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3.4.24.35: gelatinase B

This is an abbreviated version!
For detailed information about gelatinase B, go to the full flat file.

Word Map on EC 3.4.24.35

Reaction

Cleavage of gelatin types I and V and collagen types IV and V =

Synonyms

92 kDa gelatinase, 92 kDa type IV collagenase, 92 kDa type IV collagenase proMMP-9, 92-kDa Gelatinase, 92-kDa gelatinase B, 92-kDa Type IV collagenase, 95 kDa type IV collagenase/gelatinase, Collagenase IV, Collagenase type IV, gelatinase, gelatinase B, Gelatinase MMP 9, gelatinolytic enzyme, GELB, Macrophage gelatinase, matrix metallopeptidase 9, matrix metallopeptidase 9 gelatinase B, matrix metalloprotease-9, Matrix metalloproteinase 9, matrix metalloproteinase-9, metrix metalloproteinase-9, MMP 9, MMP-9, MMP9, neutrophil collagenase, pro-matrix metalloproteinase-9, progelatinase, Type IV collagen metalloproteinase, Type IV collagenase, Type IV collagenase/gelatinase, Type V collagenase

ECTree

     3 Hydrolases
         3.4 Acting on peptide bonds (peptidases)
             3.4.24 Metalloendopeptidases
                3.4.24.35 gelatinase B

