KCNV1 Antibody - N-terminal region (ARP35233_P050)
- Known as:
- KCNV1 Antibody - N-terminal region (ARP35233_P050)
- Catalog number:
- arp35233_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KCNV1 Antibody - N-terminal region (ARP35233_P050)
Ask about this productRelated genes to: KCNV1 Antibody - N-terminal region (ARP35233_P050)
- Gene:
- KCNV1 NIH gene
- Name:
- potassium voltage-gated channel modifier subfamily V member 1
- Previous symbol:
- -
- Synonyms:
- Kv8.1
- Chromosome:
- 8q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-07-10
- Date modifiied:
- 2016-02-04
Related products to: KCNV1 Antibody - N-terminal region (ARP35233_P050)
Related articles to: KCNV1 Antibody - N-terminal region (ARP35233_P050)
- KvS proteins are voltage-gated potassium channel subunits that form functional channels when assembled into heteromers with Kv2.1 () or Kv2.2 (). Mammals have 10 KvS subunits: Kv5.1 (), Kv6.1 (), Kv6.2 (), Kv6.3 (), Kv6.4 (), Kv8.1 (), Kv8.2 (), Kv9.1 (), Kv9.2 (), and Kv9.3 (). Electrically excitable cells broadly express channels containing Kv2 subunits and most neurons have substantial Kv2 conductance. However, whether KvS subunits contribute to these conductances has not been clear, leaving the physiological roles of KvS subunits poorly understood. Here, we identify that two potent Kv2 inhibitors, used in combination, can distinguish conductances of Kv2/KvS heteromers and Kv2-only channels. We find that Kv5, Kv6, Kv8, or Kv9-containing channels are resistant to the Kv2-selective pore-blocker RY785 yet remain sensitive to the Kv2-selective voltage sensor modulator guangxitoxin-1E (GxTX). Using these inhibitors in mouse superior cervical ganglion neurons, we find predominantly RY785-sensitive conductances consistent with channels composed entirely of Kv2 subunits. In contrast, RY785-resistant but GxTX-sensitive conductances consistent with Kv2/KvS heteromeric channels predominate in mouse and human dorsal root ganglion neurons. These results establish an approach to pharmacologically distinguish conductances of Kv2/KvS heteromers from Kv2-only channels, enabling investigation of the physiological roles of endogenous KvS subunits. These findings suggest that drugs which distinguish KvS subunits could modulate electrical activity of subsets of Kv2-expressing cell types. - Source: PubMed
Publication date: 2025/05/27
Stewart Robert GMarquis Matthew JamesJo SooyeonHarris Brandon JAberra Aman SCook VerityWhiddon ZacharyYarov-Yarovoy VladimirFerns MichaelSack Jon T - HPV infection is common among women and can result in serious illnesses. This research utilizes single-cell RNA-sequencing (scRNA-seq) to study the connection between cellular heterogeneity and HPV integrations in cervical histopathology. scRNA-seq was used to examine heterogeneity among normal patients and those in three disease stages: high-grade squamous intraepithelial lesions (HSIL), microinvasive carcinoma (MIC), and cervical squamous epithelium carcinoma cancer (CSCC) tissues. A method was developed to identify HPV integration events from scRNA-seq data. Our results indicated an increase in squamous epithelial cells and a decrease in columnar epithelial cells as the disease progressed from normal to CSCC. We discovered HPV genes that were differentially expressed across normal patients and those in the three disease stages. Notably, HPV integration events were more common in squamous epithelial cells at the single-cell level. The ratio of HPV-integrated cells increased as the disease progressed from normal tissue to CSCC, eventually stabilizing. Several genes, such as EGR1, S100A11, S100A8, KRT5, RPL34, ATP1B1, RPS4X and EEF2, were frequently integrated by HPV across patients. In contrast, genes like PAN3, BABAM2, SPEN, TCIM-SIRLNT, TEX41-PABPC1P2 and KCNV1-LINC01608 showed frequent integration events across cells. KRT5, ATP1B1, RPS4X, PAN3 and SPEN were novel recurrent HPV-integrated genes we observed at the patient or cell level in this study. Additionally, we found that HPV genes from various HPV types exhibited integration preferences in various samples and disease stages. This provides a valuable insight into the mechanism of HPV-induced cervical cancer from a single-cell standpoint, highlighting its clinical relevance. - Source: PubMed
