Ask about this productRelated genes to: Cacng8 Blocking Peptide
- Gene:
- CACNG8 NIH gene
- Name:
- calcium voltage-gated channel auxiliary subunit gamma 8
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 2000-10-24
- Date modifiied:
- 2016-10-05
Related products to: Cacng8 Blocking Peptide
Related articles to: Cacng8 Blocking Peptide
- Stroke remains a major global health challenge due to its high mortality and significant socioeconomic burden. Despite advances in clinical management, effective diagnostic tools and therapeutic strategies remain limited. This study aimed to identify and expand the repertoire of biomarkers of damage and repair that could serve as potential diagnostic and prognostic tools across post-stroke phases. Twenty-three male wild-type mice were assigned according to three longitudinal time points to control pre-stroke, 24-hour acute, and 35-day chronic post-stroke groups. Ischemic injury was induced via a 30-minute middle cerebral artery occlusion Koizumi method. Magnetic resonance imaging and neurological scoring were used to assess lesion size and functional deficit acutely, as well as structural and functional recovery during the chronic phase. Proteomic profiling of the ipsilateral and contralateral cortices was performed using data-independent acquisition (DIA)-based MS method. Statistical analysis revealed 74 differentially expressed proteins showing significant temporal changes in expression, which were classified into four temporal expression clusters: acutely and chronically upregulated, acutely upregulated and chronically downregulated, acutely downregulated and chronically upregulated, and acutely and chronically downregulated. Gene ontology analysis identified 47 affected biological processes, including synaptic signaling, immune response, cell-cell communication, cytoskeletal organization, and proliferation. Thirteen proteins previously not associated with stroke pathophysiology were identified, including 10 from the ipsilateral cortex (Dbi, Cpne3, Dnm2, Eef1a1, Taldo1, Pgls, Gnb5, Phf24, Ctsz, Capg) and 3 from the contralateral cortex (Agpat3, Cacng8, Endod). The identified biomarkers provide novel molecular insights into post-stroke energy metabolism, neuroinflammation, and cellular remodeling, highlighting potential targets for further intervention. - Source: PubMed
Publication date: 2025/12/04
Hamer DominikButorac AnaPetrinec DanielaBerecki MonikaMendes Vera MManadas BrunoKelava VanjaK Hackenberger BranimirGlasnović AntonLovrić MarijaGajović SrećkoDobrivojević Radmilović Marina - Parkinson's disease (PD) is a progressive neurodegenerative disorder marked by the loss of dopaminergic neurons and widespread transcriptomic dysregulation across disease stages. Patients commonly exhibit motor symptoms such as tremors, rigidity, and bradykinesia, alongside non-motor symptoms including depression and cognitive decline. While previous research has largely focused on protein-coding genes, growing attention is being directed toward the regulatory roles of non-coding RNAs in PD pathogenesis-particularly the interplay between circular RNAs (circRNAs) and microRNAs (miRNAs). Emerging evidence indicates that circRNAs can act as competing endogenous RNAs (ceRNAs), modulating gene expression by sequestering miRNAs and thereby mitigating miRNA-mediated repression of target mRNAs. In this study, we performed a dynamic transcriptomic analysis across four PD stages using RNA-seq data to identify differentially expressed circRNA-miRNA-mRNA networks. We constructed stage-specific ceRNA networks by selecting positively co-regulated circRNAs and linear transcripts that were co-expressed exclusively within the same disease stage. Among the upregulated circRNAs with predicted ceRNA activity, circPRDM2 and circHSH2D were identified as uniquely expressed in PD patients. Additionally, we assessed the coding potential of the predicted target genes to further elucidate the regulatory impact of circRNAs on mRNA expression. Our findings provide new insights into the post-transcriptional regulatory mechanisms involved in PD and highlight candidate stage-specific ceRNA axes that may serve as potential biomarkers or therapeutic targets. - Source: PubMed
Publication date: 2025/12/01
