Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 05/2013, Volume 33, Issue 5, pp. 926 - 934
OBJECTIVE—Platelet inhibition is a major strategy to prevent acute ischemic cardiovascular and cerebrovascular events, which may, however, be associated with...
CLEC-2 | thrombosis | hemostasis | GPVI | platelets | COLLAGEN | IMMUNE THROMBOCYTOPENIC PURPURA | SYK | INTEGRIN | ANTIBODY | MECHANISMS | PERIPHERAL VASCULAR DISEASE | PLATELET ACTIVATION | HEMATOLOGY | ANTITHROMBOTIC PROTECTION | Platelet Membrane Glycoproteins - antagonists & inhibitors | Animals | Hemostasis | Mice, Inbred C57BL | Lectins, C-Type - physiology | Platelet Membrane Glycoproteins - physiology | Male | Mice | Thrombosis - prevention & control | Lectins, C-Type - antagonists & inhibitors
CLEC-2 | thrombosis | hemostasis | GPVI | platelets | COLLAGEN | IMMUNE THROMBOCYTOPENIC PURPURA | SYK | INTEGRIN | ANTIBODY | MECHANISMS | PERIPHERAL VASCULAR DISEASE | PLATELET ACTIVATION | HEMATOLOGY | ANTITHROMBOTIC PROTECTION | Platelet Membrane Glycoproteins - antagonists & inhibitors | Animals | Hemostasis | Mice, Inbred C57BL | Lectins, C-Type - physiology | Platelet Membrane Glycoproteins - physiology | Male | Mice | Thrombosis - prevention & control | Lectins, C-Type - antagonists & inhibitors
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 08/2013, Volume 123, Issue 8, pp. 3331 - 3342
Platelets are anuclear organelle-rich cell fragments derived from bone marrow megakaryocytes (MKs) that safeguard vascular integrity. The major platelet...
MEDICINE, RESEARCH & EXPERIMENTAL | GLYCOPROTEIN-VI | ALPHA-GRANULES | BLEEDING-TIME | INTEGRIN | IN-VIVO | ARTERIAL THROMBOSIS | NBEAL2 | GROWTH-FACTOR | PROTEINS | ISCHEMIC-STROKE | Care and treatment | Genetic aspects | Diagnosis | Research | Gene expression | Blood platelet disorders | Thrombosis | Blood clot | Proteins | Wound healing | Heart attacks | Blood platelets | Microscopy | Colleges & universities | Defects
MEDICINE, RESEARCH & EXPERIMENTAL | GLYCOPROTEIN-VI | ALPHA-GRANULES | BLEEDING-TIME | INTEGRIN | IN-VIVO | ARTERIAL THROMBOSIS | NBEAL2 | GROWTH-FACTOR | PROTEINS | ISCHEMIC-STROKE | Care and treatment | Genetic aspects | Diagnosis | Research | Gene expression | Blood platelet disorders | Thrombosis | Blood clot | Proteins | Wound healing | Heart attacks | Blood platelets | Microscopy | Colleges & universities | Defects
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2015, Volume 10, Issue 7, p. e0133429
Integrin alpha IIb beta 3 plays a central role in the adhesion and aggregation of platelets and thus is essential for hemostasis and thrombosis. Integrin...
