Introduction of KCND3
KCND3, also known as potassium channel, voltage-gated shal related subfamily D, member 3, potassium voltage-gated channel long, Sha1-related potassium channel Kv4.3, potassium ionic channel Kv4.3, spinocerebellar ataxia 22, spinocerebellar ataxia 19, voltage-gated K+ Channel, BRGDA9, KCND3L, KCND3S, KSHIVB, KV4.3, SCA19 or SCA22, is a 73.5 kDa membrane protein consisting of 655 amino acids. In humans, it is encoded by the KCND3 gene mapped to the chromosome 1p13.2. The KCND3 codes for KCND3, a pore-forming (alpha) subunit of Shal family of A-type voltage-gated potassium channel, which is critical in membrane repolarization in excitable cells. This gene comprises intracellular N- and C-termini and six transmembrane segments. RT-PCR and sequence analysis exhibited the existence of two splice variant, KCND3L and KCND3S.
|Basic Information of KCND3|
|Protein Name||Potassium voltage-gated channel subfamily D member 3|
|Aliases||Voltage-gated potassium channel subunit Kv4.3|
|Organism||Homo sapiens (Human)|
Function of KCND3 Membrane Protein
Voltage-gated potassium (Kv) channels are the most complex group of voltage-gated ion channels from structural and functional standpoints. KCND3 is a member of potassium channel, voltage-gated, shal-related subfamily. Members of this family form voltage-activated A-type potassium ion channels and are dominant in the repolarization phase of action potentials. This protein is likely to contribute to I(Sa) current in neurons and I(To) current in hearts. Channel properties are regulated by interactions with other alpha subunits as well as with regulatory subunits. There are several diseases related to the KCND3 including Brugada Syndrome and Spinocerebellar Ataxia. The study reported that mutations in the beta subunit KCNE3 result in the gain of function, which may cause Brugada Syndrome. KCND3 has been identified as the causative gene in 2012, whose associated pathways are transmission across chemical synapses and cardiac conduction. Additionally, an essential paralog of KCND3 is KCND2 gene.
Fig.1 Protein structure of KCND3.
Application of KCND3 Membrane Protein in Literature
Trio whole-exome sequencing resulted from the patient and his parents unclosed a novel de novo missense mutation in KCND3, the causative gene of SCA19/22, replacing for evolutionally conserved glycine (Gly). And this mutation was supposed to be functionally deleterious by an analysis of bioinformatics.
This study provided the first evidence of a concept that KV4.3 directly affected NaV1.5 current. Future research employing appropriate disease models explored the potential electrophysiological involvements in pathophysiological conditions, including BrS related to KCND3 gain-of-function mutations.
The report presented a case of one patient carrying with nonfatal cardiac arrest. Serial electrocardiograms (ECG) exhibited intermittent early repolarization pattern (ERP) and genetic testing revealed a KCND3 duplication in this patient and his 2-year-old daughter, in whom ECG also showed evident ERP.
In summary, the article identified a novel T361S mutation in KCND3 correlated with AF in Chinese Han families. The T361S mutant led to changes in channel kinetics and the up-regulation of Kv4.3 protein, which possibly was a critical driver for lone AF as found in the patient.
In this study, five hub genes were identified successfully, including LGALS4, PTPRN2, TMPRSS11E, TRIM31, and KCND3, and five biological pathways that may be potential biomarkers for the early diagnosis and treatment related to the bladder cancer revealed.
KCND3 Preparation Options
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