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ATP-sensitive inward rectifier potassium channel

In the kidney, probably plays a major role in potassium homeostasis. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. 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. The inward rectification is mainly due to the blockage of outward current by internal magnesium. This channel is activated by internal ATP and can be blocked by external barium.

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ATP-sensitive inward rectifier potassium channel 1

Also known as ATP-sensitive inward rectifier potassium channel 1 (ATP-regulated potassium channel ROM-K) (Inward rectifier K(+) channel Kir1.1) (KAB-1) (Potassium channel, inwardly rectifying subfamily J member 1).
ROMK: an inward rectifier-type potassium channel protein. Probably plays a major role in potassium homeostasis in the kidney. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. The channel is activated by internal ATP and can be blocked by external barium. High levels of expression in the kidney and pancreatic islets. Lower levels in skeletal muscle, pancreas, spleen, brain, heart and liver. Three alternatively spliced isoforms have been described.

Protein type: Channel, potassium; Membrane protein, integral; Membrane protein, multi-pass

Cellular Component: integral to plasma membrane; plasma membrane

Molecular Function: ATP-activated inward rectifier potassium channel activity; inward rectifier potassium channel activity; peptide binding; phosphatidylinositol-4,5-bisphosphate binding; potassium ion binding

Biological Process: kidney development; negative regulation of apoptosis; post-embryonic development; potassium ion import; potassium ion transport; tissue homeostasis

Disease: Bartter Syndrome, Antenatal, Type 1

ATP-sensitive inward rectifier potassium channel 10

Also known as ATP-sensitive inward rectifier potassium channel 10 (ATP-dependent inwardly rectifying potassium channel Kir4.1) (Inward rectifier K(+) channel Kir1.2) (Potassium channel, inwardly rectifying subfamily J member 10).
Kir4.1: May be responsible for potassium buffering action of glial cells in the brain. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. 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. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by extracellular barium and cesium. Defects in KCNJ10 are the cause of seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance (SESAMES). A complex disorder characterized by generalized seizures with onset in infancy, delayed psychomotor development, ataxia, sensorineural hearing loss, hypokalemia, metabolic alkalosis, and hypomagnesemia. Belongs to the inward rectifier-type potassium channel (TC 1.A.2.1) family. KCNJ10 subfamily.

Protein type: Channel, ligand-gated; Channel, potassium; Membrane protein, integral; Membrane protein, multi-pass

Chromosomal Location of Human Ortholog: 1q23.2

Cellular Component: integral to plasma membrane; plasma membrane

Molecular Function: ATP-activated inward rectifier potassium channel activity; G-protein activated inward rectifier potassium channel activity; inward rectifier potassium channel activity; protein binding

Biological Process: potassium ion import; potassium ion transport

Disease: Deafness, Autosomal Recessive 4, With Enlarged Vestibular Aqueduct; Pendred Syndrome; Seizures, Sensorineural Deafness, Ataxia, Mental Retardation, And Electrolyte Imbalance

ATP-sensitive inward rectifier potassium channel 11

Also known as ATP-sensitive inward rectifier potassium channel 11 (BIR) (Inward rectifier K(+) channel Kir6.2) (Potassium channel, inwardly rectifying subfamily J member 11).
Kir6.2: This receptor is controlled by G proteins. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. 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. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by extracellular barium. Subunit of ATP-sensitive potassium channels (KATP). Can form cardiac and smooth muscle-type KATP channels with ABCC9. KCNJ11 forms the channel pore while ABCC9 is required for activation and regulation. Defects in KCNJ11 are the cause of familial hyperinsulinemic hypoglycemia type 2 (HHF2); also known as persistent hyperinsulinemic hypoglycemia of infancy (PPHI) or congenital hyperinsulinism. HHF is the most common cause of persistent hypoglycemia in infancy and is due to defective negative feedback regulation of insulin secretion by low glucose levels. It causes nesidioblastosis, a diffuse abnormality of the pancreas in which there is extensive, often disorganized formation of new islets. Unless early and aggressive intervention is undertaken, brain damage from recurrent episodes of hypoglycemia may occur. Defects in KCNJ11 are a cause of diabetes mellitus permanent neonatal (PNDM). PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy. Defects in KCNJ11 are the cause of transient neonatal diabetes mellitus type 3 (TNDM3). Neonatal diabetes mellitus, defined as insulin-requiring hyperglycemia within the first month of life, is a rare entity. In about half of the neonates, diabetes is transient and resolves at a median age of 3 months, whereas the rest have a permanent form of diabetes. In a significant number of patients with transient neonatal diabetes mellitus, diabetes type 2 appears later in life. The onset and severity of TNDM3 is variable with childhood-onset diabetes, gestational diabetes or adult-onset diabetes described. Defects in KCNJ11 may contribute to non-insulin- dependent diabetes mellitus (NIDDM), also known as diabetes mellitus type 2. Belongs to the inward rectifier-type potassium channel (TC 1.A.2.1) family. KCNJ11 subfamily.

