Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it (PubMed:36149965, PubMed:7590287, PubMed:9490857). Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages (PubMed:7590287, PubMed:7696590). The inward rectification is mainly due to the blockage of outward current by internal magnesium (PubMed:9490857). Can be blocked by extracellular barium or cesium (PubMed:7590287, PubMed:7696590). Probably participates in establishing action potential waveform and excitability of neuronal and muscle tissues (PubMed:7590287, PubMed:7696590, PubMed:7840300).
Long QT syndrome 7
LQT7
A heart disorder characterized by a prolonged QT interval on the ECG and polymorphic ventricular arrhythmias. They cause syncope and sudden death in response to exercise or emotional stress, and can present with a sentinel event of sudden cardiac death in infancy. Long QT syndrome type 7 manifests itself as a clinical triad consisting of potassium-sensitive periodic paralysis, ventricular ectopy and dysmorphic features.
None
The disease is caused by variants affecting the gene represented in this entry.
Short QT syndrome 3
SQT3
A form of short QT syndrome, a heart disorder characterized by idiopathic persistently and uniformly short QT interval on ECG in the absence of structural heart disease in affected individuals. It can cause syncope and sudden death. SQT3 has a unique ECG phenotype characterized by asymmetrical T waves.
None
The disease is caused by variants affecting the gene represented in this entry.
Atrial fibrillation, familial, 9
ATFB9
A familial form of atrial fibrillation, a common sustained cardiac rhythm disturbance. Atrial fibrillation is characterized by disorganized atrial electrical activity and ineffective atrial contraction promoting blood stasis in the atria and reduces ventricular filling. It can result in palpitations, syncope, thromboembolic stroke, and congestive heart failure.
None
The disease is caused by variants affecting the gene represented in this entry.
S-nitrosylation increases the open probability and inward rectifying currents.
Belongs to the inward rectifier-type potassium channel (TC 1.A.2.1) family. KCNJ2 subfamily.
Heart, brain, placenta, lung, skeletal muscle, and kidney. Diffusely distributed throughout the brain.
IRK1, KCNJ2, Inward rectifier potassium channel 2, Cardiac inward rectifier potassium channel, Inward rectifier K(+) channel Kir2.1, IRK-1, hIRK1
Proteins
Cardiovascular
48288Da
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