A Disintegrin And Metalloprotease 17 Cleaved-Arg215 (ADAM17 Cleaved-R215) Antibody

Documentos del producto

Especificaciones del producto

Primary Antibodies

Target: A Disintegrin And Metalloprotease 17 Cleaved-Arg215 (ADAM17 Cleaved-R215)
Immunogen: The antiserum was produced against synthesized peptide derived from internal of human ADAM 17.

Rabbit

Human

Concentration: 1 mg/ml

WB: 1/500 - 1/3000, ELISA: 1/20000. Optimal dilutions/concentrations should be determined by the end user.

Polyclonal

Unconjugated

IgG

Purified from rabbit antiserum by affinity chromatography using epitope-specific immunogen.

10 µg

100 µg

200 µg

300 µg

1 mg

Liquid

ELISA, WB

PBS (without Mg<sup>2+</sup> and Ca<sup>2+</sup>), pH 7.4, 150 mM NaCl, 0.02% sodium azide, 50% glycerol.

Shipped within 5-10 working days.

Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles.

No

P78536

CSVP, CD156B, TACE,TNF-Alpha Convertase,TNF-Alpha Converting enzyme,adam-17

Antibody anti-ADAM17

RUO

THIS PRODUCT IS FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC, THERAPEUTIC OR COSMETIC PROCEDURES. NOT FOR HUMAN OR ANIMAL CONSUMPTION.

Background

ADAM17, also known as ADAM metallopeptidase domain 17 or tumor necrosis factor-alpha converting enzyme (TACE), is a member of the ADAM family of proteins. Like other ADAM proteins, it possesses a complex domain structure with distinct functional regions, including a metalloproteinase domain responsible for its proteolytic activity.ADAM17 is a transmembrane protein. Consists of several domains, including a metalloproteinase domain, a disintegrin domain, a cysteine-rich domain, an EGF-like domain, a transmembrane domain, and a cytoplasmic tail. Is responsible for the cleavage and release of various membrane-bound proteins, including cytokines, growth factors, receptors, and adhesion molecules. One of its most well-known substrates is tumor necrosis factor-alpha (TNF-α).ADAM17 cleaves the membrane-bound precursor form of TNF-α to release its soluble form into the extracellular space. Soluble TNF-α can then bind to its receptors on target cells, initiating signaling cascades involved in inflammation, apoptosis, and immune responses.ADAM17 also sheds and regulates the activity of other important proteins, including epidermal growth factor receptor (EGFR) ligands, transforming growth factor-alpha (TGF-α), and Notch receptor. Dysregulation of ADAM17 activity has been implicated in various diseases, including inflammatory disorders, autoimmune diseases, cancer, and cardiovascular diseases. In particular, increased ADAM17 activity and elevated levels of its substrates, such as TNF-α, have been observed in conditions like rheumatoid arthritis, inflammatory bowel disease, and certain cancers. Given its central role in inflammation and disease pathogenesis, ADAM17 is considered a promising therapeutic target

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