KCND3 is a voltage-gated potassium (Kv) channel that is involved in the repolarization of the action potential. Genetic alterations in KCND3 have been associated with Brugada syndrome and sudden unexplained death. Rabbit Anti-KCND3 antibody recognizes human, mouse, rat, rabbit, and pig KCND3.
Immunogen
Synthetic peptide directed towards the middle region of human KCND3
Application
Rabbit Anti-KCND3 antibody is suitable for western blot applications at a concentration of 1.25 μg/ml.
Biochem/physiol Actions
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). KCND3 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.
Sequence
Synthetic peptide located within the following region: KARLARIRVAKTGSSNAYLHSKRNGLLNEALELTGTPEEEHMGKTTSLIE
Physical form
Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Heritable arrhythmia syndromes, including Brugada syndrome (BrS) and idiopathic ventricular fibrillation (IVF), may serve as the pathogenic basis for autopsy-negative sudden unexplained death (SUD) and sudden infant death syndrome (SIDS). Emerging evidence has linked perturbations in the transient outward current
Brugada syndrome (BrS) is a sudden death-predisposing genetic condition characterized electrocardiographically by ST segment elevation in the leads V(1)-V(3). Given the prominent role of the transient outward current (I(to)) in BrS pathogenesis, we hypothesized that rare gain-of-function mutations in KCND3
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