overlapping yet distinct disruption of the Ca2+-dependent facilitation (CDF) of CaV2.1 channels. Moreover, while the majority of CaM variants demonstrated the ability to bind the IQ region of each channel, differences were noted between CaV1.3 and CaV2.1, demonstrating unique CaM interactions across the two channel subtypes. Further, C-lobe CaM variants display a reduced ability to sense Ca2+ when in complex with the CaV IQ domains, explaining the Ca2+/CaM regulation deficits. Overall, these results support the possibility that disrupted Ca2+/CaM regulation of multiple VGCCs may contribute to the pathogenesis of calmodulinopathies. - Source: PubMed
Publication date: 2026/04/24
Hussey John WDeMarco EmilyDiSilvestre DeborahBrohus MaleneBusuioc Ana-OctaviaIversen Emil DJensen Helene HNyegaard MetteOvergaard Michael TBen-Johny ManuDick Ivy E - Dopamine signaling is critical for cognitive and emotional regulation and is implicated in multiple neuropsychiatric disorders. One downstream effector of dopamine is the L-type calcium channel CaV1.2, encoded by the risk gene . Genome-wide association studies have consistently linked single nucleotide polymorphisms to schizophrenia, bipolar disorder, and related conditions. We previously showed that homozygous deletion of in dopamine receptor 1 (D1)-expressing cells enhances remote (30 days post-training) contextual fear memory in male mice. Here, we extend these findings by examining sex- and gene dosage-dependent behavioral consequences of loss in D1 cells. We find a sex-dependent dissociation, where females show enhanced aversive memory up to 30 days post-training even with partial loss, whereas males require complete loss to show enhanced fear. In contrast, males show impaired spatial memory in the Water Y-maze following heterozygous or homozygous deletion, an effect not observed in females. Cue-associated fear memory was transiently elevated in females but unaffected in males. Locomotor activity was reduced in females during the initial minutes of testing, with no effects in males, while social interaction and anxiety-like behaviors were unchanged across groups. These findings indicate that Ca 1.2 signaling in D1-expressing cells differentially regulates aversive versus spatial memory in a sex-dependent manner, providing insight into how risk variants may contribute to sex-specific cognitive phenotype. - Source: PubMed
Publication date: 2026/04/08
Walsh Josiah DScala-Chavez DiegoLee Andrew SMartínez-Rivera ArleneRajadhyaksha Anjali M - This study investigated the potential role of ferroptosis-associated competing endogenous RNA (ceRNA) networks in retinoblastoma (RB). In total, two independent RB gene expression datasets (GSE97508 and GSE208143) and a microRNA (miRNA) expression dataset (GSE208677) were retrieved from the Gene Expression Omnibus database. Differential expression analysis was conducted to identify ferroptosis-related (FR) differentially expressed genes (DEGs) in RB. A protein-protein interaction network for FR-DEGs was constructed using the STRING database, whereas hub genes were determined using the CytoHubba plugin. Reverse transcription-quantitative PCR (RT-qPCR) was used to verify the expression of and . Immune cell infiltration in RB was assessed using the CIBERSORT algorithm. Additionally, miRNA-targeting hub genes were predicted, where an FR miRNA-mRNA regulatory network was constructed. Finally, a ceRNA network and a drug-gene interaction network were constructed. A total of 584 FR-DEGs were identified from the GSE97508 dataset, revealing 135 upregulated and 449 downregulated genes. The intersection of FR-DEGs with FerrDb-extracted FRGs yielded 23 genes that were defined as core FR-DEGs for subsequent analysis. Functional and pathway enrichment analyses highlighted their involvement in iron and transition metal ion homeostasis, response to hypoxic and ischemic conditions and apoptotic processes. Hub genes ( and ) were identified and validated in an independent dataset, with RT-qPCR confirming and upregulation. Immune cell infiltration analysis indicated altered immune cell populations in RB, where an association analysis revealed associations between hub genes and immune cells. A comprehensive FR miRNA-mRNA regulatory network and a ceRNA network were established, shedding light on additional layers of regulatory mechanisms in RB. Furthermore, the drug-gene interaction network consisted of 20 potential candidate drugs. In conclusion, the present integrated analysis offers a comprehensive understanding of the potential role in RB, providing valuable insights into the molecular mechanisms and potential therapeutic targets for this childhood ocular tumor. - Source: PubMed
Publication date: 2026/04/08
Kang ZhengjiaLiu Gaoqin