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1. Full Text MicroRNA-150 regulates blood-brain barrier permeability via Tie-2 after permanent middle cerebral artery occlusion in rats
by Fang, Zhi and He, Quan-Wei and Li, Qian and Chen, Xiao-Lu and Baral, Suraj and Jin, Hui-Juan and Zhu, Yi-Yi and Li, Man and Xia, Yuan-Peng and Mao, Ling and Hu, Bo
FASEB Journal, ISSN 0892-6638, 06/2016, Volume 30, Issue 6, pp. 2097 - 2107
The mechanism of blood-brain barrier (BBB) disruption, involved in poststroke edema and hemorrhagic transformation, is important but elusive. We investigated... 
Claudin-5 | Ischemic stroke | BMEC | Apoptosis | ANGIOGENESIS | VEGF | BIOCHEMISTRY & MOLECULAR BIOLOGY | apoptosis | ISCHEMIA | ANGIOPOIETIN-1 | CELL BIOLOGY | STROKE | IN-VITRO | DISRUPTION | ENDOTHELIAL-CELLS | BIOLOGY | NEOVASCULARIZATION | EXPRESSION | ischemic stroke | claudin-5 | Up-Regulation | Claudin-5 - metabolism | Rats | Claudin-5 - genetics | MicroRNAs - metabolism | Middle Cerebral Artery - pathology | Permeability | Infarction, Middle Cerebral Artery - metabolism | Receptor, TIE-2 - genetics | Animals | Blood-Brain Barrier - physiology | Receptor, TIE-2 - metabolism | MicroRNAs - genetics | Endothelial Cells - physiology | Index Medicus
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2. Full Text Expression of Tie-2 by Human Monocytes and Their Responses to Angiopoietin-2
by Murdoch, Craig and Tazzyman, Simon and Webster, Steve and Lewis, Claire E
The Journal of Immunology, ISSN 0022-1767, 06/2007, Volume 178, Issue 11, pp. 7405 - 7411
Angiopoietins 1 and 2 bind to Tie-2 expressed on endothelial cells and regulate vessel stabilization and angiogenesis. Tie-2(+) monocytes have been shown to be... 
TUMOR-NECROSIS-FACTOR | HUMAN PERIPHERAL-BLOOD | ANGIOGENESIS | MACROPHAGES | INFLAMMATION | ENDOTHELIAL-CELLS | IN-VIVO | VESSEL FORMATION | RECEPTOR | IMMUNOLOGY | HYPOXIA | Cell Hypoxia - immunology | Humans | Neoplasms, Experimental - enzymology | Monocytes - metabolism | Neoplasms, Experimental - pathology | Lymphocyte Subsets - metabolism | RNA, Messenger - biosynthesis | Cell Membrane - pathology | Monocytes - pathology | Angiopoietin-2 - physiology | Granulocytes - pathology | Neovascularization, Pathologic - immunology | Granulocytes - metabolism | Receptor, TIE-2 - physiology | Inflammation Mediators - physiology | Lymphocyte Subsets - pathology | Cytokines - metabolism | Macrophages - pathology | Gene Expression Regulation - immunology | RNA, Messenger - genetics | Receptor, TIE-2 - biosynthesis | Cells, Cultured | Granulocytes - enzymology | Macrophages - enzymology | Receptor, TIE-2 - genetics | Cell Membrane - enzymology | Monocytes - enzymology | Macrophages - metabolism | Animals | Up-Regulation - immunology | Lymphocyte Subsets - enzymology | Cell Membrane - immunology | Mice | Cytokines - antagonists & inhibitors | Chemotaxis, Leukocyte - immunology | Neoplasms, Experimental - blood supply | Index Medicus | Abridged Index Medicus
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3. Full Text Wnt5a signaling induces proliferation and survival of endothelial cells in vitro and expression of MMP-1 and Tie-2
by Masckauchán, T. Néstor H and Agalliu, Dritan and Vorontchikhina, Marina and Ahn, Audrey and Parmalee, Nancy L and Li, Chi-Ming and Khoo, Alan and Tycko, Benjamin and Brown, Anthony M. C and Kitajewski, Jan
Molecular Biology of the Cell, ISSN 1059-1524, 12/2006, Volume 17, Issue 12, pp. 5163 - 5172
Wnts are lipid-modified secreted glycoproteins that regulate diverse biological processes. We report that Wnt5a, which functions in noncanonical Wnt signaling,... 
