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Journal Article
Nature, ISSN 0028-0836, 06/2017, Volume 546, Issue 7656, pp. 107 - 112
Menopause is associated with bone loss and enhanced visceral adiposity. A polyclonal antibody that targets the beta-subunit of the pituitary hormone... 
WHITE | OBESITY | ENERGY-EXPENDITURE | BROWN-FAT | OSTEOCLAST FORMATION | MULTIDISCIPLINARY SCIENCES | FOLLICLE-STIMULATING-HORMONE | RECEPTOR | BONE MASS | MENOPAUSAL TRANSITION | OVARIECTOMIZED MICE | Obesity - drug therapy | Receptors, FSH - genetics | Adipose Tissue, White - metabolism | Diet, High-Fat - adverse effects | Follicle Stimulating Hormone, beta Subunit - antagonists & inhibitors | Male | Osteoporosis - drug therapy | Adipocytes - drug effects | Uncoupling Protein 1 - biosynthesis | Adipose Tissue - metabolism | Antibodies - immunology | Female | Receptors, FSH - metabolism | Adiposity - drug effects | Ovariectomy | Mitochondria - metabolism | Mitochondria - drug effects | Receptors, FSH - antagonists & inhibitors | Haploinsufficiency | Antibodies - pharmacology | Animals | Oxygen Consumption - drug effects | Adipocytes - metabolism | Obesity - prevention & control | Follicle Stimulating Hormone, beta Subunit - immunology | Adipose Tissue, Beige - drug effects | Mice | Thermogenesis - drug effects | Adipose Tissue - drug effects | Adipose Tissue, Beige - metabolism | Adipose Tissue, White - drug effects | Adipose tissues | Physiological aspects | Physiological research | Follicle-stimulating hormone | Thermogenesis | Research | Binding | Obesity | Immunoglobulins | Adipose tissue | Pituitary hormones | Body fat | Menopause | Blocking | Adipocytes | Hormones | Metabolism | Density | Osteoporosis | Mitochondria | Biomedical materials | Bone mass | Pituitary | Biocompatibility | Bone loss | Adipose tissue (brown)
Journal Article
Proceedings of the National Academy of Sciences USA, ISSN 0027-8424, 2019, Volume 116, Issue 4, pp. 1361 - 1369
Interleukin-1 beta (IL-1 beta) is abundant in the tumor microenvironment, where this cytokine can promote tumor growth, but also antitumor activities. We... 
Antitumor immunity | Breast cancer | Anti–PD-1 | IL-1β | Immunotherapy | INTERLEUKIN-1 | RECRUITMENT | IMMUNE CONTEXTURE | MACROPHAGES | MULTIDISCIPLINARY SCIENCES | breast cancer | IL-1 beta | anti-PD-1 | antitumor immunity | CHEMOTHERAPY | MICROENVIRONMENT | CYTOKINE RELEASE SYNDROME | INFLAMMATION | immunotherapy | REGULATORY T-CELLS | SUPPRESSOR-CELLS | Tumor Necrosis Factor-alpha - metabolism | Granzymes - pharmacology | Immunosuppression - methods | Humans | Monocytes - metabolism | Programmed Cell Death 1 Receptor - antagonists & inhibitors | Interferon-gamma - metabolism | Colony-Stimulating Factors - metabolism | Breast Neoplasms - metabolism | Inflammation - metabolism | CD8-Positive T-Lymphocytes - metabolism | Dendritic Cells - drug effects | Female | Antineoplastic Agents - pharmacology | Dendritic Cells - metabolism | Interleukin-1beta - antagonists & inhibitors | Tumor Microenvironment - drug effects | Antibodies, Monoclonal - pharmacology | Mice, Inbred C57BL | Breast Neoplasms - drug therapy | Mice, Knockout | Monocytes - drug effects | Macrophages - metabolism | Animals | Cell Differentiation - drug effects | CD8-Positive T-Lymphocytes - drug effects | Cell Line, Tumor | Macrophages - drug effects | Mice | Mice, Inbred BALB C | CD11b Antigen - metabolism | PD-1 protein | CD8 antigen | Interleukin | Macrophages | Immunity | Metastases | Anticancer properties | Recruitment | Granzyme B | Lymphocytes | Colony-stimulating factor | Inhibition | CD11b antigen | Dendritic cells | Medical immunity | Macrophage colony-stimulating factor | Interleukin 12 | Inflammation | Tumor necrosis factor-α | Monocytes | Immunosuppression | Lymphocytes B | γ-Interferon | Interleukin 10 | Differentiation | Monocyte chemoattractant protein 1 | Tumors | Cancer | Biological Sciences | PNAS Plus | anti–PD-1
Journal Article
Journal of Experimental Medicine, ISSN 0022-1007, 2015, Volume 212, Issue 2, pp. 235 - 252
Progressive tissue fibrosis is a cause of major morbidity and mortality. Pulmonary fibrosis is an epithelial-mesenchymal disorder in which TGF-beta 1 plays a... 
