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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. 再加上，我们可以发Potassium Voltage-Gated Channel, Shal-Related Subfamily, Member 3 抗体 (55) 和 Potassium Voltage-Gated Channel, Shal-Related Subfamily, Member 3 蛋白 (6)和数多这个蛋白质的别的产品。
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In ERaKO but not ERaKO mice, the mRNA of Kv4.3 was selectively increased... E2 negatively regulates the density of Ito through ERa, this highlights a potential role for this female hormone in modulating cardiac electrical activity.
Data show that potassium channel (显示 KCNAB2 ELISA试剂盒) Kv4.3 outward current is presented incardiomyocyte lacking the potassium channel Kv4.2 (显示 KCND2 ELISA试剂盒) gene (Kv4.2 (显示 KCND2 ELISA试剂盒)-/-).
The gain-of-function SCNA overexpressing dopamine substantia nigra neurons was in part mediated by an increase of their intrinsic pacemaker frequency caused by a redox-dependent impairment of Kv4.3
The protein levels of KV4.3 and KV2.2 (显示 KCNB2 ELISA试剂盒) were up-regulated in the hypertrophic smooth muscle cell membrane.
The experiments here demonstrate that Kv4.2 (显示 KCND2 ELISA试剂盒), Kv4.3 and Kv1.4 (显示 KCNA4 ELISA试剂盒) 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.
Taken together, these data suggest that nerve injury causes an epigenetic silencing of K(v)4.3 gene mediated through transcriptional suppressor NRSF in the DRG.
Kv4.3 channel alpha-subunit (显示 POLG ELISA试剂盒) is found to be one of the components (along with Kv4.2 (显示 KCND2 ELISA试剂盒) and Kv1.4 (显示 KCNA4 ELISA试剂盒)) that propagates the voltage-gated potassium current in pyramidal cortical neurons.
Ativation of AT1 (显示 SLC33A1 ELISA试剂盒) receptors by Angioteinsin II or stretch specifically destabilizes cardiac myocyte Kv4.3 channel mRNA by activating NADPH oxidase (显示 NOX1 ELISA试剂盒).
The results show that Kv4.3 is concentrated in layer 1, the bottom of layer 2/3, and in layers 4 and 5/6.
The results presented here suggest that, in contrast with Kv4.2 (显示 KCND2 ELISA试剂盒), Kv4.3 is not required for the generation of functional mouse ventricular I(to,f) channels.
mutations cause a gainoffunction of KV4.3/KChIP2encoded channels by increasing membrane protein expression and slowing channel inactivation.
Altered Kv4.3 channel localization and/or functioning resulting from SCA19/22 mutations may lead to Purkinje cell loss, neurodegeneration and ataxia.
the interaction of DPP10a, expressed in human atrium, with Kv4.3 channels generates a sustained current component of Ito, which may affect late repolarization phase of atrial action potentials.
Kv4.3 K(+) channel (显示 KCNC4 ELISA试剂盒) is involved in heart hypertrophy/heart failure independently of its electric function.[review]
Demonstrate SEMA3A (显示 SEMA3A ELISA试剂盒) as a naturally occurring protein that selectively inhibits Kv4.3 and SEMA3A (显示 SEMA3A ELISA试剂盒) as a possible Brugada syndrome susceptibility gene through a Kv4.3 gain-of-function mechanism.
maps to chromosome 1p21-q21 and identification in Dutch autosomal dominant cerebellar ataxia family
These results indicate that Kv4.3 is likely the target of discrepin and highlight the importance of the basic residue K13 (显示 KCNG1 ELISA试剂盒), located in the alpha-helix of the toxin, for current blockage.
findings indicate mutations in KCND3 are not a common cause of disease among rarer types of European cerebellar ataxia; however 2 variants were identified in the SCA cases: p.L450F and p.P614S; mutations in KCND3 can cause 2 allelic disorders, SCA19/22 and Brugada syndrome which may co-occur
Report a KV4.3 gain-of-function mutation in early-onset persistent lone atrial fibrillation.
expression of the sodium (SCN5A (显示 SCN5A ELISA试剂盒)) and potassium (KCND3) channels as well as the fibrosis content in the ventricles of heart failure and of non-diseased hearts under different post-mortem intervals
biophysical 11-state Markov model of Kv4.3 gating incorporating a direct transition from the open-inactivated state to the closed-inactivated state
Our data demonstrate isoform-specific regulation of closed-state inactivation by protein kinase C (显示 PKC ELISA试剂盒) in Kv4.3
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 includes two isoforms with different sizes, which are encoded by alternatively spliced transcript variants of this gene.
potassium voltage-gated channel, Shal-related subfamily, member 3
, potassium voltage-gated channel subfamily D member 3-like
, potassium voltage-gated channel subfamily D member 3
, potassium voltage-gated channel, Shal-related family, member 3
, potassium channel Kv4.3
, potassium voltage-gated channel Shal-related subfamily member 3
, potassium channel Kv4.3L
, potassium channel Kv4.3M
, voltage-gated potassium channel subunit Kv4.3
, potassium ionic channel Kv4.3
, sha1-related potassium channel Kv4.3
, voltage-gated K+ channel
, potassium voltage gated channel, Shal-related family, member 3