ADHESION | ACTIVATION | COLLAGEN | PROTEIN | THROMBOSIS | MULTIDISCIPLINARY SCIENCES | IN-VIVO | MECHANISMS | BINDING | HEMOSTASIS | AGGREGATION | Paxillin - metabolism | Thrombosis - physiopathology | Hemostasis - physiology | Mice, Inbred C57BL | Platelet Activation - physiology | Cytoplasm - metabolism | Platelet Aggregation - physiology | Blood Platelets - physiology | Hydrogen Peroxide - metabolism | Mice, Knockout | Thrombosis - metabolism | Animals | Blood Platelets - metabolism | Focal Adhesions - metabolism | Platelet Glycoprotein GPIIb-IIIa Complex - metabolism | Female | Mice | Focal Adhesions - physiology | Flow cytometry | Immunoglobulins | Senescence | Hydrogen peroxide | Cloning | Glycoproteins | Platelet aggregation | Agglomeration | Thrombosis | Adhesion | Proteins | Medicine | Blood platelets | Hemostasis | Collagen | Stem cells | Ligands | Hemostatics | Thromboembolism | Platelets | Paxillin | Hydrogen ion concentration
ADHESION | ACTIVATION | COLLAGEN | PROTEIN | THROMBOSIS | MULTIDISCIPLINARY SCIENCES | IN-VIVO | MECHANISMS | BINDING | HEMOSTASIS | AGGREGATION | Paxillin - metabolism | Thrombosis - physiopathology | Hemostasis - physiology | Mice, Inbred C57BL | Platelet Activation - physiology | Cytoplasm - metabolism | Platelet Aggregation - physiology | Blood Platelets - physiology | Hydrogen Peroxide - metabolism | Mice, Knockout | Thrombosis - metabolism | Animals | Blood Platelets - metabolism | Focal Adhesions - metabolism | Platelet Glycoprotein GPIIb-IIIa Complex - metabolism | Female | Mice | Focal Adhesions - physiology | Flow cytometry | Immunoglobulins | Senescence | Hydrogen peroxide | Cloning | Glycoproteins | Platelet aggregation | Agglomeration | Thrombosis | Adhesion | Proteins | Medicine | Blood platelets | Hemostasis | Collagen | Stem cells | Ligands | Hemostatics | Thromboembolism | Platelets | Paxillin | Hydrogen ion concentration
Journal Article
Annals of Neurology, ISSN 0364-5134, 05/2015, Volume 77, Issue 5, pp. 784 - 803
Objective Recent evidence suggests that ischemic stroke is a thromboinflammatory disease. Plasma kallikrein (PK) cleaves high–molecular‐weight kininogen to...
ACTIVATION | INHIBITION | THROMBUS FORMATION | INFLAMMATION | ACUTE ISCHEMIC-STROKE | REGULATORY T-CELLS | REPERFUSION | MICE | NEUROSCIENCES | BRAIN | CLINICAL NEUROLOGY | PROTECTS | Plasma Kallikrein - metabolism | Stroke - prevention & control | Mice, Inbred C57BL | Plasma Kallikrein - antagonists & inhibitors | Male | Inflammation - blood | Stroke - genetics | Mice, Knockout | Brain Infarction - prevention & control | Stroke - blood | Plasma Kallikrein - genetics | Animals | Brain Infarction - blood | Inflammation - genetics | Female | Thrombosis - genetics | Inflammation - prevention & control | Mice | Thrombosis - blood | Thrombosis - prevention & control | Brain Infarction - genetics | Plasma | Stroke | Thrombosis | Rodents
ACTIVATION | INHIBITION | THROMBUS FORMATION | INFLAMMATION | ACUTE ISCHEMIC-STROKE | REGULATORY T-CELLS | REPERFUSION | MICE | NEUROSCIENCES | BRAIN | CLINICAL NEUROLOGY | PROTECTS | Plasma Kallikrein - metabolism | Stroke - prevention & control | Mice, Inbred C57BL | Plasma Kallikrein - antagonists & inhibitors | Male | Inflammation - blood | Stroke - genetics | Mice, Knockout | Brain Infarction - prevention & control | Stroke - blood | Plasma Kallikrein - genetics | Animals | Brain Infarction - blood | Inflammation - genetics | Female | Thrombosis - genetics | Inflammation - prevention & control | Mice | Thrombosis - blood | Thrombosis - prevention & control | Brain Infarction - genetics | Plasma | Stroke | Thrombosis | Rodents
Journal Article
Stroke, ISSN 0039-2499, 11/2013, Volume 44, Issue 11, pp. 3202 - 3210
Journal Article
STROKE, ISSN 0039-2499, 11/2013, Volume 44, Issue 11, pp. 3202 - 3210
Background and Purpose Lymphocytes are important players in the pathophysiology of acute ischemic stroke. The interaction of lymphocytes with endothelial cells...
MCAO | thrombo-inflammation | PROTECTION | INJURY | RECEPTOR | MECHANISMS | BLOOD-BRAIN-BARRIER | CLINICAL NEUROLOGY | RESPONSES | RECOVERY | microvascular dysfunction | inflammation | FTY720 | SPHINGOSINE-1-PHOSPHATE | PERIPHERAL VASCULAR DISEASE | FINGOLIMOD | ischemic stroke | T-LYMPHOCYTES | Neuroprotective Agents - therapeutic use | Propylene Glycols - pharmacology | Neurons - pathology | Brain Ischemia - therapy | Enzyme Inhibitors - pharmacology | Fingolimod Hydrochloride | Male | Mice, Transgenic | Middle Cerebral Artery - pathology | Lymphopenia - pathology | Homeodomain Proteins - genetics | Sphingosine - pharmacology | Inflammation - therapy | Sphingosine - analogs & derivatives | Animals | Lymphocytes - drug effects | Hypoxia | Mice | Immunosuppressive Agents - pharmacology | Stroke - therapy | Thrombosis - therapy | Index Medicus
MCAO | thrombo-inflammation | PROTECTION | INJURY | RECEPTOR | MECHANISMS | BLOOD-BRAIN-BARRIER | CLINICAL NEUROLOGY | RESPONSES | RECOVERY | microvascular dysfunction | inflammation | FTY720 | SPHINGOSINE-1-PHOSPHATE | PERIPHERAL VASCULAR DISEASE | FINGOLIMOD | ischemic stroke | T-LYMPHOCYTES | Neuroprotective Agents - therapeutic use | Propylene Glycols - pharmacology | Neurons - pathology | Brain Ischemia - therapy | Enzyme Inhibitors - pharmacology | Fingolimod Hydrochloride | Male | Mice, Transgenic | Middle Cerebral Artery - pathology | Lymphopenia - pathology | Homeodomain Proteins - genetics | Sphingosine - pharmacology | Inflammation - therapy | Sphingosine - analogs & derivatives | Animals | Lymphocytes - drug effects | Hypoxia | Mice | Immunosuppressive Agents - pharmacology | Stroke - therapy | Thrombosis - therapy | Index Medicus
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 09/2013, Volume 33, Issue 9, pp. 2212 - 2217
OBJECTIVE—We recently showed that mice lacking the lipid signaling enzyme phospholipase (PL) D1 or both PLD isoforms (PLD1 and PLD2) were protected from...
phospholipase D | thrombosis | 5-fluoro-2-indolyl des-chlorohalopemide | cerebral stroke | PLATELETS | RISK | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | MOLECULAR-MECHANISMS | HALOPEMIDE | Carotid Artery Diseases - prevention & control | Infarction, Middle Cerebral Artery - physiopathology | Infarction, Middle Cerebral Artery - prevention & control | Carotid Artery Diseases - physiopathology | Blood Platelets - enzymology | Recovery of Function | Dose-Response Relationship, Drug | Time Factors | Infarction, Middle Cerebral Artery - genetics | Indoles - pharmacology | Phospholipase D - genetics | Thrombosis - blood | Thrombosis - prevention & control | Blood Platelets - drug effects | Domperidone - analogs & derivatives | Integrins - blood | Disease Models, Animal | Hemostasis - drug effects | Thrombosis - physiopathology | Phospholipase D - deficiency | Mice, Inbred C57BL | Thrombosis - enzymology | Enzyme Inhibitors - pharmacology | Phospholipase D - antagonists & inhibitors | Infarction, Middle Cerebral Artery - blood | Mice, Knockout | Fibrinolytic Agents - pharmacology | Animals | Carotid Artery Diseases - enzymology | Carotid Artery Diseases - blood | Carotid Artery Diseases - genetics | Domperidone - pharmacology | Thrombosis - genetics | Mice | Infarction, Middle Cerebral Artery - enzymology
