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Nature (London), ISSN 1476-4687, 2015, Volume 526, Issue 7575, pp. 700 - 704
Journal Article
Nature (London), ISSN 1476-4687, 2014, Volume 517, Issue 7536, pp. 583 - 588
Journal Article
The Journal of clinical investigation, ISSN 0021-9738, 2015, Volume 125, Issue 2, pp. 665 - 680
.... Here, we demonstrated that the mitochondrial uncoupling protein-2 (UCP2) regulates NLRP3-mediated caspase-1 activation through the stimulation of lipid synthesis in macrophages... 
MEDICINE, RESEARCH & EXPERIMENTAL | OXIDATIVE STRESS | GLUCOSE-METABOLISM | ATP-CITRATE LYASE | UCP2 | SEPTIC SHOCK | CELL-GROWTH | CRITICALLY-ILL PATIENTS | INTENSIVE INSULIN THERAPY | CANCER | MITOCHONDRIAL UNCOUPLING PROTEINS | Fatty Acid Synthase, Type I - genetics | Fatty Acid Synthase, Type I - biosynthesis | Lipids - genetics | Inflammasomes - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Ion Channels - genetics | Caspase 1 - metabolism | Mitochondrial Proteins - genetics | Interleukin-1beta - genetics | Lipids - biosynthesis | Sepsis - pathology | Interleukin-1beta - metabolism | Mitochondrial Proteins - metabolism | Sepsis - metabolism | Macrophages - pathology | Down-Regulation - genetics | Inflammasomes - genetics | Sepsis - genetics | Mice, Knockout | Carrier Proteins - genetics | Enzyme Induction - genetics | Macrophages - metabolism | Animals | Carrier Proteins - metabolism | Sepsis - chemically induced | Ion Channels - metabolism | Caspase 1 - genetics | Sepsis - therapy | Mice | Uncoupling Protein 2 | Interleukin-18 - genetics | Interleukin-18 - metabolism | Cellular proteins | Immune response | Synthesis | Sepsis | Development and progression | Lipids | Genetic aspects | Properties | Enzymes | Cytokines | Pathogenesis | Mortality | Glucose | Metabolism | Gene expression | Fatty acids | Proteins | Studies | Metabolites | Consent | Rodents
Journal Article
Cancer cell, ISSN 1535-6108, 2012, Volume 22, Issue 2, pp. 153 - 166
... ALL). The genetic alterations that activate kinase signaling in Ph-like ALL are poorly understood... 
GROWTH-FACTOR RECEPTOR | BCR-JAK2 FUSION GENE | ONCOLOGY | NUCLEAR-PORE | MYELOPROLIFERATIVE NEOPLASMS | ACUTE MYELOID-LEUKEMIA | OF-FUNCTION MUTATIONS | FLT3 MUTATIONS | CHILDHOOD | B-PROGENITOR | CHRONIC MYELOMONOCYTIC LEUKEMIA | CELL BIOLOGY | Recurrence | Humans | Molecular Sequence Data | RNA, Messenger - metabolism | Receptor, Platelet-Derived Growth Factor beta - genetics | Protein-Tyrosine Kinases - genetics | DNA Mutational Analysis | Base Sequence | Trans-Activators - genetics | Phosphorylation - drug effects | Philadelphia Chromosome | Receptors, Cytokine - genetics | Genetic Predisposition to Disease | RNA, Messenger - genetics | Risk Factors | Gene Expression Regulation, Leukemic - drug effects | Signal Transduction - genetics | Enzyme Activation - drug effects | Mutation - genetics | Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics | Animals | Signal Transduction - drug effects | Cell Transformation, Neoplastic | Oncogene Proteins, Fusion - genetics | Precursor Cell Lymphoblastic Leukemia-Lymphoma - enzymology | Mice | Protein Kinase Inhibitors - pharmacology | Gene Rearrangement - genetics | Sequence Deletion - genetics | Tyrosine | Platelet-derived growth factor | Cytokines | Genes | Oncology, Experimental | Genomes | Research | Gene expression | Population genetics | Hunger | Medical genetics | Genetic research | Nucleotide sequencing | Acute lymphocytic leukemia | Cancer | DNA sequencing
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 0027-8424, 7/2014, Volume 111, Issue 30, pp. 11181 - 11186
Acute glaucoma is a sight-threatening condition characterized by a sudden and substantial rise in intraocular pressure (IOP) and consequent retinal ganglion... 
