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The Journal of immunology (1950), ISSN 1550-6606, 2004, Volume 172, Issue 1, pp. 567 - 576
The signaling mechanism by which the anti-inflammatory cytokine IL-10 mediates suppression of proinflammatory cytokine synthesis remains largely unknown.... 
RHEUMATOID-ARTHRITIS | TUMOR-NECROSIS-FACTOR | DNA-BINDING | HUMAN NEUTROPHILS | TYROSINE PHOSPHORYLATION | INTERLEUKIN-10 RECEPTOR | GENE-EXPRESSION | KAPPA-B-ALPHA | IMMUNOLOGY | HUMAN MONOCYTES | MONONUCLEAR PHAGOCYTES | Protein Binding - genetics | Protein Biosynthesis | Interleukin-6 - antagonists & inhibitors | Humans | Tumor Necrosis Factor-alpha - genetics | Immunoglobulins - genetics | Lipopolysaccharides - antagonists & inhibitors | RNA, Messenger - metabolism | Suppressor of Cytokine Signaling Proteins | Repressor Proteins - antagonists & inhibitors | Antigens, CD - metabolism | Trans-Activators - physiology | Protein Tyrosine Phosphatases - antagonists & inhibitors | RNA, Messenger - biosynthesis | Protein Tyrosine Phosphatases - genetics | Inflammation Mediators - physiology | Glycoproteins - genetics | DNA-Binding Proteins - physiology | Protein Tyrosine Phosphatases - biosynthesis | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction - genetics | DNA - metabolism | Down-Regulation - genetics | Macrophages - metabolism | Protein Tyrosine Phosphatase, Non-Receptor Type 2 | Repressor Proteins - biosynthesis | Up-Regulation - immunology | Interleukin-10 - antagonists & inhibitors | Lipopolysaccharides - pharmacology | Adenoviruses, Human - genetics | Interleukin-10 - immunology | Tumor Necrosis Factor-alpha - biosynthesis | Phosphorylation | Tissue Inhibitor of Metalloproteinase-1 - biosynthesis | Antigens, CD - biosynthesis | Receptors, Cell Surface | Receptors, IgG - biosynthesis | Receptors, IgG - antagonists & inhibitors | Interleukin-10 - physiology | Signal Transduction - immunology | Tissue Inhibitor of Metalloproteinase-1 - metabolism | Signaling Lymphocytic Activation Molecule Family Member 1 | Receptors, Tumor Necrosis Factor - antagonists & inhibitors | RNA, Messenger - antagonists & inhibitors | Receptors, Tumor Necrosis Factor, Type II | Trans-Activators - genetics | Inflammation Mediators - antagonists & inhibitors | Trans-Activators - biosynthesis | Immunoglobulins - biosynthesis | Macrophages - immunology | Inflammation Mediators - immunology | Receptors, Tumor Necrosis Factor - metabolism | Immune Sera - pharmacology | Proteins - physiology | Cells, Cultured | Glycoproteins - antagonists & inhibitors | Histocompatibility Antigens Class II - biosynthesis | Tissue Inhibitor of Metalloproteinase-1 - antagonists & inhibitors | Transcription Factors - antagonists & inhibitors | Transcription Factors - biosynthesis | Up-Regulation - genetics | DNA-Binding Proteins - genetics | DNA - antagonists & inhibitors | Glycoproteins - biosynthesis | Suppressor of Cytokine Signaling 3 Protein | Down-Regulation - immunology | Interleukin-6 - biosynthesis | Receptors, Tumor Necrosis Factor - biosynthesis | STAT3 Transcription Factor | Trans-Activators - antagonists & inhibitors | Genetic Vectors | DNA-Binding Proteins - biosynthesis | Tumor Necrosis Factor-alpha - antagonists & inhibitors
Journal Article
JNCI : Journal of the National Cancer Institute, ISSN 1460-2105, 2017, Volume 109, Issue 9
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 06/2017, Volume 292, Issue 24, pp. 10048 - 10060
IFNs are effective in inhibiting angiogenesis in preclinical models and in treating several angioproliferative disorders. However, the detailed mechanisms of... 
