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1. Full Text Coagulation factor XII genetic variation, ex vivo thrombin generation, and stroke risk in the elderly: results from the Cardiovascular Health Study
by Olson, N. C and Butenas, S and Lange, L. A and Lange, E. M and Cushman, M and Jenny, N. S and Walston, J and Souto, J. C and Soria, J. M and Chauhan, G and Debette, S and Longstreth, W. T and Seshadri, S and Reiner, A. P and Tracy, R. P
Journal of Thrombosis and Haemostasis, ISSN 1538-7933, 10/2015, Volume 13, Issue 10, pp. 1867 - 1877
The relationships of thrombin generation (TG) with cardiovascular disease risk are underevaluated in population-based cohorts. To evaluate the relationships of... 
epidemiology | XII | thrombin | cardiovascular diseases | factor | single nucleotide polymorphisms | Thrombin | Single nucleotide polymorphisms | Cardiovascular diseases | Epidemiology | Factor XIIa | United States - epidemiology | Prospective Studies | Age Factors | Humans | Brain Ischemia - genetics | Male | Stroke - genetics | Incidence | Brain Ischemia - blood | Time Factors | Female | Brain Ischemia - ethnology | European Continental Ancestry Group - genetics | Genetic Predisposition to Disease | Factor XII - genetics | Risk Assessment | Gene Frequency | Risk Factors | African Americans - genetics | Stroke - blood | Phenotype | Factor XII - metabolism | Stroke - ethnology | Blood Coagulation - genetics | Aged | Polymorphism, Single Nucleotide | Thrombin - metabolism | Stroke (Disease) | Genetic research | Genetic aspects | Chromosomes | Risk factors | Index Medicus | Single Nucleotide Polymorphisms | Cardiovascular Diseases
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2. Full Text Selective depletion of plasma prekallikrein or coagulation factor XII inhibits thrombosis in mice without increased risk of bleeding
by Revenko, Alexey S and Gao, Dacao and Crosby, Jeff R and Bhattacharjee, Gourab and Zhao, Chenguang and May, Chris and Gailani, David and Monia, Brett P and MacLeod, A. Robert
Blood, ISSN 0006-4971, 11/2011, Volume 118, Issue 19, pp. 5302 - 5311
Recent studies indicate that the plasma contact system plays an important role in thrombosis, despite being dispensable for hemostasis. For example, mice... 
PLATELET POLYPHOSPHATES | MYOCARDIAL-INFARCTION | BLOOD-COAGULATION | IN-VIVO | VENOUS THROMBOSIS | HAGEMAN-FACTOR | SURFACE-DEPENDENT ACTIVATION | CORONARY-HEART-DISEASE | HEMATOLOGY | ANTIPHOSPHOLIPID SYNDROME | TISSUE FACTOR | Factor XII Deficiency - blood | Hemostasis - physiology | Male | Prekallikrein - deficiency | RNA, Messenger - metabolism | Gene Knockdown Techniques | Hemorrhage - etiology | Factor XII Deficiency - genetics | Prekallikrein - antagonists & inhibitors | Thrombosis - blood | Thrombosis - prevention & control | Disease Models, Animal | Prekallikrein - genetics | Hemorrhage - genetics | Factor XII - genetics | Mice, Inbred C57BL | RNA, Messenger - genetics | Risk Factors | Hemostasis - genetics | Hemorrhage - blood | Animals | Oligonucleotides, Antisense - genetics | Factor XII - antagonists & inhibitors | Oligonucleotides, Antisense - administration & dosage | Thrombosis - genetics | Mice | Mice, Inbred BALB C | Index Medicus | Abridged Index Medicus | Thrombosis and Hemostasis
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3. Full Text Increased Activity of Coagulation Factor XII (Hageman Factor) Causes Hereditary Angioedema Type III
by Cichon, Sven and Martin, Ludovic and Hennies, Hans Christian and Müller, Felicitas and Van Driessche, Karen and Karpushova, Anna and Stevens, Wim and Colombo, Roberto and Renné, Thomas and Drouet, Christian and Bork, Konrad and Nöthen, Markus M
The American Journal of Human Genetics, ISSN 0002-9297, 2006, Volume 79, Issue 6, pp. 1098 - 1104
Hereditary angioedema (HAE) is characterized clinically by recurrent acute skin swelling, abdominal pain, and potentially life-threatening laryngeal edema.... 
