Kcna4 polyclonal antibody
- Known as:
- Kcna4 pab (anti-)
- Catalog number:
- PAB10103
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- Kcna4 polyclonal antibody
Related genes to: Kcna4 polyclonal antibody
- Gene:
- KCNA4 NIH gene
- Name:
- potassium voltage-gated channel subfamily A member 4
- Previous symbol:
- KCNA4L
- Synonyms:
- Kv1.4, HK1, HPCN2
- Chromosome:
- 11p14.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-13
- Date modifiied:
- 2016-10-11
Related products to: Kcna4 polyclonal antibody
Related articles to: Kcna4 polyclonal antibody
- Our previous studies demonstrate that htau mice recapitulate many of the neuropsychiatric features of early Alzheimer's disease (AD), and that the dorsal raphe nucleus (DRN) contains distinct subregions. Herein, we investigate the vulnerability of the centromedial DRN to pathologically phosphorylated tau (p-tau), a region composed predominantly of dually serotonergic/glutamatergic (5HT/glut) neurons. - Source: PubMed
Kolling Louis JBalasubramanian NagalakshmiIsmail ShafaFeller Alexander JAlberhasky Jessica Marie HunterWang RuixiangJennings LukeHefti MarcoMarcinkiewcz Catherine Anne - A large "gene desert" located far upstream from Fshb and Kcna4 contains several gonadotrope-specific accessible chromatin sites that were seen in chromatin conformation capture to make distinct contacts with both genes. Expression of Fshb and Kcna4 was strongly inhibited by JQ-1, which represses super-enhancer activity, and the region displays super-enhancer characteristics. The sites of open chromatin were seen, in chromatin immunoprecipitation, to bind Brd4 and Med1, most notably at a site -67 kb from the Fshb gene, as well as binding Ctcf further upstream (-123 kb), all of which were increased following activin exposure. The locus is transcribed to chromatin-associated long noncoding RNAs whose levels correlate with Fshb and Kcna4 mRNA levels in vivo and in cultured gonadotrope cells, indicating coordinated regulation. CRISPR interference confirmed distinct functions for each element and, together with the chromatin conformation capture data, indicate that the -67 kb locus mediates basal and activin-stimulated Fshb expression, whereas the site at -59 kb contributes to activin-stimulation of both genes. Single-cell multiomics revealed that the -67 kb locus is accessible in pituitary stem cells and throughout gonadotrope differentiation, preceding opening of the Fshb promoter, although it is closed in other differentiated cell types, suggesting a gonadotrope-specific factor that keeps it open at this stage. Foxl2 was found to bind this element, contributes to maintaining its chromatin accessibility, and recruits Supt16h, a component of the Facilitates Active Chromatin Transcription histone chaperone complex. These findings define a distal, Foxl2-bound super-enhancer that regulates Fshb transcription and shapes the gonadotrope regulatory landscape. - Source: PubMed
Refael TalGolan GilDarsa DaniellaPnueli LilachChakravarty ProbirRizzoti KarineMelamed Philippa - The number of individuals diagnosed with opioid use disorder (OUD) has risen steeply because of increased prescribing of opioid drugs including oxycodone for chronic pain relief. When rats given extended access to oxycodone only a subset of animals self-administers more drug over time. Identifying the molecular mechanism associated with this behavior can introduce novel ways to combat OUD. Herein, we sought to identify the alteration in the expression of voltage gated and calcium activated potassium channels after extended access to oxycodone self-administration. - Source: PubMed
Publication date: 2025/08/11
Wabreha Ammanuel YAdjei NasserLadenheim BruceCadet Jean LudDaiwile Atul P - Shaker-type potassium channel genes (Kv1) have been linked to human epilepsies, including KCNA1 (Kv1.1), KCNA2 (Kv1.2), and more recently, KCNA3 (Kv1.3) and KCNA6 (Kv1.6). In this study, we report three early-onset epilepsy cases with de novo missense mutations in Shaker-type channel genes, including Kv1.3, KCNA4 (Kv1.4), and Kv1.6, identified through whole exome sequencing trio study. The newly identified Kv1.3-V478M, Kv1.6-T421I, and Kv1.4-V558L mutations are located within the channel selectivity filter or S6 hinge, both critical for channel gating. These variants are in paralogous locations of previously reported pathogenic variant in KCNA2. These mutations do not significantly affect trafficking and plasma membrane localization of the Kv channels. In contrast, our patch-clamp analysis in a cell-based system reveals that all three mutations cause severe loss-of-function channel properties. Additionally, our Drosophila model highlights the detrimental effects of Kv1.3-V478M on neural circuit activity. Current findings suggest that, similar to Kv1.1, Kv1.2, and Kv1.3, both loss-of-function and gain-of-function mutations in Kv1.6 may contribute to the phenotypic variability in epilepsy severity. Our study also extends the list of potassium channel genes implicated in human epilepsy, introducing Kv1.4 as a novel epilepsy-related gene. - Source: PubMed
Tsai Meng-HanLo Chia-HuaLiu You-XuanWu Sheng-NanKuo Cheng-YenLiu Yi-HsuanChang Ying-ChaoLin Kuan-LinHung Po-ChengChen Hwei-HsienChen Jian-LiangYao Chi-KuangHwang EricWang Ya-Jean - MicroRNAs have been studied extensively in neurodegenerative diseases. In a previous study, miR-153 promoted neural differentiation and projection formation in mouse hippocampal HT-22 cells. However, the pathways and molecular mechanism underlying miR-153induced neural differentiation remain unclear. To explore the molecular mechanism of miR-153 on neural differentiation, we performed RNA sequencing on miR-153-overexpressed HT-22 cells. Based on RNA sequencing, differentially expressed genes (DEGs) and pathways in miR-153-overexpressed cells were identified. The Database for Annotation, Visualization and Integrated Discovery and Gene Set Enrichment Analysis were used to perform functional annotation and enrichment analysis of DEGs. Targetscan predicted the targets of miR-153. The Search Tool for the Retrieval of Interacting Genes and Cytoscape, were used to construct protein-protein interaction networks and identify hub genes. Q-PCR was used to detect mRNA expression of the identified genes. The expression profiles of the identified genes were compared between embryonic days 9.5 (E9.5) and E11.5 in the embryotic mouse brain of the GDS3442 dataset. Cell Counting Kit-8 assay was used to determine cell proliferation and cellular susceptibility to amyloid β-protein (Aβ) toxicity in miR-153-overexpressed cells. The results indicated that miR-153 increased cell adhesion/Ca (Cdh5, Nrcam, and P2rx4) and Bdnf/Ntrk2 neurotrophic signaling pathway, and decreased ion channel activity (Kcnc3, Kcna4, Clcn5, and Scn5a). The changes in the expression of the identified genes in miR-153-overexpressed cells were consistent with the expression profile of GDS3442 during neural differentiation. In addition, miR-153 overexpression decreased cellular susceptibility to Aβ toxicity in HT-22 cells. In conclusion, miR-153 overexpression may promote neural differentiation by inducing cell adhesion and the Bdnf/Ntrk2 pathway, and regulating electrophysiological maturity by targeting ion channels. MiR-153 may play an important role in neural differentiation; the findings provide a useful therapeutic direction for neurodegenerative diseases. - Source: PubMed
Publication date: 2024/04/26
Jiao LiJunfang ZhangYanna LiCaixia JinChen ZhangSong JiaJie XuXiaoli YanXin GuiLibo XingFeng WangLixia LuChunli XuLei Xu