APOPTOSIS | ACTIVATION | NETWORK | GENE | BIOCHEMISTRY & MOLECULAR BIOLOGY | ENDOTHELIAL-CELLS | TNF-ALPHA | INDUCTION | RAR-ALPHA | TRANSCRIPTION FACTOR | EXPRESSION | Endothelium, Vascular - cytology | Human Umbilical Vein Endothelial Cells - metabolism | Humans | Neovascularization, Pathologic - pathology | Endopeptidases - chemistry | STAT1 Transcription Factor - metabolism | Interferon-alpha - genetics | RNA Interference | Human Umbilical Vein Endothelial Cells - cytology | STAT1 Transcription Factor - agonists | Promyelocytic Leukemia Protein - metabolism | Ubiquitin Thiolesterase - metabolism | Neovascularization, Pathologic - prevention & control | Ubiquitin Thiolesterase - antagonists & inhibitors | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Promyelocytic Leukemia Protein - genetics | Recombinant Proteins - metabolism | Cell Line | Endopeptidases - metabolism | Interferon-alpha - metabolism | Cells, Cultured | STAT1 Transcription Factor - genetics | Ubiquitin Thiolesterase - genetics | Mice, Knockout | STAT2 Transcription Factor - agonists | Animals | Endopeptidases - genetics | Endothelium, Vascular - metabolism | STAT2 Transcription Factor - genetics | Promyelocytic Leukemia Protein - antagonists & inhibitors | Endothelium, Vascular - pathology | Neovascularization, Pathologic - metabolism | Protein Processing, Post-Translational | STAT2 Transcription Factor - metabolism | STAT3 Transcription Factor - antagonists & inhibitors | Neovascularization, Physiologic | signal transducers and activators of transcription 1 (STAT1) | STAT transcription factor | Signal Transduction | interferon | angiogenesis | STAT3
Journal Article
The EMBO journal, ISSN 0261-4189, 2012, Volume 31, Issue 17, pp. 3513 - 3523
Journal Article
Cancer cell, ISSN 1535-6108, 08/2017, Volume 32, Issue 2, pp. 169 - 184.e7
Journal Article
PLoS ONE, ISSN 1932-6203, 08/2013, Volume 8, Issue 8, p. e71646
Some of the signal transducer and activator of transcription (STAT) family members are constitutively activated in a wide variety of human tumors... 
TRANSFORMATION | ACTIVATION | FLUORESCENCE POLARIZATION | HIGH-THROUGHPUT SCREEN | MULTIDISCIPLINARY SCIENCES | TRANSCRIPTION | SIGNAL TRANSDUCERS | KINASE INHIBITOR | IDENTIFICATION | CANCER | SMALL-MOLECULE INHIBITOR | Recombinant Proteins - metabolism | Amino Acid Sequence | Peptides - chemistry | Humans | Molecular Sequence Data | STAT5 Transcription Factor - chemistry | Biological Assay - methods | STAT3 Transcription Factor - chemistry | Structure-Activity Relationship | Protein Transport | src Homology Domains | Digoxigenin - metabolism | STAT5 Transcription Factor - metabolism | Cell Nucleus - metabolism | Peptides - metabolism | STAT5 Transcription Factor - antagonists & inhibitors | Protein Binding | HeLa Cells | STAT3 Transcription Factor - antagonists & inhibitors | STAT3 Transcription Factor - metabolism | Proteins | Tyrosine | Biotin | Multiplexing | Phosphorylation | Transcription factors | Transcription | Peptides | Leukemia | Phosphotyrosine | Homology | Antagonists | Identification | Selectivity | Kinases | Assaying | Deletion mutant | Chlorine compounds | Cell growth | Clonal deletion | Rodents | Inhibition | Growth factors | Pharmaceutical sciences | Binding | Translocation | Cytokines | Stat3 protein | Feasibility studies | Lead compounds | Sodium chloride | Gene expression | Nuclear transport | Mutants | Sodium | Spacer | Reaction time | Ligands | Beads | Prostate cancer | Tumors
Journal Article
Journal of allergy and clinical immunology, ISSN 0091-6749, 2015, Volume 136, Issue 3, pp. 667 - 677.e7
...)–signal transducer and activator of transcription (STAT) pathway plays a critical role in skin barrier function and can be a therapeutic target for AD... 
