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3.4.24.86: ADAM 17 endopeptidase

This is an abbreviated version!
For detailed information about ADAM 17 endopeptidase, go to the full flat file.

Word Map on EC 3.4.24.86

Reaction

Narrow endopeptidase specificity. Cleaves Pro-Leu-Ala-Gln-Ala-/-Val-Arg-Ser-Ser-Ser in the membrane-bound, 26-kDa form of tumor necrosis factor alpha (TNFalpha). Similarly cleaves other membrane-anchored, cell-surface proteins to "shed" the extracellular domains =

Synonyms

(TACE/ADAM17/CD156q), (TACE:ADAM17), a disintegrin and metallo protease domain 17, a disintegrin and metalloprotease 17, a disintegrin and metalloprotease-17, a disintegrin and metalloproteinase 17, a disintegrin and metalloproteinase-17, ADAM-17, ADAM17, ADAM17 proteinase, ADAM17/tumor necrosis factor-alpha (TNF-A)converting enzyme, ADAMTS-2, CD156, H-TACE, human TACE B, metalloprotease TACE, metalloprotease-disintegrin tumour necrosis factor alpha convertase, metalloproteinase ADAM17, pro tumor necrosis factor cleavage enzyme, pro-tumor necrosis factor-alpha-processing enzyme, proteinase, pro-tumor necrosis factor (9CI), sheddase, TACE, TACE proteinase, TACE/ADAM17, TNF converting enzyme, TNF-alpha convertase, TNF-alpha converting enzyme, TNF-alpha processing protease, TNFalpha converting enzyme, tumor necrosis factor alpha convertase, tumor necrosis factor alpha converting enzyme, tumor necrosis factor alpha-converting enzyme, tumor necrosis factor-alpha converting enzyme, tumor necrosis factor-alpha-converting enzyme, tumour necrosis factor alpha-converting enzyme, tumour necrosis factor-alpha converting enzyme

ECTree

     3 Hydrolases
         3.4 Acting on peptide bonds (peptidases)
             3.4.24 Metalloendopeptidases
                3.4.24.86 ADAM 17 endopeptidase

Expression

Expression on EC 3.4.24.86 - ADAM 17 endopeptidase

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EXPRESSION
ORGANISM
UNIPROT
LITERATURE
ADAM-17 mRNA increases, but not significantly upon treatment with TNF -alpha and TGF-beta1
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ADAM-17 mRNA remains at control levels when treated with IL-1beta and IFN-gamma
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ADAM17 expression is increased in chronically inflamed tissue
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ADAM17 is expressed in most tissues and is up-regulated during inflammation and cancer
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ADAM17 is upregulated in most tumor cells
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cultured HL-60 neutrophils exposed to tobacco smoke extract show increased enzyme content
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dose-dependent increase of TACE mRNA expression in anti-Ro/SSA antibodies-treated salivary land epithelial cells, followed by internalization, pro-domain shedding and activation of TACE protein, suggesting that increased TACE activity is necessary for the release of TNF-alpha observed in anti-Ro/SSA antibodies-stimulated salivary gland epithelial cells. Adalimumab treatment brings TACE mRNA and surface TACE expression to levels similar to those observed in untreated salivary gland epithelial cells
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enzyme levels of mRNA are markedly and transiently increased 6-12 h post-human chorionic gonadotropin, and return to low baseline levels at 24 h post-human chorionic gonadotropin in granulosa and theca interna cells of preovulatory follicles. Forskolin stimulation induces a pattern of enzyme mRNA up-regulation in vitro
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expression of ADAM-17 is significantly increased in gallbladder carcinoma with high histological grade and pT stage compared with low histological grade and pT stage tumors and is not associated with patients’ gender, age, histological type, and resection margin involvement
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granulocyte-macrophage colony-stimulating factor GM-CSF and interleukin-4 in combination potently up-regulate tumor necrosis factor-alpha coverting enzyme TACE and activity in monocytes, causing ectodomain shedding of M-CSF receptor
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in aneurysmal thoracic aorta from patients, the enzyme Is increased in tunica media and intima
in proliferating cells which are stably transfected to impose the anchorage of a chimeric B12-binding protein, transcobalamin-oleosin TO, to the intracellular membrane, a 2-fold increase of p75NTR-regulated intramembraneous proteolysis is observed that is associated with an increased expression of enzymes Adam-10 and Adam-17
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increased TACE mRNA expression in anti-Ro/SSA antibodies-treated salivary gland epithelial cells is restored to normal levels by Adalimumab treatment
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infection of AGS cells with wild-type H pylori or an H pylori cagL-deficient isogenic mutant that also contains a wild-type version of cagL, P12DeltacagL/cagL, represses HKalpha promoter-Luc reporter activity and stimulates ADAM17 activity. Both responses are inhibited by point mutations in the nuclear factor-kappaB binding site of HKalpha or by infection with P12DeltacagL
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metalloproteases ADAM-9, ADAM-15, and ADAM-17 are upregulated in advanced human atherosclerotic lesions in samples from carotid, aortic, and femoral territories compared to samples from internal thoracic artery free of atherosclerotic plaques
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Porphyromonas gingivalis challenge results in a concentration-dependent enhancement of TACE messenger RNA expression and protein release by Jurkat cells. TLCK treatment or heat treatment of Porphyromonas gingivalis culture supernatants decreases TACE release to control levels
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protein kinase C-activating phorbol ester PMA, often used as a strong inducer of the enzyme, causes not only proteolysis by the enzyme but also a rapid increase of the mature protease at the cell surface. This is followed by internalisation and subsequent degradation of the protease. Eventually, this leads to a substantial downregulation of mature enzyme
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stimulation of lung epithelial A549 tumor cells with phorbol-12-myristate-13-acetate leads to the downregulation of the surface expressed mature form of the enzyme
the enzyme is significantly upregulated in gastric cancer and positive metastatic lymph node tissues
transcript levels of TACE and TNF-alpha as well as TACE protein expression are significantly upregulated in direct, but not in indirect coculture condition of marrow stromal cell and brain microvascular endothelial cell
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transcription factor Sp1 binds to the ADAM17 promoter, and Sp1 regulates ADAM17 expression under hypoxia. Suppression of Sp1 decreases invasiveness and migration in U87 tumor cells
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treatment with angiotensin II results in angiotensin II type 1 receptor AT1R-mediated increase myocardial TACE expression and activity