PATHOGENESIS | MEDICINE, RESEARCH & EXPERIMENTAL | CELLS | TGF-BETA | GREMLIN | DISEASE | MYOFIBROBLAST | LUNG DEVELOPMENT | MECHANISMS | GROWTH-FACTOR | IMMUNOLOGY | EPITHELIAL-MESENCHYMAL INTERACTIONS | Inflammation - pathology | Lung Injury - pathology | Myofibroblasts - immunology | Humans | Middle Aged | Transforming Growth Factor beta1 - metabolism | Antibiotics, Antineoplastic - adverse effects | Follistatin-Related Proteins - antagonists & inhibitors | Male | Pulmonary Fibrosis - genetics | Bone Morphogenetic Protein 4 - metabolism | Myofibroblasts - metabolism | Respiratory Mucosa - pathology | Inflammation - metabolism | Respiratory Mucosa - immunology | Lung Injury - metabolism | Female | Pulmonary Fibrosis - metabolism | Disease Models, Animal | Follistatin-Related Proteins - genetics | Follistatin-Related Proteins - metabolism | Cell Line | Gene Expression | Signal Transduction | Antibodies, Monoclonal - pharmacology | Cell Communication | Mesenchymal Stromal Cells - metabolism | Antibodies, Neutralizing - pharmacology | Inflammation - immunology | Bleomycin - adverse effects | Follistatin-Related Proteins - deficiency | Mice, Knockout | Lung Injury - genetics | Phenotype | Animals | Inflammation - genetics | Protein Binding | Pulmonary Fibrosis - chemically induced | Aged | Mice | Pulmonary Fibrosis - drug therapy | Respiratory Mucosa - metabolism | Lung Injury - chemically induced | Smad Proteins - metabolism
Journal Article
Blood, ISSN 0006-4971, 01/2008, Volume 111, Issue 2, pp. 613 - 623
Platelet a-granules constitute the major rapidly releasable reservoir of thrombospondin-1 in higher animals. Although some fragments and peptides derived from... 
ACTIVATION | INHIBITION | CELL RESPONSES | L-ARGININE | GLYCOPROTEIN-IV | CGMP | MONOCLONAL-ANTIBODY | TERMINAL PEPTIDE | HEMATOLOGY | INTEGRIN-ASSOCIATED PROTEIN | VON-WILLEBRAND-FACTOR | Cyclic GMP - pharmacology | Immunologic Capping - physiology | Cell Adhesion Molecules - genetics | CD36 Antigens - genetics | Peptides - genetics | Secretory Vesicles - metabolism | Fibrinolytic Agents - metabolism | Phosphoproteins - metabolism | Platelet Adhesiveness - genetics | Secretory Vesicles - genetics | Peptides - metabolism | Thrombin - pharmacology | CD36 Antigens - metabolism | Blood Platelets - cytology | Arginine - genetics | Platelet Glycoprotein GPIIb-IIIa Complex - metabolism | Thrombospondin 1 - genetics | Immunologic Capping - drug effects | Microfilament Proteins - metabolism | Platelet Aggregation - drug effects | Platelet Glycoprotein GPIIb-IIIa Complex - genetics | Microfilament Proteins - genetics | CD47 Antigen - genetics | rap1 GTP-Binding Proteins - metabolism | Shear Strength | Nitric Oxide - antagonists & inhibitors | Platelet Aggregation - physiology | CD47 Antigen - metabolism | Phosphoproteins - genetics | Cell Adhesion Molecules - metabolism | Thrombin - genetics | Mice, Knockout | Peptides - pharmacology | Platelet Adhesiveness - drug effects | Fibrinolytic Agents - pharmacology | Animals | Cyclic GMP - metabolism | Blood Platelets - metabolism | Nitric Oxide - genetics | Cyclic GMP - genetics | Thrombospondin 1 - pharmacology | Mice | Thrombin - metabolism | Thrombospondin 1 - metabolism | Nitric Oxide - metabolism | rap1 GTP-Binding Proteins - genetics | Arginine - metabolism | Cyclic GMP - antagonists & inhibitors | Hemostasis, Thrombosis, and Vascular Biology
Journal Article
Brain, ISSN 0006-8950, 2012, Volume 135, Issue 6, pp. 1794 - 1818
Multiple sclerosis involves demyelination and axonal degeneration of the central nervous system. The molecular mechanisms of axonal degeneration are relatively... 