Allergy and Immunology | keratinocyte differentiation | signal transducer and activator of transcription 3 | Atopic dermatitis | filaggrin | Janus kinase inhibitor | JAK INHIBITOR | MODEL | IMMUNOLOGY | CORNIFIED ENVELOPE | NC/NGA MICE | ATOPIC-DERMATITIS | RESPONSES | ALLERGY | FILAGGRIN MUTATIONS | STAT6 | DIFFERENTIATION | TH2 | RNA, Small Interfering - genetics | Dermatitis, Atopic - genetics | Humans | Interleukin-13 - immunology | Transplantation, Heterologous | STAT6 Transcription Factor - genetics | Interleukin-13 - genetics | RNA, Small Interfering - immunology | Skin, Artificial | Dermatitis, Atopic - immunology | Intermediate Filament Proteins - genetics | Skin Transplantation | STAT6 Transcription Factor - antagonists & inhibitors | Interleukin-4 - genetics | STAT3 Transcription Factor - genetics | Disease Models, Animal | Intermediate Filament Proteins - immunology | Signal Transduction | Mice, Inbred C57BL | Gene Expression Regulation | Dermatitis, Atopic - pathology | STAT6 Transcription Factor - immunology | Keratinocytes - immunology | Interleukin-4 - immunology | Keratinocytes - pathology | Animals | Dermatitis, Atopic - drug therapy | Keratinocytes - drug effects | Cell Differentiation - drug effects | Mice, Nude | Mice | Protein Kinase Inhibitors - pharmacology | Immunocompromised Host | STAT3 Transcription Factor - immunology | STAT3 Transcription Factor - antagonists & inhibitors | Circuit components | Allergens | Mutual fund industry | Skin | Genetic transcription | Proteins | Cytokines | Genes | Skin & tissue grafts | Ligands | Kinases | Potassium | Chemokines
Journal Article
Cardiovascular research, ISSN 1755-3245, 2009, Volume 84, Issue 2, pp. 201 - 208
.... We propose that IPostC confers its infarct-sparing effect via activation of the newly described prosurvival Survivor Activating Factor Enhancement (SAFE... 
Ischaemia | Infarction | Reperfusion | Postconditioning | Preconditioning | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | NECROSIS-FACTOR-ALPHA | CARDIAC MYOCYTE | MURINE MODEL | ISOLATED MOUSE HEARTS | INDUCED CARDIOPROTECTION | ACUTE MYOCARDIAL-INFARCTION | TNF-ALPHA | PROSURVIVAL KINASES | SIGNAL TRANSDUCER | Tumor Necrosis Factor-alpha - metabolism | Phosphorylation | Tumor Necrosis Factor-alpha - genetics | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Glycogen Synthase Kinase 3 beta | Male | Phosphatidylinositol 3-Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Receptors, Tumor Necrosis Factor, Type I - metabolism | Tumor Necrosis Factor-alpha - deficiency | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Myocardial Reperfusion Injury - pathology | Receptors, Tumor Necrosis Factor, Type II - metabolism | Myocardial Infarction - pathology | Myocardium - metabolism | STAT3 Transcription Factor - deficiency | Flavonoids - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Disease Models, Animal | Mice, Inbred C57BL | Myocardium - pathology | Tyrphostins - pharmacology | Myocardial Infarction - metabolism | Glycogen Synthase Kinase 3 - metabolism | Receptors, Tumor Necrosis Factor, Type I - genetics | Receptors, Tumor Necrosis Factor, Type II - genetics | Mice, Knockout | Receptors, Tumor Necrosis Factor, Type II - deficiency | Myocardial Reperfusion Injury - metabolism | Animals | Androstadienes - pharmacology | Signal Transduction - drug effects | Mice | Myocardial Infarction - prevention & control | Protein Kinase Inhibitors - pharmacology | STAT3 Transcription Factor - antagonists & inhibitors | Myocardial Reperfusion Injury - prevention & control | Proto-Oncogene Proteins c-akt - antagonists & inhibitors
Journal Article
IUBMB life, ISSN 1521-6543, 2018, Volume 70, Issue 1, pp. 81 - 91
... and activator of transcription 3. INTRODUCTION As one of the most frequently diagnosed cancer, lung cancer is the leading cause of cancer‐related mortality worldwide. Among... 