phospholipase D | thrombosis | 5-fluoro-2-indolyl des-chlorohalopemide | cerebral stroke | PLATELETS | RISK | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | MOLECULAR-MECHANISMS | HALOPEMIDE | Carotid Artery Diseases - prevention & control | Infarction, Middle Cerebral Artery - physiopathology | Infarction, Middle Cerebral Artery - prevention & control | Carotid Artery Diseases - physiopathology | Blood Platelets - enzymology | Recovery of Function | Dose-Response Relationship, Drug | Time Factors | Infarction, Middle Cerebral Artery - genetics | Indoles - pharmacology | Phospholipase D - genetics | Thrombosis - blood | Thrombosis - prevention & control | Blood Platelets - drug effects | Domperidone - analogs & derivatives | Integrins - blood | Disease Models, Animal | Hemostasis - drug effects | Thrombosis - physiopathology | Phospholipase D - deficiency | Mice, Inbred C57BL | Thrombosis - enzymology | Enzyme Inhibitors - pharmacology | Phospholipase D - antagonists & inhibitors | Infarction, Middle Cerebral Artery - blood | Mice, Knockout | Fibrinolytic Agents - pharmacology | Animals | Carotid Artery Diseases - enzymology | Carotid Artery Diseases - blood | Carotid Artery Diseases - genetics | Domperidone - pharmacology | Thrombosis - genetics | Mice | Infarction, Middle Cerebral Artery - enzymology
Journal Article
Thrombosis and Haemostasis, ISSN 0340-6245, 07/2015, Volume 113, Issue 4, pp. 870 - 880
Summary Factor VII (FVII) activating protease (FSAP) is a circulating protease with a putative function in blood coagulation and fibrinolysis. Genetic...
Stroke, Systemic or Venous Thromboembolism | Haemostasis | Fibrinolysis | FSAP | Thrombosis | HABP2 | Coagulation | LIVER FIBROSIS | RISK | PROTEOLYSIS | fibrinolysis | thrombosis | haemostasis | G534E | PERIPHERAL VASCULAR DISEASE | MARBURG-I POLYMORPHISM | HEMATOLOGY | FACTOR PATHWAY INHIBITOR | Carotid Artery Diseases - prevention & control | Serine Endopeptidases - administration & dosage | Thrombosis - chemically induced | Carotid Artery Diseases - chemically induced | Mesenteric Vascular Occlusion - genetics | Venous Thromboembolism - blood | Chlorides | Serine Endopeptidases - genetics | Carotid Arteries - enzymology | Mesenteric Vascular Occlusion - enzymology | Thrombosis - blood | Thrombosis - prevention & control | Disease Models, Animal | Genetic Predisposition to Disease | Serine Endopeptidases - deficiency | Mesenteric Vascular Occlusion - prevention & control | Mice, Inbred C57BL | Thrombosis - enzymology | Hemostasis - genetics | Lipoproteins - blood | Mesenteric Vascular Occlusion - blood | Venous Thromboembolism - enzymology | Mice, Knockout | Ferric Compounds | Phenotype | Venous Thromboembolism - genetics | Animals | Carotid Artery Diseases - enzymology | Carotid Artery Diseases - blood | Collagen | Carotid Artery Diseases - genetics | Venous Thromboembolism - chemically induced | Blood Coagulation Tests | Thrombosis - genetics | Jugular Veins - enzymology | Norepinephrine | Mesenteric Vascular Occlusion - chemically induced | Mesenteric Arteries - enzymology
Stroke, Systemic or Venous Thromboembolism | Haemostasis | Fibrinolysis | FSAP | Thrombosis | HABP2 | Coagulation | LIVER FIBROSIS | RISK | PROTEOLYSIS | fibrinolysis | thrombosis | haemostasis | G534E | PERIPHERAL VASCULAR DISEASE | MARBURG-I POLYMORPHISM | HEMATOLOGY | FACTOR PATHWAY INHIBITOR | Carotid Artery Diseases - prevention & control | Serine Endopeptidases - administration & dosage | Thrombosis - chemically induced | Carotid Artery Diseases - chemically induced | Mesenteric Vascular Occlusion - genetics | Venous Thromboembolism - blood | Chlorides | Serine Endopeptidases - genetics | Carotid Arteries - enzymology | Mesenteric Vascular Occlusion - enzymology | Thrombosis - blood | Thrombosis - prevention & control | Disease Models, Animal | Genetic Predisposition to Disease | Serine Endopeptidases - deficiency | Mesenteric Vascular Occlusion - prevention & control | Mice, Inbred C57BL | Thrombosis - enzymology | Hemostasis - genetics | Lipoproteins - blood | Mesenteric Vascular Occlusion - blood | Venous Thromboembolism - enzymology | Mice, Knockout | Ferric Compounds | Phenotype | Venous Thromboembolism - genetics | Animals | Carotid Artery Diseases - enzymology | Carotid Artery Diseases - blood | Collagen | Carotid Artery Diseases - genetics | Venous Thromboembolism - chemically induced | Blood Coagulation Tests | Thrombosis - genetics | Jugular Veins - enzymology | Norepinephrine | Mesenteric Vascular Occlusion - chemically induced | Mesenteric Arteries - enzymology
Journal Article
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Full Text
Altered BCR signalling quality predisposes to autoimmune disease and a pre‐diabetic state
The EMBO Journal, ISSN 0261-4189, 08/2012, Volume 31, Issue 15, pp. 3363 - 3374
The spleen tyrosine kinase family members Syk and Zap‐70 are pivotal signal transducers downstream of antigen receptors and exhibit overlapping expression...
B cell | autoimmunity | Syk | Zap‐70 | Zap-70 | B-CELL DEVELOPMENT | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | ANTIBODY | PROTEIN-TYROSINE KINASE | MARGINAL-ZONE | LECTIN RECEPTORS | CELL BIOLOGY | MICE | T-CELLS | Genetic Predisposition to Disease | Proto-Oncogene Proteins c-bcr - metabolism | Prediabetic State - genetics | Humans | Mice, Inbred C57BL | Cells, Cultured | B-Lymphocytes - physiology | ZAP-70 Protein-Tyrosine Kinase - genetics | Mice, Transgenic | Signal Transduction - genetics | Gene Knock-In Techniques | Autoimmune Diseases - genetics | Protein-Tyrosine Kinases - genetics | Animals | B-Lymphocytes - immunology | Proto-Oncogene Proteins c-bcr - physiology | Proto-Oncogene Proteins c-bcr - genetics | Mice | Gene Rearrangement, B-Lymphocyte - genetics | Intracellular Signaling Peptides and Proteins - genetics | Syk Kinase | B-Lymphocytes - metabolism | Signal transduction | Diabetes | Autoimmune diseases | Kinases | Molecular biology
B cell | autoimmunity | Syk | Zap‐70 | Zap-70 | B-CELL DEVELOPMENT | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | ANTIBODY | PROTEIN-TYROSINE KINASE | MARGINAL-ZONE | LECTIN RECEPTORS | CELL BIOLOGY | MICE | T-CELLS | Genetic Predisposition to Disease | Proto-Oncogene Proteins c-bcr - metabolism | Prediabetic State - genetics | Humans | Mice, Inbred C57BL | Cells, Cultured | B-Lymphocytes - physiology | ZAP-70 Protein-Tyrosine Kinase - genetics | Mice, Transgenic | Signal Transduction - genetics | Gene Knock-In Techniques | Autoimmune Diseases - genetics | Protein-Tyrosine Kinases - genetics | Animals | B-Lymphocytes - immunology | Proto-Oncogene Proteins c-bcr - physiology | Proto-Oncogene Proteins c-bcr - genetics | Mice | Gene Rearrangement, B-Lymphocyte - genetics | Intracellular Signaling Peptides and Proteins - genetics | Syk Kinase | B-Lymphocytes - metabolism | Signal transduction | Diabetes | Autoimmune diseases | Kinases | Molecular biology
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 06/2016, Volume 36, Issue 6, pp. 1247 - 1253
OBJECTIVE—Ischemic stroke, which is mainly caused by thromboembolic occlusion of brain arteries, is the second leading cause of death and disability worldwide...