Glaucoma | Reperfusion | Messenger RNA | Ischemia | Toll like receptors | Central nervous system | Retina | Brain damage | Intraocular pressure | Microglia | Retinal ischemia/reperfusion injury | Cell apoptosis | BRAIN-INJURY | MICROGLIA ACTIVATION | INTERLEUKIN-1-BETA | MULTIDISCIPLINARY SCIENCES | REPERFUSION INJURY | POPULATIONS | retinal ischemia/reperfusion injury | ANGLE-CLOSURE GLAUCOMA | cell apoptosis | TOLL-LIKE RECEPTORS | CENTRAL-NERVOUS-SYSTEM | MICE | CEREBRAL-ISCHEMIA | Inflammasomes - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Caspase 8 - metabolism | Caspase 1 - metabolism | Interleukin-1beta - genetics | Caspase 8 - genetics | Interleukin-1beta - metabolism | Apoptosis Regulatory Proteins - genetics | Eye Proteins - genetics | Glaucoma - metabolism | Disease Models, Animal | Acute Disease | Rats | Toll-Like Receptor 4 - genetics | Receptors, Cytoplasmic and Nuclear - genetics | Nerve Tissue Proteins - genetics | Rats, Sprague-Dawley | Toll-Like Receptor 4 - metabolism | Inflammasomes - genetics | Apoptosis Regulatory Proteins - metabolism | Mice, Knockout | Nerve Tissue Proteins - metabolism | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Eye Proteins - metabolism | Caspase 1 - genetics | Adaptor Proteins, Signal Transducing - genetics | Mice | Adaptor Proteins, Signal Transducing - metabolism | Enzyme Activation - genetics | Glaucoma - genetics | Receptors, Cytoplasmic and Nuclear - metabolism | Biological Sciences | reperfusion injury | retinal ischemia
Journal Article
Biochimica et biophysica acta. Molecular basis of disease, ISSN 0925-4439, 06/2013, Volume 1832, Issue 6, pp. 848 - 863
.... This study was designed to examine the effect of protein kinase B (Akt) activation on lipopolysaccharide-induced cardiac anomalies and underlying mechanism(s) involved... 
Heart | ER stress | Sepsis | Akt | Contractile function | Apoptosis | OXIDATIVE STRESS | CONTRACTILE DYSFUNCTION | BIOCHEMISTRY & MOLECULAR BIOLOGY | HEART-FAILURE | ENDOPLASMIC-RETICULUM STRESS | AUTOPHAGY | GROWTH-FACTOR I | SIGNAL-TRANSDUCTION | SYNTHASE | BIOPHYSICS | INFLAMMATORY RESPONSE | NF-KAPPA-B | Caspase 9 - genetics | Apoptosis - drug effects | Calcium - metabolism | Heat-Shock Proteins - biosynthesis | Myocardial Contraction - drug effects | bcl-2-Associated X Protein - biosynthesis | Apoptosis - genetics | Glycogen Synthase Kinase 3 beta | Heat-Shock Proteins - genetics | Phosphorylation - genetics | Caspase 3 - genetics | Phosphorylation - drug effects | Transcription Factor CHOP - biosynthesis | Proto-Oncogene Proteins c-akt - metabolism | Apoptosis Regulatory Proteins - biosynthesis | Lipopolysaccharides - toxicity | Endoplasmic Reticulum Stress - drug effects | Mice, Transgenic | Glycogen Synthase Kinase 3 - genetics | Eukaryotic Initiation Factor-2 - genetics | Mice | Enzyme Activation - genetics | Transcription Factor CHOP - genetics | Eukaryotic Initiation Factor-2 - biosynthesis | Microtubule-Associated Proteins - genetics | bcl-X Protein - genetics | Extracellular Signal-Regulated MAP Kinases - metabolism | Endoplasmic Reticulum Stress - genetics | Extracellular Signal-Regulated MAP Kinases - genetics | Proto-Oncogene Proteins c-akt - genetics | Myocardial Contraction - genetics | MAP Kinase Signaling System - genetics | Apoptosis Regulatory Proteins - genetics | Caspase 3 - biosynthesis | bcl-X Protein - biosynthesis | bcl-2-Associated X Protein - genetics | Beclin-1 | Gene Expression Regulation - genetics | Myocardium - pathology | Transcription Factors - biosynthesis | Transcription Factors - genetics | Enzyme Activation - drug effects | Glycogen Synthase Kinase 3 - metabolism | Microtubule-Associated Proteins - biosynthesis | Gene Expression Regulation - drug effects | Autophagy-Related Protein 7 | Myocardium - enzymology | Animals | MAP Kinase Signaling System - drug effects | Caspase 9 - biosynthesis
Journal Article
PLoS genetics, ISSN 1553-7404, 2015, Volume 11, Issue 8, p. e1005482
Journal Article
Nature genetics, ISSN 1546-1718, 2012, Volume 44, Issue 8, pp. 852 - 860
... p.Thr790Met alteration or MET activation. Genetic or pharmacological inhibition of AXL restored sensitivity to erlotinib in these tumor models... 
