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Literature summary for 3.4.21.73 extracted from

  • Kenny, S.; Duval, C.; Sammut, S.J.; Steele, I.; Pritchard, D.M.; Atherton, J.C.; Argent, R.H.; Dimaline, R.; Dockray, G.J.; Varro, A.
    Increased expression of the urokinase plasminogen activator system by Helicobacter pylori in gastric epithelial cells (2008), Am. J. Physiol. Gastrointest. Liver Physiol., 295, G431-G441.
    View publication on PubMedView publication on EuropePMC
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Application

Application Comment Organism
medicine expression of uPA, its receptor, and of inhibitor PAI-1 is increased in response to Helicobacter pylori, and for uPA, but not the receptor or PAI-1, requires the virulence factor CagE. Helicobacter pylori also stimulates soluble and cell surface-bound uPA activity. It stimulates epithelial cell proliferation, which is inhibited by uPA immunoneutralization and uPA receptor knock-down. Expogenous uPA also stimulates proliferation that is further increased after PAI-1 knock-down Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
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Source Tissue

Source Tissue Comment Organism Textmining
epithelial cell gastric biopsy probes. uPA, uPA receptor and inhibitor PAI-1 are expressed in H+/K+ ATPase- and vesicular monoamine transporter 2-expressing cells. uPA is also expressed in pepsinogen- and uPA receptor-containing cells. In each case, expression is increased in response to Helicobacter pylori, and for uPA, but not the receptor or PAI-1, requires the virulence factor CagE. Helicobacter pylori also stimulates soluble and cell surface-bound uPA activity Homo sapiens
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