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E412D
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site-directed mutagenesis
P574R
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the mutant is associated with a non-significant decreased risk of coronary artery disease when compared with the wild type genotype
R668Q
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the mutant is associated with a non-significant decreased risk of coronary artery disease when compared with the wild type genotype
E402H/H411E
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site-directed mutagenesis, proteolytic inactive MMP-9 mutant, application of the MMP-9 mutant decreases portal and periportal accumulation of collagen and inhibits fibrogenesis induced by CCl4 in mice
E402Q
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site-directed mutagenesis, proteolytic inactive MMP-9 mutant, application of the MMP-9 mutant decreases portal and periportal accumulation of collagen and inhibits fibrogenesis induced by CCl4 in mice, the MMP-9 mutant suppresses transdifferentiation of hepatic stellate cells to the myofibroblast-like phenotype in vitro and in vivo. Adenoviral application of the mutant leads to increased apoptosis of activated hepatic stellate cells
H401A
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site-directed mutagenesis, proteolytic inactive MMP-9 mutant, application of the MMP-9 mutant decreases portal and periportal accumulation of collagen and inhibits fibrogenesis induced by CCl4 in mice, the MMP-9 mutant suppresses transdifferentiation of hepatic stellate cells to the myofibroblast-like phenotype in vitro and in vivo. Adenoviral application of the mutant leads to increased apoptosis of activated hepatic stellate cells
E402H/H411E
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site-directed mutagenesis, proteolytic inactive MMP-9 mutant, application of the MMP-9 mutant decreases portal and periportal accumulation of collagen and inhibits fibrogenesis induced by CCl4 in mice
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E402Q
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site-directed mutagenesis, proteolytic inactive MMP-9 mutant, application of the MMP-9 mutant decreases portal and periportal accumulation of collagen and inhibits fibrogenesis induced by CCl4 in mice, the MMP-9 mutant suppresses transdifferentiation of hepatic stellate cells to the myofibroblast-like phenotype in vitro and in vivo. Adenoviral application of the mutant leads to increased apoptosis of activated hepatic stellate cells
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H401A
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site-directed mutagenesis, proteolytic inactive MMP-9 mutant, application of the MMP-9 mutant decreases portal and periportal accumulation of collagen and inhibits fibrogenesis induced by CCl4 in mice, the MMP-9 mutant suppresses transdifferentiation of hepatic stellate cells to the myofibroblast-like phenotype in vitro and in vivo. Adenoviral application of the mutant leads to increased apoptosis of activated hepatic stellate cells
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E402A
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no enzymic activity, competition with isolated collagen-binding domain and with matrix metalloproteinase MMP-2 binding to native and denatured type I collagen
E402A
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site-directed mutagenesis of the catalytic Glu402 results in an inactive enzyme
R279Q
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the mutant is associated with a non-significant decreased risk of coronary artery disease when compared with the wild type genotype
R279Q
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there is no relationship between R279Q polymorphism and atrial fibrillation hypertensive heart disease patients of Chinese Han population
additional information
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recombinant enzyme collagen-binding domain, competition with binding to gelatin of either enzyme mutant E402A or matrix metalloproteinase MMP-2 mutant E404A
additional information
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construction of proteolytically inactive truncated MMP-9 mutant: MMP-9DELTAHem, lacking the hemopexin domain, MMP-9DELTAOG, lacking the OG domain, and MMP-9DELTAOGHem, lacking both the hemopexin and the OG domain
additional information
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no difference in MMP-9 C-1562T polymorphism is observed between multiple sclerosis and healthy subjects, whereas (CA)n genotypes and alleles are associated with multiple sclerosis
additional information
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patients with bipolar mood disorder had significant preponderance of T allele versus C allele of 1562C/T polymorphism of the MMP-9 gene
additional information
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the -1562CNT polymorphism of MMP-9 gene is significantly associated with atrial fibrillation risk in Chinese Han patients with hypertensive heart disease
additional information
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the functional-1562C/T polymorphism is associated with schizophrenia
additional information
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variant genotypes -1562 CT/TT, 279 RQ/QQ, 574 PR/RR and 668 RQ/QQ have a 51% decreased risk of coronary artery disease
additional information
generation of the catalytically inactive mutant of zymogen proMMP-9, proMMP-9 MutE
additional information
in an islet culture model where human islet amyloid polypeptide transgenic mouse islets develop amyloid but nontransgenic islets do not, a broad spectrum MMP inhibitor (GM6001) and an MMP-2/9 inhibitor increases amyloid formation and the resultant beta-cell apoptosis
additional information
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in an islet culture model where human islet amyloid polypeptide transgenic mouse islets develop amyloid but nontransgenic islets do not, a broad spectrum MMP inhibitor (GM6001) and an MMP-2/9 inhibitor increases amyloid formation and the resultant beta-cell apoptosis
additional information
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enzyme-deficient MPP-9-/- mice show impaired neutrophil infiltration during zymosan peritonitis, overview
additional information
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MMP-9 deprived mice show impaired polymorphonuclear leukocyte infiltration at infalmmation sites, overview
additional information
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MMP-9 knockout mice show delayed inflammatory response and macrophage infiltration in gastritis
additional information
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MMP-9 mutants reduce type I collagen protein, TIMP-1, and MMP-2 expression in vivo, overview
additional information
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MMP-9-/- mice show reduced bacterial burdens in pulmonary and extrapulmonary tissues, less extensive histopathology predominated by neutrophils, and decreased morbidity and mortality compared to wild-type mice, MMP-9-/- mice are able to resolve infection with either the virulence-attenuated type B, live vaccine strain, or the highly virulent type A strain of Francisella tularensis, overview
additional information
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MMP-9-deficient mice show eliminated elastin breakdown in coronary artery in the Kawasaki disease
additional information
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generation of a mutant version lacking the O-glycosylated linker region and hemopexin domains and containing only the protease domain, residues 1-447
additional information
in an islet culture model where human islet amyloid polypeptide transgenic mouse islets develop amyloid but nontransgenic islets do not, a broad spectrum MMP inhibitor (GM6001) and an MMP-2/9 inhibitor increases amyloid formation and the resultant beta-cell apoptosis
additional information
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in an islet culture model where human islet amyloid polypeptide transgenic mouse islets develop amyloid but nontransgenic islets do not, a broad spectrum MMP inhibitor (GM6001) and an MMP-2/9 inhibitor increases amyloid formation and the resultant beta-cell apoptosis
additional information
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MMP-9 mutants reduce type I collagen protein, TIMP-1, and MMP-2 expression in vivo, overview
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additional information
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MMP-9 deprived mice show impaired polymorphonuclear leukocyte infiltration at infalmmation sites, overview
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additional information
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MMP-9 knockout mice show delayed inflammatory response and macrophage infiltration in gastritis
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additional information
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enzyme-deficient MPP-9-/- mice show impaired neutrophil infiltration during zymosan peritonitis, overview
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additional information
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in an islet culture model where human islet amyloid polypeptide transgenic mouse islets develop amyloid but nontransgenic islets do not, a broad spectrum MMP inhibitor (GM6001) and an MMP-2/9 inhibitor increases amyloid formation and the resultant beta-cell apoptosis
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additional information
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MMP-9-/- mice show reduced bacterial burdens in pulmonary and extrapulmonary tissues, less extensive histopathology predominated by neutrophils, and decreased morbidity and mortality compared to wild-type mice, MMP-9-/- mice are able to resolve infection with either the virulence-attenuated type B, live vaccine strain, or the highly virulent type A strain of Francisella tularensis, overview
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