3.4.24.34: neutrophil collagenase
This is an abbreviated version!
For detailed information about neutrophil collagenase, go to the full flat file.
Word Map on EC 3.4.24.34
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3.4.24.34
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mmp-9
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metalloproteinases
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zymography
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metastasis
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timp-1
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endothelial
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angiogenesis
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necrosis
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artery
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fibrosis
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cartilage
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gelatinase
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gelatin
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osteoarthritis
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joint
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periodontal
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tnf
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arthritis
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plaque
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infarct
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vessel
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rheumatoid
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myocardial
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invasiveness
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plasminogen
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basement
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synovial
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chondrocytes
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gingival
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articular
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transwell
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mt1-mmp
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aortic
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aneurysm
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collagenolytic
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aggrecan
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matrigel
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atherosclerotic
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stromelysins
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signal-regulated
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erk
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crevicular
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doxycycline
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gelatinolytic
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matrix-degrading
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anti-invasive
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diagnostics
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disintegrin
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upa
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photoaging
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membrane-type
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medicine
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biotechnology
- 3.4.24.34
- mmp-9
- metalloproteinases
-
zymography
- metastasis
- timp-1
- endothelial
- angiogenesis
- necrosis
- artery
- fibrosis
- cartilage
- gelatinase
- gelatin
- osteoarthritis
- joint
- periodontal
- tnf
- arthritis
- plaque
- infarct
- vessel
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rheumatoid
- myocardial
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invasiveness
- plasminogen
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basement
- synovial
- chondrocytes
- gingival
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articular
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transwell
- mt1-mmp
- aortic
- aneurysm
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collagenolytic
- aggrecan
- matrigel
- atherosclerotic
- stromelysins
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signal-regulated
- erk
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crevicular
- doxycycline
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gelatinolytic
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matrix-degrading
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anti-invasive
- diagnostics
-
disintegrin
- upa
-
photoaging
-
membrane-type
- medicine
- biotechnology
Reaction
Cleavage of interstitial collagens in the triple helical domain. Unlike EC 3.4.24.7, interstitial collagenase, this enzyme cleaves type III collagen additional information slowly than type I =
Synonyms
collagenase-2, collagenases-8, EC 3.4.24.7, HNC, human neutrophil collagenase, matrix metalloproteinase, Matrix metalloproteinase 8, Matrix metalloproteinase-8, metalloproteinase-8, MetMMP-8, MMP-7, MMP-8, MMP8, neutrophil collagenase, neutrophil collagenase MMP-8, neutrophil interstitial collagenase, PheMMP-8, PMNL collagenase, PMNL-CL, polymorphonuclear leukocyte collagenase, whMMP-8
ECTree
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General Information
General Information on EC 3.4.24.34 - neutrophil collagenase
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malfunction
physiological function
additional information
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abrogation of MMP-8 activity by specific inhibitors as well as transfection with MMP-8 siRNA abolishes production of the cleavage fragment and occludin remained attached to the cell periphery
malfunction
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MMP-8-/- mice with acute lung injury have greater increases in lung polymorphonuclear neutrophils (PMNs) and macrophage counts, measures of alveolar capillary barrier injury, lung elastance, and mortality than wild-type mice with acute lung injury
malfunction
intracerebroventricular microinjection of MMP8-specific shRNA lentivirus reduces the extent of ischemia-induced brain damage, as assessed by infarct volume, neurological score, microglial activation, and TNF-alpha expression. Administration of an MMP8 inhibitor (M8I) immediately after reperfusion reduced brain damage
malfunction
ischemia-reperfusion (I/R) injury leads to increased expression of intestinal and systemic MMP8. Inhibition of MMP8 prevents intestinal barrier dysfunction following I/R injury. MMP8-null mice have reduced intestinal permeability to FD-40 compared with wild-type mice. Wild-type mice treated with MMP8 inhibitor also have a significant reduction of intestinal neutrophil infiltration as compared with wild-type mice treated with vehicle. Claudin-3 expression is reduced after I/R injury, relative to the respective sham-treated animals, and this effect is ameliorated by either genetic ablation or pharmacologic inhibition of MMP8. Inhibition of MMP8 decreases neutrophil infiltration in the intestine and lung and prevents intestinal damage, myeloperoxidase activity is reduced, overview
malfunction
