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PLoS ONE, ISSN 1932-6203, 02/2010, Volume 5, Issue 2, p. e9258
Background: The Notch pathway is essential for proper epidermal differentiation during embryonic skin development. Moreover, skin specific loss of Notch... 
B-CELL DEVELOPMENT | HUMAN EPITHELIAL-CELLS | STEM-CELLS | IN-VITRO | MOUSE KERATINOCYTES | BIOLOGY | MICE | T-CELL | GROWTH-FACTOR | EXPRESSION | THYMIC STROMAL LYMPHOPOIETIN | Dermatitis, Atopic - genetics | Skin - metabolism | Humans | Receptor, Notch2 - genetics | Receptors, Notch - genetics | Myeloproliferative Disorders - genetics | Granulocyte Colony-Stimulating Factor - genetics | Dermatitis, Atopic - mortality | Flow Cytometry | Receptors, Cytokine - metabolism | Receptors, Cytokine - genetics | Granulocyte Colony-Stimulating Factor - metabolism | Skin - pathology | Immunoglobulins | Cytokines - metabolism | Mice, Inbred C57BL | Receptors, Notch - physiology | Mice, Transgenic | Survival Rate | Signal Transduction - genetics | Dermatitis, Atopic - physiopathology | Reverse Transcriptase Polymerase Chain Reaction | Mice, Knockout | Receptor, Notch2 - physiology | Animals | Mice, Nude | Models, Biological | Survival Analysis | Myeloproliferative Disorders - physiopathology | Signal Transduction - physiology | Mice | Skin - physiopathology | Receptor, Notch1 - genetics | Myeloproliferative Disorders - mortality | Receptor, Notch1 - physiology | Embryonic development | Psoriasis | Atopic dermatitis | Bone marrow | Transplantation | Skin | B cells | Syngeneic grafts | Pathogenesis | Bone marrow transplantation | Homeostasis | Lichen planus | Inactivation | Dermatitis | Thymus | Signal transduction | Embryogenesis | Biomedical materials | Immunology | Granulocytes | Granulocyte colony-stimulating factor | Lymphocytes | Rodents | Biocompatibility | Drug dosages | Osteopenia | Neutropenia | Spleen | Repressing | Deactivation | Cytokines | Developmental biology | Dermatology | Leukocytes (eosinophilic) | Neutrophils | Keratinocytes | Breast cancer | Gene expression | Myeloproliferative diseases | Hemopoiesis | Signaling | Thymic stromal lymphopoietin | Stem cells | Mast cells | Infiltration | Notch protein | Bone | Hematopoietic system | Mutation | Eosinophils
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 2017, Volume 292, Issue 44, pp. 18178 - 18191
Unlike age-matched men, premenopausal women benefit from cardiovascular protection. Estrogens protect against apoptosis of endothelial cells (ECs), one of the... 
Endothelium, Vascular - cytology | Tumor Necrosis Factor-alpha - metabolism | Apoptosis - drug effects | Humans | Receptor, Notch1 - chemistry | Endothelium, Vascular - drug effects | Estrogen Receptor beta - metabolism | Protease Inhibitors - pharmacology | Estrogen Receptor alpha - agonists | Estrogen Receptor beta - agonists | Estrogen Receptor beta - genetics | Protein Processing, Post-Translational - drug effects | RNA Interference | Receptor, Notch1 - agonists | Human Umbilical Vein Endothelial Cells - cytology | Estrogen Receptor alpha - metabolism | Protein Interaction Domains and Motifs | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Estrogen Receptor beta - antagonists & inhibitors | Peptide Fragments - genetics | Endothelium, Vascular - immunology | Recombinant Proteins - metabolism | Estradiol - metabolism | Peptide Fragments - metabolism | Cells, Cultured | Recombinant Proteins - chemistry | Estrogen Receptor alpha - antagonists & inhibitors | Receptor, Notch1 - metabolism | Amyloid Precursor Protein Secretases - metabolism | Peptide Fragments - chemistry | Estrogen Receptor alpha - genetics | Signal Transduction - drug effects | Endothelium, Vascular - metabolism | Peptide Fragments - agonists | Proto-Oncogene Proteins c-akt - agonists | Protein Kinase Inhibitors - pharmacology | Amyloid Precursor Protein Secretases - antagonists & inhibitors | Receptor, Notch1 - genetics | Tumor Necrosis Factor-alpha - antagonists & inhibitors | estrogen | Notch pathway | tumor necrosis factor (TNF) | ERβ | estrogen receptor | Notch1 | apoptosis | Akt | endothelial dysfunction | Cell Biology
Journal Article
Cancer Research, ISSN 0008-5472, 10/2009, Volume 69, Issue 19, pp. 7569 - 7576
Journal Article
Breast Cancer Research, ISSN 1465-5411, 06/2014, Volume 16, Issue 3, pp. R62 - R62
Introduction: Resistance to anti-estrogen therapies is a major cause of disease relapse and mortality in estrogen receptor alpha (ERa)-positive breast cancers.... 