ACTIVATION | PROTEIN | PATHWAY | CLONING | TUMOR ANGIOGENESIS | WNT-5A | BETA-CATENIN | IDENTIFICATION | DISHEVELLED PHOSPHORYLATION | FRIZZLED-4 | CELL BIOLOGY | Phosphorylation | Cell Proliferation | Blood Vessels - metabolism | Humans | Extracellular Signal-Regulated MAP Kinases - metabolism | Wnt-5a Protein | Phosphoproteins - metabolism | RNA, Messenger - metabolism | Wnt Proteins - metabolism | Wnt Proteins - genetics | Microarray Analysis | Receptor, TIE-2 - metabolism | Dishevelled Proteins | Matrix Metalloproteinase 1 - genetics | Proto-Oncogene Proteins - metabolism | Signal Transduction | Cell Survival | RNA, Messenger - genetics | Gene Expression Regulation | Proto-Oncogene Proteins - genetics | Receptor, TIE-2 - genetics | Animals | Frizzled Receptors - genetics | Endothelial Cells - cytology | Mice | Adaptor Proteins, Signal Transducing - metabolism | Matrix Metalloproteinase 1 - metabolism | Cell Movement | Index Medicus
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4. Full Text Fibulin-5 regulates angiopoietin-1/Tie-2 receptor signaling in endothelial cells
by Chan, Wilson and Ismail, Hodan and Mayaki, Dominique and Sanchez, Veronica and Tiedemann, Kerstin and Davis, Elaine C and Hussain, Sabah N. A
PLoS ONE, ISSN 1932-6203, 06/2016, Volume 11, Issue 6, pp. e0156994 - e0156994
Background Fibulin-5 is an extracellular matrix glycoprotein that plays critical roles in vasculogenesis and embryonic development. Deletion of Fibulin-5 in... 
EXTRACELLULAR-MATRIX PROTEINS | ANGIOGENESIS | MECHANISM | TIE2 | PATHWAY | ROLES | MULTIDISCIPLINARY SCIENCES | IN-VIVO | ALPHA-5-BETA-1 | EXPRESSION | Cricetulus | Gene Expression - drug effects | Human Umbilical Vein Endothelial Cells - metabolism | Humans | Immunoblotting | Angiopoietin-1 - metabolism | Early Growth Response Protein 1 - genetics | HEK293 Cells | Receptor, TIE-2 - metabolism | Extracellular Matrix Proteins - metabolism | Angiopoietin-1 - pharmacology | CHO Cells | Recombinant Proteins - metabolism | Cell Survival - drug effects | Cricetinae | Human Umbilical Vein Endothelial Cells - drug effects | Signal Transduction | Extracellular Matrix Proteins - genetics | Cells, Cultured | Extracellular Matrix Proteins - pharmacology | Recombinant Proteins - pharmacology | Reverse Transcriptase Polymerase Chain Reaction | Receptor, TIE-2 - genetics | Angiopoietin-1 - genetics | Animals | Inhibitor of Differentiation Protein 1 - genetics | Protein Binding | Mutation | Kruppel-Like Transcription Factors - genetics | Transcription factors | Phosphorylation | Id1 protein | Laboratories | Toxicity | Angiopoietin | Cytotoxicity | AKT protein | Kinases | Caspase-3 | Cell surface | Cell adhesion & migration | Proteins | Angiogenesis | Signal transduction | Embryogenesis | Cell growth | Clonal deletion | Penicillin | Deletion | Extracellular matrix | Deoxyribonucleic acid--DNA | Kruppel protein | Recombinant | Binding | Deprivation | Proteoglycans | Cell survival | EGR-1 protein | Incubation | Research & development--R&D | Glycoprotein | Extracellular signal-regulated kinase | Caspase | Gene expression | Endothelial cells | Embryonic growth stage | Medicine | Signaling | Inhibitors | Respiratory diseases | Skin | Lung Kruppel-like factor | Heparin | Angiogenesis inhibitors | Viability | Integrins | Index Medicus | Research & development | R&D | Deoxyribonucleic acid | DNA
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5. Full Text Gamma-tocotrienol induces apoptosis in prostate cancer cells by targeting the Ang-1/Tie-2 signalling pathway
by Tang, Kai Dun and Tang, Kai Dun and Liu, Ji and Liu, Ji and Russell, Pamela J and Russell, Pamela J and Clements, Judith A and Clements, Judith A and Ling, Ming-Tat and Ling, Ming-Tat
International Journal of Molecular Sciences, ISSN 1661-6596, 03/2019, Volume 20, Issue 5, p. 1164
Emerging evidence suggests that gamma-tocotrienol (-T3), a vitamin E isomer, has potent anti-cancer properties against a wide-range of cancers. -T3 not only... 
Angiopoietin-1 | Gamma-tocotrienol and autophagy | Tie-2 | Prostate cancer | angiopoietin-1 | VITAMIN-E | gamma-tocotrienol and autophagy | FACTOR-C | BIOCHEMISTRY & MOLECULAR BIOLOGY | RISK | AUTOPHAGY | CHEMISTRY, MULTIDISCIPLINARY | prostate cancer | DISEASE | AMPK | EXPRESSION | ENDOTHELIAL GROWTH-FACTOR | Cell Survival - drug effects | Prostatic Neoplasms - metabolism | Down-Regulation | Humans | Vitamin E - analogs & derivatives | Male | Angiopoietin-1 - metabolism | Autophagy | Receptor, TIE-2 - genetics | Angiopoietin-1 - genetics | Prostatic Neoplasms - genetics | Chromans - pharmacology | Signal Transduction - drug effects | Cell Line, Tumor | Receptor, TIE-2 - metabolism | Cell Proliferation - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Prostatic Neoplasms - drug therapy | Vitamin E - pharmacology | Index Medicus
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6. Full Text Somatic Activating PIK3CA Mutations Cause Venous Malformation
by Limaye, Nisha and Kangas, Jaakko and Mendola, Antonella and Godfraind, Catherine and Schlögel, Matthieu J and Helaers, Raphael and Eklund, Lauri and Boon, Laurence M and Vikkula, Miikka
The American Journal of Human Genetics, ISSN 0002-9297, 12/2015, Volume 97, Issue 6, pp. 914 - 921
Somatic mutations in , the gene encoding endothelial cell tyrosine kinase receptor TIE2, cause more than half of sporadically occurring unifocal venous... 
