| KCNJ13 | |||||||||||||||||||||||||||||||||||||||||||||||||||
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| Identifiers | |||||||||||||||||||||||||||||||||||||||||||||||||||
| Aliases | KCNJ13 , KIR1.4, KIR7.1, LCA16, SVD, potassium voltage-gated channel subfamily J member 13, potassium inwardly rectifying channel subfamily J member 13 | ||||||||||||||||||||||||||||||||||||||||||||||||||
| External IDs | OMIM: 603208; MGI: 3781032; HomoloGene: 55638; GeneCards: KCNJ13; OMA:KCNJ13 - orthologs | ||||||||||||||||||||||||||||||||||||||||||||||||||
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| Wikidata | |||||||||||||||||||||||||||||||||||||||||||||||||||
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Potassium inwardly-rectifying channel, subfamily J, member 13 (KCNJ13) is a human gene encoding the Kir7.1 protein. [5]
The renal outer medullary potassium channel (ROMK) is an ATP-dependent potassium channel (Kir1.1) that transports potassium out of cells. It plays an important role in potassium recycling in the thick ascending limb (TAL) and potassium secretion in the cortical collecting duct (CCD) of the nephron. In humans, ROMK is encoded by the KCNJ1 gene. Multiple transcript variants encoding different isoforms have been found for this gene.
Inward-rectifier potassium channels (Kir, IRK) are a specific lipid-gated subset of potassium channels. To date, seven subfamilies have been identified in various mammalian cell types, plants, and bacteria. They are activated by phosphatidylinositol 4,5-bisphosphate (PIP2). The malfunction of the channels has been implicated in several diseases. IRK channels possess a pore domain, homologous to that of voltage-gated ion channels, and flanking transmembrane segments (TMSs). They may exist in the membrane as homo- or heterooligomers and each monomer possesses between 2 and 4 TMSs. In terms of function, these proteins transport potassium (K+), with a greater tendency for K+ uptake than K+ export. The process of inward-rectification was discovered by Denis Noble in cardiac muscle cells in 1960s and by Richard Adrian and Alan Hodgkin in 1970 in skeletal muscle cells.
The Kir2.1 inward-rectifier potassium channel is a lipid-gated ion channel encoded by the KCNJ2 gene.
Kir6.2 is a major subunit of the ATP-sensitive K+ channel, a lipid-gated inward-rectifier potassium ion channel. The gene encoding the channel is called KCNJ11 and mutations in this gene are associated with congenital hyperinsulinism.
G protein-activated inward rectifier potassium channel 2 is a protein that in humans is encoded by the KCNJ6 gene. Mutation in KCNJ6 gene has been proposed to be the cause of Keppen-Lubinsky Syndrome (KPLBS).
Potassium inwardly-rectifying channel, subfamily J, member 4, also known as KCNJ4 or Kir2.3, is a human gene.
Potassium inwardly-rectifying channel, subfamily J, member 8, also known as KCNJ8, is a human gene encoding the Kir6.1 protein. A mutation in KCNJ8 has been associated with cardiac arrest in the early repolarization syndrome.
G protein-activated inward rectifier potassium channel 4(GIRK-4) is a protein that in humans is encoded by the KCNJ5 gene and is a type of G protein-gated ion channel.
ATP-sensitive inward rectifier potassium channel 12 is a lipid-gated ion channel that in humans is encoded by the KCNJ12 gene.
G protein-activated inward rectifier potassium channel 1(GIRK-1) is encoded in the human by the gene KCNJ3.
ATP-sensitive inward rectifier potassium channel 10 is a protein that in humans is encoded by the KCNJ10 gene.
Potassium inwardly-rectifying channel, subfamily J, member 15, also known as KCNJ15 is a human gene, which encodes the Kir4.2 protein.
Potassium channel subfamily K member 1 is a protein that in humans is encoded by the KCNK1 gene.
Potassium inwardly-rectifying channel, subfamily J, member 16 (KCNJ16) is a human gene encoding the Kir5.1 protein.
Potassium inwardly-rectifying channel, subfamily J, member 14 (KCNJ14), also known as Kir2.4, is a human gene.
G protein-activated inward rectifier potassium channel 3 is a protein that in humans is encoded by the KCNJ9 gene.
The G protein-coupled inwardly rectifying potassium channels (GIRKs) are a family of lipid-gated inward-rectifier potassium ion channels which are activated (opened) by the signaling lipid PIP2 and a signal transduction cascade starting with ligand-stimulated G protein-coupled receptors (GPCRs). GPCRs in turn release activated G-protein βγ- subunits (Gβγ) from inactive heterotrimeric G protein complexes (Gαβγ). Finally, the Gβγ dimeric protein interacts with GIRK channels to open them so that they become permeable to potassium ions, resulting in hyperpolarization of the cell membrane. G protein-coupled inwardly rectifying potassium channels are a type of G protein-gated ion channels because of this direct interaction of G protein subunits with GIRK channels. The activation likely works by increasing the affinity of the channel for PIP2. In high concentration PIP2 activates the channel absent G-protein, but G-protein does not activate the channel absent PIP2.
Potassium channel, subfamily K, member 10, also known as KCNK10 is a human gene. The protein encoded by this gene, K2P10.1, is a potassium channel containing two pore-forming P domains.
Potassium channel, subfamily K, member 12, also known as KCNK12 is a human gene. The protein encoded by this gene, K2P12.1, is a potassium channel containing two pore-forming P domains.
Potassium channel, subfamily K, member 13, also known as KCNK13 is a human gene. The protein encoded by this gene, K2P13.1 is a potassium channel containing two pore-forming P domains.
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This article incorporates text from the United States National Library of Medicine, which is in the public domain.
