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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. Zusätzlich bieten wir Ihnen KCND2 Proteine (7) und viele weitere Produktgruppen zu diesem Protein an.
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Mammalian Monoclonal KCND2 Primary Antibody für ISt, IHC - ABIN1304770
Mulholland, Spencer, Hu, Kroener, Chandler: Neuroplasticity of A-type potassium channel complexes induced by chronic alcohol exposure enhances dendritic calcium transients in hippocampus. in Psychopharmacology 2015
Show all 64 Pubmed References
Human Polyclonal KCND2 Primary Antibody für IHC, IHC (p) - ABIN4329445
Chang, Atzmon, Bergman, Brugmann, Atwood, Chang, Barzilai: Identification of genes promoting skin youthfulness by genome-wide association study. in The Journal of investigative dermatology 2014
The results reveal an important role for miR (zeige MLXIP Antikörper)-324-5p-mediated silencing of Kv4.2 in seizure onset.
Ca(2 (zeige CA2 Antikörper)+)/calcineurin (CaN)/nuclear factor of activated T-cells (NFAT (zeige NFATC1 Antikörper)) c4 axis is required for neuritin (zeige NRN1 Antikörper)-induced Kv4.2 transcriptional expression and potentiation of IA densities in cerebellum granule neurons.
Data show that suprachiasmatic nucleus (SCN (zeige SRI Antikörper)) explants from potassium channel (zeige KCNAB2 Antikörper) Kv1.4 (zeige KCNA4 Antikörper)(-/-)period2 protein Per2 (zeige PER2 Antikörper)(Luc) and potassium channel Kv4.2(-/-) period2 protein Per2 (zeige PER2 Antikörper)(Luc) mice have significantly shorter circadian periods in PER2 (zeige PER2 Antikörper) rhythms.
Data show that potassium channel (zeige KCNAB2 Antikörper) Kv4.3 (zeige KCND3 Antikörper) 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 (zeige IAPP Antikörper) precursor mutation mice.
Real-time RT-PCR and Western blotting revealed that Kv4.2 expression was downregulated in both BSO-treated groups, whereas KChIP2 (zeige KCNIP2 Antikörper) expression was downregulated only in the H/M-Sod2 (zeige SOD2 Antikörper)(+/-)+BSO group (P<0.05).
WT PrP(C (zeige PRNP Antikörper)), in a DPP6 (zeige DPP6 Antikörper)-dependent manner, modulated Kv4.2 channel properties, causing an increase in peak amplitude
MiR (zeige MLXIP Antikörper)-301a may be a central regulator for the expression of Kv4.2 in diabetes.
The experiments here demonstrate that Kv4.2, Kv4.3 (zeige KCND3 Antikörper) and Kv1.4 (zeige KCNA4 Antikörper) 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 (zeige CA1 Antikörper) hippocampal pyramidal neurons.
Our results do not support the notion that accessory KChIP2 (zeige KCNIP2 Antikörper) binding is a prerequisite for dendritic trafficking and functional surface expression of Kv4.2 channels, however, accessory KChIP2 (zeige KCNIP2 Antikörper) 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 (zeige KCNIP2 Antikörper) demonstrated a gain-of-function phenotype.
S-glutathionylation of an auxiliary subunit confers redox sensitivity to Kv4 (zeige KCNC1 Antikörper) 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 (zeige KCNIP4 Antikörper) in each Kv4.2.KChIP4 (zeige KCNIP4 Antikörper) complex was dependent on the expression level of KChIP4 (zeige KCNIP4 Antikörper).
reflected in the immunoblotting data KV4.2 receptors were detected at higher levels of expression in patient with cortical dysplasia with intractable epilepsy.
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