STEM-CELLS | ACTIVATION | INHIBITION | ONCOLOGY | PATHWAY | TAMOXIFEN RESISTANCE | GROWTH | ALPHA | EXPRESSION | ESTROGEN-RECEPTOR | MODULATION | Amyloid Precursor Protein Secretases - genetics | Receptors, Notch - metabolism | CD24 Antigen - metabolism | Epithelial-Mesenchymal Transition - physiology | Humans | Membrane Glycoproteins - biosynthesis | Gene Expression Regulation, Neoplastic | Receptors, Notch - genetics | Membrane Glycoproteins - antagonists & inhibitors | MCF-7 Cells | RNA Interference | Hyaluronan Receptors - metabolism | Estrogen Receptor alpha - metabolism | Female | Tumor Cells, Cultured | Spheroids, Cellular | Proto-Oncogene Proteins - metabolism | Antineoplastic Agents, Hormonal - pharmacology | Neoplasm Invasiveness | Antibodies, Monoclonal - pharmacology | Valine - analogs & derivatives | Receptor, Notch2 - metabolism | Proto-Oncogene Proteins - genetics | Receptor, Notch1 - metabolism | Breast Neoplasms - drug therapy | Membrane Glycoproteins - genetics | Cell Movement - drug effects | Drug Resistance, Neoplasm - genetics | Breast Neoplasms - pathology | Tetrahydronaphthalenes - pharmacology | Tamoxifen - pharmacology | RNA, Small Interfering | Amyloid Precursor Protein Secretases - antagonists & inhibitors | Valine - pharmacology | Selective Estrogen Receptor Modulators - pharmacology | Receptor, Notch4 | Amyloid Precursor Protein Secretases - biosynthesis | Medical equipment and supplies industry | Pharmaceutical industry | Health aspects | Medical test kit industry
Journal Article
Nature, ISSN 0028-0836, 04/2010, Volume 464, Issue 7291, pp. 1052 - 1057
The four receptors of the Notch family are widely expressed transmembrane proteins that function as key conduits through which mammalian cells communicate to... 
B-CELLS | ANTI-P185HER2 ANTIBODY | ANGIOGENESIS | MULTIDISCIPLINARY SCIENCES | REGULATORY REGION | MALIGNANT-MELANOMA | MUTATIONS | LEUKEMIA | GAMMA-SECRETASE | CANCER-THERAPY | INHIBITS TUMOR-GROWTH | Angiogenesis Inhibitors - immunology | Neoplasms - metabolism | NIH 3T3 Cells | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - pathology | Receptor, Notch2 - antagonists & inhibitors | Receptors, Notch - metabolism | Humans | Goblet Cells - drug effects | Receptors, Notch - genetics | Peptide Library | Receptors, Notch - antagonists & inhibitors | Antibody Specificity - immunology | Angiogenesis Inhibitors - therapeutic use | Antibodies - immunology | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - metabolism | Antibodies - therapeutic use | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - drug therapy | Angiogenesis Inhibitors - pharmacology | Receptor, Notch1 - immunology | Neoplasms - blood supply | Receptor, Notch2 - immunology | Antibodies - adverse effects | Neoplasms - drug therapy | Antibodies - pharmacology | Animals | Signal Transduction - drug effects | Neovascularization, Pathologic - drug therapy | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Mice, Inbred BALB C | Goblet Cells - pathology | Receptor, Notch1 - antagonists & inhibitors | Neoplasms - pathology | Receptors, Notch - immunology | Viral antibodies | Proteases | Proteolysis | Physiological aspects | Antibodies | Research | Properties | Membrane proteins | Cell growth | Cell cycle | Cancer | Crystal structure | Apoptosis | Receptors | Inhibitors | Toxicity | Notches | Mathematical models | Inhibition | Signalling | Diseases | Index Medicus
Journal Article
Angiogenesis, ISSN 0969-6970, 10/2013, Volume 16, Issue 4, pp. 921 - 937
Notch is an intercellular signaling pathway related mainly to sprouting neo-angiogenesis. The objective of our study was to evaluate the angiogenic mechanisms... 
