Ask about this productRelated genes to: KCNC3 Blocking Peptide
- Gene:
- KCNC3 NIH gene
- Name:
- potassium voltage-gated channel subfamily C member 3
- Previous symbol:
- SCA13
- Synonyms:
- Kv3.3
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-13
- Date modifiied:
- 2019-04-23
Related products to: KCNC3 Blocking Peptide
Related articles to: KCNC3 Blocking Peptide
- Traumatic brain injury (TBI) is a prevalent cause of secondary neuropsychiatric disorders, with post-traumatic anxiety significantly worsening long-term outcomes. However, the key neural circuits and molecular mechanisms underlying post-TBI anxiety remain poorly understood. Here, we show that TBI patients with frontal lobe injuries and anxiety exhibited increased activity and enhanced functional connectivity in the anterior insular cortex (aIC) and lateral orbitofrontal cortex (lOFC). Mechanistically, we established a mouse model of moderate frontal lobe TBI, categorizing animals into anxious and non-anxious TBI groups. BOLD-fMRI and c-Fos expression analyses revealed that mice with post-traumatic anxiety also exhibited increased activity in the aIC and lOFC, as well as heightened activity in the aIC-lOFC glutamatergic circuit. Optogenetic and chemogenetic modulation of this circuit bidirectionally regulated post-traumatic anxiety. Single-cell RNA sequencing of aIC glutamatergic neurons identified a specific downregulation of KCNC3 in anxious TBI mice. Functional validation confirmed that KCNC3 downregulation mediates hyperactivity in the aIC-lOFC glutamatergic circuit and induces post-traumatic anxiety. Together, these findings unveil a critical role of TBI‑induced KCNC3 downregulation in aIC glutamatergic neurons in driving hyperactivity of the aIC-lOFC glutamatergic circuit and resulting post‑traumatic anxiety, and they suggest KCNC3 and the aIC-lOFC circuit as promising therapeutic targets for post‑TBI anxiety. - Source: PubMed
Publication date: 2026/07/27
Li Meng-GeQian Xiao-BoZhang Hai-LongLi DiJi LingXu Xin-ChunDing Jia-ShengYin Li-JunZhang LiXu Guang-YinGao Rong
- Source: PubMed
- Kv3.3 voltage-gated K (Kv) channels are highly expressed in cerebellar Purkinje neurons and some hippocampal neurons, aligning with the motor and cognitive impairments observed in spinocerebellar ataxia 13 (SCA13) caused by Kv3.3 mutations. Despite their functional significance, the mechanisms governing Kv3.3 subcellular localization remain poorly understood. Here we report microtubule-associated protein 6 (MAP6) regulates Kv3.3 axon-dendrite targeting. MAP6 deletion reduces Kv3.3 levels in the processes of Purkinje neurons. Mechanistically, MAP6's 1st and 2nd Mn modules directly bind the external surface of the Kv3.3 N-terminal T1 tetramer, while its 3rd Mn module indirectly associates with Cav2 Ca channels. In Purkinje neurons, shRNA-mediated MAP6 knockdown decreases somatodendritic levels of both Kv3.3 and Cav2.1 (associated with SCA6). Notably, expression of Mn1/2-GFP selectively reduces Kv3.3, but not Cav2.1, levels. Purkinje neuron burst firing is reduced in both conditions. These findings uncover a MAP6-dependent mechanism for targeting two key ion channels linked to SCAs. - Source: PubMed
Publication date: 2026/04/30
Ma DiNalinakshan NandithaMarshall Alec HJukkola PeterBosc ChristopheGory-Fauré SylvieAndrieux AnnieWester Jason CGu Chen - An aberrant expression of the voltage-gated potassium (Kv) channel family has been verified in a variety of tumors, which can contribute to tumor proliferation and migration by regulating the cell cycle, suppressing apoptosis, facilitating the epithelial-mesenchymal transition (EMT), and activating downstream tumor-associated pathways. Kv3.3 is encoded by the Kv channel subfamily C member 3 (). Previous studies on focused primarily on nervous system diseases rather than tumors. Therefore, our aim is to explore the potential biological roles and clinical significance of in the field of oncology. - Source: PubMed
Publication date: 2025/12/19
Xia KunZhu Hong-ChaoLai Fang-YeLi Zi-HaoWang WeiWang Nan - This study explores the cell fate reprogrammability of H3K27M-mutant pediatric high-grade gliomas (pHGG) using neuronal transdifferentiation as a potential targeted therapy. We treated the BT245 patient-derived glioma cell line with pharmacological combinations targeting neuronal differentiation pathways and performed bulk RNA sequencing to characterize gene expression patterns driving cell fate transitions. Our findings reveal that the drug combinations induce transcriptomic changes consistent with differentiation towards neuronal phenotypes, including the upregulation of synaptic and dendritic signaling genes and the downregulation of malignant signatures. In comparison, astrocytic differentiation media (DM) and H3K27M knockout (KO) promote residual astrocytic phenotypes, suggesting neuronal transdifferentiation as a more effective strategy for mitigating tumor aggressiveness and progression. Differentially expressed genes such as GRIK1, GRIN1, NRXN3, NRXN1, CALB2, SCGN, SLC32A1, SLC1A2, KCNC3, and neurodevelopmental regulators including WNT7A, DLX6, ERBB4, ARX, BCL11B, SEMA3C, and FGFBP3 were identified as key markers regulating the neuron-like lineage transition. This study demonstrates that pHGGs can be phenotypically redirected toward neuronal-like identities through modulating cell fate differentiation programs. These findings advance the concept of 'differentiation therapy' as a promising intervention to reduce phenotypic plasticity and malignancy in pHGG ecosystems. While these are early in vitro findings, the potential ability to steer and control glioma cells toward stable, less malignant fates offers promising translational potential for patient-centered targeted therapies. - Source: PubMed
Publication date: 2025/12/30
Uthamacumaran AbicumaranHorth CynthiaBareke EricGravel MichelMajewski Jacek