KCNG4 antibody - N-terminal region (ARP35473_P050)
- Known as:
- KCNG4 (anti-) - N-terminal region (ARP35473_P050)
- Catalog number:
- arp35473_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KCNG4 antibody - N-terminal region (ARP35473_P050)
Related genes to: KCNG4 antibody - N-terminal region (ARP35473_P050)
- Gene:
- KCNG4 NIH gene
- Name:
- potassium voltage-gated channel modifier subfamily G member 4
- Previous symbol:
- -
- Synonyms:
- Kv6.4
- Chromosome:
- 16q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-20
- Date modifiied:
- 2016-02-04
Related products to: KCNG4 antibody - N-terminal region (ARP35473_P050)
Related articles to: KCNG4 antibody - N-terminal region (ARP35473_P050)
- Fast-spiking parvalbumin-positive (PV) neurons provide precisely timed, context-dependent inhibition within cortical circuits. PV neuron firing properties are specialized among cortical neurons, suggesting that they express a unique complement of ion channels. Here, we show that the PV-specific silent voltage-gated potassium (Kv) channel subunit Kv6.4 (encoded by ) modulates both intrinsic and synaptic properties of cortical PV neurons. Kv6.4 does not form functional channels on its own but, as shown in prior work, assembles with Kv2 subunits to create heterotetrameric channel complexes, effectively reducing Kv2-mediated delayed rectifier current. We find that expression is enriched within a distinct -expressing subclass in primary somatosensory (S1) and motor (M1) cortex and emerges during postnatal development. In PV neurons, Kv6.4 loss reduces action potential (AP) height and width, hyperpolarizes the threshold and interspike potential, and accelerates AP upstroke particularly during repetitive firing. Kv6.4 loss, potentially due to the changes in AP waveform, also alters GABA release and paired-pulse depression at synapses made by PV onto pyramidal (PYR) neurons. The effects of Kv6.4 loss are amplified during high-frequency firing, within the physiological range of fast-spiking PV neurons, likely due to altered repolarization dynamics that accumulate across successive APs. These findings are thus consistent with the function of Kv6.4 in modifying Kv2-mediated delayed rectifier currents. Hence, Kv6.4 tunes the temporal precision of PV inhibitory output, a feature that may be critical for stable excitation-inhibition ratios and adaptive circuit function underlying learning and behavior. - Source: PubMed
Publication date: 2026/02/03
Ganesh SanikaCanty Theresa MSabatini Bernardo L - Fast-spiking parvalbumin-positive (PV) neurons provide precisely timed, context-dependent inhibition within cortical circuits. PV neuron firing properties are specialized among cortical neurons, suggesting that they express a unique complement of ion channels. Here, we identify the PV-specific silent voltage-gated potassium (Kv) channel subunit Kv6.4 (encoded by ), whose role in cortical PV neuron physiology was previously unknown, as a modulator of both intrinsic and synaptic properties. Kv6.4 does not form functional channels on its own but, as shown in prior work, assembles with Kv2 subunits to create heterotetrameric channel complexes, effectively reducing Kv2-mediated delayed rectifier current. We find that expression is enriched within a distinct -expressing subclass in primary somatosensory (S1) and motor (M1) cortex and emerges during postnatal development. In PV neurons, Kv6.4 loss reduces action potential (AP) height and width, hyperpolarizes the threshold and interspike potential, and accelerates AP upstroke particularly during repetitive firing. Kv6.4 loss, potentially due to the changes in AP waveform, also alters GABA release and paired-pulse depression at synapses made by PV onto pyramidal (PYR) neurons. The effects of Kv6.4 loss are amplified during high-frequency firing, within the physiological range of fast-spiking PV neurons, likely due to altered repolarization dynamics that accumulate across successive APs. These findings are thus consistent with the function of Kv6.4 in modifying Kv2-mediated delayed rectifier currents. Hence, Kv6.4 tunes the temporal precision of PV inhibitory output, a feature that may be critical for stable excitation-inhibition ratios and adaptive circuit function underlying learning and behavior. - Source: PubMed
Publication date: 2025/12/22
Ganesh SanikaCanty Theresa MSabatini Bernardo L - 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 - Toxoplasma gondii can cause severe damage to immunodeficient hosts, and also compromise brain structure and function in immunocompetent hosts during latent infection. In China, the two different isolates, Chinese I (ToxoDB#9) and Chinese III are dominant epidemic strains widely spreading in humans and domestic animals and can lead to latent infection in host brain tissues, but the comparison of their manipulation patterns and mechanisms remains unclear. - Source: PubMed
Publication date: 2025/05/26
Zhou Bei-BeiDong Hong-JieSun HangXie Xiao-ManXie Huan-HuanZhu Wen-JuLi Ya-NanXu ChaoCao Jian-PingZhao Gui-HuaYin Kun - Hibernation, an adaptive mechanism to extreme environmental conditions, is prevalent among mammals. Its main characteristics include reduced body temperature and metabolic rate. However, the mechanisms by which hibernating animals re-enter deep sleep during the euthermic phase to sustain hibernation remain poorly understood. We selected the as a model organism and conducted transcriptomic sequencing of its hypothalamus at multiple time points throughout hibernation. Through the strategies of gene set filtering and intersection analysis, we effectively filtered out redundant data, identifying a subset of genes whose expression was downregulated during the euthermic phase potentially inducing re-enter deep sleep, thereby maintaining the periodic cycles of torpor and arousal. These cycles are crucial for sustaining the overall hibernation process. Notably, genes associated with sodium and potassium ion channels were significantly enriched. Specifically, potassium ion-related genes such as Kcnc1, Kcna2, Kcng4, and Kcna6, along with sodium ion-related genes such as Scn1a and Hcn2, were markedly downregulated. qRT-PCR validation of four of these genes (Kcnc1, Kcna6, Scn1a, and Hcn2) confirmed significant downregulation during the euthermic phase compared to the deep sleep phase, further supporting our transcriptomic findings. This study provides novel insights into the hypothalamic transcriptome dynamics at various hibernation stages. Although the functional roles of these genes require further investigation, our findings lay the groundwork for future studies to elucidate the molecular mechanisms underlying hibernation. - Source: PubMed
Publication date: 2024/12/23
Zhang TianYang ChaoGuo YaxiuXu ZihanZhao MinboWu FengZhang HongyuWang HailongSui XiukunJiang SiyuHe RongqiaoDai ZhongquanLiu YingLi Yinghui