DIAGNOSIS | OVERGROWTH | GENE | PI3K | LYMPHATIC ENDOTHELIAL-CELLS | GENETICS & HEREDITY | Humans | Vascular Malformations - enzymology | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Neovascularization, Pathologic - pathology | Neovascularization, Pathologic - enzymology | Transfection | Veins - enzymology | Receptor, TIE-2 - metabolism | Receptor, TIE-2 - antagonists & inhibitors | Human Umbilical Vein Endothelial Cells - drug effects | Genetic Association Studies | Signal Transduction | Gene Frequency | Gene Expression Regulation | Vascular Malformations - pathology | Receptor, TIE-2 - genetics | Phosphatidylinositol 3-Kinases - genetics | Class I Phosphatidylinositol 3-Kinases | Human Umbilical Vein Endothelial Cells - enzymology | Alleles | Human Umbilical Vein Endothelial Cells - pathology | Neovascularization, Pathologic - genetics | High-Throughput Nucleotide Sequencing | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Mutation | Vascular Malformations - genetics | Veins - pathology | Arteriovenous malformations | Causes of | Genetic aspects | Gene mutations | Health aspects | Phosphotransferases | Genotype & phenotype | Kinases | Morphology | Cells | Cancer | Index Medicus | Report
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7. Full Text Endothelial destabilization by angiopoietin-2 via integrin β1 activation
by Hakanpaa, Laura and Sipila, Tuomas and Leppanen, Veli-Matti and Gautam, Prson and Nurmi, Harri and Jacquemet, Guillaume and Eklund, Lauri and Ivaska, Johanna and Alitalo, Kari and Saharinen, Pipsa
Nature Communications, ISSN 2041-1723, 01/2015, Volume 6, Issue 1, pp. 5962 - 5962
Angiopoietins regulate vascular homeostasis via the endothelial Tie receptor tyrosine kinases. Angiopoietin-1 (Ang1) supports endothelial stabilization via... 
Cell Line | Endothelial Cells - metabolism | Angiopoietin-2 - genetics | Humans | Male | Mice, Transgenic | Angiopoietin-1 - metabolism | Angiopoietin-2 - metabolism | Receptor, TIE-2 - genetics | Integrin beta1 - metabolism | Pregnancy | Angiopoietin-1 - genetics | Animals | Female | Receptor, TIE-2 - metabolism | Mice | Integrin beta1 - genetics | Real-Time Polymerase Chain Reaction | Index Medicus
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8. Full Text Apelin gene therapy increases myocardial vascular density and ameliorates diabetic cardiomyopathy via upregulation of sirtuin 3
by Zeng, Heng and He, Xiaochen and Hou, Xuwei and Li, Lanfang and Chen, Jian-Xiong
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 02/2014, Volume 306, Issue 4, pp. H585 - H597
Microvascular insufficiency contributes to cardiac hypertrophy and worsens heart dysfunction in diabetic cardiomyopathy. Our recent study shows that apelin may... 
VEGF/VEGFR2 | Diabetic cardiomyopathy | Angiogenesis | Sirtuin 3 | Ang-1/Tie-2 | Apelin | NADPH OXIDASE | METABOLIC SYNDROME | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | apelin | sirtuin 3 | angiogenesis | HEART-FAILURE | diabetic cardiomyopathy | TUMOR ANGIOGENESIS | PEPTIDE APELIN | IMPAIRED ANGIOGENESIS | CARDIAC-HYPERTROPHY | PERIPHERAL VASCULAR DISEASE | ORPHAN RECEPTOR APJ | EXPRESSION | ENDOTHELIAL GROWTH-FACTOR | Diabetic Cardiomyopathies - metabolism | Reactive Oxygen Species - metabolism | Sirtuin 3 - metabolism | Male | Vascular Endothelial Growth Factor A - metabolism | Angiopoietin-1 - metabolism | Vascular Endothelial Growth Factor A - genetics | Angiopoietin-2 - metabolism | Diabetic Cardiomyopathies - physiopathology | Receptors, Vascular Endothelial Growth Factor - metabolism | Myocardium - metabolism | Neovascularization, Pathologic - physiopathology | Receptor, TIE-2 - metabolism | Diabetic Cardiomyopathies - therapy | Receptors, Vascular Endothelial Growth Factor - genetics | Neovascularization, Pathologic - therapy | Heart - physiopathology | Sirtuin 3 - genetics | Endothelium, Vascular - physiopathology | Intercellular Signaling Peptides and Proteins - genetics | Up-Regulation - genetics | Adipokines | Receptor, TIE-2 - genetics | Diabetic Cardiomyopathies - genetics | Angiopoietin-1 - genetics | Animals | Endothelium, Vascular - metabolism | Neovascularization, Pathologic - genetics | Mice | Neovascularization, Pathologic - metabolism | Apoptosis - physiology | Prevention | Cardiomyopathy | Physiological aspects | Genetic research | Genetic aspects | Research | Diabetes | Gene therapy | Heart diseases | Heart failure | Rodents | Glucose | Apoptosis | Index Medicus | VEGFR2 | Tie-2 | VEGF | Ang-1 | Integrative Cardiovascular Physiology and Pathophysiology
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9. Full Text Tie-2 regulates the stemness and metastatic properties of prostate cancer cells
by Tang, Kai-Dun and Holzapfel, Boris M and Liu, Ji and Lee, Terence Kin-Wah and Ma, Stephanie and Jovanovic, Lidija and An, Jiyuan and Russell, Pamela J and Clements, Judith A and Hutmacher, Dietmar W and Ling, Ming-Tat
Oncotarget, ISSN 1949-2553, 2016, Volume 7, Issue 3, pp. 2572 - 2584
Ample evidence supports that prostate tumor metastasis originates from a rare population of cancer cells, known as cancer stem cells (CSCs). Unfortunately,... 
