HPA014722
Anti-KCNJ5 antibody produced in rabbit
Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
Synonym(s):
Anti-CIR, Anti-GIRK4, Anti-KATP1, Anti-Kir3.4, Anti-LQT13
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About This Item
Recommended Products
biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
product line
Prestige Antibodies® Powered by Atlas Antibodies
form
buffered aqueous glycerol solution
species reactivity
human
technique(s)
immunohistochemistry: 1:500- 1:1000
immunogen sequence
TPVLTLEKGFYEVDYNTFHDTYETNTPSCCAKELAEMKREGRLLQYLPSPPLLGGCAEAGLDAEAEQNEEDEPKGLGG
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... KCNJ5(3762)
General description
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.
Immunogen
G protein-activated inward rectifier potassium channel 4 recombinant protein epitope signature tag (PrEST)
Application
All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project 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. We also provide Prestige Antibodies® protocols and other useful information.
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. We also provide Prestige Antibodies® protocols and other useful information.
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).
Features and Benefits
Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.
Every Prestige Antibody is tested in the following ways:
Every Prestige Antibody is tested in the following ways:
- IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
- Protein array of 364 human recombinant protein fragments.
Linkage
Corresponding Antigen APREST72857
Physical form
Solution in phosphate-buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide
Legal Information
Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany
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Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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L Gomez et al.
Genes, brain, and behavior, 13(6), 535-542 (2014-05-21)
Linkage and association of Tourette Syndrome (TS) and Attention-Deficit/Hyperactivity Disorder (ADHD) have previously been reported in the 11q24 chromosomal region. To identify the risk gene within the region we studied the potassium inwardly-rectifying channel J5 (KCNJ5) gene in a sample
Jingjing Zhang et al.
Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics, 32(1), 21-25 (2015-01-31)
To investigate the prevalence of KCNJ5 gene missense mutations and their role in patients with unilateral adrenal hyperplasia (UAH). Fourteen UAH tissues were collected through surgical resection, and all the tissues were confirmed by pathology. Peripheral blood samples of the
Silvia Monticone et al.
The Journal of clinical endocrinology and metabolism, 98(11), E1861-E1865 (2013-09-17)
Primary aldosteronism is a heterogeneous group of disorders comprising both sporadic and familial forms. Mutations in the KCNJ5 gene, which encodes the inward rectifier K(+) channel 4 (G protein-activated inward rectifier K(+) channel 4, Kir3.4), cause familial hyperaldosteronism type III
Meena Murthy et al.
Hypertension (Dallas, Tex. : 1979), 63(4), 783-789 (2014-01-15)
Primary aldosteronism (autonomous aldosterone production with suppressed renin) plays an important pathophysiological role in what has been previously labeled as essential hypertension. Besides the recently described germline mutations in the KCNJ5 potassium channel associated with familial primary aldosteronism, somatic mutations
Carolina Velarde-Miranda et al.
Clinical and experimental pharmacology & physiology, 40(12), 895-901 (2013-07-09)
The G-protein-activated inwardly rectifying potassium channel Kir3.4 is expressed in the zona glomerulosa cell membrane and transports potassium out of the cell. Angiotensin II stimulation of aldosterone secretion is mediated, in part, by suppression of the transcription of KCNJ5, the
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