KCNC2 Antibody
- Known as:
- KCNC2 Antibody
- Catalog number:
- XW-7716
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- KCNC2 Antibody
Related genes to: KCNC2 Antibody
- Gene:
- KCNC2 NIH gene
- Name:
- potassium voltage-gated channel subfamily C member 2
- Previous symbol:
- -
- Synonyms:
- Kv3.2
- Chromosome:
- 12q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-13
- Date modifiied:
- 2016-10-11
Related products to: KCNC2 Antibody
Related articles to: KCNC2 Antibody
- Histone deacetylases (HDACs) regulate neuroprotection; however, Trichostatin A (TSA), an HDAC inhibitor, lacks clear molecular mechanisms and core targets in Alzheimer's disease (AD), limiting clinical translation. This study aimed to decipher TSA's AD-regulating network, screen core genes, and support AD early diagnosis and multi-target therapies. - Source: PubMed
Publication date: 2026/04/20
Ou ChangzeChen BinbinDeng JunLong Huajun - Methamphetamine (METH) use disorder (MUD) is characterized by high relapse rates driven by craving, yet the underlying neural mechanisms remain unclear. Here, we reveal the temporal and circuit-specific contributions of somatostatin (SST) and parvalbumin (PV) interneurons (INs) in the prelimbic cortex (PL) in the incubation of METH craving. SST INs mediated drug seeking during early withdrawal (day 1) via lateral hypothalamus (LH) GABAergic inputs, while PV INs drove seeking following prolonged withdrawal (day 15) via anteromedial thalamus (AM) glutamatergic inputs. Single-cell RNA sequencing (scRNA-seq) revealed upregulated KCNC2 (encoding the Kv3.2 potassium channel) in both subtypes, with specific protein modifications. Selective KCNC2 knockdown in SST or PV INs significantly suppressed drug seeking during early or prolonged withdrawal, respectively. These findings uncover the distinct contributions of PL IN subtypes to the incubation of craving and identify KCNC2 as a potential phase-specific therapeutic target in MUD. - Source: PubMed
Publication date: 2026/03/26
Shi SaiSun Yi-WenDing Jin-JunCheng Ying-JieWu Man-QingSu HangGong Wan-KunLiu FangYuan Ti-FeiZhao Min - The Kv3.2 subfamily of voltage activated potassium channels encoded by the gene is abundantly expressed in neurons that fire trains of fast action potentials that are a major source of cortical inhibition. Gain-of-function (GOF) pathogenic variants in and , encoding Kv3.1 and Kv3.2 respectively, cause several types of epilepsy including developmental and epileptic encephalopathy (DEE). Fluoxetine (Prozac) is a known inhibitor of the Kv3.1 current and was reported to improve seizure control in a single patient with a GOF variant. Here, we describe fluoxetine treatment of two siblings with a V473A variant associated with DEE, which resulted in improved seizure control, ability to wean antiepileptic medications, and improved development. The V437A variant showed GOF activity as demonstrated by HEK293 cells expressing variant subunits activating at more hyperpolarized potentials than WT channels. Fluoxetine reduced currents equally for both Kv3.2 WT and Kv3.2-V473A variant channels, with an IC of ∼12 µM. Further analysis of this repurposed drug showed that norfluoxetine, a long-lasting metabolite of fluoxetine which is produced in the liver and accumulates in the brain, was more effective than fluoxetine itself in selectively inhibiting the dominant pathogenic channel activity of the pathogenic allele. Norfluoxetine showed 7-fold greater selectivity in inhibiting Kv3.2 variant currents (IC of ∼0.4 µM) compared to WT currents (IC of ∼2.9 µM). Combined with a previous report of improved outcomes for a variant, our results suggest that fluoxetine or its metabolite, norfluoxetine, may be beneficial for patients with GOF variants in and other neuronal potassium channels. - Source: PubMed
Publication date: 2025/01/15
Li PingButler AliceZhou YuMagleby Karl LGurnett Christina ASalkoff Lawrence - Atherosclerosis and aneurysm of the aorta are relatively common pathological conditions that remain asymptomatic for a long period of time and have life-threatening and disabling complications. DNA methylation profiling in several regions (a dilated area, a nondilated area, and an atherosclerotic plaque) of the ascending aorta was carried out in patients with aortic aneurysm. DNA methylation was analyzed by reduced representation bisulfite sequencing (RRBS). Differences in methylation level between dilated and normal aortic tissues were detected for two CpG sites of the NR2F1-AS1 gene (|Δβ| > 0.2 and FDR < 0.05). In total, 586/480 differentially methylated CpG sites (DMSs) were identified by comparing atherosclerotic plaque samples with dilated/normal aortic tissues; 323/234 of the DMSs were hypermethylated and 263/246 were hypomethylated in atherosclerotic plaques. Most DMSs were in introns and intergenic regions; 88.2% of the DMSs were in the binding sites of transcription factors, among which ZNf263, ZFP148, PATZ1, NRF1, TCF12, and EGR1 play a role in the pathogenesis of atherosclerosis of various arteries and ELK1, ETS1, and KLF15 play a role in aortic aneurysms. Sixteen DMSs were found in the regions of the genes CMIP, RPH3AL, XRCC1, GATA5, EXD3, KCNC2, HIVEP3, ADCY9, CDCP2, FOLR1, WT1, MGMT, GAS2, CA1, PRSS16, and ANK3, whose protein products are involved in both aortic dissection and atherosclerosis in various arterial circulation regions. The protein products of the genes are involved in a wide range of biological processes, including mesenchyme development (GO:0060485; FOLR1, WT1, GATA5, HIVEP3, and KCNC2) and positive regulation of DNA metabolic processes (GO:0051054; MGMT, WT1, and XRCC1). - Source: PubMed
Goncharova I AZarubin A AShipulina S AKoroleva Iu APanfilov D SKozlov B NNazarenko M S - Spontaneous preterm birth (SPTB) is the leading cause of neonatal morbidity and mortality. It is a final common pathway for multiple etiologies, some of which are well known while others likely remain to be identified. Despite recent advancements in identifying genetic risk factors, the mechanisms of many SPTBs remain poorly understood due to the phenotypic heterogeneity and complexity. Large family-based studies decrease heterogeneity and improve power to identify genetic causes of SPTB. - Source: PubMed
Publication date: 2024/12/06
Workalemahu TsegaselassieClark Erin A SMadsen Michael JYu ZheDalton Susan EEsplin M SeanManuck TracyNeklason DeborahWu Chen-Han WilfredJorde Lynn BCamp Nicola JSilver Robert MVarner Michael W