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BRENDA support

Literature summary for 3.4.24.23 extracted from

  • Chen, P.; McGuire, J.K.; Hackman, R.C.; Kim, K.H.; Black, R.A.; Poindexter, K.; Yan, W.; Liu, P.; Chen, A.J.; Parks, W.C.; Madtes, D.K.
    Tissue inhibitor of metalloproteinase-1 moderates airway re-epithelialization by regulating matrilysin activity (2008), Am. J. Pathol., 172, 1256-1270.
    View publication on PubMedView publication on EuropePMC

Inhibitors

Inhibitors Comment Organism Structure
tissue inhibitor of metalloproteinase i.e. TIMP-1. TIMP-1 and matrilysin co-localize and co-immunoprecipitate in wounded primary airway epithelial cultures. TIMP-1-deficient cultures migrate faster, and epithelial cells spread to a greater extent compared with wild-type cultures. TIMP-1 also inhibits matrilysin-mediated cell migration and spreading in vitro. In vivo, TIMP-1 deficiency enhances airway re-epithelialization after naphthalene injury. TIMP-1 and matrilysin co-localize in airway epithelial cells adjacent to the wound edge Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus Q10738
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Source Tissue

Source Tissue Comment Organism Textmining
epithelial cell primary airway epithelial cell air-liquid interface culture. Tissue inhibitor of metalloproteinase TIMP-1 and matrilysin co-localize and co-immunoprecipitate in wounded primary airway epithelial cultures. TIMP-1-deficient cultures migrate faster, and epithelial cells spread to a greater extent compared with wild-type cultures. TIMP-1 also inhibits matrilysin-mediated cell migration and spreading in vitro. In vivo, TIMP-1 deficiency enhances airway re-epithelialization after naphthalene injury. TIMP-1 and matrilysin co-localize in airway epithelial cells adjacent to the wound edge Mus musculus
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