3.4.24.B9: ADAM9 endopeptidase
This is an abbreviated version!
For detailed information about ADAM9 endopeptidase, go to the full flat file.
Word Map on EC 3.4.24.B9
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3.4.24.B9
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adams
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metastasis
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ectodomains
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metalloproteases
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alpha-secretase
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hb-egf
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medicine
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adam-15
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non-amyloidogenic
- 3.4.24.B9
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adams
- metastasis
- ectodomains
- metalloproteases
- alpha-secretase
- hb-egf
- medicine
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adam-15
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non-amyloidogenic
Reaction
proteolytic degradation of proteins =
Synonyms
a disintegrin and metalloproteinase domain 9, ADAM 9, ADAM metallopeptidase domain 9, ADAM-9, ADAM-9 sheddase, ADAM9, cellular disintegrin-related protein, M12.209, MDC, MDC-9, MDC9, MDC9/meltrin-gamma/ADAM9, meltrin gamma, meltrin-gamma, metallo protease desintegrin 9, metalloprotease ADAM9, metalloprotease disintegrin 9, metalloprotease/disintegrin/cysteine-rich protein 9, MLTNG, More, myeloma cell metalloproteinase
ECTree
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General Information
General Information on EC 3.4.24.B9 - ADAM9 endopeptidase
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malfunction
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silencing of ADAM-9 in melanoma cells significantly reduces cell adhesion to fibroblasts. Ablation of ADAM-9 in fibroblasts almost completely abolishes these cellular interactions and melanoma cell invasion in vitro
physiological function
additional information
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ADAM-9 interaction with alpha6beta1 integrin regulates fibroblast motility, and alpha6beta1 integrin can induce the mobility of several cell types including macrophages. ADAM-9 is involved in advanced human atherosclerosis and might play roles in the monocyte homing, migration, or proliferation in aorta, carotid, and femoral arteries. ADAM-9 is also involved both in ectodomain shedding and cell interactions through integrin binding. Potential ADAM-9 sheddase substrates include growth factors and cytokines, which are linked to atherosclerosis
physiological function
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ADAM9 is a member of the ADAM family which is involved in cellular processes like cell adhesion, migration and signalling, involvement of this protease in cervical carcinogenesis, overview
physiological function
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fibroblasts adhere to the adhesive domains of ADAM-9 in the presence of Mn2+ ions. ADAM-9 expression plays an important role in mediating cell-cell contacts between fibroblasts and melanoma cells. These interactions contribute to proteolytic activities required during invasion of melanoma cells
physiological function
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the enzyme is implicated in auto and paracrine regulation of invasiveness in A-549 cells
physiological function
coculture of melanoma cells in the presence of ADAM-9-/- fibroblasts leads to increased melanoma cell proliferation and reduced apoptosis as compared with control cocultures. TIMP-1 and sTNFRI are the two relevant factors expressed in increased amounts in culture supernatants from ADAM-9-/- fibroblasts. TIMP-1 is associated with induced melanoma cell proliferation, whereas soluble TNFR1 mediates the reduced cellular apoptosis in vitro. In vivo, injection of murine melanoma cells into the flank of ADAM-9-/- animals results in the development of significantly larger tumors than in wild-type animals as a result of increased proliferation and decreased apoptosis of melanoma cells
physiological function
aberrant overexpression of ADAM9 is found in both gastric cancer tissues and cell lines. Knockdown of ADAM9 in gastric cancer SGC-7901 cells induces a dramatic suppression of cell proliferation along with the arrest of the cell cycle in the G0/G1 phase. The 3' untranslated region of ADAM9 mRNA may be bound by miR-126, a suppressor in gastric cancer. Overexpression of miR-126 significantly downregulates ADAM9 in the gastric cancer cells
physiological function
ADAM9 enhances the expression of the pro-migratory protein CDCP1 to promote lung metastasis. Endogenous miR-218, which is abundant in normal lung tissue but suppressed in lung tumors, is regulated during the process of ADAM9-mediated CDCP1 expression. Suppression of miR-218 is associated with high migration ability in lung cancer cells
physiological function
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Adam9-/- mice are protected from emphysema development, small-airway fibrosis, and airway mucus metaplasia. Cigarette smoke-exposed Adam9-/- mice have reduced lung macrophage counts, alveolar septal cell apoptosis, lung elastin degradation, and shedding of vascular endothelial growth factor receptor-2 and epidermal growth factor receptor in BAL fluid samples
physiological function
cells lacking ADAM9 show a significant reduction in infection efficiency by encephalomyocarditis virus EMCV. Pharmacological inhibition of the metalloproteinase activity of ADAM9 does not affect virus infection. Reconstitution of inactive ADAM9 in knockout cells restores susceptibility to EMCV. ADAM9 facilitates attachment of EMCV to the cell surface
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ADAM9 is a widely expressed and particularly polyvalent member of the multifunctional ADAM family of proteins
additional information
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ADAM9 is a widely expressed and particularly polyvalent member of the multifunctional ADAM family of proteins
additional information
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promoter polymorphisms, which regulate ADAM9 transcription, are protective against sporadic Alzheimer's disease