Introduction of KCNJ16
Inward rectifier potassium channel 16 (KCNJ16), also known as Kir5.1, belongs to Kir5 subfamily, inward-rectifier potassium channels (Kir, IRK) family. Activated by phosphatidylinositol 4,5-bisphosphate (PIP2), the Kir members play a wide range of roles in the establishment of resting membrane potential, inhibition of neurotransmitter responses, regulation of nitric oxide synthase, the decision of insulin release, etc. KCNJ16, which was mapped to chromosome 17q25, has a greater tendency to uptake potassium rather than spit out potassium. It has been well documented that KCNJ16 can form functional heterodimers with KCNJ10 which increase the potassium current, alter the responsiveness during hyperpolarizing pulses, and increase the unitary conductance of KCNJ10. Human KCNJ16 is predominantly expressed in kidney, pancreas and thyroid gland, especially in convoluted tubule cells of the kidney and in the acinar and ductal cells of the pancreas. Like other Kir channels, KCNJ16 also possesses a pore domain, homologous to that of voltage-gated ion channels, and flanking transmembrane segments (TMSs).
|Basic Information of KCNJ16|
|Protein Name||Inward rectifier potassium channel 16|
|Organism||Homo sapiens (Human)|
Function of KCNJ16 Membrane Protein
The physiological roles of the KCNJ16 channel are performed by selective co-assembly with either KCNJ10 or KCNJ15 subunits to form novel heteromeric channels because KCNJ16 alone cannot produce functional K+ channels. The heteromeric KCNJ16/KCNJ10 are highly sensitive to inhibition by intracellular H+ (pHi) but insensitive to extracellular pH, providing a link between changes in intracellular pH and control of the resting membrane potential. So KCNJ16 is involved in the regulation of fluid and pH balance. Abundant co-expression in the brainstem, especially in several CO2-chemosensitive nuclei, such as locus coeruleus (LC) neurons, KCNJ16/ KCNJ10 complex plays a crucial role in defining the pH sensitivity of LC neurons and may, therefore, affect their response to hypercapnic acidosis. In the kidney, KCNJ16/ KCNJ10 mediates basolateral K+ recycling in distal convoluted tubule (DCT), which is critical for Na+ reabsorption at the tubules. Disruption of Kcnj16 gene in mice induces a severe renal phenotype, including hypokalemic, hyperchloremic metabolic acidosis with hypercalciuria. As a pH-sensitive regulator of salt transport in DCT, KCNJ16 has great potentiality in genetic diagnosis of renal tubulopathies.
Fig.1 A cellular model for enhanced salt transport caused by deletion of Kcnj16. (Paulais, 2011)
Application of KCNJ16 Membrane Protein in Literature
In this review, the authors provide evidence that KCNJ10 mutations will display differential sensitivity to heteromerisation with KCNJ16. Co-expression with KCNJ10, KCNJ16 play widely roles in seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance (SeSAME)/epilepsy, ataxia, sensorineural deafness, and renal tubulopathy (EAST) syndrome.
This article demonstrates that lacking the Kir5.1 (Kcnj16) K+ channel subunit in mice is the opposite of the phenotype seen in electrolyte imbalance (SeSAME)/epilepsy, ataxia, sensorineural deafness, and renal tubulopathy (EAST) syndrome, and they present hypokalemic, hyperchloremic metabolic acidosis with hypercalciuria.
The authors use Kir5.1 knockout mice (Kir5.1(-/-)) to study the role of KCNJ16 in the chemosensory control of breathing and they find that the transgenic mice present persistent metabolic acidosis and a clear respiratory phenotype.
This article reveals that KCNJ16 channels are key regulators of renal salt regulation in salt-sensitive hypertension. Kcnj16 knockout in Dahl salt-sensitive (SS) rats (SSKcnj16-/-) exhibit hypokalemia and reduced blood pressure.
This article identifies the novel human Kir5.1 through database searches and demonstrates that Kir5.1 is mainly expressed in kidney, pancreas and thyroid gland.
KCNJ16 Preparation Options
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