Expression

Expression on EC 3.4.24.35 - gelatinase B

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EXPRESSION
ORGANISM
UNIPROT
LITERATURE
0.025 mM panduratin A markedly down-regulates MMP-9 expression
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0.025-0.1 mM 6-hydroxydopamine and 0.05-0.5 mM 1-methyl-4-phenylpyridinium ion increase MMP-9 gene expression in a dose-dependent manner by inducing nuclear factor-kappaB and AP-1 binding to the MMP-9 promoter, N-acetylcysteine suppresses both 6-hydroxydopamine- and 1-methyl-4-phenylpyridinium ion-induced MMP-9 promoter activities, LY294002, suppresses 6-hydroxydopamine- and 1-methyl-4-phenylpyridinium ion-induced MMP-9 promoter activities, whereas SB203580 inhibits 6-hydroxydopamine-, but not 1-methyl-4-phenylpyridinium ion-induced promoter activity, neither PD98059 nor SP600125 influence 6-hydroxydopamine or 1-methyl-4-phenylpyridinium ion-induced MMP-9 promoter activity
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10 ng/ml transforming growth factor-beta1 and 10 ng/ml transforming growth factor-beta2 enhance the secretion of matrix metalloproteinase-9 in PC-3 cells 5.4fold and 4.3fold, respectively
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10 nM 12-O-tetradecanoyl phorbol-13-acetate induces MMP-9 expression (9728.9% of the control) after 24 h by the suppression of the Raf/MEK/ERK pathway in MCF-7 human breast cancer cells, 12-O-tetradecanoyl phorbol-13-acetate-induced MMP-9 expression is significantly inhibited by UO126, but not by SP600125 and SB203580
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10% (v/v) Porphyromonas gingivalis supernatant induces about 2.5fold increased MMP-9 expression in human oral epidermoid cells
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12-O-tetradecanoyl phorbol-13-acetate-induced MMP-9 expression is decreased by 324.8% by 0.1 mM silibinin
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20 mg doxycycline decreases MMP-9 levels after 1 month, 20 mg doxycycline decreases endometrial MMP-9 at 1 and 6 months compared to baseline
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50 mg/kg (-)-epigallocatechin gallate administration significantly inhibits the induction of the active form of MMP-9
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a significant increase in MMP-9 is observed in pulmonary tuberculosis patients as compared to healthy controls
-
A3 receptor stimulation induces an increase of MMP-9 protein levels in cellular extracts of U87MG cells by phosphorylation of extracellular signal-regulated protein kinases, c-Jun N-terminal kinase/stress-activated protein kinase, protein kinase B, and activator protein 1. A3 receptor activation stimulates also an increase of extracellular MMP-9 in the supernatants from U87MG glioblastoma cells
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acrolein exposure induces MMP-9 expression at both protein and mRNA levels in the lung tissue
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activation of phosphatidylinositol 3-kinase is required for tumor necrosis factor-alpha-induced upregulation of matrix metalloproteinase-9. Red wine extrac and quercetin inhibit significantly the tumor necrosis factor-alpha-induced upregulation of MMP-9 whereas resveratrol does not have significant inhibitory effects
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activation of the nitric oxide-cyclic guanosine 3’,5’-monophosphate pathway with nitrite or sildenafil, but not with BAY 41-2272, increases MMP-9 levels, lung microembolization is associated with significant increases in pro-MMP-9 levels
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active treatment with uric acid (0.5 or 1.0 mg) is associated with reduced levels of active MMP-9 at the end of infusion
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after 24 h incubation, 0.05 mg/ml aspirin inhibits MMP-9 mRNA expression by 50%. MMP-9 mRNA expression and release are inhibited by fenofibrate (0.1 mM) and 15d-prostaglandin J2 (0.005 mM)
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aqueous extract isolated from Prunella vulgaris suppresses 12-phorbol 13-myristate acetate-enhanced expression of MMP-9 protein, mRNA and transcription activity levels through suppression of nuclear factor-kappaB activation
auto-amplified NFATc1 plays a key role in upregulating MMP-9
berberine inhibits the expression of MMP-9 at both the mRNA and protein levels in a dose-dependent manner (0.005-0.05 mM) by suppressing the activation of p38 pathway in phorbol 12-myristate 13-acetate-induced macrophages
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Borrelia burgdorferi induces the host protease, matrix metalloproteinase 9, the induction of MMP-9 may allow the organism to disseminate and produce local tissue destruction
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C-reactive protein increases the expression and activity of MMP-9 in a dose-dependent manner in human THP-1 cells
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circulating MMP-9 concentrations are higher in patients with abdominal aortic aneurysm than those in subjects without abdominal aortic aneurysm
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diet-induced long-term weight loss decreases MMP-9
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Dz13 upregulates the matrix metalloproteinase-9 in cultured tumor cells
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elevated plasma levels of MMP-9 are correlated with brain levels within 24 h of acute cerebral ischemia in rats
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epidermal growth factor contributes to prostate cancer metastasis through stimulating MMP-9 secretion from prostate cancer cells
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ethanol extracts of Ocimum sanctum suppresses MMP-9 enzymatic activity in Lewis lung carcinoma cells in a dose-dependent manner (0.025-0.2 mg/ml)
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exposure of KB cells to Porphyromonas gingivalis supernatant (10% v/v) up-regulates the expression of MMP-9 protein and gene, the JNK inhibitor SP600125 (0.02 mM) significantly attenuates MMP-9 gene expression in KB cells in response to Porphyromonas gingivalis supernatant. JNK and AP-1 are the major signaling for Porphyromonas gingivalis supernatant-stimulated MMP-9 expression in KB cells
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expression of MMP9 protein and mRNA increases in rat brain tissue after cardiopulmonary resuscitation
