KCNJ5 (potassium channel, inwardly rectifying subfamily J, member 5) is an inward rectifier K+ channel 4, which is activated by G-protein. This protein is also called Kir3.4, and is expressed in zona glomerulosa, and forms either homotetramers or heterotetramers with Kir3.1 (KCNJ3), Kir3.2 (KCNJ6) or Kir3.3 (KCNJ9). The pore of this channel has a GYG motif at its narrowest position, which acts as a selectivity filter against K+. KCNJ5 contains four subunits, with each of them spanning the membrane twice. The pore is present in between the four subunits. This gene is localized to human chromosome 11q24.
Synonyms: Anti-CIR; Anti-GIRK4; Anti-KATP1; Anti-Kir3.4; Anti-LQT13
MDL Number: MFCD07370456
Storage: -20C
Application: All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project (www.proteinatlas.org)and as a result, are supported by the most extensive characterization in the industry. The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. To view these protocols and other useful information about Prestige Antibodies and the HPA, visit sigma.com/prestige.
Biochem Physiol Actions: KCNJ5 (potassium channel, inwardly rectifying subfamily J, member 5) is a channel that acts as a filter to reduce the K+ selectivity of cells. This leads to the movement of Na+ ions inside the cell, causing depolarization, which eventually results in enhanced synthesis of aldosterone. Hyperpolarization of membrane by this channel leads to inhibition of prolactin secretion by pituitary lactotropes, when acted upon by dopamine. Mutations in this gene are associated with familial hyperaldosteronism type III (FH-III), and are also involved in the pathophysiology of sporadic aldosterone-producing adenomas. Polymorphisms in this gene are linked to common as well as rare forms of primary aldosteronism. Mutations in KCNJ5 might also be linked with unilateral adrenal hyperplasia. Polymorphisms in this gene are also associated with Tourette Syndrome (TS) and attention-deficit/hyperactivity disorder (ADHD).
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