Gao YulanTakenaka KoniiSantucci KristinaLindner GraceXu Si-MeiCheng YuningJanitz Michael - The Transmembrane AMPA Receptor Regulatory Protein Gamma-8 (TARP γ-8), encoded by , regulates AMPA receptor (AMPAR) trafficking, gating, and synaptic localization. Although well-characterized in central synapses, its role in retinal development and disease remains underexplored. This study investigates within the context of inherited retinal dystrophies (IRDs) by integrating human genetics within silico structural analysis. Whole Exome Sequencing (WES) was performed on IRD-affected families with atypical phenotypes-such as residual photoreceptor activity alongside severe optic atrophy or abnormal electroretinogram (ERG) profiles-yet no biallelic mutations in known IRD genes. In all families, rare heterozygous or compound heterozygous variants were identified, including a recurrent stop-gain (p.Arg123Ter) and two missense variants (p.Leu96Val, p.Val102Met), suggesting a potential modifier role. To explore their functional impact, we modeled 14 AMPAR-associated postsynaptic complexes, comparing wild-type and mutant TARP γ-8 configurations. These included auxiliary subunits (CACNG2-7, CNIH2/3), scaffolding proteins (PSD93, PSD95), and regulators (PPP3CA, RIMBPs). Docking and MM-PBSA/MM-GBSA analyses revealed that truncation or destabilization of CACNG8 severely reduced complex stability (ΔΔG > 20 kcal/mol) and altered binding geometry. Molecular dynamics simulations highlighted increased structural perturbations, reduced hydrogen bonding, and greater conformational disorder in mutant assemblies. Grid Inhomogeneous Solvation Theory (GIST) and PCA/TICA analyses further revealed diminished water structuring and constrained conformational landscapes. Altogether, our findings support the potential role of as a genetic modifier in IRDs, pending further validation in larger cohorts. The study illustrates how combining genomic and structural approaches can uncover hidden contributors to complex retinal disorders. - Source: PubMed
Publication date: 2025/10/03
Alibrandi SimonaMordà DomenicoScimone ConcettaAbate GiorgiaChust Ignacio BabiloniRinaldi CarmelaPoggi LuciaScalinci Sergio ZaccariaD'Angelo RosaliaSidoti AntoninaDonato Luigi - Lymphoma is one of the leading causes of cancer and cancer deaths and yet has not been amenable to population screening. The role of methylated DNA markers (MDMs) in the detection of lymphoma has not been extensively studied. We aimed to discover, validate, and test tissue-derived MDMs of lymphoma in archival plasma specimens. Reduced representation bisulfite sequencing (RRBS) was performed on a discovery set of frozen tissues. MDMs identified were converted to methylation-specific PCR assays and validated on independent formalin-fixed, paraffin-embedded (FFPE) tissues. Target enrichment long-probe quantitative-amplified signal (TELQAS) assays were developed and assayed in plasma-extracted, bisulfite-converted DNA from independent treatment-naïve lymphoma patients and healthy controls. Prediction of cancer status was modeled using random forest model with in silico cross-validation. After discovery and validation in tissue, 16 TELQAS assays (ZNF503, VWA5B1, HOXA9, GABRG3, ITGA5, MAX.chr17.7190, BNC1, CDK20, MAX.chr4.4069, TPBG, DNAH14, SYT6, CACNG8, FAM110B, ADRA1D, and NRN1) were selected for testing in plasma. These detected 78% (95% CI, 74%-82%) of lymphoma cases at 90% specificity. Excluding marginal zone and T-cell lymphomas, sensitivity increased to 84% (80%-88%). MDMs in plasma show promise to detect lymphoma and are candidates for inclusion in multi-cancer detection studies. - Source: PubMed
Publication date: 2024/11/20
Witzig Thomas ETaylor William RMahoney Douglas WBamlet William RFoote Patrick HBurger Kelli NDoering Karen ADevens Mary EArndt Jacquelyn RO'Connell Maria CBerger Calise KNovak Anne JCerhan James RHennek JacquelynKaterov SlavaAllawi Hatim TJevremovic DraganDao Linda NGraham Rondell PKisiel John B - Neurological disorders such as Alzheimer's, Parkinson's, amyotrophic lateral sclerosis, and schizophrenia are associated with altered neuronal excitability, resulting from dysfunctions in the molecular architecture and physiological regulation of ion channels and synaptic transmission. Ion channels and synapses are regarded as suitable therapeutic targets in modern pharmacology. Cannabinoids have received great attention as an original therapeutic approach for their effects on human health due to their ability to modulate the neurotransmitter release through interaction with the endocannabinoid system. In our study, we explored the effect of cannabinol (CBN) through next-generation sequencing analysis of NSC-34 cell physiology. Our findings revealed that CBN strongly influences the ontologies related to ion channels and synapse activity at all doses tested. Specifically, the genes coding for calcium and potassium voltage-gated channel subunits, and the glutamatergic and GABAergic receptors (, , , , , , , , , , ), were up-regulated. Conversely, the genes involved into serotoninergic and cholinergic pathways (, , , , , ), were down-regulated. These findings highlight the influence of CBN in the expression of genes involved into ion influx and synaptic transmission. - Source: PubMed
Publication date: 2024/09/19
Trainito AlessandraMuscarà ClaudiaGugliandolo AgneseChiricosta LuigiSalamone StefanoPollastro FedericaMazzon EmanuelaD'Angiolini Simone