C1 INHIBITOR | SYSTEM | ACTIVATION | FRENCH-CANADIANS | HUMAN GENOME | PLASMA | GENE | GENETICS & HEREDITY | POPULATIONS | MUTATIONS | NORMAL C1-INHIBITOR | Kinins - metabolism | Markov Chains | Factor XII - genetics | Factor XII - analysis | Humans | Male | Angioedema - genetics | Linkage Disequilibrium | Founder Effect | Haplotypes - genetics | Time Factors | Pedigree | Factor XII - metabolism | Bayes Theorem | Female | Heterozygote | Models, Genetic | Mutation | Microsatellite Repeats | Angioneurotic edema | Genetic aspects | Blood coagulation factors | Research | Gene mutations | Estrogen | Genetic research | Pathology | Genetic disorders | Protease inhibitors | Index Medicus | Haplotypes | Hematology | Angioedema | Kinins | Innate immunity | Factor XII | Life Sciences | Human health and pathology | Immunology | Report
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4. Full Text Factor XII regulates the pathological process of thrombus formation on ruptured plaques
by Kuijpers, Marijke J. E and van der Meijden, Paola E. J and Feijge, Marion A. H and Mattheij, Nadine J. A and May, Frauke and Govers-Riemslag, José and Meijers, Joost C. M and Heemskerk, Johan W. M and Renné, Thomas and Cosemans, Judith M. E. M
Arteriosclerosis, thrombosis, and vascular biology, ISSN 1079-5642, 2014, Volume 34, Issue 8, pp. 1674 - 1680
Atherothrombosis is the main cause of myocardial infarction and ischemic stroke. Although the extrinsic (tissue factor-factor VIIa [FVIIa]) pathway is... 
Blood coagulation | Fibrin | Plaque rupture | Blood platelets | Thrombus | Tissue factor | Factor XII | blood platelets | ACTIVATION | tissue factor | blood coagulation | plaque rupture | thrombus | COAGULATION-FACTOR-XII | INHIBITION | PLASMA | HUMAN ATHEROSCLEROTIC PLAQUES | IN-VIVO | PERIPHERAL VASCULAR DISEASE | PLATELET GLYCOPROTEIN-VI | GENERATION | PROVIDES PROTECTION | fibrin | HEMATOLOGY | factor XII | Carotid Arteries - metabolism | Factor XIIa - metabolism | Apolipoproteins E - deficiency | Factor XII Deficiency - blood | Atherosclerosis - genetics | Humans | Aortic Diseases - blood | Carotid Artery Diseases - complications | Time Factors | Carotid Artery Diseases - pathology | Blood Coagulation | Factor XII Deficiency - genetics | Thrombosis - blood | Aorta, Thoracic - pathology | Aortic Diseases - pathology | Disease Models, Animal | Atherosclerosis - pathology | Factor XII - genetics | Mice, Inbred C57BL | Aorta, Thoracic - metabolism | Atherosclerosis - complications | Plaque, Atherosclerotic | Factor VIIa - metabolism | Mice, Knockout | Atherosclerosis - blood | Thrombosis - pathology | Aortic Diseases - genetics | Animals | Blood Platelets - metabolism | Thrombosis - etiology | Apolipoproteins E - genetics | Carotid Artery Diseases - blood | Factor XII - metabolism | Carotid Artery Diseases - genetics | Aortic Diseases - complications | Thrombosis - genetics | Carotid Arteries - pathology | Mice | Factor XI - metabolism | Thromboplastin - metabolism | Cholesterol, Dietary | Rupture, Spontaneous | Index Medicus
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5. Full Text Selective depletion of factor XI or factor XII with antisense oligonucleotides attenuates catheter thrombosis in rabbits
by Yau, Jonathan W and Liao, Peng and Fredenburgh, James C and Stafford, Alan R and Revenko, Alexey S and Monia, Brett P and Weitz, Jeffrey I
Blood, ISSN 0006-4971, 03/2014, Volume 123, Issue 13, pp. 2102 - 2107
Central venous catheter thrombosis can cause venous obstruction and pulmonary embolism. To determine the extent to which catheter thrombosis is triggered by... 
COAGULATION-FACTOR-XII | INTRINSIC PATHWAY | IN-VITRO | CANCER-PATIENTS | INHIBITION | MOLECULAR-WEIGHT KININOGEN | SURFACE MODIFICATION | BLEEDING RISK | BLOOD FACTOR-XII | CONTACT ACTIVATION | HEMATOLOGY | Rabbits | Factor XI - genetics | Factor XII - genetics | Oligonucleotides, Antisense - pharmacology | Male | Substrate Specificity - genetics | Factor XI - antagonists & inhibitors | Gene Expression Regulation - drug effects | Animals | Substrate Specificity - drug effects | Catheter Obstruction | Catheters - adverse effects | Factor XII - antagonists & inhibitors | Thrombosis - genetics | Thrombosis - prevention & control | RNA Interference - physiology | Disease Models, Animal | Genetic Therapy - methods | Index Medicus | Abridged Index Medicus
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6. Full Text Defective glycosylation of coagulation factor XII underlies hereditary angioedema type III
by Björkqvist, Jenny and De Maat, Steven and Lewandrowski, Urs and Di Gennaro, Antonio and Oschatz, Chris and Schönig, Kai and Nöthen, Markus M and Drouet, Christian and Braley, Hal and Nolte, Marc W and Sickmann, Albert and Panousis, Con and Maas, Coen and Renné, Thomas
Journal of Clinical Investigation, ISSN 0021-9738, 08/2015, Volume 125, Issue 8, pp. 3132 - 3146
Hereditary angioedema type III (HAEIII) is a rare inherited swelling disorder that is associated with point mutations in the gene encoding the plasma protease... 
