KCNJ3

	KCNJ3 G protein-activated inward rectifier potassium channel 1 (GIRK-1) is encoded in the human by the gene ''KCNJ3''. 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 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 and plays an important role in regulating heartbeat. It associates with three other G-protein-activated potassium channels to form a hetero-tetrameric pore-forming complex. Interactions KCNJ3 has been shown to Protein-protein interaction, interact with KCNJ5. See also * G protein-coupled inwardly-rectifying potassium channel * Inward-rectifier potassium ion channel References Further reading * * * * * * * * * * * * * * * * * * * External links * Ion channels {{membrane-protein-stub ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu]
	G Protein-coupled Inwardly-rectifying Potassium Channel 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. GIRK ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu]
	Inward-rectifier Potassium Ion Channel 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. Overview of inward rectification A channel that is "inwardly-rectifying" is one that passes current (positive cha ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu]
	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. Function 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 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 adrenal gland and pituitary, although it is also detected at low levels in 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. Inter ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu]