Any feedback?
Please rate this page
(all_enzymes.php)
(0/150)

BRENDA support

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

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

     3 Hydrolases
         3.4 Acting on peptide bonds (peptidases)
             3.4.21 Serine endopeptidases
                3.4.21.5 thrombin

Source Tissue

Source Tissue on EC 3.4.21.5 - thrombin

Please wait a moment until all data is loaded. This message will disappear when all data is loaded.
SOURCE TISSUE
ORGANISM
UNIPROT
COMMENTARY hide
LITERATURE
SOURCE
-
sections from Alzheimer's disease brains show reactivity to thrombin antibody in blood vessel walls but not in vessels from controls
Manually annotated by BRENDA team
-
high levels of thrombin are detected in cerebrospinal fluid obtained from Alzheimer's disease but not control patients
Manually annotated by BRENDA team
-
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
Manually annotated by BRENDA team
-
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
Manually annotated by BRENDA team
-
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
Manually annotated by BRENDA team
-
human capsular bag model
Manually annotated by BRENDA team
-
thrombin is highly expressed in microvessels from Alzheimer's disease brains but is not detectable in control vessels
Manually annotated by BRENDA team
-
a metastatic melanoma cell line
Manually annotated by BRENDA team
-
a metastatic melanoma cell line
Manually annotated by BRENDA team
additional information