C1 INHIBITOR | MEDICINE, RESEARCH & EXPERIMENTAL | CONTACT SYSTEM | PLASMA KALLIKREIN | MOLECULAR-WEIGHT KININOGEN | FACTOR 12 GENE | IN-VIVO | HAGEMAN-FACTOR | VASCULAR-PERMEABILITY | NORMAL C1-INHIBITOR | MISSENSE MUTATIONS | Bradykinin - metabolism | Factor XII - genetics | Humans | Hereditary Angioedema Type III - metabolism | Antibodies, Neutralizing - pharmacology | Mutation, Missense | Glycosylation - drug effects | Hereditary Angioedema Type III - genetics | Mice, Knockout | Hereditary Angioedema Type III - pathology | Animals | Factor XII - metabolism | Blood Coagulation | Hereditary Angioedema Type III - drug therapy | Adult | Female | Mice | Amino Acid Substitution | Bradykinin - genetics | Disease Models, Animal | Angioneurotic edema | Abnormalities | Physiological aspects | Genetic aspects | Glycosylation | Research | Blood coagulation factors | Risk factors | Peptides | Rodents | Mutation | Permeability | Gene expression | Patients | Molecular weight | Index Medicus | Abridged Index Medicus
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7. Full Text Factor XII deficiency is common in domestic cats and associated with two high frequency F12 mutations
by Maruyama, Haruhiko and Brooks, Marjory B and Stablein, Alyssa and Frye, Amelia
Gene, ISSN 0378-1119, 07/2019, Volume 706, pp. 6 - 12
Factor XII (FXII) is a coagulation protein that initiates surface-activation of the coagulation cascade in vitro. The protein's in vivo role, however, remains... 
Cat diseases | Genetics | Single nucleotide | Hageman factor | Coagulation | Polymorphism | CONTACT SYSTEM | THROMBOSIS | COAGULATION-FACTOR-XII | PHASE | GENE | ROLES | INFLAMMATION | DOGS | GENETICS & HEREDITY | HEMOSTASIS | Sequence Deletion | Animals | Factor XII - genetics | United States | Factor XII Deficiency - genetics | Cats - genetics | Exons - genetics | Factor XII Deficiency - veterinary | Polymorphism, Genetic - genetics | Retrospective Studies | Mutation | Factor XII - physiology | Pets | Medical research | Cats | Medical examination | Genes | Analysis | Prothrombin | Medicine, Experimental | Thrombin | Genetic aspects | Genetic polymorphisms | Blood | Index Medicus
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8. Full Text Plasmin is a natural trigger for bradykinin production in patients with hereditary angioedema with factor XII mutations
by de Maat, Steven, MSc and Björkqvist, Jenny, PhD and Suffritti, Chiara, PhD and Wiesenekker, Chantal P., MSc and Nagtegaal, Willem and Koekman, Arnold, BSc and van Dooremalen, Sanne, BSc and Pasterkamp, Gerard, PhD and de Groot, Philip G., PhD and Cicardi, Marco, PhD and Renné, Thomas, PhD and Maas, Coen, PhD
Journal of Allergy and Clinical Immunology, The, ISSN 0091-6749, 2016, Volume 138, Issue 5, pp. 1414 - 1423.e9
Background Patients with angioedema experience unpredictable attacks of tissue swelling in which bradykinin is implicated. Several distinct mutations in Factor... 
Allergy and Immunology | kininogen | Angioedema | plasmin | bradykinin | plasma kallikrein | Factor XII | C1 esterase inhibitor | KALLIKREIN CLEAVAGE | CONTACT SYSTEM ACTIVATION | IMMUNOLOGY | FIBRINOLYTIC SYSTEM | NORMAL C1-INHIBITOR | DEFICIENCY | C1 INHIBITOR | F12 GENE | ALLERGY | HAGEMAN-FACTOR | COAGULATION | ALTEPLASE TREATMENT | Pregnancy | Bradykinin - metabolism | Factor XII - genetics | Angioedemas, Hereditary - metabolism | Factor XII - metabolism | Humans | Antifibrinolytic Agents - pharmacology | Female | Complement C1 Inhibitor Protein - metabolism | Mutation | Fibrinolysin - metabolism | Aminocaproic Acid - pharmacology | Angioneurotic edema | Care and treatment | Genetic aspects | Bradykinin | Medical research | Medicine, Experimental | Kallikrein | Proteins | Plasma | Life sciences | Patients | Index Medicus | Abridged Index Medicus
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9. Full Text Missense mutations in the coagulation factor XII (Hageman factor) gene in hereditary angioedema with normal C1 inhibitor
by Dewald, Georg and Bork, Konrad
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 2006, Volume 343, Issue 4, pp. 1286 - 1289
Hereditary angioedema is characterized by recurrent skin swelling, abdominal pain attacks, and potentially life-threatening upper airway obstruction. The two... 
