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Serpin peptidase inhibitor, clade C

antithrombin III, AT III
The protein encoded by this gene is a plasma protease inhibitor and a member of the serpin superfamily. This protein inhibits thrombin as well as other activated serine proteases of the coagulation system, and it regulates the blood coagulation cascade. The protein includes two functional domains: the heparin binding-domain at the N-terminus of the mature protein, and the reactive site domain at the C-terminus. The inhibitory activity is enhanced by the presence of heparin. More than 120 mutations have been identified for this gene, many of which are known to cause antithrombin-III deficiency. [provided by RefSeq, Jul 2009] (from NCBI)
Top mentioned proteins: HAD, AGE, Plasminogen, CAN, Thromboplastin
Papers on antithrombin III
Effect of DNase I treatment and neutrophil depletion on acute limb ischemia-reperfusion injury in mice.
Watkins et al., Boston, United States. In J Vasc Surg, Jan 2016
DNase I treatment did enhance postischemic hindlimb perfusion, decreased infiltrating inflammatory cells, and reduced the expression of thrombin-antithrombin III.
Effect of heart rate control on coagulation status in patients of rheumatic mitral stenosis with atrial fibrillation - A pilot study.
Trehan et al., New Delhi, India. In Indian Heart J, Dec 2015
thrombin antithrombin III 22.0ng/ml [IQR 18.6-28.0],
Paralytic Ileus due to Superior Mesenteric Venous Thrombosis after Transarterial Injection for Hepatocellular Carcinoma.
Ohira et al., Fukushima, Japan. In Intern Med, Dec 2015
The thrombosis was reduced after anticoagulation therapy (heparin, antithrombin III, danaparoid sodium and warfarin).
Left ventricular intracardiac thrombus in a patient with Behçet disease successfully treated with immunosuppressive agents without anticoagulation: a case report and review of the literature.
Nasonov et al., Moscow, Russia. In Rheumatol Int, Nov 2015
Known thrombophilic factors such as methylenetetrahydrofolate reductase gene mutations, factor V Leiden mutation, proteins S and C, antithrombin III, activated protein C resistance, and antiphospholipid antibodies may contribute to the formation of intracardiac thrombi in BD.
Antithrombin III: Plasma Activity and Reference Range Among Nigerian Blood Donors.
Ngwuli et al., Lagos, Nigeria. In Niger Postgrad Med J, Oct 2015
BACKGROUND: Diagnosis of antithrombin III (ATIII) deficiency as a common cause of thrombophilia is primarily based on the determination of antithrombin levels in plasma using a functional activity assay or an immunological assay, but local reference interval is lacking.
Prevalence and role of antithrombin III, protein C and protein S deficiencies and activated protein C resistance in Kosovo women with recurrent pregnancy loss during the first trimester of pregnancy.
Mekaj et al., Pristina, Serbia. In J Hum Reprod Sci, Oct 2015
In both groups, we determined the biological activities of antithrombin III (ATIII) and protein C (PC) using the chromogenic method and the biological activity of protein S (PS) and the activated protein C resistance (APCR) were examined using a clotting method.
Caspases and Thrombin Activity Regulation by Specific Serpin Inhibitors in Bovine Skeletal Muscle.
Sentandreu et al., Constantine, Algeria. In Appl Biochem Biotechnol, Sep 2015
These are two members of the bovSERPINA3 family, i.e., bovSERPINA3-1 and A3-3, and the last one is antithrombin III (AT-III or BovSERPINC1).
Use of blood products in pediatric cardiac surgery.
Durandy, Le Plessis-Robinson, France. In Artif Organs, 2015
The same remark can be made regarding the treatment of antithrombin III deficiency.
Associations Between Inflammatory Markers, Hemostatic Markers, and Microvascular Complications in 182 Chinese Patients With Type 2 Diabetes Mellitus.
