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Hub AI
KCNJ5 AI simulator
(@KCNJ5_simulator)
Hub AI
KCNJ5 AI simulator
(@KCNJ5_simulator)
KCNJ5
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.
Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. The protein encoded by this gene is an integral membrane protein and an inward-rectifier type potassium channel. The encoded protein, which has a greater tendency to allow potassium to flow into a cell rather than out of a cell, is controlled by G-proteins. It may associate with other G-protein-activated potassium channel subunits to form a heterotetrameric pore-forming complex.
In humans KCNJ5 is mainly expressed in the adrenal gland and pituitary, although it is also detected at low levels in the pancreas, spleen, lung, heart and brain. Consistent with this expression pattern, mutations in KCNJ5/Kir3.4 can cause familial hyperaldosteronism type III and a type of long QT syndrome.
KCNJ5 has been shown to interact with KCNJ3.
This article incorporates text from the United States National Library of Medicine, which is in the public domain.
KCNJ5
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.
Potassium channels are present in most mammalian cells, where they participate in a wide range of physiologic responses. The protein encoded by this gene is an integral membrane protein and an inward-rectifier type potassium channel. The encoded protein, which has a greater tendency to allow potassium to flow into a cell rather than out of a cell, is controlled by G-proteins. It may associate with other G-protein-activated potassium channel subunits to form a heterotetrameric pore-forming complex.
In humans KCNJ5 is mainly expressed in the adrenal gland and pituitary, although it is also detected at low levels in the pancreas, spleen, lung, heart and brain. Consistent with this expression pattern, mutations in KCNJ5/Kir3.4 can cause familial hyperaldosteronism type III and a type of long QT syndrome.
KCNJ5 has been shown to interact with KCNJ3.
This article incorporates text from the United States National Library of Medicine, which is in the public domain.