Protein type: Channel, potassium; Membrane protein, integral; Membrane protein, multi-pass

ATP-sensitive inward rectifier potassium channel 12

Also known as ATP-sensitive inward rectifier potassium channel 12 (Inward rectifier K(+) channel Kir2.2) (IRK-2) (Inward rectifier K(+) channel Kir2.2v) (Potassium channel, inwardly rectifying subfamily J member 12).
KCNJ12: Probably participates in establishing action potential waveform and excitability of neuronal and muscle tissues. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. 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. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by extracellular barium and cesium. Belongs to the inward rectifier-type potassium channel (TC 1.A.2.1) family. KCNJ12 subfamily.

Protein type: Membrane protein, integral; Membrane protein, multi-pass

Chromosomal Location of Human Ortholog: 17p11.2

Cellular Component: integral to plasma membrane; intrinsic to membrane; plasma membrane

Molecular Function: G-protein activated inward rectifier potassium channel activity; inward rectifier potassium channel activity

Biological Process: muscle contraction; potassium ion import; potassium ion transport; protein homotetramerization; regulation of heart contraction

ATP-sensitive inward rectifier potassium channel 14

Also known as ATP-sensitive inward rectifier potassium channel 14 (Inward rectifier K(+) channel Kir2.4) (IRK-4) (Potassium channel, inwardly rectifying subfamily J member 14).
inwardly rectifying K+ channel; involved in controlling excitability of motoneurons [RGD, Feb 2006]

ATP-sensitive inward rectifier potassium channel 15

Also known as ATP-sensitive inward rectifier potassium channel 15 (Inward rectifier K(+) channel Kir1.3) (Inward rectifier K(+) channel Kir4.2) (Potassium channel, inwardly rectifying subfamily J member 15).
Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. 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. The inward rectification is mainly due to the blockage of outward current by internal magnesium ().

ATP-sensitive inward rectifier potassium channel 8

Also known as ATP-sensitive inward rectifier potassium channel 8 (Inward rectifier K(+) channel Kir6.1) (Potassium channel, inwardly rectifying subfamily J member 8) (uKATP-1).
KCNJ8: This potassium channel is controlled by G proteins. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. 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. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by external barium. Defects in KCNJ8 may be associated with susceptibility to J-wave syndromes, a group of heart disorders characterized by early repolarization events as indicated by abnormal J-wave manifestation on electrocardiogram (ECG). The J point denotes the junction of the QRS complex and the ST segment on the ECG, marking the end of depolarization and the beginning of repolarization. An abnormal J wave is a deflection with a dome or hump morphology immediately following the QRS complex of the surface ECG. Examples of J-wave disorders are arrhythmias associated with an early repolarization pattern in the inferior or mid to lateral precordial leads, Brugada syndrome, some cases of idiopathic ventricular fibrillation (VF) with an early repolarization pattern in the inferior, inferolateral or global leads, as well as arrhythmias associated with hypothermia. Defects in KCNJ8 may be a cause of susceptibility to sudden infant death syndrome (SIDS). SIDS is the sudden death of an infant younger than 1 year that remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of clinical history. Pathophysiologic mechanisms for SIDS may include respiratory dysfunction, cardiac dysrhythmias, cardiorespiratory instability, and inborn errors of metabolism, but definitive pathogenic mechanisms precipitating an infant sudden death remain elusive. Belongs to the inward rectifier-type potassium channel (TC 1.A.2.1) family. KCNJ8 subfamily.

Protein type: Channel, potassium; Membrane protein, integral; Membrane protein, multi-pass

Chromosomal Location of Human Ortholog: 12p11.23

Cellular Component: plasma membrane; voltage-gated potassium channel complex

Molecular Function: ATP-activated inward rectifier potassium channel activity; inward rectifier potassium channel activity

Biological Process: potassium ion import; potassium ion transport

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