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Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Additionally we are shipping KCND2 Antibodies (101) and many more products for this protein.
Showing 3 out of 7 products:
The results reveal an important role for miR (show MLXIP Proteins)-324-5p-mediated silencing of Kv4.2 in seizure onset.
Ca(2 (show CA2 Proteins)+)/calcineurin (CaN)/nuclear factor of activated T-cells (NFAT (show NFATC1 Proteins)) c4 axis is required for neuritin (show NRN1 Proteins)-induced Kv4.2 transcriptional expression and potentiation of IA densities in cerebellum granule neurons.
Data show that suprachiasmatic nucleus (SCN (show SRI Proteins)) explants from potassium channel (show KCNAB2 Proteins) Kv1.4 (show KCNA4 Proteins)(-/-)period2 protein Per2 (show PER2 Proteins)(Luc) and potassium channel Kv4.2(-/-) period2 protein Per2 (show PER2 Proteins)(Luc) mice have significantly shorter circadian periods in PER2 (show PER2 Proteins) rhythms.
Data show that potassium channel (show KCNAB2 Proteins) Kv4.3 (show KCND3 Proteins) outward current is presented incardiomyocyte lacking the potassium channel Kv4.2 gene (Kv4.2-/-).
This study demonstrated that Dendritic hyperexcitability induced by Kv4.2 deficiency exacerbated behavioral deficits and increased epileptiform activity amyloid protein (show IAPP Proteins) precursor mutation mice.
Real-time RT-PCR and Western blotting revealed that Kv4.2 expression was downregulated in both BSO-treated groups, whereas KChIP2 (show KCNIP2 Proteins) expression was downregulated only in the H/M-Sod2 (show SOD2 Proteins)(+/-)+BSO group (P<0.05).
WT PrP(C (show PRNP Proteins)), in a DPP6 (show DPP6 Proteins)-dependent manner, modulated Kv4.2 channel properties, causing an increase in peak amplitude
MiR (show MLXIP Proteins)-301a may be a central regulator for the expression of Kv4.2 in diabetes.
The experiments here demonstrate that Kv4.2, Kv4.3 (show KCND3 Proteins) and Kv1.4 (show KCNA4 Proteins) all contribute to the generation of potassium channels in mature cortical pyramidal (CP) neurons; these channels play distinct roles in regulating the intrinsic properties of mature CP neurons.
Kv4.2 regulation of excitability determines synaptic maturation site in CA1 (show CA1 Proteins) hippocampal pyramidal neurons.
A mutation, V404M, in the Kv4.2 channel subunit is associated with infant-onset epilepsy and autism. V404M enhances inactivation of channels that have not opened but dramatically impairs inactivation after opening. Authors show that increased side-chain volume is largely responsible for these seemingly paradoxical effects.
Our results do not support the notion that accessory KChIP2 (show KCNIP2 Proteins) binding is a prerequisite for dendritic trafficking and functional surface expression of Kv4.2 channels, however, accessory KChIP2 (show KCNIP2 Proteins) binding may play a potential role in Kv4.2 modulation during intrinsic plasticity processes.
closed-state inactivation in Kv4.2 channels is a multistep process
The stoichiometry of the Kv4.2-DPP10 complex was variable depending on the relative expression level of each subunit, with a preference for 4:2 stoichiometry
The findings of this study suggest that variations in KCND2 genes are associated with both mild and severe persistent breast pain after breast cancer surgery.
A rare genetic mutation of the KCND2 gene, p.D612N, was identified in a single patient. Co-expression of mutant and wild-type KCND2 with KChIP2 (show KCNIP2 Proteins) demonstrated a gain-of-function phenotype.
S-glutathionylation of an auxiliary subunit confers redox sensitivity to Kv4 (show KCNC1 Proteins) channel inactivation.
study identified a de novo variant p.Val404Met in KCND2 in a family with identical twins affected with autism and severe seizures; findings suggest KCND2 is the causal gene for epilepsy in this family and has a role in the etiology of autism
Subunit counting by single-molecule imaging revealed that the bound number of KChIP4 (show KCNIP4 Proteins) in each Kv4.2.KChIP4 (show KCNIP4 Proteins) complex was dependent on the expression level of KChIP4 (show KCNIP4 Proteins).
Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. Four sequence-related potassium channel genes - shaker, shaw, shab, and shal - have been identified in Drosophila, and each has been shown to have human homolog(s). This gene encodes a member of the potassium channel, voltage-gated, shal-related subfamily, members of which form voltage-activated A-type potassium ion channels and are prominent in the repolarization phase of the action potential. This member mediates a rapidly inactivating, A-type outward potassium current which is not under the control of the N terminus as it is in Shaker channels.
potassium voltage-gated channel, Shal-related subfamily, member 2
, potassium voltage-gated channel Sha1-related subfamily member 2
, potassium voltage-gated channel subfamily D member 2
, potassium channel Kv4.2
, voltage-gated potassium channel subunit Kv4.2
, voltage-gated potassium channel Kv4.2
, voltage-sensitive potassium channel
, Potassium voltage-gated channel subfamily D member 2
, Voltage-gated potassium channel subunit Kv4.2
, potassium channel alpha subunit Kv4.2
, potassium voltage gated channel, Shal-related family, member 2