GEFITINIB | RECEPTOR TYROSINE KINASES | MET AMPLIFICATION | GROWTH | GENETICS & HEREDITY | ACQUIRED-RESISTANCE | MUTATIONS | NF-KAPPA-B | TUMORS | MUTANT EGFR | ERLOTINIB | Erlotinib Hydrochloride | Proto-Oncogene Proteins c-met - metabolism | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Humans | Lung Neoplasms - metabolism | Middle Aged | Lung Neoplasms - pathology | Male | Intercellular Signaling Peptides and Proteins - metabolism | Epithelial-Mesenchymal Transition | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Adult | Female | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Proto-Oncogene Proteins - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | Signal Transduction | Carcinoma, Non-Small-Cell Lung - genetics | Carcinoma, Non-Small-Cell Lung - metabolism | Intercellular Signaling Peptides and Proteins - genetics | Proto-Oncogene Proteins - genetics | Receptor Protein-Tyrosine Kinases - metabolism | Proto-Oncogene Proteins c-met - genetics | Xenograft Model Antitumor Assays | Drug Resistance, Neoplasm - genetics | Animals | Receptor Protein-Tyrosine Kinases - genetics | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Aged | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Enzyme Activation | Mutation | Quinazolines - pharmacology | Erlotinib | Physiological aspects | Genetic aspects | Research | Lung cancer, Non-small cell | Drug therapy | Health aspects | Protein kinases | Studies | Medical research | Rodents | Lung cancer | Genomics | Kinases | Gene expression | Acquisitions & mergers | Tumors
Journal Article
The Journal of biological chemistry, ISSN 0021-9258, 03/2011, Volume 286, Issue 11, pp. 9107 - 9119
.... In human cells, the activation process involves autophosphorylation on three sites (Ser(367), Ser(1893), and Ser(1981)) and acetylation on Lys... 
RECRUITMENT | STRAND BREAK REPAIR | PROTEIN | PHOSPHORYLATION | DNA-DAMAGE RESPONSE | NBS1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | NUCLEAR FOCI | MRN COMPLEX | N-TERMINUS | ATAXIA-TELANGIECTASIA | Humans | DNA Repair Enzymes - genetics | Multiprotein Complexes - genetics | DNA Breaks, Double-Stranded | DNA-Binding Proteins - metabolism | MRE11 Homologue Protein | Multiprotein Complexes - metabolism | Phosphorylation - genetics | Tumor Suppressor Proteins - genetics | DNA Repair Enzymes - metabolism | Cell Cycle Proteins - genetics | Phosphorylation - drug effects | Nuclear Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Radiation, Ionizing | Tumor Suppressor Proteins - metabolism | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Nuclear Proteins - metabolism | Ataxia Telangiectasia - metabolism | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Enzyme Activation - drug effects | Enzyme Activation - radiation effects | S Phase - genetics | Phosphorylation - radiation effects | S Phase - radiation effects | Animals | Ataxia Telangiectasia - genetics | Mice | Protein Kinase Inhibitors - pharmacology | S Phase - drug effects | Enzyme Activation - genetics | Cell Line, Transformed | Ataxia-telangiectasia | Signal Transduction | Post-translational Modification | Mass Spectrometry (MS) | DNA Damage | Protein Phosphorylation | Serine Threonine Protein Kinase | ATM Kinase
Journal Article