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F(ab')2 fragments or stimulation with lipopolysaccharide have no effect on MMP-9 production
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heregulin-beta1 stimulates MMP-9 secretion and activation via a transcriptional regulation in human breast cancer cells
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higher plasma MMP-9 concentrations are found in periodontal disease patients compared with healthy controls
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homocysteine increases mRNA expression of MMP-9
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immune cell secretion of MMP-9 decreases by 58% after 3 months of omega-3 fatty acid supplementation when compared with baseline levels in patients with relapsing-remitting multiple sclerosis
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in sections of ectopic tumors treated with Dz13, MMP-9 is downregulated
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in the extract from the small intestine 24 h after indomethacin administration, the MMP-9 activation is significantly attenuated by 10 mg/kg 2-[4-(5-fluoro-3-methylbenzo[b]thiophen-2-yl)sulfonamido-3-methanesulfonylphenyl] thiazole-4-carboxylic acid
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in the human vascular endothelium, simvastatin and atorvastatin (0.0001-0.01 mM) reduce MMP-9 expression and activity
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in vivo administration of a nuclear factor-kappa B inhibitory peptide blocks the expression of MMP-9 in dystrophic muscle of mdx mice
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induction of MMP-9 expression and activity is significantly inhibited by 0.001 mM of the specific cPLA2alpha inhibitor
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interferon-gamma suppresses MMP-9 expression
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interleukin 1beta, interleukin-6, and tumor necrosis factor -alpha stimulate MMP-9 expression
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ischemia and reperfusion induce an upregulation of MMP-9 in the ischemic hemispheric microvessels
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islet MMP-9 mRNA levels are decreased in type 2 diabetic subjects
leucine-zipper and sterile-alpha motif kinase reduces MMP-9 activity by increasing TIMP-1/2 expression in H9c2 cardiomyoblast cells
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levels of MMP-9 in choriodecidua and amnion increases 4 and 8fold, respectively, after simultaneous infection with Escherichia coli added to either the amniotic or the choriodecidual face or to both
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levonorgestrel subcutaneous implant increases serum MMP-9 levels after 1 month
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low-energy laser irradiation (wavelength of 810 nm with continuous waves at 100 mW output power) facilitates MMP-9 expression in rats 7 days after treatment
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matrix metalloproteinase-9 is significantly increased after 8 weeks of very low energy diet-induced weight loss
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mild nonischemic cerebral venous hypertension results in increased MMP-9 activity. MMP-9 activity increases 10fold 1 day after surgery, gradually decreases afterwards, and returns to baseline 2 weeks after surgery
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MMP-9 activity is increased in fibroblasts when the cells are in contact with fibronectin and laminin, while in myoblasts, enhanced activity of the secreted enzyme occurs only in presence of collagen
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MMP-9 activity is significantly increased to 5.0 and 6.1times of the normal intestinal value 12 and 24 h after indomethacin administration, respectively
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MMP-9 expression and activity significantly increase on day 3 after status epilepticus after pilocarpine injection
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MMP-9 expression in the retinal ganglion cell layer significantly increases in the endothelin-1-induced chronic optic nerve ischemia model
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MMP-9 is markedly increased in both the bronchoalveolar lavage fluid and in the lung parenchyma of bleomycin-treated rats, especially in the early phase with the peak on the 4th day
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MMP-9 is moderately induced by Fusobacterium nucleatum and considerably induced by phorbol 12-myristate-13-acetate in gingival epithelial cells, MMP-9 mRNA up-regulation occurs at 3 h, whereas MMP-9 secretion and activity in cell-free supernatants occurs at 12 h
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MMP-9 is significantly increased in the infarcted tissue compared to the contralateral hemisphere after ischemic stroke
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MMP-9 is upregulated during inflammatory bowel disease, MMP-9 activity is highly upregulated in wild type mice treated with dextran sodium sulfate, Salmonella typhimurium, or trinitrobenzene sulfonic acid
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MMP-9 mRNA expression and release are induced by 0.002 mM prostaglandin E2
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MMP-9 mRNA expression and release is significantly decreased after treatment with 0.0125-0.05 mg/ml aspirin for 24 h. The aspirin-induced down-regulation of MMP-9 mRNA expression and reduction of MMP-9 release are notably alleviated after pretreatment with specific inhibitors of peroxisome proliferator-activated receptor alpha/gamma
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MMP-9 mRNA expression is induced by interleukin 17, at 200 ng/ml the mRNA level increases about 17times compared with the untreated group
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MMP-9 protein activity is decreased in the media samples of cells from large-healthy follicles compared with those from medium-healthy follicles
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MMP-9 protein activity is detected as early as 2 h after the focal ischemic insult (focal cerebral ischemia by photothrombosis), it rapidly increases at 6 h after ischemia, and reaches a maximum level 48 h after the ischemic event. Thereafter, the MMP-9 level abruptly decreases and returns to the baseline at 72 h after the insult
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MMP-9 protein and mRNA levels are decreased up to 43% after treatment with 0.025 mM panduratin A
