potassium inwardly-rectifying channel, subfamily J, member 4 Synonyms: Kir2.3 HIR HRK1 IRK3 HIRK2. Symbol: Kcnj4
One class of potassium channels is activated by depolarization whereas a second class is not. The latter are referred to as inwardly rectifying K+ channels, and they have a greater tendency to allow potassium to flow into the cell rather than out of it. This asymmetry in potassium ion conductance plays a key role in the excitability of muscle cells and neurons. The protein encoded by KCNJ4 (also known as HIR; HRK1; IRK3; HIRK2; IRK-3; Kir2.3; MGC142066; MGC142068) encodes the potassium inwardly-rectifying channel, subfamily J, member 4, named Kir2.3, which is an integral membrane protein. The encoded protein has a small unitary conductance compared to other members of this protein family. Two transcript variants encoding the same protein have been found for this gene.
Kcnj4 : potassium inwardly-rectifying channel, subfamily J, member 4
The portion of a neuron that includes the nucleus, but excludes all cell projections such as axons and dendrites.
Double layer of lipid molecules that encloses all cells, and, in eukaryotes, many organelles; may be a single or double lipid bilayer; also includes associated proteins.
integral to membrane
Penetrating at least one phospholipid bilayer of a membrane. May also refer to the state of being buried in the bilayer with no exposure outside the bilayer. When used to describe a protein, indicates that all or part of the peptide sequence is embedded in the membrane.
A neuron projection that has a short, tapering, often branched, morphology, receives and integrates signals from other neurons or from sensory stimuli, and conducts a nerve impulse towards the axon or the cell body. In most neurons, the impulse is conveyed from dendrites to axon via the cell body, but in some types of unipolar neuron, the impulse does not travel via the cell body.
Free intracellular polyamines (PAs) are the key determinants of
rectification in IK1 and Kir2 channels (Lopatin ). Yan et al.  provided evidence that different concentrations of free PAs may underlie differences
between atrial and ventricular IK1 in the guinea pig heart.
Inclusion of only one Kir2.3
subunit to a Kir2.1 channel led to an approximate threefold slowing of
activation kinetics, with greater slowing on subsequent additions of
Kir2.3 subunits. Activation kinetics of IK1 in both ventricles and both
atria was found to correspond to fast-activating Kir2.1/Kir2.2 channels, suggesting no major contribution of Kir2.3 subunits. Panama 
Kir2.3 is modulated by ATP (Collins et al., 1996 ), protein
kinase C (PKC) (Henry et al., 1996 ), G protein beta-gamma subunits
(Cohen et al., 1996 ), Mg2+ (Chuang et al., 1997 ), pH (Coulter
et al., 1995 ; Zhu et al., 1999a ), arachidonic acid (AA) (Liu et
al., 2001 ) and the membrane phospholipid phosphatidyl inositol 4,5-bisphosphate (PIP2) (Du et al., 2004 ). Listed by Wang .
Subcellular Localization of Kir2.3
Immunoelectron microscopy of the OB revealed that Kir2.3 immunoreactivity was specifically clustered on the postsynaptic membrane of asymmetric synapses between granule cells and mitral/tufted cells 
Expression of Kir2.3 in Mouse Brain
Although Kir2.3 is known to be expressed abundantly in the forebrain, its precise localization has not been identified. Using an antibody specific to Kir2.3, we examined the subcellular localization of Kir2.3 in mouse brain. Kir2.3 immunoreactivity was detected in a granular pattern in restricted areas of the brain, including the olfactory bulb (OB) 
Expression of Kir2.3 in Rat Brain
we have provided both immunohisto- chemical and electrophysiological evidence that the Kir2.3 strong inward rectifier channel is expressed in astrocytes of both polygonal and stellate morphology, from both adult and neonatal rat brain, both in vivo and in vitro. Given the importance of this channel in maintaining the resting potential of polygonal reactive astrocytes 
Expression of Kir2.3 in Mammalian CNS
Kir2.3 has previously been identified in mammalian CNS forebrain (Lesage et al., 1994; Morishige et al., 1994; Bredt et al., 1995; Karschin et al., 1996; Stone- house et al., 1999), in nodes of Ranvier (Mi et al., 1996), and in renal epithelial cells (Welling, 1997) 
Kir2.3 is highly expressed in the heart and brain (Perier 1994 [14).
Kirs2.3 function in Rat Cardiomyocytes
A major finding of this study is that Kir2.3 channel subunit is essential for normal native IK1 currents in the neonatal rat cardiomyocytes. Previous studies showed that the deletion of Kir2.1 subunit almost eliminated the IK1 currents, and the deletion of Kir2.2 subunit reduced the IK1 currents by 50% . Our data demonstrated that IK1 current densities in the Kir2.3 knock-down cardiomyocytes were decreased by about 80%. Therefore, Kir2.3 subunit also plays an important role in IK1 currents.
IN cardiac myocytes the inward rectifier potassium current,
IK1, regulates the late phase of action potential (AP) repolarization and stabilizes the resting membrane potential. IK1 channels are believed to be homo- and/or heterotetramers
of Kir2.1, Kir2.2, and Kir2.3 subunits from the Kir2 family of
inward rectifier potassium channels (Lopatin , Nichols ). A number of studies consistently indicated that the species-dependent (Dhamoon )
and tissue-specific expression (Schram ) of different Kir2 subunits
may contribute, at least in part, to its variability.
There is evidence that, in mouse ventricles, Kir2.1 is the
major isoform with a significant contribution of Kir2.2, although
knockout of both genes revealed the presence of another slowly
activating component characteristic of Kir2.3 subunits (Zaritzki ).
Temporal Lobe Epilepsy
Kir2.3, has been found down-regulated in the hippocampus of chronic temporal lobe epileptic (cTLE) patients which may underline the mechanism of epilepsy. Our results suggest that the down-regulation of the Kir2.3 channel expression might contribute to the pathogenesis of TLE, which may be ameliorated by the administration of tenidap 
Human Kir2.3 in CHO cells Kinetics
whole-cell Kir2.3 currents in response to a series of 250 ms voltage steps from −127 mV to +23 mV (10 mV increments) before (ctrl), during Arachidonic Acid (AA), and after (wash) application of 10 μM AA