juvenile MMP8 null mice have greater mortality and higher bacterial burden than wild-type mice. Leukocyte counts and cytokine concentrations in the peritoneal fluid are increased in the MMP8 null mice relative to the wild-type mice. Peritoneal macrophages from MMP8 null mice have reduced phagocytic capacity compared to wild-type macrophages. There is no quantitative difference in NET formation, but fewer bacteria are adherent to NETs from MMP8 null animals
malfunction
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ischemia-reperfusion (I/R) injury leads to increased expression of intestinal and systemic MMP8. Inhibition of MMP8 prevents intestinal barrier dysfunction following I/R injury. MMP8-null mice have reduced intestinal permeability to FD-40 compared with wild-type mice. Wild-type mice treated with MMP8 inhibitor also have a significant reduction of intestinal neutrophil infiltration as compared with wild-type mice treated with vehicle. Claudin-3 expression is reduced after I/R injury, relative to the respective sham-treated animals, and this effect is ameliorated by either genetic ablation or pharmacologic inhibition of MMP8. Inhibition of MMP8 decreases neutrophil infiltration in the intestine and lung and prevents intestinal damage, myeloperoxidase activity is reduced, overview
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malfunction
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juvenile MMP8 null mice have greater mortality and higher bacterial burden than wild-type mice. Leukocyte counts and cytokine concentrations in the peritoneal fluid are increased in the MMP8 null mice relative to the wild-type mice. Peritoneal macrophages from MMP8 null mice have reduced phagocytic capacity compared to wild-type macrophages. There is no quantitative difference in NET formation, but fewer bacteria are adherent to NETs from MMP8 null animals
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MMP-8 inactivates macrophage inflammatory protein-1alpha to reduce acute lung inflammation and injury in mice
physiological function
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MMP-8 is involved in the proteolytic cleavage of the tight junction protein occludin, resulting in its disappearance from the cell periphery and cleavage to a lower-sized 50-kDa protein in infected human brain microvascular endothelial cells
physiological function
aortic rings isolated from MMP8 -/- apoE -/- mice have less endothelial cell sprouting, and endothelial cells in MMP8 -/- apoE -/- mice have a lower ability to migrate into Matrigel plugs and less capacity of proliferation and angiogenesis. MMP8 -/- apoE -/- and MMP8 +/+- apoE -/- mice fed a Western diet for 12 have small lesion size and less endothelial cells within atherosclerotic lesions
physiological function
knockdown of MMP-8 in human umbilical vein endothelial cells with MMP-8 shRNA lentivirus results in a decrease in in vitro capillary-like network formation, cell proliferation and migration, and impairs its capacity of in vivo angiogenesis. Less nuclear accumulation of beta-catenin and lower beta-catenin target gene expression levels are observed in the HuVECs expressing lower levels of endogenous MMP-8. MMP8 is expressed in microvessels within human atherosclerotic plaques and aneurysm. Knockdown of endogenous MMP-8 down-regulates platelet/endothelial cell adhesion molecule PECAM-1 expression by converting less angiotensin I to II, which is an inducer for PECAM-1 gene expression
physiological function
MMP-8 is upregulated in LPS-stimulated BV2 microglial cells and primary cultured microglia, and treatment with MMP-8 inhibitor or MMP-8 short hairpin RNA suppresses proinflammatory molecules, particularly TNF-alpha secretion. Treatment with MMP-8 inhibitor inhibits TNF-alpha-converting enzyme activity more efficiently than TAPI-0, a general TNF-alpha converting enzyme inhibitor. It inhibits MAPK phosphorylation, NF-kappaB/AP-1 activity, and reactive oxygen species production
physiological function
MMP-8 is upregulated in septic conditions, particularly in microglia. Administration of MMP-8 inhibitor or MMP-8 short hairpin RNA significantly inhibits microglial activation and expression/secretion of TNF-alpha in brain tissue, serum, and cerebrospinal fluid of lipopolysaccharid-induced septic mice
physiological function
matrix metalloproteinase-8 augments bacterial clearance in a juvenile sepsis model. Developmental age influences the role of MMP8 in sepsis, mechanism by which MMP8 influences outcomes in sepsis, analysis of local cytokine response in juvenile wild-type and MMP8 null mice with peritoneal sepsis, overview
physiological function
MMP-8 is a collagen cleaving enzyme, produced by neutrophils and epithelial cells under inflammatory conditions, has been implicated in numerous tissue remodeling processes
physiological function
MMP-8 participates in cancer, arthritis, asthma, and failure of dental fillings
physiological function
neutrophil collagenase matrix metalloproteinase-8 (MMP8) belongs to the MMPs that have important roles in various inflammation-related disorders. MMP8 is a neuroinflammatory mediator in activated microglia by regulating TNF-alpha productivity. Pathogenetic role of MMP8
physiological function
role of matrix metalloproteinase-8 (MMP8) as a mediator of injury in intestinal ischemia and reperfusion. MMP8 is induced during intestinal injury
physiological function
role of salivary matrix metalloproteinase-8 (MMP-8) in chronic periodontitis diagnosis
physiological function
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role of matrix metalloproteinase-8 (MMP8) as a mediator of injury in intestinal ischemia and reperfusion. MMP8 is induced during intestinal injury
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physiological function
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MMP-8 is a collagen cleaving enzyme, produced by neutrophils and epithelial cells under inflammatory conditions, has been implicated in numerous tissue remodeling processes
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physiological function
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matrix metalloproteinase-8 augments bacterial clearance in a juvenile sepsis model. Developmental age influences the role of MMP8 in sepsis, mechanism by which MMP8 influences outcomes in sepsis, analysis of local cytokine response in juvenile wild-type and MMP8 null mice with peritoneal sepsis, overview
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MMP-8 differs from other MMPs in that it has an insertion that enlarges its active site
additional information
MMP-8 is critical for dexamethasone therapy in alkali-burned corneas under dry eye conditions. The anti-inflammatory effects of Dex are mediated through increased MMP-8 expression
additional information
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MMP-8 is critical for dexamethasone therapy in alkali-burned corneas under dry eye conditions. The anti-inflammatory effects of Dex are mediated through increased MMP-8 expression
additional information
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MMP-8 is critical for dexamethasone therapy in alkali-burned corneas under dry eye conditions. The anti-inflammatory effects of Dex are mediated through increased MMP-8 expression
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