HPA010738
Anti-ADAM17 antibody produced in rabbit
Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
Synonym(s):
Anti-A disintegrin and metalloproteinase domain 17 antibody produced in rabbit, Anti-ADAM 17 precursor antibody produced in rabbit, Anti-CD156b antigen antibody produced in rabbit, Anti-Snake venom-like protease antibody produced in rabbit, Anti-TNF-α convertase antibody produced in rabbit, Anti-TNF-α-converting enzyme antibody produced in rabbit
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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)
immunofluorescence: 0.25-2 μg/mL
immunohistochemistry: 1:20-1:50
immunogen sequence
SEYTVKWQDFFTGHVVGEPDSRVLAHIRDDDVIIRINTDGAEYNIEPLWRFVNDTKDKRMLVYKSEDIKNVSRLQSPKVCGYLKVDNEELLPKGLVDREPPEELVHRVKRRADPDPMKNTCKLLVVADHRFYR
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... ADAM17(6868)
Related Categories
General description
A disintegrin and metallopeptidase domain 17 (ADAM17) belongs to ADAM family of genes, which has a characteristic cysteine rich region called disintegrin and a metalloproteinase domain. This gene is located on chromosome 2, spans 55kb and has 9 exons. In adult humans, ADAM17 is expressed on multiple tissues such as, heart, muscle, kidney, placenta, pancreas, thymus, small intestine, ovaries, testes and prostate. In fetus, it is expressed in brain, lung, liver and kidney.
Immunogen
ADAM 17 precursor 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
ADAMs (A disintegrin and metallopeptidases) are called ectodomain sheddases and ADAM17 is an angiotensin-converting enzyme 2 (ACE2) sheddase. It also processes and sheds multiple cell surface molecules such as, adhesion molecules and cytokines. It produces the soluble form of tumor necrosis factor α (TNF-α), along with the processing of I-CAM, V-CAM, IL-6R, L-selectin etc. These, in turn, play a role in development, regeneration and inflammation of the circulatory system. Polymorphism rs12692386 in ADAM17 gene is associated with an increased susceptibility to abdominal aortic aneurysm. This gene is also up-regulated in myocardial infarction patients, as well as in atherosclerosis patients. It also plays a role in the pathophysiology of ischemic strokes (IS). ADAM17 aids in tumor progression by facilitating tumor proliferation and invasion, as in the case of non-small cell lung cancer.
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 APREST72102
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
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
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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Kai Wang et al.
Frontiers in immunology, 13, 923516-923516 (2022-06-21)
SARS-Cov-2 caused the COVID-19 pandemic worldwide. ADAM17 functions as a disintegrin and transmembrane metalloproteinase domain protein involved in the regulation of SARS-CoV-2 receptor ACE2. However, its impact on cancer patients infected with COVID-19 and its correlation with immune cell infiltration
Henriette Ebsen et al.
PloS one, 8(10), e76853-e76853 (2013-10-17)
A disintegrin and metalloproteases (ADAMs) have been implicated in many processes controlling organismic development and integrity. Important substrates of ADAM proteases include growth factors, cytokines and their receptors and adhesion proteins. The inducible but irreversible cleavage of their substrates alters
You Li et al.
Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 33(5), 1426-1438 (2014-05-24)
Accumulating evidence suggests that the principal TNF-α converting enzyme, a disintegrin and metalloproteinase 17 (ADAM17), is involved in the development of human abdominal aortic aneurysm (AAA). However, the association between ADAM17 gene polymorphisms and AAA has not been explored. The
You Li et al.
Journal of atherosclerosis and thrombosis, 21(8), 878-893 (2014-04-15)
Stroke is a leading cause of death and disability worldwide. Most ischemic strokes (IS) are caused by atherosclerosis. Recently, the pivotal role of ADAM17 in atherosclerosis has been thoroughly addressed. However, the association between ADAM17 and IS has not yet
Xiaohong Lv et al.
Molecular medicine reports, 9(5), 1935-1940 (2014-03-15)
A disintegrin and metalloprotease (ADAM) 17 has been implicated in the tumor progression of various types of solid tumor; however, little is known about its role in non-small cell lung carcinoma (NSCLC). The present study evaluated whether the downregulation of
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