Metastasis | Cancer stem cells | Tie-2 | Prostate cancer | Prostatic Neoplasms - metabolism | RNA, Small Interfering - genetics | Cell Proliferation | Stromal Cells - pathology | Humans | Male | Immunoenzyme Techniques | Prostatic Neoplasms - genetics | Neoplastic Stem Cells - metabolism | Neoplastic Stem Cells - pathology | Receptor, TIE-2 - metabolism | Tumor Cells, Cultured | Real-Time Polymerase Chain Reaction | Receptor, TIE-2 - antagonists & inhibitors | RNA, Messenger - genetics | Stromal Cells - metabolism | Mice, SCID | Reverse Transcriptase Polymerase Chain Reaction | Cell Adhesion | Receptor, TIE-2 - genetics | Xenograft Model Antitumor Assays | Osteoblasts - pathology | Prostatic Neoplasms - secondary | Animals | Endothelium, Vascular - metabolism | Endothelium, Vascular - pathology | Mice, Inbred NOD | Mice | Osteoblasts - metabolism | Apoptosis | Index Medicus
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10. Full Text Developmental Heterogeneity of Cardiac Fibroblasts Does Not Predict Pathological Proliferation and Activation
by Ali, Shah R and Ranjbarvaziri, Sara and Talkhabi, Mahmood and Zhao, Peng and Subat, Ali and Hojjat, Armin and Kamran, Paniz and Müller, Antonia M.S and Volz, Katharina S and Tang, Zhaoyi and Red-Horse, Kristy and Ardehali, Reza
Circulation Research, ISSN 0009-7330, 09/2014, Volume 115, Issue 7, pp. 625 - 635
RATIONALE:Fibrosis is mediated partly by extracellular matrix–depositing fibroblasts in the heart. Although these mesenchymal cells are reported to have... 
Aging | Growth and development | Cardiac fibroblasts | Fibrosis | CELLS | PRESSURE-OVERLOAD | CONTRIBUTE | CARDIAC & CARDIOVASCULAR SYSTEMS | cardiac fibroblasts | EPICARDIUM | HEART | growth and development | PERIPHERAL VASCULAR DISEASE | fibrosis | aging | NEURAL CREST | HEMATOLOGY | EXPRESSION | LINEAGE | TRANSGENIC MICE | Paired Box Transcription Factors - genetics | PAX3 Transcription Factor | Cell Proliferation | Myocytes, Cardiac - cytology | Bone Marrow Cells - cytology | Mice, Inbred C57BL | Antigens, CD - genetics | T-Box Domain Proteins - genetics | Pericardium - cytology | T-Box Domain Proteins - metabolism | Antigens, CD - metabolism | Receptor, TIE-2 - genetics | Cell Lineage | Animals | Myocytes, Cardiac - metabolism | Receptor, TIE-2 - metabolism | Cell Differentiation | Fibroblasts - cytology | Mice | Pericardium - growth & development | Bone Marrow Cells - metabolism | Paired Box Transcription Factors - metabolism | Cross Circulation | Fibroblasts - metabolism | Index Medicus
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11. Full Text A distinguishing gene signature shared by tumor-infiltrating Tie2-expressing monocytes, blood "resident" monocytes, and embryonic macrophages suggests common functions and developmental relationships
by Pucci, Ferdinando and Venneri, Mary Anna and Biziato, Daniela and Nonis, Alessandro and Moi, Davide and Sica, Antonio and Di Serio, Clelia and Naldini, Luigi and De Palma, Michele
Blood, ISSN 0006-4971, 2009, Volume 114, Issue 4, pp. 901 - 914
We previously showed that Tie2-expressing monocytes (TEMs) have nonredundant proangiogenic activity in tumors. Here, we compared the gene expression profile of... 