Zeng XiPeng FangWang ZiyingTeng QiuliSha YingLeung Ross Ka-KitChristopher L A I Koon ChiLi GuoliangHuang XiaoyuanLin Shitong - Hundreds of novel candidate human epilepsy-associated genes have been identified thanks to advancements in next-generation sequencing and large genome-wide association studies, but establishing genetic etiology requires functional validation. We generated a list of >2,200 candidate epilepsy-associated genes, of which 48 were developed into stable loss-of-function (LOF) zebrafish models. Of those 48, evidence of seizure-like behavior was present in 5 (, , , , and ). Further characterization provided evidence for epileptiform activity via electrophysiology in and mutants. Additionally, and mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further, RNA sequencing (RNA-seq) revealed convergent transcriptional abnormalities between mutant lines, consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of , , and in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes. - Source: PubMed
Publication date: 2024/06/05
LaCoursiere Christopher MarkUllmann Jeremy F PKoh Hyun YongTurner LauraBaker Cristina MRobens BarbaraShao WanqingRotenberg AlexanderMcGraw Christopher MPoduri Annapurna H - While voltage-gated potassium channels have critical roles in controlling neuronal excitability, they also have non-ion-conducting functions. Kv8.1, encoded by the KCNV1 gene, is a 'silent' ion channel subunit whose biological role is complex since Kv8.1 subunits do not form functional homotetramers but assemble with Kv2 to modify its ion channel properties. We profiled changes in ion channel expression in amyotrophic lateral sclerosis patient-derived motor neurons carrying a superoxide dismutase 1(A4V) mutation to identify what drives their hyperexcitability. A major change identified was a substantial reduction of KCNV1/Kv8.1 expression, which was also observed in patient-derived neurons with C9orf72 expansion. We then studied the effect of reducing KCNV1/Kv8.1 expression in healthy motor neurons and found it did not change neuronal firing but increased vulnerability to cell death. A transcriptomic analysis revealed dysregulated metabolism and lipid/protein transport pathways in KCNV1/Kv8.1-deficient motor neurons. The increased neuronal vulnerability produced by the loss of KCNV1/Kv8.1 was rescued by knocking down Kv2.2, suggesting a potential Kv2.2-dependent downstream mechanism in cell death. Our study reveals, therefore, unsuspected and distinct roles of Kv8.1 and Kv2.2 in amyotrophic lateral sclerosis-related neurodegeneration. - Source: PubMed
Publication date: 2024/06/11
Huang XuanLee SeungkyuChen KuchuanKawaguchi RikiWiskow OleGhosh SulagnaFrost DevlinPerrault LauraPandey RoshanKlim Joseph RBoivin BrunoHermawan CrystalLivak Kenneth JGeschwind Daniel HWainger Brian JEggan Kevin CBean Bruce PWoolf Clifford J - Hundreds of novel candidate human epilepsy-associated genes have been identified thanks to advancements in next-generation sequencing and large genome-wide association studies, but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy-associated genes, of which 81 were determined suitable for the generation of loss-of-function zebrafish models via CRISPR/Cas9 gene editing. Of those 81 crispants, 48 were successfully established as stable mutant lines and assessed for seizure-like swim patterns in a primary F screen. Evidence of seizure-like behavior was present in 5 () of the 48 mutant lines assessed. Further characterization of those 5 lines provided evidence for epileptiform activity via electrophysiology in and mutants. Additionally, and mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Furthermore, RNAseq revealed convergent transcriptional abnormalities between mutant lines, consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of , , and in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes. - Source: PubMed
Publication date: 2024/02/08
LaCoursiere Christopher MarkUllmann Jeremy F PKoh Hyun YongTurner LauraBaker Cristina MRobens BarbaraShao WanqingRotenberg AlexanderMcGraw Christopher MPoduri Annapurna