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ADAM17 - Revision history
2026-05-11T18:04:58Z
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<p><b>New page</b></p><div>{{Infobox enzyme<br />
| Name = ADAM metallopeptidase domain 17<br />
| EC_number = 3.4.24.86<br />
| CAS_number = 603639-49-0<br />
| IUBMB_EC_number = 3/4/24/86<br />
| GO_code = 0004222<br />
| image = <br />
| width = <br />
| caption = <br />
}}<br />
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'''ADAM17''', also known as '''tumor necrosis factor-α converting enzyme''' (TACE), is an enzyme that in humans is encoded by the ''ADAM17'' gene. This enzyme belongs to the [[ADAM family]], which is a group of [[peptidase]]s known for their role in the shedding of membrane-anchored proteins. ADAM17 is particularly important in the regulation of [[proinflammatory]] cytokines such as [[tumor necrosis factor-alpha|tumor necrosis factor-α (TNF-α)]].<br />
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== Function ==<br />
ADAM17 is a [[membrane protein]] that cleaves several membrane-bound [[cytokines]], [[growth factors]], [[receptors]], and other proteins. Its most notable substrate is TNF-α, a cytokine involved in systemic inflammation and a member of a group of cytokines that stimulate the acute phase reaction. By cleaving the membrane-bound precursor of TNF-α, ADAM17 releases the soluble form of this cytokine, which is a key player in inflammatory processes.<br />
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Besides TNF-α, ADAM17 also acts on substrates like [[transforming growth factor-alpha|transforming growth factor-α (TGF-α)]], [[L-selectin]], and [[amyloid precursor protein]]. Through the shedding of these molecules, ADAM17 regulates various biological processes including cell proliferation, adhesion, and migration.<br />
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== Structure ==<br />
ADAM17 is a type I transmembrane protein and consists of a prodomain that maintains the enzyme in an inactive state until it is removed, a metalloprotease domain that contains the catalytic site, a disintegrin domain, a cysteine-rich domain, and a cytoplasmic domain. The metalloprotease domain of ADAM17 contains a zinc-binding site essential for its proteolytic activity.<br />
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== Clinical Significance ==<br />
Given its role in shedding TNF-α and other regulatory molecules, ADAM17 has been implicated in various pathological conditions including [[cancer]], [[rheumatoid arthritis]], and [[Alzheimer's disease]]. Inhibitors of ADAM17 are being studied for their potential to treat these diseases by controlling the bioavailability of TNF-α and other growth factors.<br />
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== Genetic Studies ==<br />
Mutations in the ''ADAM17'' gene have been associated with inflammatory diseases and certain cancers, highlighting the importance of regulated proteolysis in human health.<br />
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== See Also ==<br />
* [[Metalloproteinase]]<br />
* [[Enzyme]]<br />
* [[Cytokine]]<br />
* [[Membrane protein]]<br />
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[[Category:EC 3.4.24]]<br />
[[Category:Human proteins]]<br />
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