CACNA1C siRNA_Lentivectors
- Known as:
- CACNA1C siRNA_Lentivectors
- Catalog number:
- i003619b
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CACNA1C siRNA_Lentivectors
Related genes to: CACNA1C siRNA_Lentivectors
- Gene:
- CACNA1C NIH gene
- Name:
- calcium voltage-gated channel subunit alpha1 C
- Previous symbol:
- CCHL1A1, CACNL1A1
- Synonyms:
- Cav1.2, CACH2, CACN2, TS, LQT8
- Chromosome:
- 12p13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1991-01-30
- Date modifiied:
- 2019-04-23
Related products to: CACNA1C siRNA_Lentivectors
Related articles to: CACNA1C siRNA_Lentivectors
- Male obesity-associated secondary hypogonadism(MOSH) is a common disease among severely obese male patients. Although surgical interventions have demonstrated clinical benefits, a subset of patients continue to experience MOSH following surgery. Therefore, this study aims to investigate epigenetic changes associated with the use of the weight-loss drug Semaglutide in MOSH, focusing on DNA methylation and miRNA expression. In this exploratory study, samples were classified into three groups: a control group (n = 2), a MOSH group (n = 7), and a follow-up group (n = 4). DNA methylation analysis was performed on all samples, while miRNA sequencing was conducted on a subset of the samples: 2 from the control group, 7 from the MOSH group, and 2 from the follow-up group. Differentially expressed miRNAs (DEMs) were analyzed through the R package "limma", and the methylation level of CpG sites was analyzed based on the methylation β value, obtaining differentially methylated genes (DMGs). The functional enrichment analysis of miRNA target genes and methylation change genes was conducted using the R package "clusterProfiler". Finally, the regulatory networks of miRNA and methylation genes as well as the protein-protein interaction (PPI) network were analyzed. A total of 6 DEMs were screened out. The target genes of these DEMs were mainly enriched in pathways such as ATP binding, phosphorylation, cell adhesion, and Glycosphingolipid biosynthesis. Eighty DMGs were identified, and the largest number of DMGs were found in the X chromosome. In the regulatory network of DMGs and DEMs, hsa-miR-423-5p regulates most of these DMGs. Moreover, the PPI network shows that DPP6, DPP10, CACNA1C, and CNTNAP2 are the proteins with the strongest connectivity. Notably, differential CpG methylation changes were observed on chromosome 7, indicating a potential region of epigenetic alteration in MOSH; however, the biological and functional relevance of these changes remains unclear. Collectively, these findings suggest that Semaglutide treatment in MOSH may be associated with concurrent alterations in DNA methylation and miRNA expression, implicating genes related to energy and glycolipid metabolism, including DPP6, DPP10, CACNA1C, and CNTNAP2. These results are exploratory and hypothesis-generating, providing preliminary observations to inform future validation studies. - Source: PubMed
Publication date: 2026/06/23
Guo YunchongSu JunleiShen LijunDing ChenzhaoWen YaqingLi ZetingLi Fangping - This paper reviews the molecular differences across the cortical hierarchy in primates that expand in dorsolateral prefrontal cortex (dlPFC) to generate working memory and top-down control, but which confer vulnerability in mental disorders. Research on molecular mechanisms early in the primate cortical hierarchy, e.g. in primary visual cortex (V1), are often in concert with rodent, e.g. neurotransmission relies greatly on AMPAR, while modulation with attention involves NMDAR and cholinergic mechanisms. However, there are also significant differences in cortical specializations and cholinergic receptor localization between rodent and primate V1. In contrast to V1, the recurrent excitatory microcircuits in layer III of primate dlPFC that generate working memory express many distinct mechanisms: neurotransmission depends on NMDAR and acetylcholine (and thus arousal state), not AMPAR; extended neuronal firing underlying working memory depends on magnified calcium signaling in spines; however, excessive cytosolic calcium reduces firing, with powerful mechanisms to take the dlPFC "off-line" during uncontrollable stress and/or inflammation, e.g. opening potassium channels on spines to rapidly weaken connections. Regulation of these powerful mechanisms is lost due to inflammation and/or genetic insults (e.g. gain-of-function mutations in CACNA1C, loss of function in GRM3), which may interact to induce loss of dendritic spines and/or tau pathology, cognitive impairments and reduced top-down control. Many of the genetic risks for schizophrenia weaken layer III dlPFC spine connections, suggesting that multiple genotypes would produce a shared phenotype. The review also suggests new therapeutic targets that can act to reduce inflammation, regulate calcium and strengthen synaptic efficacy in the primate dlPFC. - Source: PubMed
Publication date: 2026/06/19
