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Carboxypeptidases are enzymes that hydrolyze C-terminal peptide bonds. Additionally we are shipping Carboxypeptidase B2 (Plasma) Kits (47) and Carboxypeptidase B2 (Plasma) Proteins (27) and many more products for this protein.
Showing 10 out of 179 products:
Human Polyclonal CPB2 Primary Antibody for ICC, IF - ABIN4287866
Kato, Nicholson, Neiman, Rantalainen, Holmes, Barrett, Uhlén, Nilsson, Spector, Schwenk: Variance decomposition of protein profiles from antibody arrays using a longitudinal twin model. in Proteome science 2011
Dog (Canine) Polyclonal CPB2 Primary Antibody for WB - ABIN2781326
Ricart, Ramón, Vayá, España, Santaolaria, Todolí, Castelló, Fontcuberta, Estellés: Fibrinolytic inhibitor levels and polymorphisms in Behçet disease and their association with thrombosis. in British journal of haematology 2008
Human Polyclonal CPB2 Primary Antibody for EIA, WB - ABIN452866
Valnickova, Thogersen, Christensen, Chu, Pizzo, Enghild: Activated human plasma carboxypeptidase B is retained in the blood by binding to alpha2-macroglobulin and pregnancy zone protein. in The Journal of biological chemistry 1996
Cpb2-deficient mice had decreased pneumococcal meningitis mortality and attenuated cytokine levels and bacterial outgrowth in the syst (show SET Antibodies)emic compartment but not in the brain (show CSF2 Antibodies)compartment, as compared with wild-type mice.
with strain there was significant PKCepsilon (show PRKCE Antibodies) translocation to the Z-disc and co-localization with CapZbeta1 or alpha-actinin (show ACTN1 Antibodies), which was quantified on confocal images.
Carboxypeptidase B2 deficiency reveals that complement C3a (show C3 Antibodies) limits infection and C5a exacerbates infection in a murine polymicrobial sepsis model.
Combination of TAFI (show SET Antibodies)-I and a low dose of rtPA was not as effective as the standard dose of rtPA in treating thromboembolic stroke, while TAFI (show SET Antibodies) inhibition alone was not effective at all.
Capping protein-beta (show CAPZB Antibodies) 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 (show SET Antibodies) 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 Antibodies) and Capzb2 accompanies adequate brain reserve in the initial stages of AD pathology.
The unique NFkappaB site in the mouse CPB2 promoter is functional and mediates the upregulation of mouse CPB2 expression by TNFalpha (show TNF Antibodies).
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.
Protein C (show PROC Antibodies) and TAFI are concurrently activated in a thrombomoulin-dependent manner and do not compete for the thrombin (show F2 Antibodies)-TM complex, raising the possibility that they interact with distinct activation complexes.
Acute myocardial infarction patients have higher plasma CPU levels and lower proCPU levels than controls. This finding indicates in vivo generation of functional active CPU in patients with AMI (show CFD Antibodies).
Arg12-Glu28 and Cys383-Val401 in TAFI are involved in thrombomodulin (show THBD Antibodies)-mediated TAFI activation. Gly205-Asp232 is involved in binding to thrombin (show F2 Antibodies).
CPB2 polymorphisms (reference sequences: rs1926447 and rs3742264) were related to systemic complications in bacterial meningitis. TAFI levels correlated positively with CSF (show CSF2 Antibodies) complement. rs1926447 (TT) was associated with higher levels of TAFI in CSF (show CSF2 Antibodies).
Pro-inflammatory cytokines or lipopolysaccharide decreased TAFI protein levels via binding of tristetraprolin (show ZFP36 Antibodies) to the CPB2 3'-UTR (show UTS2R Antibodies), which mediates CPB2 mRNA destabilisation. HuR (show ELAVL1 Antibodies) can bind the CBP2 (show SERPINH1 Antibodies) 3'UTR (show UTS2R Antibodies). This is reduced by pro-inflammatory mediators.
Review/Meta-analysis: failed to confirm the influence of Ala147Thr and Thr325Ile TAFI variants on the susceptibility to CVD. Increased risk of CHD (show CHDH Antibodies) was detected in TAFI Ile325 allele carriers.
TAFI deficiency results in increased brain damage in a model of thrombolysis after ischemic stroke, which was not associated with bleeding but with neuronal degeneration and MP production.
Generated stable deletion mutant of TAFI with full carboxypeptidase activity without activation.
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.
F-actin-capping protein subunit beta
, capZ beta
, capping protein beta 1
, 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