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Results 1 - 10 of 43 > >>
EC Number General Information Commentary Reference
Display the word mapDisplay the reaction diagram Show all sequences 3.4.21.5malfunction high glucose enhances smooth muscle cell responsiveness to thrombin through transcriptional upregulation of PAR-4, which may play an important role in the vascular complications of diabetes 717167
Display the word mapDisplay the reaction diagram Show all sequences 3.4.21.5malfunction in the transgenic TRAMP mouse model of prostate cancer inhibition of endogenous thrombin by hirudin retards spontaneous tumor growth. Inhibition of thrombin may lead to tumor dormancy 708032
Display the word mapDisplay the reaction diagram Show all sequences 3.4.21.5metabolism PAR-1 signaling to NF-kappaB in endothelial cells via protein kinase C signaling, CARMA3/Bcl10/MALT1, CBM, signalosome, and IkappaB kinase, and involving thrombin, pathway regulation, overview. The CBM signalosome controls thrombin-dependent monocyte/endothelial adhesion. The process is different in lymphocytes where CARMA1 is active instead of CARMA3 717814
Display the word mapDisplay the reaction diagram Show all sequences 3.4.21.5metabolism thrombin induces NF-kappaB activation and IL-8/CXCL8 expression in human lung epithelial cells by a Rac1-dependent PI3K/Akt pathway. Treatment of cells with thrombin causes activation of Rac and Akt. Thrombin induces NF-kappaB activation and protein expression through multiple signaling pathways such as PKCalpha/c-Src, Rac1, extracellular signal-regulated kinase, p38 mitogen-activated protein kinase, c-Jun N-terminal kinase, IkappaB kinases, and PI3K/Akt, overview 717817
Display the word mapDisplay the reaction diagram Show all sequences 3.4.21.5metabolism thrombin induces NF-kappaB activation and IL-8/CXCL8 expression in lung epithelial cells by a Rac1-dependent PI3K/Akt pathway. Treatment of cells with thrombin causes activation of Rac and Akt. Thrombin induces NF-kappaB activation and protein expression through multiple signaling pathways such as PKCalpha/c-Src, Rac1, extracellular signal-regulated kinase, p38 mitogen-activated protein kinase, c-Jun N-terminal kinase, IkappaB kinases, and PI3K/Akt, overview 717817
Display the word mapDisplay the reaction diagram Show all sequences 3.4.21.5more peptides of the C-terminal region of human thrombin are released upon proteolysis and identified in human wounds displaying length- and sequence-dependent antimicrobial, e.g. against Gram-negative bacteria Escherichia coli and Pseudomonas aeruginosa, the Gram-positive bacterium Staphylococcus aureus, and the fungus Candida albicans, as well as immunomodulating effects. A peptide length of at least 20 amino acids is required for effective anti-inflammatory effects in macrophage models, as well as optimal antimicrobial activity 717098
Display the word mapDisplay the reaction diagram Show all sequences 3.4.21.5more the thrombin catalytic triad comprises residues His57, Asp102, and Ser195 718297
Display the word mapDisplay the reaction diagram Show all sequences 3.4.21.5more thrombin and trypsin directly activate vagal C-fibres in C57BL6 mouse lung via protease-activated receptor-1,i.e. PAR1, not via PAR3, PAR2, and PAR4, overview 718033
Display the word mapDisplay the reaction diagram Show all sequences 3.4.21.5physiological function after treating JR-FL Env-expressing 293T cells with various concentrations of thrombin and subsequent coculture for 14 h, thrombin effect turns out to be a concentration-dependent fusion enhancement, thrombin can enhance the fusion mediated by R5-tropic HIV-1 gp160 707386
Display the word mapDisplay the reaction diagram Show all sequences 3.4.21.5physiological function HUVEC cells stimulated with thrombin (10 nM) exhibit an increased amount of actin filaments (show increased cell stiffness) when compared to unstimulated cells 709588
Results 1 - 10 of 43 > >>