Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
TAFI and TAFIa levels were increased in patients with APS (show SH2B2 Proteins) as a potential response to complement activation. Interestingly, TAFI activation was associated with arterial thrombotic APS (show SH2B2 Proteins) manifestations.
Reprot altered in vivo TAFI activation in patients with abdominal aortic aneurysms, as shown by the increased plasma levels of TAFI(activated)/TAFIai(inactivated) and TAFI-activation peptide.
Lys (show LYZ Proteins) 42, Lys (show LYZ Proteins) 43, Lys (show LYZ Proteins) 44 and Arg 12 are critical for the interaction of TAFI with the thrombin (show F2 Proteins)-thrombomodulin (show THBD Proteins) complex, which modulates its antifibrinolytic potential.
CPU generation during in vitro clot (show TXNDC17 Proteins) lysis follows a biphasic pattern in pooled plasma. A first CPU activity peak is mediated by the action of thrombin (show F2 Proteins)-(thrombomodulin (show THBD Proteins)), a second by the action of plasmin (show PLG Proteins).
The data suggested that suppression of TAFI by siRNA inhibits invasion and migration of breast cancer cells and that TAFI may be a new target for breast cancer therapy.
Report direct crosstalk between coagulation and fibrinolysis, which takes place on activated platelets' surface that is further controlled by thrombin-activatable fibrinolysis inhibitor (TAFI).
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
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.
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.
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.
The unique NFkappaB site in the mouse CPB2 promoter is functional and mediates the upregulation of mouse CPB2 expression by TNFalpha (show TNF Proteins).
These findings suggest that plasma carboxypeptidase B plays a critical role in dampening local, C5a-mediated inflammation and represents a molecular link between inflammation and coagulation in autoimmune arthritis.
In another mouse experiment, animals infected with isogenic Bacillus anthracis inhA (show INHA Proteins) deletion mutants restored TAFI levels, while the levels in the parent strain decreased.
Protective roles for fibrin, tissue factor (show F3 Proteins), plasminogen activator inhibitor-1 (show SERPINE1 Proteins), and thrombin activatable fibrinolysis inhibitor, but not factor XI, during defense against the gram-negative bacterium Yersinia enterocolitica.
Apo-E (show APOE Proteins) deficiency alone is not associated with tumors but a lack of TAFI appears to make the mice permissive for tumor formation in ApoE (show APOE Proteins) mice
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
, carboxypeptidase U
, plasma carboxypeptidase B