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1. Full Text Ruthenium-catalyzed isoquinolone synthesis through C-H activation using an oxidizing directing group
by Li, Bin and Feng, Huiliang and Xu, Shansheng and Wang, Baiquan
Chemistry - A European Journal, ISSN 0947-6539, 11/2011, Volume 17, Issue 45, pp. 12573 - 12577
The oxidant directs: A mild, practical, efficient, and regioselective Ru-catalyzed isoquinolone synthesis with a broad substrate scope was reported (see... 
ruthenium | CiH activation | homogeneous catalysis | directing group | alkynes | DIRECT ARYLATION | BOND FORMATION | INTERNAL ALKYNES | CHEMISTRY, MULTIDISCIPLINARY | CARBON-HYDROGEN | FUNCTIONALIZATION | C-H activation | BENZAMIDES | OXIDATIVE COUPLING/CYCLIZATION | COUPLING REACTIONS | METAL | BENZOIC-ACIDS | Synthesis | Oxidants | Oxidizing agents | Activation | Oxidation | Bonding | Substrates
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2. Full Text Rhodium-catalyzed annulation of N-benzoylsulfonamide with isocyanide through C-H activation
by Zhu, Chen and Xie, Weiqing and Falck, John R
Chemistry - A European Journal, ISSN 0947-6539, 11/2011, Volume 17, Issue 45, pp. 12591 - 12595
The first rhodium-catalyzed annulation of N-benzoylsulfonamide (1) with isocyanide (2) through C--H activation is described. The transformation is broadly... 
annulations | CiH activation | heterocycles | isocyanide | rhodium | C(SP)-H BONDS | CARBON-HYDROGEN BONDS | ISONITRILES | ALKYNES | CLEAVAGE | CHEMISTRY, MULTIDISCIPLINARY | ALKENES | C-H activation | CARBONYLATION | BENZAMIDES | CARBOXYLIC-ACIDS | BENZOIC-ACIDS | Sulfonamides - chemical synthesis | Combinatorial Chemistry Techniques | Cyclization | Models, Chemical | Sulfonamides - chemistry | Stereoisomerism | Nitriles - chemistry | Molecular Structure | Catalysis | Rhodium - chemistry | Organic chemistry | Electronic properties | Rhodium | Chemical reactions | Activation | Transformations | Compatibility
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3. Full Text TLR activation of the transcription factor XBP1 regulates innate immune responses in macrophages
by Martinon, Fabio and Chen, Xi and Lee, Ann-Hwee and Glimcher, Laurie H
Nature Immunology, ISSN 1529-2908, 05/2010, Volume 11, Issue 5, pp. 411 - 418
Sensors of pathogens, such as Toll-like receptors (TLRs), detect microbes to activate transcriptional programs that orchestrate adaptive responses to specific... 
UNFOLDED PROTEIN RESPONSE | PATHWAY | ER STRESS | HOST-DEFENSE | ENDOPLASMIC-RETICULUM STRESS | FRANCISELLA-TULARENSIS INFECTION | IMMUNOLOGY | LIVE VACCINE STRAIN | INFLAMMATORY RESPONSE | NEGATIVE REGULATOR | SYSTEMS BIOLOGY | RNA, Small Interfering - genetics | Endoribonucleases - genetics | Tularemia - metabolism | Toll-Like Receptor 2 - genetics | Membrane Glycoproteins - metabolism | Lipopeptides - pharmacology | Transcriptional Activation - drug effects | NADPH Oxidases - metabolism | Tularemia - genetics | Protein Splicing - genetics | Transcriptional Activation - immunology | X-Box Binding Protein 1 | Protein Splicing - drug effects | NADPH Oxidases - genetics | Stress, Physiological - drug effects | TNF Receptor-Associated Factor 6 - genetics | Transcription Factor CHOP - biosynthesis | Transcription Factors - immunology | Cytokines - genetics | Protein-Serine-Threonine Kinases - metabolism | DNA-Binding Proteins - immunology | Endoribonucleases - metabolism | Macrophages - pathology | Stress, Physiological - genetics | Myeloid Differentiation Factor 88 - genetics | Toll-Like Receptor 4 - genetics | Signal Transduction - genetics | Toll-Like Receptor 4 - immunology | Toll-Like Receptor 2 - metabolism | Toll-Like Receptor 4 - metabolism | Mice, Knockout | Macrophages - metabolism | Signal Transduction - drug effects | Tunicamycin - pharmacology | Lipopolysaccharides - pharmacology | Toll-Like Receptor 2 - immunology | Mice | Stress, Physiological - immunology | Endoribonucleases - immunology | Transcription Factor CHOP - genetics | NADPH Oxidases - immunology | DNA-Binding Proteins - metabolism | Signal Transduction - immunology | Macrophages - virology | Mice, Mutant Strains | Tularemia - immunology | Membrane Glycoproteins - immunology | Macrophages - immunology | Cytokines - immunology | Cell Line | Francisella tularensis - immunology | Protein Splicing - immunology | Protein-Serine-Threonine Kinases - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Immunity, Innate | NADPH Oxidase 2 | Regulatory Factor X Transcription Factors | Mice, Inbred C3H | Membrane Glycoproteins - genetics | Transcription Factors - metabolism | Animals | TNF Receptor-Associated Factor 6 - metabolism | Macrophages - drug effects | Protein-Serine-Threonine Kinases - immunology | Francisella tularensis - pathogenicity | Myeloid Differentiation Factor 88 - metabolism | Cytokines - biosynthesis | Cell receptors | Transcription factors | Immune response | Physiological aspects | Genetic aspects | Research | Health aspects | Francisella tularensis
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4. Full Text Fas ligation and tumor necrosis factor alpha activation of murine astrocytes promote heat shock factor‐1 activation and heat shock protein expression leading to chemokine induction and cell survival
by Choi, Kuicheon and Ni, Li and Jonakait, G. Miller
Journal of Neurochemistry, ISSN 0022-3042, 02/2011, Volume 116, Issue 3, pp. 438 - 448
P>Death-inducing ligands tumor necrosis factor alpha (TNF alpha) and Fas ligand (FasL) do not kill cultured astrocytes; instead they induce a variety of... 
NF‐κB | astrocytes | chemokines | heat shock factor‐1 | heat shock proteins | NF-κB | heat shock factor-1 | DEATH RECEPTOR | DENDRITIC CELLS | HSP70 PROTECTS | BIOCHEMISTRY & MOLECULAR BIOLOGY | LIGAND-INDUCED APOPTOSIS | BINDING ACTIVITY | DOWN-REGULATION | HUMAN FETAL ASTROCYTES | MEDIATED APOPTOSIS | NEUROSCIENCES | NF-kappa B | GENE-EXPRESSION | NF-KAPPA-B | Tumor Necrosis Factor-alpha - metabolism | Cell Line | Chemokines - biosynthesis | Fas Ligand Protein - metabolism | Transcriptional Activation - genetics | Cells, Cultured | Cell Survival - genetics | Chemokines - physiology | Heat-Shock Proteins - biosynthesis | Apoptosis - genetics | fas Receptor - metabolism | Mice, Inbred C3H | Heat Shock Transcription Factors | DNA-Binding Proteins - metabolism | Fas Ligand Protein - physiology | Transcription Factors - metabolism | Heat-Shock Proteins - genetics | Astrocytes - physiology | Animals | Tumor Necrosis Factor-alpha - physiology | Mice | Enzyme Activation - genetics | Heat-Shock Proteins - physiology | Astrocytes - metabolism | Tumor necrosis factor | DNA | Heat shock proteins | Protein biosynthesis | Necrosis | Tumors | Protein binding | Cell culture | Cell survival | Fas antigen | Astrocytes | Extracellular signal-regulated kinase | CCL3 protein | Data processing | Signal transduction | NF- Kappa B protein | FasL protein | CXC chemokines | CXCL10 protein | Hsp72 protein | Quercetin | Interleukin 8 | Monocyte chemoattractant protein 1 | Tumor necrosis factor- alpha
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5. Full Text Toll-like Receptor 4-Dependent Activation of Dendritic Cells by β-Defensin 2
by Arya Biragyn and Pier Adelchi Ruffini and Cynthia A. Leifer and Elena Klyushnenkova and Alexander Shakhov and Oleg Chertov and Aiko K. Shirakawa and Joshua M. Farber and David M. Segal and Joost J. Oppenheim and Larry W. Kwak
Science, ISSN 0036-8075, 11/2002, Volume 298, Issue 5595, pp. 1025 - 1029
β-Defensins are small antimicrobial peptides of the innate immune system produced in response to microbial infection of mucosal tissue and skin. We demonstrate... 
