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Literature summary for 3.4.17.20 extracted from

  • Bruno, N.E.; Yano, Y.; Takei, Y.; Qin, L.; Suzuki, T.; Morser, J.; D'Alessandro-Gabazza, C.N.; Mizoguchi, A.; Suzuki, K.; Taguchi, O.; Gabazza, E.C.; Sumida, Y.
    Immune complex-mediated glomerulonephritis is ameliorated by thrombin-activatable fibrinolysis inhibitor deficiency (2008), Thromb. Haemost., 100, 90-100.
    View publication on PubMed
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Application

Application Comment Organism
medicine TAFI-mediated inhibition of plasmin generation plays a role in the pathogenesis of glomerulonephritis, and it might constitute a novel molecular target for therapy Mus musculus

Protein Variants

Protein Variants Comment Organism
additional information the development of immune complex-mediated glomerulonephritis in wild-type and TAFI-deficient mice is compared. After six weeks of treatment with horse spleen apoferritin and lipoplysaccharide to induce glomerulonephritis, mice deficient in TAFI have significantly better renal function as shown by lower concentrations of albumin in urine and blood urea nitrogen compared to wild-type mice. The activity of plasmin and matrix metalloproteinases is significantly increased, and mesangial matrix expansion and the deposition of collagen and fibrin in kidney tissues are significantly decreased in TAFI-knockout mice as compared to their wild-type counterparts Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus Q9JHH6
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Synonyms

Synonyms Comment Organism
TAFI
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 Mus musculus
thrombin-activatable fibrinolysis inhibitor
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 Mus musculus