|CSC-DC007968||Panoply™ Human KCNJ2 Knockdown Stable Cell Line||Inquriy|
|CSC-RI0024||Human KCNJ2 Stable Cell Line-HEK293||Inquriy|
|CSC-RI0066||Human CACNA1C/NEUROD1/CACNA2D1/KCNJ2 Stable Cell Line-HEK293||Inquriy|
|CSC-RI0070||Human CACNA1D/CACNB3/CACNA2D1 + KCNJ2(tetracycline-inducible) Stable Cell Line-HEK293||Inquriy|
|CSC-RI0072||Human CACNA1A/AP4B1/CACNA2D1/KCNJ2 Stable Cell Line-HEK293||Inquriy|
|CSC-RI0074||Human CACNA1B/BHLHE22/CACNA2D1/KCNJ2 Stable Cell Line-HEK293||Inquriy|
|CSC-RI0080||Human CACNA1H/CACNB2/CACNA2D1/KCNJ2 Stable Cell Line-HEK293||Inquriy|
|CSC-RI0115||Human KCNJ2 Stable Cell Line-HEK293||Inquriy|
|CSC-RI0116||Human KCNJ2 Stable Cell Line-CHO||Inquriy|
|CSC-SC007968||Panoply™ Human KCNJ2 Over-expressing Stable Cell Line||Inquriy|
|CDCB167340||Chicken KCNJ2 ORF Clone (NM_205370)||Inquriy|
|CDCB180461||Rabbit KCNJ2 ORF clone (NM_001082198.1)||Inquriy|
|CDCR245297||Mouse Kcnj2 ORF Clone(NM_008425.4)||Inquriy|
|CDCR337937||Human KCNJ2 ORF Clone(NM_000891.2)||Inquriy|
|CDCR378397||Rat Kcnj2 ORF Clone(NM_017296.1)||Inquriy|
|CDFH009651||Human KCNJ2 cDNA Clone(NM_000891.2)||Inquriy|
|CDFR011343||Rat Kcnj2 cDNA Clone(NM_017296.1)||Inquriy|
|MiUTR1H-05137||KCNJ2 miRNA 3'UTR clone||Inquriy|
|MiUTR1R-02822||KCNJ2 miRNA 3'UTR clone||Inquriy|
|SHH323275||shRNA set against Human KCNJ2 (NM_000891.2)||Inquriy|
|SHH323279||shRNA set against Mouse KCNJ2 (NM_008425.4)||Inquriy|
|SHH323283||shRNA set against Rat KCNJ2 (NM_017296.1)||Inquriy|
|SHL189804||shRNA set against Human KCNJ2(NM_000891.2)||Inquriy|
|SHL189876||shRNA set against Rat Kcnj2(NM_017296.1)||Inquriy|
|SHW005865||shRNA set against Chicken KCNJ2 (NM_205370)||Inquriy|
KCNJ2, encodes Kir2.1, is a member of the classical inwardly rectifying potassium channel family (Kir2 subfamily). It is a 427 amino acid, double-channel transmembrane protein, located at both ends in the cytoplasm. It conducts a strong inward rectifier K+ current in a wide range of tissues and cell types, including neurons, skeletal muscle, cardiac myocytes, immune system, hippocampus, caudate, putamen and carcinoma cells. The KCNJ2 gene was first cloned by Kubo from a macrophage cell line. Similar to the other members of the Kir family, KCNJ2 is tetrameric, containing two transmembrane helix domains (M1 and M2), an ion-selective P-loop between M1 and M2, and cytoplasmic N-and C-terminal domains. Functionally, KCNJ2 plays a key role in maintaining the resting membrane potential and regulating cellular excitability in cardiac myocytes, skeletal muscle and neurons. Changes in the expression levels of K+ channels induced by aberrant KCNJ2 expression have substantial effects on cellular processes such as cell death, proliferation, apoptosis and adhesion, which are linked to a variety of cardiac and neurological disorders.
It is reported that KCNJ2 loss-of-function mutations result in four distinct arrhythmia syndromes, including Andersen-Tawil syndrome type 1 (ATS1, also denoted as long QT syndrome type 7 [LQT7]), short QT syndrome type 3(SQT), familial atrial fibrillation and CPVT3. ATS1 is a rare autosomal-dominant disorder. It is characterized by a phenotypic triad consisting of cardiac abnormalities (premature ventricular complexes, ventricular bigeminy, ventricular tachycardia and supraventricular, torsades de pointes, prominent electrocardiographic U waves and prolonged QT intervals) in addition to dysmorphic features and periodic paralysis.
In addition, gain-of-function KCNJ2 mutations cause atrial fibrillation (AF). Atrial fibrillation is the most common arrhythmia characterized by complex and irregular atrial electrical activity. One rare, genetic condition associated with increased risk of AF is the SQT, which is caused by mutations in genes involved in normal electrical function of the heart. SQT results in QT shortening and increased risk of sudden cardiac death.
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