Mouse Gene Set: BIOCARTA_FIBRINOLYSIS_PATHWAY

For the Human gene set with the same name, see BIOCARTA_FIBRINOLYSIS_PATHWAY

Standard name BIOCARTA_FIBRINOLYSIS_PATHWAY
Systematic name MM1398
Brief description Fibrinolysis Pathway
Full description or abstract Clot formation and fibrinolysis is a balance of plasmin activation/inhibition and thrombin-thrombomodulin activity that regulates fibrin polymer formation and degradation. Active thrombin is produced by the cleavage of prothrombin in the intrinsic thrombin activation pathway or the extrinsic thrombin activation pathway. Cleavage of fibrinogen by thrombin releases the fibrin monomers that auto-polymerize within seconds into fibrin threads or fibers. The coagulation cascade has many feedback loops. One example is the binding of thrombin to the fibrin polymers resulting in a reduction in soluble thrombin. The fibers form a more stable clot as a result of the covalent bonds formed by activated factor XIII enzyme (also known as Fibrin stabilizing factor). These fibers form a mesh the traps platelets, blood cells and plasma to form a clot. The removal of the clot is caused by plasmin cleavage of the fibrin monomers into soluble fibrin degradation products. Plasmin is formed by the cleavage of plasminogen between Arg561 and Val562. Plasmin is a two-chain trypsin-like serine protease. Plasminogen activator inhibitor 1 (PAI1) and plasminogen activator inhibitor 2 (PAI2) inhibit cleavage of plasminogen by tissue-type plasminogen activator (tPA) or urokinase plasminogen activator (uPA). The presence of fibrin fibers and fibrin degradation products exert a two-fold stimulation of tPA and uPA. Plasmin activity is also inhibited by alpha2-antiplasmin. Thrombin activatable fibrinolysis inhibitor (TAFI) is a carboxy-peptidase B-like proenzyme activated by the thrombin-thrombomodulin dimer. TAFI cleaves (DD)E2 to separate DD and E fragments which do not enhance the activation of tPA or uPA and results in a reduced feedback signal. Disease Significance: Overabundance or increased activity of the plamsminogen activator inhibitors or reduced presence or function of tPA or uPA can result in atherosclerotic disease and venous thrombosis due to an increase in fibrin deposition or formation of a thrombus. Thrombosis can also result from plasminogen deficiency caused by a lack of protein or lack of functional protein. Reduced or depleted levels of alpha2-antiplamin can result in severe bleeding disorders.
Collection M2: Curated
      CP: Canonical Pathways
            CP:BIOCARTA: BioCarta Pathways
Source publication  
Exact source  
Related gene sets  
External links https://data.broadinstitute.org/gsea-msigdb/msigdb/biocarta/mouse/m_fibrinolysisPathway...
Filtered by similarity ?
Source species Mus musculus
Contributed by BioCarta
Source platform or
identifier namespace
MOUSE_SEQ_ACCESSION
Dataset references  
Download gene set format: grp | gmt | xml | json | TSV metadata
Compute overlaps ? (show collections to investigate for overlap with this gene set)
Compendia expression profiles ? NG-CHM interactive heatmaps
(Please note that clustering takes a few seconds)
Mouse Transcriptomic BodyMap compendium

Legacy heatmaps (PNG)
Mouse Transcriptomic BodyMap compendium
Advanced query Further investigate these 11 genes
Show members (show 11 source identifiers mapped to 11 genes)
Version history 2022.1.Mm: First Introduced.

See MSigDB license terms here. Please note that certain gene sets have special access terms.