Syk kinase | thrombosis | mice | stroke | platelets | ACTIVATION | DISCOVERY | GLYCOPROTEIN VI | TRIAL | SPLEEN TYROSINE KINASE | ACUTE ISCHEMIC-STROKE | CHRONIC LYMPHOCYTIC-LEUKEMIA | PERIPHERAL VASCULAR DISEASE | SEPARATION | HEMATOLOGY | HEMOSTASIS | Arterial Occlusive Diseases - blood | Infarction, Middle Cerebral Artery - prevention & control | Brain - enzymology | Motor Activity - drug effects | Blood Platelets - enzymology | Syk Kinase - antagonists & inhibitors | Arterial Occlusive Diseases - genetics | Dose-Response Relationship, Drug | Time Factors | Syk Kinase - genetics | Infarction, Middle Cerebral Artery - genetics | Thrombosis - blood | Thrombosis - prevention & control | Blood Platelets - drug effects | Disease Models, Animal | Hemostasis - drug effects | Administration, Oral | Mice, Inbred C57BL | Thrombosis - enzymology | Genotype | Syk Kinase - deficiency | Arterial Occlusive Diseases - enzymology | Infarction, Middle Cerebral Artery - blood | Mice, Knockout | Brain - drug effects | Protein Kinase Inhibitors - administration & dosage | Phenotype | Animals | Signal Transduction - drug effects | Brain - pathology | Thrombosis - genetics | Fibrinolytic Agents - administration & dosage | Arterial Occlusive Diseases - prevention & control | Syk Kinase - blood | Infarction, Middle Cerebral Artery - enzymology
Syk kinase | thrombosis | mice | stroke | platelets | ACTIVATION | DISCOVERY | GLYCOPROTEIN VI | TRIAL | SPLEEN TYROSINE KINASE | ACUTE ISCHEMIC-STROKE | CHRONIC LYMPHOCYTIC-LEUKEMIA | PERIPHERAL VASCULAR DISEASE | SEPARATION | HEMATOLOGY | HEMOSTASIS | Arterial Occlusive Diseases - blood | Infarction, Middle Cerebral Artery - prevention & control | Brain - enzymology | Motor Activity - drug effects | Blood Platelets - enzymology | Syk Kinase - antagonists & inhibitors | Arterial Occlusive Diseases - genetics | Dose-Response Relationship, Drug | Time Factors | Syk Kinase - genetics | Infarction, Middle Cerebral Artery - genetics | Thrombosis - blood | Thrombosis - prevention & control | Blood Platelets - drug effects | Disease Models, Animal | Hemostasis - drug effects | Administration, Oral | Mice, Inbred C57BL | Thrombosis - enzymology | Genotype | Syk Kinase - deficiency | Arterial Occlusive Diseases - enzymology | Infarction, Middle Cerebral Artery - blood | Mice, Knockout | Brain - drug effects | Protein Kinase Inhibitors - administration & dosage | Phenotype | Animals | Signal Transduction - drug effects | Brain - pathology | Thrombosis - genetics | Fibrinolytic Agents - administration & dosage | Arterial Occlusive Diseases - prevention & control | Syk Kinase - blood | Infarction, Middle Cerebral Artery - enzymology
Journal Article
British Journal of Haematology, ISSN 0007-1048, 06/2016, Volume 173, Issue 5, pp. 769 - 778
Summary Haemostasis including blood coagulation is initiated upon vessel wall injury and indispensable to limit excessive blood loss. However, unregulated...