Wang MinGalvin Veronica CJoyce Mary Kate PDatta DibyadeepYang ShengtaoDisney Anita AArnsten Amy F T - Anorexia nervosa (AN) is a severe metabo-psychiatric disorder with the highest mortality rate among psychiatric conditions. Its characteristic onset during adolescence suggests that disrupted neurodevelopmental processes during critical periods may contribute to disease pathophysiology. In this exploratory study, we conducted an integrated multi-layered omics analysis to identify molecular alterations affecting neurodevelopmental pathways in individuals with AN. We employed three complementary approaches: DNA methylation sequencing via Reduced Representation Bisulfite Sequencing (RRBS), microRNA (miRNA) expression profiling using panel-based qPCR, and microbiome characterization through 16S rRNA sequencing in a sample of 38 patients with AN and 40 healthy controls. Analyses focused on molecular mechanisms involved in neurodevelopmental processes. RRBS analysis identified methylation differences in neurodevelopmentally relevant genes, particularly (voltage-gated calcium channel) and (transcription factor). miRNA profiling revealed extensive dysregulation, with 74 miRNAs showing altered levels in the AN pools. Network analysis highlighted that miR-135 family targets (SK3 channel involved in neuronal excitability), while miR-374b regulates (IGF-1 signaling modulator). Microbiome analysis revealed that 42% of the AN group exhibited dramatic oral dysbiosis characterized by Proteobacteria dominance. Our findings demonstrate coordinated multi-level dysregulation of mechanisms governing neural circuit maturation during adolescence, supporting a neurodevelopmental framework for understanding AN. The convergence of molecular alterations on ion channels and growth factor signaling suggests systems-level perturbations in developmental regulatory mechanisms. The identified miRNAs represent potential biomarkers and therapeutic targets, while microbiome heterogeneity suggests distinct clinical subgroups. While exploratory in nature, this work provides novel insights into AN molecular architecture and generates testable hypotheses for future mechanistic studies incorporating individual-level data essential to validate these candidates and establish robust clinical correlations. - Source: PubMed
Publication date: 2026/05/19
Gilardini FedericaSabatucci AnnalauraCifani CarloSegura-Garcia CristinaPucci MariangelaRania MariannaD'Addario Claudio - Autism spectrum disorder (ASD) may be a predisposing factor in the development of catatonia, which has been demonstrated to be effectively treated using electroconvulsive therapy (ECT). CACNA1 channelopathy mutations have been associated with autism spectrum disorder, intellectual disability, and epilepsy. The single published case report of ECT use in CACNA1 subunit mutations demonstrated a negative outcome, and no current case reports on CACNA1B, CACNA1C, CACNA1D, or CACNA1E mutations have been published. We present a case of an adolescent with a known CACNA1D mutation and symptoms of excited catatonia who experienced a reduction in the frequency and severity of self-injurious and violent behavior following treatment with ECT. Our case demonstrates the use of ECT for catatonia in an individual with a CACNA1 mutation without complication and with a positive therapeutic response. - Source: PubMed
Publication date: 2026/05/26
Mancine RyleyKuang JoannaRaghunandan ChristinaPalffy Alexander - Painful diabetic neuropathy (PDN) is frequently accompanied by anxiety, yet the neural circuit mechanisms associated with nociceptive hypersensitivity to affective dysfunction remain unclear. Here we combined brain-wide c-Fos mapping, viral tracing, in vivo fiber photometry, whole-cell recordings, and projection-specific opto/chemogenetics in a mouse model of streptozotocin-induced PDN to define a thalamo-cortex circuit for pain-anxiety comorbidity. Within the posterior insular cortex (pIC), CaMKIIα⁺ excitatory neurons were recruited in PDN mice with comorbid anxiety, exhibiting heightened neuronal excitability and enhanced excitatory synaptic input. Bidirectional chemogenetic modulation of pIC neurons oppositely regulated anxiety-like behavior and mechanical hypersensitivity without locomotor or glycemic confounds. Circuit mapping identified a monosynaptic excitatory projection from the paraventricular thalamus (PVT) to the pIC; PVT neurons were hyperactive in PDN, and projection-defined manipulation of the PVT to pIC pathway bidirectionally controlled the behavioral phenotypes. Cacna1c was upregulated in the PVT of PDN mice; its knockdown in pIC-projecting PVT neurons attenuated both pain and anxiety-like behaviors. Together, these results delineate a thalamo-cortex excitatory pathway that couples nociceptive and affective dimensions of PDN and suggest that selective targeting of the PVT to pIC circuit may provide coordinated relief of pain and anxiety-related symptoms. - Source: PubMed
Publication date: 2026/05/27
Wei MinShou JiayinYang JingCai SiqingBai QiyuanHou JinwenJiang YeShen ShixiongYu ZhuoyingZhao XinruHan YongzhengCai JieYang Xue-WeiLi ZhengqianMa DaqingXing Guo-GangLi Min