CACNa1D ELISA kit
- Known as:
- CACNa1D Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CACNa1D-Mu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CACNa1D ELISA kit
Related genes to: CACNa1D ELISA kit
- Gene:
- CACNA1D NIH gene
- Name:
- calcium voltage-gated channel subunit alpha1 D
- Previous symbol:
- CCHL1A2, CACNL1A2
- Synonyms:
- Cav1.3, CACH3, CACN4
- Chromosome:
- 3p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-12-12
- Date modifiied:
- 2016-10-05
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- Glioblastoma (GBM) is the most common aggressive brain tumor in adults. The development of therapy resistance in GBM necessitates the identification of novel biomarkers to guide molecularly targeted treatment strategies. This study aims to identify potential tumor suppressor genes in GBM and to evaluate their potential as therapeutic targets. Genes localized on deletion regions in GBM tumors were selected using the BioMart database. Microarray datasets containing GBM tumor and normal brain tissue samples were analyzed with GEO2R. A protein-protein interaction (PPI) network was constructed for dDEGs on deletion regions using the String database to identify hub genes. The expression and structural changes of hub genes were examined using GEPIA2 and cBioPortal, respectively. GROMACS software was used to perform molecular dynamics (MD) simulations. A total of 1704 dDEGs located within the deletion regions of GBM tumors were identified. Expression levels of 11 hub genes, including subunits of the entire GABA(A) receptor complex, were significantly downregulated in TCGA GBM samples. Additionally, mutations in , , and were predicted to disrupt protein structure and function. Meprobamate was selected as the agonist for GABA(A) receptor-related hub genes. MD simulations indicated that meprobamate remained associated with the GABA(A) receptor but exhibited time-dependent repositioning during the later stages of the simulation. , , and may have potential tumor-suppressive roles in GBM. In addition, GABA(A) receptors may represent potential molecular targets in GBM, warranting further experimental investigation. - Source: PubMed
Publication date: 2026/09/17
Caglar Hasan OnurMeral BerkayCaglar Fulya - Improved access to genetic testing is accelerating identification of variants underlying common sleep traits and rare Mendelian disorders. This review highlights advances over the past two years. - Source: PubMed
Publication date: 2026/09/09
Mani HaritaCuddapah Vishnu Anand - Alternative splicing is a critical determinant of protein diversity in the heart, where it drives the postnatal functional maturation of cardiomyocytes and specifies the ion-channel and calcium-handling isoforms required for mature contractile function; dysregulated splicing programs have in turn been implicated in cardiomyopathies and arrhythmias. However, the splicing regulators that control cardiomyocyte calcium handling remain largely unknown. - Source: PubMed
Publication date: 2026/07/28
Murphy SeanWang HanwenZureick NadineKoakutsu MisatoSuh DavidLee Dong IkKwon Chulan - The germline genetic basis of bilateral primary aldosteronism (PA) remains poorly understood, particularly in apparently sporadic disease. We investigated rare germline variants in canonical and candidate genes in patients with bilateral PA associated with resistant hypertension and/or hypertension diagnosed before 40 years of age. - Source: PubMed
Publication date: 2026/07/27
Santana Lucas SAlves-Fernandes Débora KLima Sobrinho Jose Antonio BFreitas-Castro FelipeRossetti Lucas BOkubo JessicaFagundes Gustavo F CKawahara Eduardo ZMendes Thiago SBortolotto Luiz APio-Abreu AndreaSilva Giovanio VDrager Luciano FLatronico Ana ClaudiaAlmeida Madson Q - Voltage-gated calcium channels (VGCCs) regulate differentiation, function, and survival of excitable cells, and pathogenic variants cause diverse disorders. Most known disease-associated VGCC mutations affect well-characterized regions controlling voltage-dependent gating and channel kinetics, while many residues remain functionally unannotated. We developed an evolutionary model to predict the pathogenic potential of residues in the pore-forming Ca1.3 subunit, previously validated with de novo gain-of-function variants linked to neurodevelopmental diseases. Here we show that the model recapitulates established functional regions and prospectively identifies functional sites at single-amino acid resolution. Electrophysiological analyses of five predicted variants across multiple channel domains confirmed functional alterations. The approach also captures loss-of-function variants typically pathogenic only in the homozygous state, establishing a predictive framework for identifying and functionally characterizing pathogenic variants in Ca1.3 and related ion channels. - Source: PubMed
Publication date: 2026/08/03
Tang XuechenHermenean Horia CYakimchyk AlesiaTuluc PetronelOrtner Nadine JLiedl Klaus R