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AB65794

Anti-Kv4.3/KCND3 antibody

0

(1 Review)

|

(4 Publications)

Rabbit Polyclonal Kv4.3/KCND3 antibody. Suitable for WB, IHC-P, IHC-Fr and reacts with Human samples. Cited in 4 publications.

View Alternative Names

A-type voltage-gated potassium channel KCND3, Potassium voltage-gated channel subfamily D member 3, Voltage-gated potassium channel subunit Kv4.3, KCND3

Key facts

Host species

Rabbit

Clonality

Polyclonal

Isotype

IgG

Carrier free

No

Reacts with

Human

Applications

IHC-P, IHC-Fr, WB

applications

Immunogen

The exact immunogen used to generate this antibody is proprietary information.

Reactivity data

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Properties and storage information

Form
Liquid
Purity
Whole antiserum
Storage buffer
Constituents: Whole serum
Shipped at conditions
Blue Ice
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
-20°C
Aliquoting information
Upon delivery aliquot
Storage information
Avoid freeze / thaw cycle

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Kv4.3 also known as KCND3 is a voltage-gated potassium channel subunit with an important role in membrane repolarization. This protein with a mass of approximately 71 kDa is extensively expressed in the heart and brain. Kv4.3 contributes to the formation of transient outward potassium currents (Ito) that are essential for shaping the action potentials in neurons and cardiac myocytes. These currents help in the rapid repolarization phase that restores the resting membrane potential after depolarization.
Biological function summary

Kv4.3 influences electrical signaling and cellular excitability in the cardiovascular and nervous systems. It often forms complexes with auxiliary subunits such as KChIP1-4 (Kv channel-interacting proteins) which modulate its current properties and localization. In neurons Kv4.3 helps regulate firing patterns while in cardiac tissue it affects heart rate and contractility. The presence of these complexes ensures precise control of channel function fitting the specific needs of tissue type and physiological condition.

Pathways

Kv4.3 integrates into critical signaling networks that involve ion homeostasis and action potential propagation. It belongs to the pathway that manages membrane potential dynamics interacting with proteins like Kv4.2 and Kv2.1 as part of a broader set of voltage-gated potassium channels. This network plays a role in the Wnt signaling pathway impacting cellular processes such as cell cycle regulation and differentiation.

Kv4.3 has been linked with cardiac arrhythmias and neurological disorders. Altered Kv4.3 functionality can lead to improper cardiac electrical activity resulting in arrhythmic events such as Long QT Syndrome. In the brain aberrations in Kv4.3 channel activity can correlate with epilepsy where disrupted ion channel regulation triggers excessive neuronal firing. Its involvement in these conditions highlights its participation in concert with other related proteins like SCN5A in cardiac tissues and CACNA1H in neuronal contexts.

Product protocols

For this product, it's our understanding that no specific protocols are required. You can visit:

Target data

Pore-forming (alpha) subunit of voltage-gated A-type potassium channels that mediates transmembrane potassium transport in excitable membranes, in brain and heart (PubMed : 10200233, PubMed : 17187064, PubMed : 21349352, PubMed : 22457051, PubMed : 23280837, PubMed : 23280838, PubMed : 34997220, PubMed : 9843794). In cardiomyocytes, may generate the transient outward potassium current I(To) (By similarity). In neurons, may conduct the transient subthreshold somatodendritic A-type potassium current (ISA) (By similarity). Kinetics properties are characterized by fast activation at subthreshold membrane potentials, rapid inactivation, and quick recovery from inactivation (PubMed : 10200233, PubMed : 17187064, PubMed : 21349352, PubMed : 22457051, PubMed : 23280837, PubMed : 23280838, PubMed : 34997220, PubMed : 9843794). Channel properties are modulated by interactions with regulatory subunits (PubMed : 17187064, PubMed : 34997220). Interaction with the regulatory subunits KCNIP1 or KCNIP2 modulates the channel gating kinetics namely channel activation and inactivation kinetics and rate of recovery from inactivation (PubMed : 17187064, PubMed : 34997220). Likewise, interaction with DPP6 modulates the channel gating kinetics namely channel activation and inactivation kinetics (PubMed : 34997220).
See full target information KCND3

Publications (4)

Recent publications for all applications. Explore the full list and refine your search

The Journal of neuroscience : the official journal of the Society for Neuroscience 44: PubMed38664011

2024

Calcium-Dependent Regulation of Neuronal Excitability Is Rescued in Fragile X Syndrome by a Tat-Conjugated N-Terminal Fragment of FMRP.

Applications

Unspecified application

Species

Unspecified reactive species

Xiaoqin Zhan,Hadhimulya Asmara,Paul Pfaffinger,Ray W Turner

Frontiers in cardiovascular medicine 9:957903 PubMed36304536

2022

Cardiac-specific knockdown of Bhlhe40 attenuates angiotensin II (Ang II)-Induced atrial fibrillation in mice.

Applications

Unspecified application

Species

Unspecified reactive species

Kai-Wen Ren,Xiao-Hong Yu,Yu-Hui Gu,Xin Xie,Yu Wang,Shi-Hao Wang,Hui-Hua Li,Hai-Lian Bi

Nature communications 11:2755 PubMed32488011

2020

FMRP(1-297)-tat restores ion channel and synaptic function in a model of Fragile X syndrome.

Applications

Unspecified application

Species

Unspecified reactive species

Xiaoqin Zhan,Hadhimulya Asmara,Ning Cheng,Giriraj Sahu,Eduardo Sanchez,Fang-Xiong Zhang,Gerald W Zamponi,Jong M Rho,Ray W Turner

Circulation research 106:166-75 PubMed19893015

2009

MicroRNA-133a protects against myocardial fibrosis and modulates electrical repolarization without affecting hypertrophy in pressure-overloaded adult hearts.

Applications

WB

Species

Human

Scot J Matkovich,Wei Wang,Yizheng Tu,William H Eschenbacher,Lisa E Dorn,Gianluigi Condorelli,Abhinav Diwan,Jeanne M Nerbonne,Gerald W Dorn
View all publications

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