coagulation factor XII | inhibitors | contact activation | Thrombosis | experimental animal models | Experimental animal models | Inhibitors | Contact activation | Coagulation factor XII | ACTIVATION | MECHANISMS | FACTOR-XII | SUPPORT | THERAPY | ROLES | TARGETS | HEMATOLOGY | CEREBRAL-ISCHEMIA | CONTACT PATHWAY | INFESTIN-4 | Hemostasis - drug effects | Rabbits | Insect Proteins - pharmacology | Recombinant Fusion Proteins - pharmacology | Venous Thrombosis - drug therapy | Recombinant Fusion Proteins - therapeutic use | Treatment Outcome | Serum Albumin, Human | Venous Thrombosis - etiology | Arterial Occlusive Diseases - etiology | Serum Albumin - therapeutic use | Fibrinolytic Agents - pharmacology | Animals | Factor XIIa - antagonists & inhibitors | Serum Albumin - pharmacology | Arterial Occlusive Diseases - drug therapy | Thrombosis - etiology | Insect Proteins - therapeutic use | Mice | Thrombosis - drug therapy | Kinetics | Disease Models, Animal | Anticoagulants (Medicine) | Glycosaminoglycans | Analysis | Blood clot
coagulation factor XII | inhibitors | contact activation | Thrombosis | experimental animal models | Experimental animal models | Inhibitors | Contact activation | Coagulation factor XII | ACTIVATION | MECHANISMS | FACTOR-XII | SUPPORT | THERAPY | ROLES | TARGETS | HEMATOLOGY | CEREBRAL-ISCHEMIA | CONTACT PATHWAY | INFESTIN-4 | Hemostasis - drug effects | Rabbits | Insect Proteins - pharmacology | Recombinant Fusion Proteins - pharmacology | Venous Thrombosis - drug therapy | Recombinant Fusion Proteins - therapeutic use | Treatment Outcome | Serum Albumin, Human | Venous Thrombosis - etiology | Arterial Occlusive Diseases - etiology | Serum Albumin - therapeutic use | Fibrinolytic Agents - pharmacology | Animals | Factor XIIa - antagonists & inhibitors | Serum Albumin - pharmacology | Arterial Occlusive Diseases - drug therapy | Thrombosis - etiology | Insect Proteins - therapeutic use | Mice | Thrombosis - drug therapy | Kinetics | Disease Models, Animal | Anticoagulants (Medicine) | Glycosaminoglycans | Analysis | Blood clot
Journal Article
HAEMATOLOGICA, ISSN 0390-6078, 08/2019, Volume 104, Issue 9, pp. 1892 - 1905
Ca2+ entry via Orai1 store-operated Ca2+ channels in the plasma membrane is critical to cell function, and Orai1 loss causes severe immunodeficiency and...
ACTIVATION | VWF | PORE | DEEP-VEIN THROMBOSIS | TETRASPANIN | ADAM10 | PLATELET-ADHESION | HEMATOLOGY | MYOCARDIAL ISCHEMIA/REPERFUSION INJURY | HEMOSTASIS | CRAC CHANNEL | Index Medicus
ACTIVATION | VWF | PORE | DEEP-VEIN THROMBOSIS | TETRASPANIN | ADAM10 | PLATELET-ADHESION | HEMATOLOGY | MYOCARDIAL ISCHEMIA/REPERFUSION INJURY | HEMOSTASIS | CRAC CHANNEL | Index Medicus
Journal Article
Annals of Neurology, ISSN 0364-5134, 05/2015, Volume 77, Issue 5, pp. 784 - 803
Journal Article
Circulation Research: Journal of the American Heart Association, ISSN 0009-7330, 04/2002, Volume 90, Issue 7, pp. 807 - 813
Coronary microembolization results in progressive myocardial dysfunction, with causal involvement of tumor necrosis factor-α (TNF-α). TNF-α uses a signal...
