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
-
invasiveness
- plasminogen
-
basement
- synovial
- chondrocytes
- gingival
-
articular
-
transwell
- mt1-mmp
- aortic
- aneurysm
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collagenolytic
- aggrecan
- matrigel
- atherosclerotic
- stromelysins
-
signal-regulated
- erk
-
crevicular
- doxycycline
-
gelatinolytic
-
matrix-degrading
-
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
3.4.24.34 neutrophil collagenaseAdvanced search results
results (
results (Engineering
Engineering on EC 3.4.24.34 - neutrophil collagenase
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
E198A
N188G
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25% decrease in collagen cleavage, 30% decrease in cleavage of (7-methoxycoumarin-4-yl)acetyl-Pro-Leu-Gly-Leu-[3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl]-Ala-Arg-NH2
Y189F
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88% of wild-type activity with (7-methoxycoumarin-4-yl)acetyl-Pro-Leu-Gly-Leu-[3-(2,4-dinitrophenyl)-L-2,3-diaminopropionyl]-Ala-Arg-NH2. Activity against type I collagen dripps 3fold compared with wild-type enzyme
additional information
E198A
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mutant enzyme is not activated by 4-aminophenylmercuric acetate, no collagen cleavage activity
additional information
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genotyping and identification of the MMP8 single nucleotide polymorphism rs11225395, located 0.8 kB 5' of the transcription start site
additional information
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construction of MMP-8 knockout mice by gene targeting, MMP-8-deficient female mice develop tongue squamous cell carcinoma at a significantly higher incidence than wild-type mice exposed to carcinogen 4-nitroquinoline-N-oxide, overview
additional information
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MMP8-/- mice, of a mixed C57BL/6J/129 background, deficient in collagenase-2/MMP-8 are more susceptible to develop skin cancer compared to wild-type mice, mutant mice show a significant delay in wound closure and an altered inflammatory response in their wounds, with a delay of neutrophil infiltration during the first days and a persistent inflammation at later time points, alterations in the TGF-beta1 signaling pathway and by an apoptosis defect in MMP8-/- mice, phenotype, overview
additional information
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polymorphonuclear cell infiltration towards lipopolysaccharides is abrogated in MMP-8-null mice
additional information
construction of MMP8-null mice, phenotype of I/R injury mice and non-ischemic mice. Genetic ablation of MMP8 preserves claudin-3 expression
additional information
generation of MMP-8 knockout mutant mice. In contrast to septic adult mice, genetic ablation of MMP8 increases mortality following bacterial peritonitis in juvenile mice. This increase in mortality is associated with rexadduced bacterial clearance and reduced NET efficiency. Juvenile MMP8 null mice have greater mortality and higher bacterial burden than wild-type mice. Genetic ablation of MMP8 in juvenile mice increases mortality following sepsis from polymicrobial peritonitis
additional information
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generation of MMP-8 knockout mutant mice. In contrast to septic adult mice, genetic ablation of MMP8 increases mortality following bacterial peritonitis in juvenile mice. This increase in mortality is associated with rexadduced bacterial clearance and reduced NET efficiency. Juvenile MMP8 null mice have greater mortality and higher bacterial burden than wild-type mice. Genetic ablation of MMP8 in juvenile mice increases mortality following sepsis from polymicrobial peritonitis
additional information
topical dexamethasone (Dex)-treated MMP-8 knockout mice in the corneal alkali burn murine model show reduced corneal clarity, increased expression of inflammatory mediators (IL-6, CXCL1, and MMP-1 mRNA) and increased neutrophil infiltration at 2D and 5D compared to Dex-treated wild-type mice. The accumulation of neutrophils is reduced in wounded corneas of MMP-8 knockout mice subjected to the corneal alkali burn murine (CM) model
additional information
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topical dexamethasone (Dex)-treated MMP-8 knockout mice in the corneal alkali burn murine model show reduced corneal clarity, increased expression of inflammatory mediators (IL-6, CXCL1, and MMP-1 mRNA) and increased neutrophil infiltration at 2D and 5D compared to Dex-treated wild-type mice. The accumulation of neutrophils is reduced in wounded corneas of MMP-8 knockout mice subjected to the corneal alkali burn murine (CM) model
additional information
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MMP8-/- mice, of a mixed C57BL/6J/129 background, deficient in collagenase-2/MMP-8 are more susceptible to develop skin cancer compared to wild-type mice, mutant mice show a significant delay in wound closure and an altered inflammatory response in their wounds, with a delay of neutrophil infiltration during the first days and a persistent inflammation at later time points, alterations in the TGF-beta1 signaling pathway and by an apoptosis defect in MMP8-/- mice, phenotype, overview
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additional information
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construction of MMP8-null mice, phenotype of I/R injury mice and non-ischemic mice. Genetic ablation of MMP8 preserves claudin-3 expression
-
additional information
-
topical dexamethasone (Dex)-treated MMP-8 knockout mice in the corneal alkali burn murine model show reduced corneal clarity, increased expression of inflammatory mediators (IL-6, CXCL1, and MMP-1 mRNA) and increased neutrophil infiltration at 2D and 5D compared to Dex-treated wild-type mice. The accumulation of neutrophils is reduced in wounded corneas of MMP-8 knockout mice subjected to the corneal alkali burn murine (CM) model
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additional information
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generation of MMP-8 knockout mutant mice. In contrast to septic adult mice, genetic ablation of MMP8 increases mortality following bacterial peritonitis in juvenile mice. This increase in mortality is associated with rexadduced bacterial clearance and reduced NET efficiency. Juvenile MMP8 null mice have greater mortality and higher bacterial burden than wild-type mice. Genetic ablation of MMP8 in juvenile mice increases mortality following sepsis from polymicrobial peritonitis
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