Angiogenesis | Biomedicine | Notch signaling | EphrinB2/EphB4 | Cancer Research | Oncology | Ophthalmology | Molecular regulation of intussusceptive angiogenesis | SDF-1/CXCR4 | Cardiology | Biomedicine general | Cell Biology | ACTIVATION | RECEPTOR | LIGAND DELTA-LIKE-4 | SPECIFICATION | VASCULAR MORPHOGENESIS | PATHWAY | ENDOTHELIAL-CELLS | GROWTH | PERIPHERAL VASCULAR DISEASE | TIP | EXPRESSION | Liver - pathology | Male | Receptor, EphB4 - genetics | RNA, Messenger - biosynthesis | Receptor, Notch1 - deficiency | Receptors, Notch - antagonists & inhibitors | Chemokine CXCL12 - genetics | Receptor, EphB2 - biosynthesis | Pericytes - pathology | Bone Marrow Transplantation | Leukocytes, Mononuclear - transplantation | Neovascularization, Pathologic - physiopathology | Neovascularization, Pathologic - prevention & control | Receptors, CXCR4 - genetics | Receptors, Vascular Endothelial Growth Factor - genetics | Liver - metabolism | Mice, Inbred C57BL | RNA, Messenger - genetics | Receptor, TIE-2 - biosynthesis | Receptors, Vascular Endothelial Growth Factor - biosynthesis | Gene Expression Regulation | Receptors, Notch - physiology | Receptor, EphB2 - genetics | Chick Embryo | Receptor, TIE-2 - genetics | Animals | Receptors, CXCR4 - biosynthesis | Signal Transduction - drug effects | Chemokine CXCL12 - biosynthesis | Neovascularization, Pathologic - genetics | Signal Transduction - physiology | Mice | Mice, Inbred BALB C | Receptor, EphB4 - biosynthesis | Amyloid Precursor Protein Secretases - antagonists & inhibitors | Oligopeptides - pharmacology
Journal Article
Cancer Research, ISSN 0008-5472, 07/2008, Volume 68, Issue 13, pp. 5226 - 5235
Journal Article
Journal of Allergy and Clinical Immunology, The, ISSN 0091-6749, 2015, Volume 136, Issue 2, pp. 441 - 453
Background Traffic-related particulate matter (PM) has been linked to a heightened incidence of asthma and allergic diseases. However, the molecular mechanisms... 
