3.4.21.5: thrombin
This is an abbreviated version!
For detailed information about thrombin, go to the full flat file.
Word Map on EC 3.4.21.5
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3.4.21.5
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platelet
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anticoagulant
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heparin
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thrombosis
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bleeding
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endothelial
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artery
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thromboplastin
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collagen
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agonist
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thromboembolism
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coronary
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procoagulant
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adp
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antithrombotic
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venous
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fibrinolysis
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thrombus
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hemorrhage
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hemostatic
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hirudin
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plasminogen
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antiplatelet
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thrombomodulin
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protease-activated
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arachidonic
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plasmin
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thromboxane
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intravascular
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viii
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d-dimers
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atrial
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thrombocytopenia
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aspirin
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aptamer
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hypercoagulability
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willebrand
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warfarin
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percutaneous
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p-selectin
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rivaroxaban
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platelet-rich
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unfractionated
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coagulopathy
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prothrombotic
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embolism
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haemostasis
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diagnostics
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analysis
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hemophilia
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biotechnology
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thrombolytic
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nutrition
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synthesis
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clopidogrel
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medicine
- 3.4.21.5
- platelet
-
anticoagulant
- heparin
- thrombosis
- bleeding
- endothelial
- artery
- thromboplastin
- collagen
- agonist
- thromboembolism
- coronary
-
procoagulant
- adp
-
antithrombotic
- venous
-
fibrinolysis
- thrombus
- hemorrhage
-
hemostatic
- hirudin
- plasminogen
-
antiplatelet
- thrombomodulin
-
protease-activated
-
arachidonic
- plasmin
-
thromboxane
-
intravascular
- viii
-
d-dimers
- atrial
- thrombocytopenia
- aspirin
- aptamer
- hypercoagulability
- willebrand
- warfarin
-
percutaneous
-
p-selectin
- rivaroxaban
-
platelet-rich
-
unfractionated
- coagulopathy
-
prothrombotic
- embolism
-
haemostasis
- diagnostics
- analysis
- hemophilia
- biotechnology
-
thrombolytic
- nutrition
- synthesis
- clopidogrel
- medicine
Reaction
selective cleavage of Arg-/-Gly bonds in fibrinogen to form fibrin and release fibrinopeptides A and B =
Synonyms
activated factor II, alpha-thrombin, alphaTh, beta-thrombin, blood-coagulation factor II, activated, blood-coagulation factor IIa, clotting factor IIa, EC 3.4.4.13, factor IIa, fibrinogenase, thrombase, thrombin, E, thrombin-C, thrombofort, TLE2, topical, tropostasin
ECTree
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Source Tissue
Source Tissue on EC 3.4.21.5 - thrombin
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sections from Alzheimer's disease brains show reactivity to thrombin antibody in blood vessel walls but not in vessels from controls
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high levels of thrombin are detected in cerebrospinal fluid obtained from Alzheimer's disease but not control patients
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thrombin induces a phosphoinositide 3-kinase-Akt pathway-dependent acquisition of dermal-sheath-like properties by dermal papilla cells in vitro, involving increased proliferation rate, acquisition of myofibroblastic contractile properties and a decreased capacity to sustain growth and survival of keratinocytes. The thrombin inhibitor protease nexin 1 regulates all those effects in vitro. Control of thrombin signaling interferes with hair follicle dermal cells plasticity to regulate their function
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both thrombin and thrombin receptor agonist peptide enhance the permeability barrier of cells, both exhibit a potent barrier protective effect when cells are treated with inactive mutant S195A of protein C prior to stimulation. Thrombin exhibits a potent cytoprotective activity in the lipopolysaccharide-induced permeability and tumor necrosis factor alpha-induced apoptosis and adhesion assays in the protein C mutant S195A treated cells. Treatment with the cholesterol depleting molecule methyl-beta-cyclodextrin eliminates the protective effect
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both thrombin and thrombin receptor agonist peptides initiate proinflammatory responses in cells. The occupancy of endothelial protein C receptor by the inactive protein C mutant S195A switches the receptor PAR-1-dependent signaling specificity of thrombin leading to thrombin inhibition of the expression of cell surface adhesion molecules CCAM-I, ICAM-I and E-selectin as well as the binding of neutrophils to tumor necrosis factor alpha-activated endothelial cells. Both thrombin and thrombin receptor agonist peptides activate Rac I and inhibit the activation of RhoA and nuclear factor kappaB pathways in response to tumor necrosis factor alpha in cells pretreated with protein C mutant S195A
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thrombin is highly expressed in microvessels from Alzheimer's disease brains but is not detectable in control vessels
additional information
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701289, 707386, 707408, 707941, 707944, 707945, 708154, 708178, 708274, 708363, 709161, 709693, 710224, 710610, 710634, 717955
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exogenous oxidative stress, thrombin activation, progression of ageing and type 2 diabetes lead to protein carbonyls formation in platelets, and this modification can be attenuated by antioxidant enzymes
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exogenous oxidative stress, thrombin activation, progression of ageing and type 2 diabetes lead to protein carbonyls formation in platelets, and this modification can be attenuated by antioxidant enzymes
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exogenous oxidative stress, thrombin activation, progression of ageing and type 2 diabetes lead to protein carbonyls formation in platelets, and this modification can be attenuated by antioxidant enzymes
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brain endothelial cells can synthesize thrombin and thus be a source of this neurotoxin in Alzheimer's disease brains
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650344, 652054, 652062, 652618, 652872, 653290, 653969, 653978, 699865, 717199, 717496, 731132, 731294, 731307, 732938
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craniocerebral trauma patients present a state of hypercoagulability at early stage and thrombin content is very high level at the site of injury
additional information
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the presence of thrombin induces a significant increase in matrix metalloprotease-9 activity and also increases its mRNA expression in primary astrocytes. Thrombin-induced matrix metalloprotease-9 production is inhibited by the selective inhibitor of protease-activated receptor PAR-1, SCH 79797 and by PDS98059