T lymphocytes | Antigens | Receptors | Cytokines | Dendritic cells | Vaccination | Toll like receptors | Reports | Mice | Immunity | Chemokines | PROTEIN | MULTIDISCIPLINARY SCIENCES | COMPLEXES | ANTITUMOR IMMUNITY | CD14 | LPS | INNATE IMMUNITY | Toll-Like Receptor 4 | Recombinant Fusion Proteins - pharmacology | Dendritic Cells - immunology | Humans | Lipopolysaccharides - immunology | Lymphocyte Culture Test, Mixed | Toll-Like Receptors | Membrane Glycoproteins - physiology | Neoplasms - therapy | Transfection | Female | Receptors, Cell Surface - physiology | Cell Line | Drosophila Proteins | Signal Transduction | Antigens, Neoplasm - immunology | Mice, Inbred C57BL | Receptors, Chemokine - metabolism | beta-Defensins - physiology | Mice, Inbred C3H | Membrane Glycoproteins - genetics | Cancer Vaccines - immunology | Animals | Neoplasms - immunology | Lipopolysaccharides - pharmacology | beta-Defensins - pharmacology | Ligands | Receptors, CCR6 | Mice, Inbred BALB C | Cytokines - biosynthesis | Interferon-alpha - physiology | Receptors, Cell Surface - genetics | Infections | Peptides | Cellular biology | Immune system
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6. Full Text NK-cell activation by LIGHT triggers tumor-specific CD8 + T-cell immunity to reject established tumors
by Fan, Zusen and Yu, Ping and Wang, Yang and Wang, Yugang and Fu, May Lynne and Liu, Wenhua and Sun, Yonglian and Fu, Yang-Xin
Blood, ISSN 0006-4971, 02/2006, Volume 107, Issue 4, pp. 1342 - 1351
Natural killer (NK) cells are generally reported as innate effector cells for killing virally infected and transformed cells. It is unclear how NK cells evoke... 
NATURAL-KILLER-CELLS | CONSTITUTIVE EXPRESSION | HERPESVIRUS ENTRY MEDIATOR | DENDRITIC CELLS | INTERFERON-GAMMA | IFN-GAMMA | IN-VIVO | RECEPTOR | HEMATOLOGY | CYTOTOXICITY | CUTTING EDGE | Lymphocyte Activation | Mice, Inbred C57BL | Tumor Necrosis Factor Ligand Superfamily Member 14 | Fibrosarcoma - immunology | Membrane Proteins - immunology | Mice, Inbred C3H | Mice, Knockout | Animals | Interferon-gamma - immunology | Neoplasms, Experimental - immunology | Interferon-gamma - antagonists & inhibitors | Tumor Necrosis Factor-alpha - immunology | Cell Line, Tumor | Killer Cells, Natural - immunology | Female | Mice | CD8-Positive T-Lymphocytes - immunology | Gene Therapy
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7. Full Text A novel intracellular pool of LFA-1 is critical for asymmetric CD8+ T cell activation and differentiation
by Capece, Tara and Walling, Brandon L and Lim, Kihong and Kim, Kyun-Do and Bae, Seyeon and Chung, Hung-Li and Topham, David J and Kim, Minsoo
Journal of Cell Biology, ISSN 0021-9525, 11/2017, Volume 216, Issue 11, pp. 3817 - 3829
The integrin lymphocyte function-associated antigen 1 (LFA-1; CD11a/CD18) is a key T cell adhesion receptor that mediates stable interactions with... 
