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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Carboxypeptidase B2

Carboxypeptidase U, TAFI, Thrombin activatable fibrinolysis inhibitor, CPB2
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. Available sequence data analyses indicate splice variants that encode different isoforms. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Plasminogen, carboxypeptidase, thrombomodulin, HAD, CAN
Papers on Carboxypeptidase U
Histones Differentially Modulate the Anticoagulant and Profibrinolytic Activities of Heparin, Heparin Derivatives, and Dabigatran.
Semeraro et al., Bari, Italy. In J Pharmacol Exp Ther, Feb 2016
Thrombin generation was assessed by calibrated automated thrombinography, inhibition of factor Xa and thrombin by synthetic substrates, tissue plasminogen activator-mediated clot lysis by turbidimetry, and thrombin-activatable fibrinolysis inhibitor (TAFI) activation by a functional assay.
Reduced plasma fibrin clot permeability and susceptibility to lysis are associated with increased risk of post-thrombotic syndrome.
Undas et al., Kraków, Poland. In J Thromb Haemost, Feb 2016
RESULTS: During one-year follow-up PTS developed in 48 (24%) patients, who were characterized by lower Ks, prolonged fibrin clot lysis time (CLT) and slower release of D-dimer from clots (D-Drate ), together with higher plasma D-dimer, C-reactive protein and thrombin-activatable fibrinolysis inhibitor (TAFI).
Structure-function relationships in Thrombin-activatable Fibrinolysis Inhibitor.
Meijers et al., Amsterdam, Netherlands. In J Thromb Haemost, Feb 2016
UNASSIGNED: Thrombin-activatable fibrinolysis inhibitor (TAFI) is an important regulator in the balance of coagulation and fibrinolysis.
Impacts of laparoscopic hysterectomy on functions of coagulation and fibrinolysis system.
Yang et al., Harbin, China. In Blood Coagul Fibrinolysis, Feb 2016
The prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), fibrinogen, D-dimer, von Willebrand factor, α-granule membrane protein-140, thrombin-activated fibrinolysis inhibitor (TAFI) and platelet count were detected at preoperative 24 h (N0), postoperative 24 h (N1) and postoperative 48 h (N2).
Multidrug resistance in Clostridium perfringens isolated from diarrheal neonatal piglets in Thailand.
Janvilisri et al., Nakhon Pathom, Thailand. In Anaerobe, Feb 2016
All isolates were cpb2-encoding C. perfringens type A and enterotoxin gene negative.
Activation of Protein C and Thrombin Activable Fibrinolysis Inhibitor on Cultured Human Endothelial Cells.
Weitz et al., Hamilton, Canada. In J Thromb Haemost, Jan 2016
BACKGROUND: When bound to thrombomodulin (TM), thrombin is a potent activator of protein C (PC) and thrombin activable fibrinolysis inhibitor (TAFI).
Association between thrombin-activatable fibrinolysis inhibitor gene polymorphisms and venous thrombosis risk: a meta-analysis.
Lu et al., Xuzhou, China. In Blood Coagul Fibrinolysis, Jan 2016
UNASSIGNED: Thrombin-activatable fibrinolysis inhibitor (TAFI) is an important antifibrinolytic factor that has been shown in increased concentrations to be associated with an increased risk for venous thrombosis.
Data supporting the structural and functional characterization of Thrombin-Activatable Fibrinolysis Inhibitor in breast cancer.
Toraih et al., Ismailia, Egypt. In Data Brief, Dec 2015
In the current study, in silico data analysis of Thrombin-Activatable Fibrinolysis Inhibitor (TAFI) gene and protein has been done.
The lectin complement pathway serine proteases (MASPs) represent a possible crossroad between the coagulation and complement systems in thromboinflammation.
Nilsson et al., Uppsala, Sweden. In J Thromb Haemost, Dec 2015
BACKGROUND: The activated forms of the complement lectin pathway (LP) proteases MASP-1 and -2 are able to cleave the coagulation factors prothrombin, fibrinogen, factor XIII and TAFI in vitro.
