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The current study revealed a significant increase level of TAFI and PAI-1, coupled with a decrease in PAI-2 in women with severe preeclampsia in comparison with the control group.
The abundance of free PAI-1 (show SERPINE1 Proteins) and TAFI in the plaque may inhibit plasmin (show PLG Proteins) generation and thereby counteract plaque destabilization by fibrinolysis, cell migration and inflammation
thrombin activatable fibrinolysis inhibitor pathway impairment, largely caused by a hitherto unknown TAFIa resistance, appears to be one main cause of decreased fibrinolytic resistance in FXI (show F11 Proteins) deficiency
analysis of the a204-VHH-i83 complex, which demonstrates that two nanobodies can simultaneously bind to TAFI
TAFIa elicited anti-angiogenic responses by endothelial cells: decreased endothelial cell proliferation, cell invasion, cell migration, tube formation, and collagen degradation. It decreased tube formation and proteolysis in endothelial cell culture grown alone and in co-culture with breast cancer cell lines. TAFIa inhibition increased secretion of matrix metalloprotease proenzymes by endothelial and breast cancer cells.
Plasma levels of TAFI are elevated in patients with chronic thromboembolic pulmonary hypertension and are correlated with resistance to clot (show TXNDC17 Proteins) lysis in those patients.
R12 (show GPR17 Proteins) is a critical residue for the activation of TAFI by thrombin (show F2 Proteins)-thrombomodulin (show THBD Proteins)
Thrombin activatable fibrinolysis inhibitor, particularly its preoperative levels but also levels during the immediate postoperative period, may be key for understanding coagulopathy during liver transplantation, and it may have a role as predictor of increased mortality rates in the liver transplant population
The results suggest that although the TAFI S438G>T polymorphism is not correlated with venous thrombosis risk in all genetic models of venous thrombosis, a trend toward a reduced risk still could be observed. (Meta-analysis)
The results of the present study demonstrated that the CPB2 expression in patients with chronic hepatitis C was inversely correlated with several risk factors of hepatic fibrosis or steatosis, although ectopic CPB2 expression did not suppress the expression of fibrogenic or lipogenic genes.
Capping protein CAPZB participates in stereocilia widening in auditory hair cells by preventing newly elongating actin filaments from depolymerizing.
Cpb2-deficient mice had decreased pneumococcal meningitis mortality and attenuated cytokine levels and bacterial outgrowth in the systemic compartment but not in the brain compartment, as compared with wild-type mice.
with strain there was significant PKCepsilon (show PRKCE Proteins) translocation to the Z-disc and co-localization with CapZbeta1 or alpha-actinin (show ACTN1 Proteins), which was quantified on confocal images.
Carboxypeptidase B2 deficiency reveals that complement C3a (show C3 Proteins) limits infection and C5a exacerbates infection in a murine polymicrobial sepsis model.
Combination of TAFI-I and a low dose of rtPA was not as effective as the standard dose of rtPA in treating thromboembolic stroke, while TAFI inhibition alone was not effective at all.
Capping protein-beta (show CAPZB Proteins) knockdown decreases filopodial length, alters filopodial shape, and reduces filopodial dynamics.
In an induced osteoarthritis model, CPB2 knockout mice developed dramatically greater cartilage damage than did wild-type mice, had a greater number of osteophytes, and a greater degree of synovitis.
TAFI deficiency results in accelerated fibrogenesis and increased liver damage in murine models of chronic and acute liver disease, which may be related to increased inflammation.
Actin-capping protein is a novel regulator of microtubule stability that functions by antagonizing mDia1 activity toward actin filaments.
This study suggested that increased expression of TrkB (show NTRK2 Proteins) and Capzb2 accompanies adequate brain reserve in the initial stages of AD pathology.
analysis of the crystal structure of thrombin-activable fibrinolysis inhibitor (TAFI) and description of the structural basis for its intrinsic activity and the short half-life of TAFIa
Purified bovine TAFI activated in the presence of a proteinaceous inhibitor renders a stable enzyme-inhibitor complex.
Findings presented here suggest that the properties of these two orthologous proteins are similar and that conclusions reached using the bovine TAFI may be extrapolated to the human TAFI protein.
Carboxypeptidases are enzymes that hydrolyze C-terminal peptide bonds. The carboxypeptidase family includes metallo-, serine, and cysteine carboxypeptidases. According to their substrate specificity, these enzymes are referred to as carboxypeptidase A (cleaving aliphatic residues) or carboxypeptidase B (cleaving basic amino residues). The protein encoded by this gene is activated by trypsin and acts on carboxypeptidase B substrates. After thrombin activation, the mature protein downregulates fibrinolysis. Polymorphisms have been described for this gene and its promoter region.
carboxypeptidase B-like protein
, carboxypeptidase B2
, carboxypeptidase B2 (plasma, carboxypeptidase U)
, carboxypeptidase R
, thrombin-activable fibrinolysis inhibitor
, thrombin-activatable fibrinolysis inhibitor
, F-actin-capping protein subunit beta
, capZ beta
, capping protein beta 1
, carboxypeptidase U
, plasma carboxypeptidase B