EFFECTOR | LYMPHOCYTE MIGRATION | DENDRITIC CELLS | MEMORY | AFFINITY | INTEGRIN LFA-1 | ICAM-1 | IMMUNOLOGICAL SYNAPSE | DIVISION | CUTTING EDGE | CELL BIOLOGY | Chemotaxis, Leukocyte | CD18 Antigens - immunology | Mitosis | Lymphocyte Function-Associated Antigen-1 - metabolism | Lymphocyte Function-Associated Antigen-1 - immunology | CD11a Antigen - genetics | Time Factors | CD8-Positive T-Lymphocytes - metabolism | Cell Differentiation | CD11a Antigen - metabolism | rab GTP-Binding Proteins - metabolism | Antigen-Presenting Cells - metabolism | Receptors, Antigen, T-Cell - metabolism | Signal Transduction | CD18 Antigens - genetics | Lymphocyte Activation | Mice, Inbred C57BL | Cells, Cultured | Mice, Transgenic | Antigen-Presenting Cells - immunology | Mice, Inbred C3H | Protein Transport | CD18 Antigens - metabolism | Animals | Lymphocyte Function-Associated Antigen-1 - genetics | CD11a Antigen - immunology | Receptors, Antigen, T-Cell - genetics | CD8-Positive T-Lymphocytes - immunology
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8. Full Text Toll-Like Receptor 4–Dependent Microglial Activation Mediates Spinal Cord Ischemia–Reperfusion Injury
by Bell, Marshall T and Puskas, Ferenc and Agoston, Viktor A and Cleveland, Joseph C and Freeman, Kirsten A and Gamboni, Fabia and Herson, Paco S and Meng, Xianzhong and Smith, Phillip D and Weyant, Michael J and Fullerton, David A and Reece, T Brett
Circulation, ISSN 0009-7322, 09/2013, Volume 128, Issue 26_suppl_1 Suppl 1, pp. S152 - S156
BACKGROUND—Paraplegia continues to complicate thoracoabdominal aortic interventions. The elusive mechanism of spinal cord ischemia–reperfusion injury has... 
Spinal cord | Reperfusion | Ischemia | Aorta | Inflammation | Aortic surgery | Macrophages | CELLS | CARDIAC & CARDIOVASCULAR SYSTEMS | aortic surgery | INITIATION | MOUSE | RATS | NEURODEGENERATION | CNS | RELEASE | MODEL | ischemia | RECOVERY | macrophages | inflammation | PERIPHERAL VASCULAR DISEASE | aorta | spinal cord | reperfusion | AXOTOMY | Microglia - metabolism | Reperfusion Injury - pathology | Cells, Cultured | Male | Mice, Inbred C3H | Mice, Knockout | Spinal Cord Ischemia - metabolism | Toll-Like Receptor 4 - physiology | Animals | Toll-Like Receptor 4 - deficiency | Spinal Cord Ischemia - pathology | Inflammation Mediators - metabolism | Mice | Reperfusion Injury - metabolism | Cell Survival - physiology | Complications and side effects | Care and treatment | Physiological aspects | Central nervous system diseases | Research | Cardiovascular diseases | TLR4
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9. Full Text JAK2 activation by growth hormone and other cytokines
by Waters, Michael J and Brooks, Andrew J
Biochemical Journal, ISSN 0264-6021, 02/2015, Volume 466, Issue 1, pp. 1 - 11
Growth hormone (GH) and structurally related cytokines regulate a great number of physiological and pathological processes. They do this by coupling their... 