ENDOTHELIAL PROGENITOR CELLS | RECRUITMENT | HUMAN PERIPHERAL-BLOOD | DENDRITIC CELLS | ANGIOGENESIS | VASCULOGENESIS | VESSEL FORMATION | RECEPTOR | HEMATOLOGY | CANCER | EXPRESSION | Macrophages - physiology | Oligonucleotide Array Sequence Analysis | Blood Cells - metabolism | Mice, Transgenic | Monocytes - metabolism | Gene Expression Profiling | Embryo, Mammalian - metabolism | Blood Cells - immunology | Receptor, TIE-2 - genetics | Chemotaxis, Leukocyte - genetics | Macrophages - metabolism | Animals | Neoplasms - genetics | Embryo, Mammalian - immunology | Neoplasms - immunology | Monocytes - pathology | Receptor, TIE-2 - metabolism | Mice | Monocytes - physiology | Gene Expression Regulation, Developmental - physiology | Index Medicus | Abridged Index Medicus
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12. Full Text Localization of Ang-1, -2, Tie-2, and VEGF expression at endothelial-pericyte interdigitation in rat angiogenesis
by Wakui, Shin and Yokoo, Kiyofumi and Muto, Tomoko and Suzuki, Yoshihiko and Takahashi, Hiroyuki and Furusato, Masakuni and Hano, Hiroshi and Endou, Hitoshi and Kanai, Yoshikatsu
Laboratory Investigation, ISSN 0023-6837, 11/2006, Volume 86, Issue 11, pp. 1172 - 1184
Endothelial cells and pericytes play critical role in angiogenesis, which is controlled, in part, by the angiopoietin (Ang)/Tie-2 system and vascular... 
Ang-2 | Angiogenesis | Ang-1 | Tie-2 | VEGF | EPI | MEDICINE, RESEARCH & EXPERIMENTAL | angiogenesis | LIGAND ANGIOPOIETIN-2 | BLOOD-VESSEL FORMATION | TUMOR ANGIOGENESIS | PATHOLOGY | SYNTHETIC HYDROGEL | GROWTH-FACTOR-BETA | THERMOREVERSIBLE GELATION | HUMAN GRANULATION-TISSUE | IN-VIVO | EMBRYONIC ANGIOGENESIS | RECEPTOR TYROSINE KINASE | Angiopoietin-2 - genetics | Male | Pericytes - ultrastructure | Vascular Endothelial Growth Factor A - metabolism | Angiopoietin-1 - metabolism | RNA, Messenger - metabolism | Vascular Endothelial Growth Factor A - genetics | Angiopoietin-2 - metabolism | Microscopy, Immunoelectron | Neovascularization, Pathologic - pathology | Receptor, TIE-2 - metabolism | Capillaries - metabolism | Disease Models, Animal | Capillaries - ultrastructure | Fluorescent Antibody Technique, Direct | Pericytes - metabolism | Gene Expression Regulation | Rats | Rats, Sprague-Dawley | Blotting, Western | Receptor, TIE-2 - genetics | Angiopoietin-1 - genetics | Animals | Angiopoietin-1 - analogs & derivatives | Neovascularization, Pathologic - metabolism | Index Medicus
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13. Full Text Angiopoietins assemble distinct Tie2 signalling complexes in endothelial cell-cell and cell-matrix contacts
by Koh, Gou Young and Wirkkala, Riikka and Olsen, Bjorn R and Saharinen, Pipsa and Nottebaum, Astrid and Alitalo, Kari and Anisimov, Andrey and Winderlich, Mark and Vestweber, Dietmar and Deutsch, Urban and Eklund, Lauri and Miettinen, Juho
Nature Cell Biology, ISSN 1465-7392, 05/2008, Volume 10, Issue 5, pp. 527 - 537
The receptor tyrosine kinase Tie2, and its activating ligand Angiopoietin-1 (Ang1), are required for vascular remodelling and vessel integrity, whereas Ang2... 
