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Mouse Anti-KCND3 Recombinant Antibody (S75-41) (CBMAB-K0527-LY)


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Summary

Host Animal
Mouse
Specificity
Mouse, Rat, Human, Frog
Clone
S75-41
Antibody Isotype
IgG1
Application
WB, IHC-P, IP, IHC-Fr, FC, ICC/IF

Basic Information

Specificity
Mouse, Rat, Human, Frog
Antibody Isotype
IgG1
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Concentration
1 mg/mL
Purity
> 95% Purity determined by SDS-PAGE.
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
Potassium Voltage-Gated Channel Subfamily D Member 3
Introduction
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. [provided by RefSeq, Jul 2008]
Entrez Gene ID
Human3752
Mouse56543
Rat65195
Frog100125015
UniProt ID
HumanQ9UK17
MouseQ9Z0V1
RatQ62897
FrogA4IIK9
Function
Pore-forming (alpha) subunit of voltage-gated rapidly inactivating A-type potassium channels. May contribute to I(To) current in heart and I(Sa) current in neurons. Channel properties are modulated by interactions with other alpha subunits and with regulatory subunits.
Biological Process
Membrane repolarizationManual Assertion Based On ExperimentIDA:BHF-UCL
Membrane repolarization during cardiac muscle cell action potentialManual Assertion Based On ExperimentTAS:BHF-UCL
Membrane repolarization during ventricular cardiac muscle cell action potentialIEA:GOC
Potassium ion export across plasma membraneManual Assertion Based On ExperimentIDA:BHF-UCL
Potassium ion transmembrane transportManual Assertion Based On ExperimentIBA:GO_Central
Potassium ion transportManual Assertion Based On ExperimentTAS:ProtInc
Protein homooligomerizationIEA:InterPro
Regulation of heart rate by cardiac conductionManual Assertion Based On ExperimentIMP:BHF-UCL
Regulation of ion transmembrane transportIEA:UniProtKB-KW
Ventricular cardiac muscle cell membrane repolarizationManual Assertion Based On ExperimentIMP:BHF-UCL
Cellular Location
Cell membrane; Cell membrane, sarcolemma; Cell projection, dendrite. Interaction with palmitoylated KCNIP2 and KCNIP3 enhances cell surface expression.
Involvement in disease
Spinocerebellar ataxia 19 (SCA19):
A form of spinocerebellar ataxia, a clinically and genetically heterogeneous group of cerebellar disorders. Patients show progressive incoordination of gait and often poor coordination of hands, speech and eye movements, due to degeneration of the cerebellum with variable involvement of the brainstem and spinal cord. SCA19 is a relatively mild, cerebellar ataxic syndrome with cognitive impairment, pyramidal tract involvement, tremor and peripheral neuropathy, and mild atrophy of the cerebellar hemispheres and vermis.
Brugada syndrome 9 (BRGDA9):
A tachyarrhythmia characterized by right bundle branch block and ST segment elevation on an electrocardiogram (ECG). It can cause the ventricles to beat so fast that the blood is prevented from circulating efficiently in the body. When this situation occurs, the individual will faint and may die in a few minutes if the heart is not reset.
Topology
Cytoplasmic: 1-181
Helical: 182-202
Helical: 222-242
Cytoplasmic: 243-256
Helical: 257-277
Helical: 287-307
Cytoplasmic: 308-320
Helical: 321-341
Pore-forming: 360-380
Helical: 382-402
Cytoplasmic: 403-655
PTM
Regulated through phosphorylation at Ser-569 by CaMK2D.
More Infomation

Ye, D., Zhou, W., Hamrick, S. K., Tester, D. J., Kim, C. J., Barajas-Martinez, H., ... & Ackerman, M. J. (2022). Acacetin, a potent transient outward current blocker, may be a novel therapeutic for KCND3-encoded Kv4. 3 gain-of-function-associated J-Wave syndromes. Circulation: Genomic and Precision Medicine, 15(5), e003238.

Zanni, G., Hsiao, C. T., Fu, S. J., Tang, C. Y., Capuano, A., Bosco, L., ... & Jeng, C. J. (2021). Novel KCND3 variant underlying nonprogressive congenital ataxia or SCA19/22 disrupt KV4. 3 protein expression and K+ currents with variable effects on channel properties. International Journal of Molecular Sciences, 22(9), 4986.

Paucar, M., Ågren, R., Li, T., Lissmats, S., Bergendal, Å., Weinberg, J., ... & Svenningsson, P. (2021). V374A KCND3 pathogenic variant associated with paroxysmal ataxia exacerbations. Neurology Genetics, 7(1).

Pollini, L., Galosi, S., Tolve, M., Caputi, C., Carducci, C., Angeloni, A., & Leuzzi, V. (2020). KCND3-related neurological disorders: from old to emerging clinical phenotypes. International journal of molecular sciences, 21(16), 5802.

Li, X., Li, Z., Wang, D. W. W., Wang, D. W., & Wang, Y. (2020). A novel gain-of-function KCND3 variant associated with Brugada syndrome. Cardiology, 145(10), 623-632.

Nakajima, T., Kawabata-Iwakawa, R., Kaneko, Y., Hamano, S. I., Sano, R., Tamura, S., ... & Kurabayashi, M. (2020). Novel cardiocerebral channelopathy associated with a KCND3 V392I mutation. International Heart Journal, 61(5), 1049-1055.

Hsiao, C. T., Fu, S. J., Liu, Y. T., Lu, Y. H., Zhong, C. Y., Tang, C. Y., ... & Jeng, C. J. (2019). Novel SCA19/22‐associated KCND3 mutations disrupt human KV4. 3 protein biosynthesis and channel gating. Human Mutation, 40(11), 2088-2107.

Takayama, K., Ohno, S., Ding, W. G., Ashihara, T., Fukumoto, D., Wada, Y., ... & Horie, M. (2019). A de novo gain-of-function KCND3 mutation in early repolarization syndrome. Heart Rhythm, 16(11), 1698-1706.

Teumer, A., Trenkwalder, T., Kessler, T., Jamshidi, Y., van den Berg, M. E., Kaess, B., ... & Lifelines Cohort Study. (2019). KCND3 potassium channel gene variant confers susceptibility to electrocardiographic early repolarization pattern. JCI insight, 4(23).

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For research use only. Not intended for any clinical use.

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