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MMP-9 secretion is CnA-isoform specific, i.e. the CnAbeta isoform contributes to the CsA-induced upregulation of MMP-9 while the CnAalpha does not
monomeric alpha-synuclein dose-dependently increases MMP-9 activity as well as mRNA level from cultured rat primary astrocytes and microglial cells (about 3fold stimulation at 200 nM). Same concentration of alpha-synuclein aggregates do not induce MMP-9 activity
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Mycobacterium tuberculosis stimulates matrix metalloproteinases secretion in the host
myricetin, i.e. 3,3',4',5,5',7-hexahydroxyflavone, suppresses UVB-induced MMP-9 expression through the suppression of Raf kinase activity
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N-2-(4-bromophenyl) ethyl caffeamide inhibits MMP-9 production through the nuclear-targeted down-regulation of nuclear factor-kappaB signaling in human monocytic cells
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no significant difference is observed in the levels of MMP-9 in culture filtrate antigen and live Mycobacterium tuberculosis-stimulated as well as unstimulated cultures of both healthy controls and pulmonary tuberculosis patients
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non-surgical periodontal therapy decreases blood plasma MMP-9 concentration by 39%
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norcantharidin downregulates MMP-9 mRNA and protein expression by inhibiting Sp1 transcriptional activity in colorectal cancer cells, norcantharidin at 0.1 mM completely abolishes the expression of MMP-9 mRNA at 48 h
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normobaric hyperoxia inhibits MMP-9-mediated occludin degradation in the ischemic hemispheric microvessels
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nuclear factor-kappaB is a key transcription factor for the production of MMP-9, tumor necrosis factor-alpha induces expression of MMP-9 at both mRNA and protein levels, tumor necrosis factor-alpha-induced expression of MMP-9 is completely blocked by N-2-(4-bromophenyl) ethyl caffeamide in a concentration-dependent (0.001-0.02 mM) manner
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obese individuals show increased activity of MMP-9/LCN2 complex, while a positive correlation between MMP-9 activity and body mass index is observed
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orthodontic pressure induces gene transcription MMP-9 in pressure gingival soft tissue
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overexpression of reversion-inducing cysteine-rich protein with Kazal motifs in HT-1080 cells decreases MMP-9 mRNA levels, reversion-inducing cysteine-rich protein with Kazal motifs-mediated suppression of MMP-9 promoter activity requires 12-O-tetradecanoylphorbol-13-acetate-responsive element and KB sites
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penta-O-galloyl-beta-D-glucose inhibits epidermal growth factor-induced MMP-9 expression in a dose- and time-dependent manner by reducing the MMP-9 transcriptional activity
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peroxisome proliferators-activated receptor gamma antagonist GW9662 has little effect on MMP-9 expression
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polyclonal immunoglobulins (IVIg) induce expression of MMP-9 in microglia
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propranolol significantly reduces MMP-9 secretion upon treatment with phorbol 12-myristate 13-acetate which is correlated with a decrease in MMP-9 gene expression
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pterostilbene (i.e. trans-3,5-dimethoxy-4'-hydroxystilbene) down-regulates matrix metalloproteinase-9 activity and inhibits protein and mRNA expression of MMP-9 driven by heregulin-beta1
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resveratrol (i.e. trans-3,4',5-trihydroxystilbene) inhibits MMP-9 mRNA and protein expression in a concentration-dependent manner (0.0025-0.01 mM) by up-regulating peroxisome proliferators-activated receptor alpha expression, The effect of resveratrol on MMp-9 can be offset partially by MK886
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serum MMP-9 concentrations are significantly higher in patients with non-herpetic acute limbic encephalitis in acute and convalescent stages than in control patients
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significant increases of MMP9 activity and protein expression are detected in B19-VP1u IgG group, phosphatidylinositol 3-phosphate kinase and phosphorylated extracellular signal-regulated kinase proteins are involved in the induction of MMP9
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silibinin suppresses 12-O-tetradecanoyl phorbol-13-acetate-induced MMP-9 expression through inhibition of COX-2 (106% decrease of expression at 0.2 mM silibinin), 12-O-tetradecanoyl phorbol-13-acetate-induced MMP-9 expression is inhibited by celecoxib in a dose-dependent fashion, 12-O-tetradecanoyl phorbol-13-acetate-induced MMP-9 expression is decreased by UO126
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Skp2 overexpression increases the expression of MMP-9, Sp1 is involved in the induction of MMP-9 by Skp2
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superparamagnetic iron oxide nanoparticle-mmp9 retention in global cerebral ischemia animals shows that striatal mmp-9 mRNA expression is 2fold greater than that of the control group and the elevation in cortical mmp-9 mRNA is less than 2fold in live brains, global cerebral ischemia in mice induces MMP-9 activity in regions with hyperintense diffusion-weighted imaging
tear MMP-9 activity is significantly higher in patients with dysfunctional tear syndrome, this activity is associated with increased mRNA expression of MMP-9
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the antihemorrhagic effect of PJ34, a potent PARP inhibitor, is associated with a 57% decrease in MMP-9 overexpression, glucocorticoid increases TIMP-1 in the brain endothelial cell line cEND to reduce the levels of MMP-9
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the broad-spectrum matrix metalloproteinase inhibitor doxycycline reduces pulmonary expression of active MMP-9
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the early increase in MMP-9 blood plasma activity in patients with acute coronary syndrome is related to MMPs activation in the unstable atherosclerotic plaque
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the enzyme expression is induced in chick embryonic tibias cultured with lipopolysaccharide