Allergy and Immunology | airway hyperresponsiveness | Traffic-related particulate matter | diesel exhaust particles | ultrafine particles | Jagged 1 | Notch | asthma | allergic airway inflammation | aryl hydrocarbon receptor | AMBIENT PARTICULATE MATTER | OXIDATIVE STRESS | DENDRITIC CELLS | IMMUNOLOGY | POLLUTION | NRF2 | ALLERGY | CHEMICALS | airway hyper-responsiveness | HEALTH | TRANSCRIPTION FACTOR | Allergens - adverse effects | Bronchial Hyperreactivity - immunology | Dendritic Cells - immunology | Humans | Dendritic Cells - pathology | Gene Expression Profiling | Monocytes - immunology | Bronchial Hyperreactivity - genetics | CD11c Antigen - immunology | Respiratory Hypersensitivity - pathology | CD11c Antigen - genetics | Immunoglobulin E - genetics | Calcium-Binding Proteins - immunology | Serrate-Jagged Proteins | T-Lymphocytes, Helper-Inducer - immunology | Monocytes - pathology | Vehicle Emissions | T-Lymphocytes, Helper-Inducer - pathology | Disease Models, Animal | Jagged-1 Protein | Bronchial Hyperreactivity - chemically induced | Signal Transduction | Membrane Proteins - genetics | Particulate Matter - adverse effects | Respiratory Hypersensitivity - chemically induced | Gene Expression Regulation | Intercellular Signaling Peptides and Proteins - genetics | Receptors, Aryl Hydrocarbon - genetics | Receptor, Notch1 - immunology | Membrane Proteins - immunology | Mice, Transgenic | Respiratory Hypersensitivity - immunology | Receptors, Cell Surface - immunology | Respiratory Hypersensitivity - genetics | Bronchial Hyperreactivity - pathology | Animals | Alleles | Mice | Primary Cell Culture | Receptor, Notch1 - genetics | Receptors, Aryl Hydrocarbon - immunology | Intercellular Signaling Peptides and Proteins - immunology | Calcium-Binding Proteins - genetics | Receptors, Cell Surface - genetics | Medical colleges | Air pollution | Asthma | Antigens | Aqueous solutions | Cytokines | Dendritic cells | Lymphocytes | Atherosclerosis | Traffic | Atoms & subatomic particles | Hydrocarbons | Inflammation | Pollutants
Journal Article
PLoS ONE, ISSN 1932-6203, 11/2013, Volume 8, Issue 11, p. e78439
Neuroinflammation mediated by the activated microglia is suggested to play a pivotal role in the pathogenesis of hypoxic brain injury; however, the underlying... 
MURINE BV-2 CELLS | MULTIDISCIPLINARY SCIENCES | NITRIC-OXIDE | RECEPTOR | NEURAL PROGENITOR CELLS | RAT-BRAIN | DIFFERENTIATION | INFLAMMATORY RESPONSE | EXPRESSION | AMEBOID MICROGLIA | INNATE IMMUNITY | Amyloid Precursor Protein Secretases - genetics | Microglia - metabolism | Transcription Factor HES-1 | Homeodomain Proteins - metabolism | NF-kappa B - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Hypoxia - metabolism | Basic Helix-Loop-Helix Transcription Factors - metabolism | Gene Expression Regulation, Developmental | Microglia - pathology | Membrane Proteins - metabolism | TNF Receptor-Associated Factor 6 - genetics | Immunoglobulin J Recombination Signal Sequence-Binding Protein - genetics | Intracellular Signaling Peptides and Proteins - genetics | Animals, Newborn | Immunoglobulin J Recombination Signal Sequence-Binding Protein - metabolism | Basic Helix-Loop-Helix Transcription Factors - genetics | Signal Transduction | Membrane Proteins - genetics | Dipeptides - pharmacology | Enzyme Inhibitors - pharmacology | Myeloid Differentiation Factor 88 - genetics | Rats | Toll-Like Receptor 4 - genetics | Receptor, Notch1 - metabolism | Toll-Like Receptor 4 - metabolism | Homeodomain Proteins - genetics | Amyloid Precursor Protein Secretases - metabolism | Hypoxia - genetics | Animals | NF-kappa B - genetics | Hypoxia - pathology | TNF Receptor-Associated Factor 6 - metabolism | Cell Line, Tumor | Mice | Amyloid Precursor Protein Secretases - antagonists & inhibitors | Receptor, Notch1 - antagonists & inhibitors | Cell Hypoxia - genetics | Receptor, Notch1 - genetics | Myeloid Differentiation Factor 88 - metabolism | Brain | Mental disorders | Laboratories | Pathogenesis | Crosstalk | Activation | Neurogenesis | Signal transduction | Embryology | Head injuries | Pathways | Rodents | Cerebrum | Toll-like receptors | Microglial cells | Inhibition | Pretreatment | Casualties | Translocation | NF-κB protein | Adenosine | TRAF6 protein | Cytokines | Histology | Exposure | Inflammation | TLR4 protein | Gene expression | Microglia | Medicine | Studies | Signaling | Brain research | DELTA protein | Stem cells | MyD88 protein | Hypoxia | Ligands | Brain damage | Notch protein | Brain injury | Secretase
Journal Article
Nature Immunology, ISSN 1529-2908, 08/2010, Volume 11, Issue 8, pp. 717 - 724
Journal Article