collapsin response mediator protein 2 | Nogo receptor | axonal degeneration | experimental autoimmune encephalomyelitis | Nogo-A | ENCEPHALOMYELITIS | FUNCTIONAL RECOVERY | RESPONSE MEDIATOR PROTEIN-2 | ALZHEIMERS-DISEASE | AXONAL REGENERATION | RHO-KINASE | NEUROSCIENCES | LESIONS | CLINICAL NEUROLOGY | MYELIN OLIGODENDROCYTE GLYCOPROTEIN | HYPERPHOSPHORYLATION | INHIBITOR | Humans | Middle Aged | Myelin Proteins - deficiency | Encephalomyelitis, Autoimmune, Experimental - immunology | tau Proteins - metabolism | Male | Green Fluorescent Proteins - genetics | Receptors, Cell Surface - antagonists & inhibitors | Nerve Degeneration - metabolism | Retinal Ganglion Cells - pathology | Time Factors | Nogo Receptor 1 | GPI-Linked Proteins - antagonists & inhibitors | Disease Models, Animal | Transduction, Genetic | Encephalomyelitis, Autoimmune, Experimental - drug therapy | Myelin Proteins - antagonists & inhibitors | Silver Staining | Myelin-Oligodendrocyte Glycoprotein | Glycoproteins - adverse effects | Mutation - genetics | CD3 Complex - metabolism | Receptors, Cell Surface - immunology | Mice, Knockout | Analysis of Variance | Axons - pathology | Encephalomyelitis, Autoimmune, Experimental - complications | Receptors, Cell Surface - deficiency | Cell Line, Tumor | Mice | Peptide Fragments - adverse effects | Nerve Degeneration - etiology | Neurofilament Proteins - metabolism | Optic Nerve - metabolism | Optic Nerve - pathology | Phosphorylation | Immunoprecipitation | Spinal Cord - metabolism | Demyelinating Diseases - metabolism | Retinal Ganglion Cells - metabolism | Intercellular Signaling Peptides and Proteins - metabolism | Tubulin - metabolism | GPI-Linked Proteins - deficiency | Spinal Cord - pathology | Axons - ultrastructure | Myelin Proteins - immunology | Adult | Female | Demyelinating Diseases - etiology | Demyelinating Diseases - pathology | Neuroblastoma - pathology | Severity of Illness Index | Antibodies - therapeutic use | Green Fluorescent Proteins - metabolism | GPI-Linked Proteins - immunology | Gene Expression Regulation - genetics | Mice, Inbred C57BL | Intercellular Signaling Peptides and Proteins - genetics | Axons - metabolism | Nerve Tissue Proteins - genetics | Multiple Sclerosis - complications | Nerve Tissue Proteins - metabolism | Animals | Multiple Sclerosis - pathology | Original
Journal Article
Journal Article
Nature, ISSN 0028-0836, 07/2008, Volume 454, Issue 7204, pp. 656 - 660
Journal Article