Srk family kinases | Class I cytokine receptors | Janus kinase 2 (JAK2) | Cytokine receptor signalling | Growth hormone | Growth hormone receptor | STIMULATING FACTOR-RECEPTOR | PROLACTIN RECEPTOR | growth hormone receptor | CRYSTAL-STRUCTURE | BIOCHEMISTRY & MOLECULAR BIOLOGY | LYN TYROSINE KINASE | TRANSMEMBRANE DOMAIN | COMMON BETA-SUBUNIT | cytokine receptor signalling | SRC-FAMILY KINASES | SIGNAL-TRANSDUCTION | ERYTHROPOIETIN RECEPTOR | growth hormone | class I cytokine receptors | THROMBOPOIETIN RECEPTOR | Receptors, Somatotropin - metabolism | Receptor Cross-Talk | Cytokines - metabolism | Signal Transduction | Growth Hormone - metabolism | Humans | Protein Multimerization | Gene Expression Regulation | Janus Kinase 2 - genetics | Models, Molecular | Receptors, Somatotropin - genetics | Growth Hormone - genetics | Animals | Janus Kinase 2 - metabolism | Protein Binding | Protein Interaction Domains and Motifs | Enzyme Activation | Receptors, Cytokine - metabolism | Cytokines - genetics | Receptors, Cytokine - genetics | CT-1, cardiotropin-1 | TPO, thrombopoietin | JM, juxtamembrane | OSM, oncostatin-M | Review | GH, growth hormone | FNIII, fibronectin III-like | ECD, extracellular domain | JAK, Janus kinase | MAb, monoclonal antibody | CRH, cytokine receptor homology | EPO, erythropoietin | CNTF, ciliary neurotropic factor | GM-CSF, granulocyte-macrophage colony-stimulating factor | PK, pseudokinase | TMD, transmembrane domain
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10. Full Text Anti-dengue virus nonstructural protein 1 antibodies cause NO-mediated endothelial cell apoptosis via ceramide-regulated glycogen synthase kinase-3β and NF-κB activation
by Chen, Chia-Ling and Lin, Chiou-Feng and Wan, Shu-Wen and Wei, Li-Shiung and Chen, Mei-Chun and Yeh, Trai-Ming and Liu, Hsiao-Sheng and Anderson, Robert and Lin, Yee-Shin
Journal of Immunology, ISSN 0022-1767, 08/2013, Volume 191, Issue 4, pp. 1744 - 1752
Immunopathogenetic mechanisms of dengue virus (DENV) infection are involved in hemorrhagic syndrome resulting from thrombocytopenia, coagulopathy, and... 
SIGNAL-TRANSDUCTION | MEMBRANE DOMAINS | HEMORRHAGIC-FEVER | C-TERMINAL REGION | LIPID RAFT | DISEASE | IMMUNOPATHOGENESIS | THROMBOCYTOPENIA | CYTOKINE | IMMUNOLOGY | EXPRESSION | Recombinant Fusion Proteins - immunology | Glycogen Synthase Kinase 3 - physiology | Humans | Glycogen Synthase Kinase 3 beta | Male | Nitric Oxide Synthase Type II - physiology | beta-Cyclodextrins - pharmacology | Ceramides - biosynthesis | Enzyme Activation - immunology | Dengue Virus - immunology | Immunoglobulin G - immunology | Sphingomyelin Phosphodiesterase - physiology | Viral Nonstructural Proteins - immunology | Cell Line | Gene Expression Regulation - immunology | Nitric Oxide - physiology | Mice, Inbred C3H | Cross Reactions | Endothelial Cells - immunology | Antibodies, Viral - physiology | Animals | Sphingomyelin Phosphodiesterase - antagonists & inhibitors | Membrane Microdomains - drug effects | NF-kappa B - physiology | Antibodies, Viral - immunology | Mice | Mice, Inbred BALB C | Apoptosis - physiology | Endothelial Cells - pathology | Ceramides - physiology
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11. Full Text Opposing actions of angiopoietin-2 on Tie2 signaling and FOXO1 activation
by Kim, Minah and Allen, Breanna and Korhonen, Emilia A and Nitschké, Maximilian and Yang, Hee Won and Baluk, Peter and Saharinen, Pipsa and Alitalo, Kari and Daly, Christopher and Thurston, Gavin and McDonald, Donald M
Journal of Clinical Investigation, ISSN 0021-9738, 09/2016, Volume 126, Issue 9, pp. 3511 - 3525
Angiopoietin-2 (ANG2) regulates blood vessel remodeling in many pathological conditions through differential effects on Tie2 signaling. While ANG2 competes... 
