KCNJ2
KCNJ2, also known as Kir2.1, IRK1 and LQT7, is an inward-rectifier potassium channel that allows potassium to flow into the cell more readily than out of it. It probably helps establish action potential waveform and excitability in neuronal and muscle tissues. Browse Assay Genie's current range of KCNJ2 research reagents below, or read on for the biology behind the target.
KCNJ2 encodes an integral membrane protein that forms an inward-rectifier type potassium channel. Inward rectifier channels have a greater tendency to allow potassium to flow into the cell than out of it. Their voltage dependence is regulated by extracellular potassium concentration: as external potassium rises, the voltage range over which the channel opens shifts to more positive voltages. The inward rectification is mainly due to internal magnesium blocking outward current, and the channel can also be blocked by extracellular barium or cesium. The KCNJ2 protein probably participates in establishing action potential waveform and excitability of neuronal and muscle tissues.
Potassium channels are present in most mammalian cells, where they take part in a wide range of physiological responses. The KCNJ2 protein belongs to the inward rectifier-type potassium channel family (TC 1.A.2.1) and to the KCNJ2 subfamily. It localises to the cell membrane, including the sarcolemma and T-tubules of muscle. The human gene sits within the HGNC group of potassium inwardly rectifying channel subfamily J genes, and mouse and rat each have a Kcnj2 ortholog, which supports comparative work in rodent models.
The gene is known by the aliases Kir2.1, IRK1 and LQT7, and was previously named potassium inwardly-rectifying channel, subfamily J, member 2. Mutations in the KCNJ2 gene have been associated with Andersen syndrome, which is characterised by periodic paralysis, cardiac arrhythmias and dysmorphic features. This makes KCNJ2 a relevant target for researchers studying ion channel physiology, excitable-cell biology and channelopathies.
KCNJ2 is an inward-rectifier potassium channel whose gating depends on extracellular potassium and is blocked by internal magnesium, making it a model for rectification.
Mutations in KCNJ2 are associated with Andersen syndrome, which features cardiac arrhythmias, and the LQT7 alias reflects this link.
The channel probably shapes action potential waveform and excitability in neuronal and muscle tissues, and Andersen syndrome includes periodic paralysis.
KCNJ2 is found at the cell membrane, including the sarcolemma and T-tubules, which is relevant to studies of channel trafficking in muscle.
KCNJ2 forms an inward-rectifier potassium channel that lets potassium enter the cell more readily than leave it. Internal magnesium blocks outward current. It probably helps set action potential waveform and excitability in neuronal and muscle tissues. Check the datasheet of any product for its validated reactivity.
KCNJ2 is also called Kir2.1, IRK1 and LQT7. UniProt lists the protein as inward rectifier potassium channel 2, and the gene was previously named potassium inwardly-rectifying channel, subfamily J, member 2.
Yes. Mutations in the KCNJ2 gene have been associated with Andersen syndrome, characterised by periodic paralysis, cardiac arrhythmias and dysmorphic features. Mouse and rat both carry a Kcnj2 ortholog, so rodent systems are commonly used to study the gene.
Other members of the potassium inwardly rectifying channel subfamily J group with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt P63252; product specifications from Assay Genie datasheets.