MIGRATION | IN-VITRO | ACTIVATION | ANGIOGENESIS | PHOSPHORYLATION | GROWTH-FACTORS | BLOOD-VESSEL FORMATION | VE-CADHERIN | EXPRESSION | RECEPTOR TYROSINE KINASE | CELL BIOLOGY | Endothelial Cells - metabolism | Humans | Cells, Cultured | Intercellular Junctions - metabolism | Extracellular Matrix - metabolism | Receptor, TIE-1 - metabolism | Angiopoietin-1 - metabolism | Lung - cytology | Angiopoietin-2 - metabolism | Recombinant Fusion Proteins - metabolism | Receptor, TIE-2 - genetics | Animals | Cell Adhesion - physiology | Endothelial Cells - cytology | Recombinant Fusion Proteins - genetics | Receptor, TIE-2 - metabolism | Signal Transduction - physiology | Cell Movement | Receptor, TIE-1 - genetics | Physiological aspects | Cell interaction | Growth factors | Protein kinases | Index Medicus
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14. Full Text Host genetic diversity enables Ebola hemorrhagic fever pathogenesis and resistance
by Rasmussen, Angela L and Okumura, Atsushi and Ferris, Martin T and Green, Richard and Feldmann, Friederike and Kelly, Sara M and Scott, Dana P and Safronetz, David and Haddock, Elaine and LaCasse, Rachel and Thomas, Matthew J and Sova, Pavel and Carter, Victoria S and Weiss, Jeffrey M and Miller, Darla R and Shaw, Ginger D and Korth, Marcus J and Heise, Mark T and Baric, Ralph S and De Villena, Fernando Pardo-Manuel and Feldmann, Heinz and Katze, Michael G
Science, ISSN 0036-8075, 11/2014, Volume 346, Issue 6212, pp. 987 - 991
Existing mouse models of lethal Ebola virus infection do not reproduce hallmark symptoms of Ebola hemorrhagic fever, neither delayed blood coagulation and... 
COAGULATION | GUINEA-PIGS | OUTBREAK | VIRUS INFECTION | MAP | MULTIDISCIPLINARY SCIENCES | Genetic Predisposition to Disease | Liver - pathology | Neovascularization, Physiologic - genetics | Liver - metabolism | Mice, Inbred C57BL | Endothelium, Vascular - physiopathology | Capillary Permeability - genetics | Receptor, TIE-2 - genetics | Hemorrhagic Fever, Ebola - blood | Liver - blood supply | Lymphocyte Activation - immunology | Animals | Host-Pathogen Interactions - genetics | Alleles | Blood Coagulation - genetics | Hemorrhagic Fever, Ebola - genetics | Hemorrhagic Fever, Ebola - immunology | Mice | Disease Models, Animal | Prevention | Genetic research | Ebola virus infections | Genetic aspects | Research | Virus research | Biological diversity | Ebola virus | Genetic diversity | Drug resistance | Pathogenesis | Hemorrhage | Fever | Index Medicus | Panels | Viral diseases | Coagulation | Genetics | Viruses
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