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the ethanolic extract from Kaempferia pandurata significantly decreases MMP-9 expression at both protein and mRNA levels in a dose-dependent manner(0.002-0.01 mg/ml). Treatment of ethanolic Kaempferia pandurata extract at 0.002, 0.005 and 0.01 mg/ml shows decreases in MMP-9 mRNA levels up to 10%, 13%, and 45%, respectively. Kaempferia pandurata interfers Porphyromonas gingivalis supernatant-induced MMP-9 expression in the oral epidermoid cell line ATCC CCL-17
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the expression of MMP-9 in neoplastic and inflammatory cells increases with more advance tumor stage, depth of tumor invasion and presence of lymph node as well as distant metastases
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the expression of MMP-9 is elevated after cerebral ischemia, expression of MMP-9 increases after permanent middle cerebral artery occlusion and transient middle cerebral artery occlusion. interleukin-1beta, tissue necrosis factor-alpha, fibroblast growth facor, and epidermal growth factor can stimulate the secretion of MMP-9
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the gelatinolytic activity of MMP-9 is constitutively activated in Lewis lung carcinoma cells
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the inability of iNOS-deficient mice to generate iNOS-derived nitric oxide profoundly inhibits MMP-9 activity in livers after ischemia/reperfusion injury, exposure of isolated murine neutrophils and macrophages to exogenous nitric oxide increases MMP-9 activity in both cell types, nitric oxide may activate MMP-9 in leukocytes by either autocrine or paracrine mechanisms
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the interleukin-1beta-induced MMP-9 gene expression is mediated through the activation of p42/p44 mitogen-activated protein kinase, p38 mitogen-activated protein kinase, and JNK1/2 in A-549 cells. The interleukin-1beta-induced MMP-9 gene expression is also mediated through the translocation of NF-kappaB (p65) into the nucleus and the degradation of IkappaBalpha
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the intracerebroventricular injection of amyloid beta25-35, amyloid beta1-40, and amyloid beta1-42, but not amyloid beta40-1, transiently increases MMP-9 activity and protein expression in the hippocampus, the expression of MMP-9 is increased in both neurons and glial cells in the hippocampus after amyloid beta treatment
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the level of MMP-9 expression was significantly increased by 4945% and 4412% of the control level following treatment with 20 nM 12-O-tetradecanoyl phorbol-13-acetate in breast cancer cells
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the levels of MMP-9 and reactive oxygen species in the gut of rats with severe acute pancreatitis are significantly higher than those of the rats treated with anti-rat polymorphonuclear neutrophil granulocytes serum or BB-94
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the levels of MMP-9 are increased in the brain and in the peripheral organs after induction of experimental autoimmune encephalomyelitis. After 40 days all the animals recover and do not show signs of experimental autoimmune encephalomyelitis. The absence of MMP-9 in the remission phase suggests a protective role of MMP-9 in the late phase of the disease, because single mmp-9-/- mice present a delayed remission in comparison with wild-type animals suggesting a phase-dependent role of MMP-9 in the disease. MMP-9 levels remain increased in the brains and, to a higher extend, in the spleens of the wild-type mice even during the remission phase, which is in line with the role of MMP-9 as a useful marker and a protective factor for experimental autoimmune encephalomyelitis in the remission phase
the mRNA levels of MMP-9 are significantly higher in diaphragm muscle from 3-, 6- and 8-week-old mdx mice compared with age-matched C57BL/10 control mice
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the mRNA of MMP9 in the granulosa cells is induced by TGFB1 but not follicle-stimulating hormone, luteinizing hormone, progesterone, or estrogen. Luciferase reporter and mutagenesis analysis indicate the AP1 and NFkappaB elements located in the promoter region from -1700 to -2400 bp are critical for both basal and TGFB1-induced MMP9 transcription
the serum MMP-9 level is significantly higher in moyamoya disease than in healthy controls
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there are significant increases in MMP-9 protein expression and enzyme activity 7 h after thermal injury
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there is a highly significant relationship between the expression of MMP-9 and macrophage count in eosinophilic granulomas
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there is an increase in the active form of MMP-9 after ischemia
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there is no difference in expression of MMP-9 for any follicle size or health status class
-
there is no MMP-9 mRNA elevation in mononuclear cells
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there is significant reduction in MMP-9 expression on day 7 in all cases, it decreases considerably on day 14 and is almost negligible on day 21 reflecting corneal healing with succinylated collagen bandage lenses
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thrombin stimulation induces MMP-9 secretion of monocytes dose- and time-dependently through activation of extracellular signaling-regulated protein kinase 1/2 and p38. Thrombin up-regulates mRNA and protein levels of MMP-9. NFkappaB activation is necessary for thrombin-induced MMP-9 upregulation in human monocytes. 1,2-bis (aminophenoxy) ethane-N,N,N',N'-tetraacetoxymethyl ester, a Ca2+ chelator, abolishes the thrombin-induced MMP-9 secretion
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total Panax notoginsenosides downregulate expression of MMP-9 apolipoprotein E-knockout mice
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treatment with 0.05 mM glycitein downregulates MMP-9 gene expression and inhibits the phorbol myristate acetate-induced MMP-9 secretion in U87MGcells
-
TX-1877 significantly inhibits expression of MMP-9
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vitamin D3 significantly reduces the MMP-9 level in antigen stimulated and unstimulated cultures of pulmonary tuberculosis as compared to healthy controls
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