Lv et al., Hangzhou, China. In Lab Med, 2014
RESULTS: C-reactive protein (CRP) and interleukin-6 (IL-6) were significantly correlated with fibrinogen, thrombin-antithrombin III complex (TAT III), plasminogen activator inhibitor-1 (PAI-1), von Willebrand factor (vWF), and coagulation factors (F) VII in patients with T2DM who had microvascular complications (P <.05).
Interventions for prophylaxis of hepatic veno-occlusive disease in people undergoing haematopoietic stem cell transplantation.
Chan et al., Hong Kong, Hong Kong. In Cochrane Database Syst Rev, 2014
One trial (30 participants) compared antithrombin III with heparin versus heparin.
A specific antidote for reversal of anticoagulation by direct and indirect inhibitors of coagulation factor Xa.
Sinha et al., San Francisco, United States. In Nat Med, 2013
This recombinant protein (r-Antidote, PRT064445) is catalytically inactive and lacks the membrane-binding γ-carboxyglutamic acid domain of native fXa but retains the ability of native fXa to bind direct fXa inhibitors as well as low molecular weight heparin-activated antithrombin III (ATIII).
Amelioration of the severity of heparin-binding antithrombin mutations by posttranslational mosaicism.
Corral et al., Murcia, Spain. In Blood, 2012
Heparin-binding antithrombin mutations are associated with thrombosis.
Molecular basis of type I antithrombin deficiency in two women with recurrent venous thromboembolism in the first trimester of pregnancy.
Wang et al., Shanghai, China. In Blood Cells Mol Dis, 2012
results revealed that the type I AT deficiency in two patients was caused by impaired secretion of the AT-Trp225Cys and AT-Ala404Asp mutant proteins.
Molecular analysis and genotype-phenotype correlation in patients with antithrombin deficiency from Southern Italy.
Di Minno et al., Napoli, Italy. In Thromb Haemost, 2012
analysis of genotype-phenotype correlation of SERPIN C1 in patients with antithrombin deficiency from Southern Italy
Regulatory regions of SERPINC1 gene: identification of the first mutation associated with antithrombin deficiency.
Corral et al., Murcia, Spain. In Thromb Haemost, 2012
identification of the first mutation located in regulatory region, which is associated with antithrombin deficiency
The infective polymerization of conformationally unstable antithrombin mutants may play a role in the clinical severity of antithrombin deficiency.
Corral et al., Murcia, Spain. In Mol Med, 2011
Under mild heating conditions, purified antithrombin London recruited WT monomers into growing polymers, reducing the anticoagulant activity.
Protein biomarker identification in the CSF of patients with CNS lymphoma.
Rubenstein et al., Menlo Park, United States. In J Clin Oncol, 2008
High antithrombin III in cerebrospinal fluid is associated with CNS lymphoma
Randomized dose-ranging trial of tamoxifen at low doses in hormone replacement therapy users.
Bonanni et al., Milano, Italy. In J Clin Oncol, 2007
The primary end point was the change of plasma insulinlike growth factor 1 (IGF-I) through 12 months, and secondary end points were IGF-I/IGF binding protein-3 (IGFBP-3) ratio, fibrinogen, antithrombin III, C reactive protein, C-telopeptide, mammographic percent density, and endometrial thickness.
Generation of C5a in the absence of C3: a new complement activation pathway.
Ward et al., Ulm, Germany. In Nat Med, 2006
Injury in lungs of C3-/- mice and C5a levels in bronchoalveolar lavage (BAL) fluids from these mice were greatly reduced in the presence of antithrombin III (ATIII) or hirudin but were not reduced in similarly treated C3+/+ mice.
Enzymatic synthesis of antithrombin III-binding heparan sulfate pentasaccharide.
Rosenberg et al., Cambridge, United States. In Nat Biotechnol, 2003
We rapidly and efficiently assembled the antithrombin III-binding pentasaccharide in just 6 steps, in contrast to the approximately 60 steps needed for its chemical synthesis, with an overall yield at least twofold greater and a completion time at least 100 times faster than for the chemical process.
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