Coronary microembolization | Tumor necrosis factor-α | Nitric oxide | Sphingosine | nitric oxide | CARDIAC & CARDIOVASCULAR SYSTEMS | ADENOSINE | ISCHEMIA | RECEPTOR | BLOOD-FLOW | sphingosine | tumor necrosis factor-alpha | HEART | CELLULAR BASIS | ANGIOPLASTY | PERIPHERAL VASCULAR DISEASE | coronary microembolization | TNF-ALPHA | HEMATOLOGY | EXPRESSION | DISTAL EMBOLIZATION | Tumor Necrosis Factor-alpha - metabolism | Ethanolamines - pharmacology | Apoptosis - drug effects | Myocardial Contraction - drug effects | Nitric Oxide Synthase - antagonists & inhibitors | Coronary Disease - physiopathology | Nitric Oxide Synthase - genetics | RNA, Messenger - metabolism | Nitric Oxide Synthase Type II | Embolism - physiopathology | Microspheres | Ceramidases | Myocardium - metabolism | Leukocyte Count | Sphingosine - metabolism | Endocannabinoids | Disease Models, Animal | Coronary Circulation | NG-Nitroarginine Methyl Ester - pharmacology | Embolism - complications | Enzyme Inhibitors - pharmacology | Coronary Disease - etiology | Oleic Acids | Amidohydrolases - antagonists & inhibitors | Myocardium - pathology | Coronary Disease - pathology | Animals | Signal Transduction - drug effects | Blood Flow Velocity | Dogs | Nitric Oxide Synthase - metabolism | Nitric Oxide - metabolism
Coronary microembolization | Tumor necrosis factor-α | Nitric oxide | Sphingosine | nitric oxide | CARDIAC & CARDIOVASCULAR SYSTEMS | ADENOSINE | ISCHEMIA | RECEPTOR | BLOOD-FLOW | sphingosine | tumor necrosis factor-alpha | HEART | CELLULAR BASIS | ANGIOPLASTY | PERIPHERAL VASCULAR DISEASE | coronary microembolization | TNF-ALPHA | HEMATOLOGY | EXPRESSION | DISTAL EMBOLIZATION | Tumor Necrosis Factor-alpha - metabolism | Ethanolamines - pharmacology | Apoptosis - drug effects | Myocardial Contraction - drug effects | Nitric Oxide Synthase - antagonists & inhibitors | Coronary Disease - physiopathology | Nitric Oxide Synthase - genetics | RNA, Messenger - metabolism | Nitric Oxide Synthase Type II | Embolism - physiopathology | Microspheres | Ceramidases | Myocardium - metabolism | Leukocyte Count | Sphingosine - metabolism | Endocannabinoids | Disease Models, Animal | Coronary Circulation | NG-Nitroarginine Methyl Ester - pharmacology | Embolism - complications | Enzyme Inhibitors - pharmacology | Coronary Disease - etiology | Oleic Acids | Amidohydrolases - antagonists & inhibitors | Myocardium - pathology | Coronary Disease - pathology | Animals | Signal Transduction - drug effects | Blood Flow Velocity | Dogs | Nitric Oxide Synthase - metabolism | Nitric Oxide - metabolism
Journal Article
The EMBO Journal, ISSN 0261-4189, 08/2012, Volume 31, Issue 15, pp. 3363 - 3374
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 08/2013, Volume 123, Issue 8, pp. 3331 - 3331
Platelets are anuclear organelle-rich cell fragments derived from bone marrow megakaryocytes (MKs) that safeguard vascular integrity. The major platelet...
Journal Article
Haematologica, 09/2019, Volume 104, Issue 9, p. 1892
Ca entry Orai1 store-operated Ca channels in the plasma membrane is critical to cell function, and Orai1 loss causes severe immunodeficiency and developmental...
Journal Article