MEDICINE, RESEARCH & EXPERIMENTAL | ANGIOGENESIS | LIGAND ANGIOPOIETIN-2 | AIRWAY INFLAMMATION | GENE-EXPRESSION | BLOOD-VESSEL FORMATION | CELL-SURVIVAL | TRANSDUCTION PATHWAY | TRANSCRIPTION FACTOR | ENDOTHELIAL GROWTH-FACTOR | FKHR FOXO1 | Vascular Remodeling | Endothelial Cells - metabolism | Humans | Mice, Inbred C57BL | Male | Mice, Transgenic | Inflammation | Phosphatidylinositol 3-Kinases - metabolism | Vascular Endothelial Growth Factor A - metabolism | Angiopoietin-2 - metabolism | Mice, Inbred C3H | Animals | Endothelium, Vascular - metabolism | Mycoplasma pulmonis | Protein Domains | Female | Receptor, TIE-2 - metabolism | Mice | Forkhead Box Protein O1 - antagonists & inhibitors | Antibodies, Monoclonal - chemistry | Infection | Development and progression | Cellular signal transduction | Health aspects | Vascular endothelial growth factor | Pathogens | Phosphorylation | Data analysis | Cytokines | Funding | Software | Infections | Design of experiments
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12. Full Text Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor 4
by Junker, Yvonne and Zeissig, Sebastian and Kim, Seong-Jun and Barisani, Donatella and Wieser, Herbert and Leffler, Daniel A and Zevallos, Victor and Libermann, Towia A and Dillon, Simon and Freitag, Tobias L and Kelly, Ciaran P and Schuppan, Detlef
Journal of Experimental Medicine, ISSN 0022-1007, 12/2012, Volume 209, Issue 13, pp. 2395 - 2408
Ingestion of wheat, barley, or rye triggers small intestinal inflammation in patients with celiac disease. Specifically, the storage proteins of these cereals... 
MEDICINE, RESEARCH & EXPERIMENTAL | GLIADIN PEPTIDES | IMMUNE-RESPONSES | IN-VIVO | GENE-EXPRESSION | DOUBLE-BLIND | BLOOD MONOCYTES | IMMUNOLOGY | TISSUE TRANSGLUTAMINASE | T-CELLS | CELIAC-DISEASE | GLUTEN PROTEINS | Triticum - immunology | Humans | Trypsin Inhibitors - adverse effects | Molecular Sequence Data | Triticum - adverse effects | Celiac Disease - etiology | Toll-Like Receptor 4 - deficiency | Celiac Disease - immunology | U937 Cells | HEK293 Cells | Amino Acid Sequence | Cell Line | Gliadin - immunology | Signal Transduction | Trypsin Inhibitors - immunology | Gliadin - adverse effects | Mice, Inbred C57BL | Myeloid Differentiation Factor 88 - genetics | Toll-Like Receptor 4 - genetics | Plant Proteins - immunology | Immunity, Innate | Toll-Like Receptor 4 - metabolism | Mice, Inbred C3H | Mice, Knockout | Plant Proteins - adverse effects | Sequence Homology, Amino Acid | Triticum - genetics | Plant Proteins - genetics | Animals | Myeloid Differentiation Factor 88 - deficiency | Hordeum - adverse effects | Trypsin Inhibitors - genetics | Mice | Hordeum - immunology | Hordeum - genetics | Myeloid Differentiation Factor 88 - metabolism | Celiac Disease - metabolism
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13. Full Text Toll-like receptor 4-mediated ROS signaling pathway involved in Ganoderma atrum polysaccharide-induced tumor necrosis factor-α secretion during macrophage activation
by Yu, Qiang and Nie, Shao-Ping and Wang, Jun-Qiao and Yin, Peng-Fei and Huang, Dan-Fei and Li, Wen-Juan and Xie, Ming-Yong
Food and Chemical Toxicology, ISSN 0278-6915, 04/2014, Volume 66, pp. 14 - 22
has been used as Chinese traditional medicine and healthful mushroom for thousands of years. The polysaccharide is regarded as the major bioactive substances... 
Macrophage activation | TNF-α | TLR4 | ROS | Ganoderma atrum polysaccharide | OXIDATIVE STRESS | RECOGNITION | TNF-alpha | PROTEIN-KINASE | FOOD SCIENCE & TECHNOLOGY | RAW264.7 CELLS | HYDROGEN-PEROXIDE | RADICALS | TOXICOLOGY | NF-KAPPA-B | INNATE IMMUNITY | Protein Kinases - metabolism | Cell Line | Reactive Oxygen Species - metabolism | Signal Transduction | Tumor Necrosis Factor-alpha - secretion | NF-kappa B - metabolism | Mice, Inbred C3H | Polysaccharides - pharmacology | Macrophage Activation | Macrophages - enzymology | Toll-Like Receptor 4 - physiology | Macrophages - secretion | Animals | Female | Macrophages - drug effects | Mice | Ganoderma | Index Medicus
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