MiR‐204 | signal transducer and activator of transcription 3 | angiogenesis | Janus kinase 2 | lung adenocarcinoma | MiR-204 | METASTASIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | CANCER | EXPRESSION | CELL BIOLOGY | Human Umbilical Vein Endothelial Cells - metabolism | Adenocarcinoma of Lung - pathology | Apoptosis - drug effects | Heterocyclic Compounds, 3-Ring - pharmacology | Humans | Gene Expression Regulation, Neoplastic | Neovascularization, Pathologic | MicroRNAs - metabolism | Vascular Endothelial Growth Factor A - metabolism | Vascular Endothelial Growth Factor A - antagonists & inhibitors | Vascular Endothelial Growth Factor A - genetics | Platelet-Derived Growth Factor - genetics | Pyrrolidines - pharmacology | Adenocarcinoma of Lung - genetics | Oligoribonucleotides - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Human Umbilical Vein Endothelial Cells - cytology | Janus Kinase 2 - metabolism | Adenocarcinoma of Lung - drug therapy | Cyclic S-Oxides - pharmacology | Janus Kinase 2 - antagonists & inhibitors | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | A549 Cells | Human Umbilical Vein Endothelial Cells - drug effects | Signal Transduction | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Janus Kinase 2 - genetics | Sulfonamides - pharmacology | Xenograft Model Antitumor Assays | Cell Movement - drug effects | Platelet-Derived Growth Factor - metabolism | Animals | Mice, Nude | Cell Proliferation - drug effects | Mice | Mice, Inbred BALB C | MicroRNAs - genetics | Adenocarcinoma of Lung - metabolism | STAT3 Transcription Factor - antagonists & inhibitors | Platelet-Derived Growth Factor - antagonists & inhibitors | Oligoribonucleotides - genetics | Adenocarcinoma | Chemical inhibitors | Platelet-derived growth factor | MicroRNA | Endothelial growth factors | Lung cancer | Analysis | Mutual fund industry | Genetic transcription | Endothelium
Journal Article
Nature communications, ISSN 2041-1723, 2017, Volume 8, Issue 1, pp. 2099 - 13
...., NSC-311068 and NSC-370284) that selectively suppress TET1 transcription and 5-hydroxymethylcytosine (5hmC... 
STEM-CELLS | ACTIVATION | B-CELL | SIGNALING PATHWAY | MULTIDISCIPLINARY SCIENCES | STAT3 | RESISTANCE | ADULTS | TET1 | CANCER | MLL-REARRANGED LEUKEMIA | Humans | Leukemia, Myeloid, Acute - metabolism | Mixed Function Oxygenases - metabolism | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Enzyme Inhibitors - administration & dosage | STAT5 Transcription Factor - genetics | STAT5 Transcription Factor - metabolism | RNA Interference | STAT5 Transcription Factor - antagonists & inhibitors | Leukemia, Myeloid, Acute - drug therapy | Daunorubicin - administration & dosage | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Leukemia, Experimental - genetics | Proto-Oncogene Proteins - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | Leukemia, Experimental - drug therapy | Mice, Inbred C57BL | Enzyme Inhibitors - pharmacology | Kaplan-Meier Estimate | THP-1 Cells | Gene Expression Regulation, Leukemic - drug effects | Proto-Oncogene Proteins - genetics | Mixed Function Oxygenases - antagonists & inhibitors | Animals | Cell Line, Tumor | Mixed Function Oxygenases - genetics | STAT3 Transcription Factor - antagonists & inhibitors | Leukemia, Experimental - metabolism | Leukemia, Myeloid, Acute - genetics | Translocation | Dioxygenase | Data analysis | Transcription factors | Transcription | Myeloid leukemia | Leukemia | Stat3 protein | Data processing | Drug screening | Synergistic effects | Chemotherapy | Acute myeloid leukemia | Deoxyribonucleic acid--DNA
Journal Article