Intrinsic coagulation pathway | Kinin system | Contact activation | Hageman factor | F12 | Angioedema | Bradykinin | Coagulation | C1 inhibitor | Factor XII | BIOCHEMISTRY & MOLECULAR BIOLOGY | kinin system | bradykinin | contact activation | coagulation | REGION | angioedema | WOMEN | BIOPHYSICS | intrinsic coagulation pathway | factor XII | SURFACES | Factor XII - genetics | Pedigree | Humans | Female | Male | Angioedema - etiology | Complement C1 Inhibitor Protein - genetics | Mutation, Missense | Angioedema - genetics | Genetic Linkage | Index Medicus
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10. Full Text Activation of the factor XII-driven contact system in Alzheimer's disease patient and mouse model plasma
by Zamolodchikov, Daria and Chen, Zu-Lin and Conti, Brooke A and Renné, Thomas and Stricklan, Sidney
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 03/2015, Volume 112, Issue 13, pp. 4068 - 4073
Alzheimer's disease (AD) is characterized by accumulation of the beta-amyloid peptide (A beta), which likely contributes to disease via multiple mechanisms.... 
High molecular-weight kininogen | Alzheimer's disease | Factor XII | Plasma kallikrein | high molecular-weight kininogen | RISK-FACTORS | DEMENTIA | MULTIDISCIPLINARY SCIENCES | NEURODEGENERATION | CEREBROSPINAL-FLUID | HEPARIN | BLOOD-BRAIN-BARRIER | AMYLOID-BETA | IN-VIVO | HAGEMAN-FACTOR | COAGULATION | plasma kallikrein | factor XII | Factor XIIa - metabolism | Humans | Male | Dementia - genetics | Factor XIIa - genetics | Case-Control Studies | Dementia - metabolism | Amyloid beta-Peptides - metabolism | Aged, 80 and over | Female | Kallikreins - blood | Kininogens - metabolism | Disease Models, Animal | Biomarkers - metabolism | Microscopy, Electron, Transmission | Peptide Fragments - metabolism | Factor XII - genetics | Mice, Inbred C57BL | Mice, Transgenic | Inflammation | Disease Progression | Animals | Factor XII - metabolism | Alzheimer Disease - metabolism | Aged | Mice | Alzheimer Disease - genetics | Transferrin - metabolism | Care and treatment | Molecular weights | Diagnosis | Analysis | Plasma | Peptides | Alzheimers disease | Rodents | Index Medicus
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11. Full Text Platelet Polyphosphates Are Proinflammatory and Procoagulant Mediators In Vivo
by Müller, Felicitas and Mutch, Nicola J and Schenk, Wolfdieter A and Smith, Stephanie A and Esterl, Lucie and Spronk, Henri M and Schmidbauer, Stefan and Gahl, William A and Morrissey, James H and Renné, Thomas
Cell, ISSN 0092-8674, 12/2009, Volume 139, Issue 6, pp. 1143 - 1156
Platelets play a central role in thrombosis, hemostasis, and inflammation. We show that activated platelets release inorganic polyphosphate (polyP), a polymer... 
HUMDISEASE | COAGULATION-FACTOR-XII | SYSTEM | INORGANIC POLYPHOSPHATE | INTRINSIC PATHWAY | ACTIVATION | BLOOD-COAGULATION | THROMBUS FORMATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | DISEASE | DEFICIENCY | CONTACT-PHASE | CELL BIOLOGY | Plasma | Bradykinin - metabolism | Factor XII - genetics | Hermanski-Pudlak Syndrome - metabolism | Humans | Polyphosphates - metabolism | Thrombosis - metabolism | Animals | Receptors, Bradykinin - metabolism | Blood Platelets - metabolism | Factor XII - metabolism | Inflammation Mediators - metabolism | Mice | Fibrin - metabolism | Peptide Hydrolases - metabolism | Pulmonary embolism | Phosphates | Medical colleges | Phosphatases | Proteases | Bradykinin | Medical genetics | Permeability | Peptide hormones | Thrombosis | Blood clot | Index Medicus
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