Impact of genetic polymorphisms in thrombin activatable fibrinolysis inhibitor (TAFI) on venous thrombosis disease: A meta-analysis.
Liu et al., Guangzhou, China. In Gene, Oct 2015
BACKGROUND: Reported studies have showed that Thrombin Activatable Fibrinolysis Inhibitor (TAFI) may be associated with an increased risk of venous thromboembolism.
PI3-Kinase Inhibitor LY294002 Repressed the Expression of Thrombin-Activatable Fibrinolysis Inhibitor in Human Hepatoma HepG2 Cells.
Takada et al., In Biol Pharm Bull, 2014
Thrombin-activatable fibrinolysis inhibitor (TAFI) is a carboxypeptidase B-like proenzyme biosynthesized in the liver and released into the blood circulation.
Genetic variations in the thrombin-activatable fibrinolysis inhibitor gene and risk of cardiovascular disease: a systematic review and meta-analysis.
Tan et al., Guangzhou, China. In Thromb Res, 2014
It has been identified that elevated plasma thrombin-activatable fibrinolysis inhibitor (TAFI) concentration, an anti-fibrinolytic factor, is associated with an increased risk of cardiovascular disease (CVD).
Insight into the Protein Composition of Immunoglobulin Light Chain Deposits of Eyelid, Orbital and Conjunctival Amyloidosis.
Enghild et al., Århus, Denmark. In J Proteomics Bioinform, 2013
Five proteins, apolipoprotein A-I, carboxypeptidase B2 (TAFI), complement component C9, fibulin-1 and plasminogen were found solely across all amyloid but not in the control tissue.
Thrombomodulin--a new target for treating stroke at the crossroad of coagulation and inflammation.
Schwaninger et al., Lübeck, Germany. In Curr Med Chem, 2013
TM binds thrombin and promotes the cleavage of protein C and the thrombin activatable fibrinolysis inhibitor (TAFI), thereby inhibiting coagulation and fibrinolysis.
Fibrinolytic and coagulative activities of Yersinia pestis.
Westerlund-Wikström et al., Helsinki, Finland. In Front Cell Infect Microbiol, 2012
Pla also inactivates the protease inhibitors alpha-2-antiplasmin and plasminogen activator inhibitor 1 (PAI-1) and prevents the activation of thrombin-activatable fibrinolysis inhibitor (TAFI).
Identification of tristetraprolin as a factor that modulates the stability of the TAFI transcript through binding to the 3'-untranslated region.
Boffa et al., Windsor, Canada. In J Thromb Haemost, 2012
Suggest a role for tristetraprolin in constitutive, and perhaps regulated, control of TAFI mRNA stability and hence abundance.
Convalescent plasma levels of TAFI activation peptide predict death and recurrent vascular events in ischemic stroke survivors.
Jern et al., In J Thromb Haemost, 2012
Letter: convalescent plasma TAFI-activation peptide, but not intact TAFI, showed association with future death and/or recurrent vascular events in ischemic stroke survivors.
Regulation of the mouse gene encoding TAFI by TNFα: role of NFκB binding site.
Boffa et al., Windsor, Canada. In Cytokine, 2012
The unique NFkappaB site in the mouse CPB2 promoter is functional and mediates the upregulation of mouse CPB2 expression by TNFalpha.
Plasma carboxypeptidase B downregulates inflammatory responses in autoimmune arthritis.
Robinson et al., Stanford, United States. In J Clin Invest, 2011
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.
Plasma thrombin-activatable fibrinolysis inhibitor levels and Thr325Ile polymorphism as a risk marker of myocardial infarction in Egyptian patients.
Elbaz et al., Ismailia, Egypt. In Acta Cardiol, 2011
Data provide evidence that TAFI Thr325IIe SNP (rs1926447) could be one of the genetic factors that increas the risk for myocardial infarct in the Egyptian population.
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