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Cell death and differentiation, ISSN 1476-5403, 2016, Volume 23, Issue 9, pp. 1565 - 1576
Necroptosis is a caspase-independent form of cell death that is triggered by activation of the receptor interacting serine/threonine kinase 3 (RIPK3... 
MYOCARDIAL-INFARCTION | RECEPTOR-INTERACTING PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | DOMAIN-LIKE PROTEIN | REPERFUSION INJURY | MIXED LINEAGE KINASE | PROGRAMMED NECROSIS | MEDIATES NECROPTOSIS | TNF-ALPHA | NECROPTOTIC CELL-DEATH | NF-KAPPA-B | CELL BIOLOGY | Protein Kinases - metabolism | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Inflammation - pathology | Protein Kinases - genetics | Sepsis - etiology | Apoptosis - drug effects | Colitis - pathology | Male | Inflammation - metabolism | Sepsis - pathology | Sepsis - metabolism | Colitis - chemically induced | Female | Protein Kinases - deficiency | Reperfusion Injury - metabolism | Disease Models, Animal | Systemic Inflammatory Response Syndrome - metabolism | Lipopolysaccharides - toxicity | Reperfusion Injury - pathology | Mice, Inbred C57BL | Ceruletide - toxicity | Reperfusion Injury - mortality | Pancreatitis - chemically induced | Dextran Sulfate - toxicity | Mice, Knockout | Tumor Necrosis Factor alpha-Induced Protein 3 - genetics | Receptor-Interacting Protein Serine-Threonine Kinases - genetics | Systemic Inflammatory Response Syndrome - pathology | Animals | Colitis - metabolism | Pancreatitis - pathology | Systemic Inflammatory Response Syndrome - etiology | Mice | Receptor-Interacting Protein Serine-Threonine Kinases - deficiency | Pancreatitis - metabolism | Receptor-Interacting Protein Serine-Threonine Kinases - antagonists & inhibitors | Tumor Necrosis Factor alpha-Induced Protein 3 - deficiency | Original Paper
Journal Article
American journal of physiology. Renal physiology, ISSN 1522-1466, 2016, Volume 311, Issue 2, pp. F330 - F342
.... In this context, serum- and glucocorticoid-induced kinase (SGK)1, a ubiquitously expressed kinase, is one of the primary aldosterone-induced proteins in the aldosterone-sensitive distal nephron... 
Epithelial transport | Phosphorylation | Neural precursor cell expressed developmentally downregulated protein 4-2 | Serum- and glucocorticoid-induced kinase 1 | Ubiquitylation | channel | Aldosterone | With no lysine kinase 1 | Potassium | Epithelial Na | PROTEOLYTIC CLEAVAGE | PHYSIOLOGY | potassium | serum- and glucocorticoid-induced kinase 1 | CL-COTRANSPORTER NCC | UBIQUITIN LIGASE | aldosterone | CELL-SURFACE EXPRESSION | SODIUM-CHANNEL | neural precursor cell expressed developmentally downregulated protein 4-2 | POTASSIUM HOMEOSTASIS | epithelial transport | CORTICAL COLLECTING DUCT | INDUCIBLE KINASE SGK1 | ALDOSTERONE-INDUCED KINASE | UROLOGY & NEPHROLOGY | with no lysine kinase 1 | epithelial Na+ channel | phosphorylation | ubiquitylation | Amino Acid Sequence | Protein-Serine-Threonine Kinases - deficiency | Potassium, Dietary - pharmacology | Endosomal Sorting Complexes Required for Transport - metabolism | Gene Expression Regulation | Protein-Serine-Threonine Kinases - genetics | Ubiquitin-Protein Ligases - metabolism | Male | Antibodies, Blocking - pharmacology | Epithelial Sodium Channels - metabolism | Mice, Knockout | Minor Histocompatibility Antigens - metabolism | Animals | Immediate-Early Proteins - genetics | WNK Lysine-Deficient Protein Kinase 1 | Diet | Potassium - urine | Potassium Channels, Inwardly Rectifying - immunology | Immediate-Early Proteins - deficiency | Nedd4 Ubiquitin Protein Ligases | Potassium Channels, Inwardly Rectifying - antagonists & inhibitors | Mice | Kidney Tubules - metabolism | Protein-Serine-Threonine Kinases - metabolism | Index Medicus
Journal Article
Journal Article
Journal Article
Nature (London), ISSN 1476-4687, 2007, Volume 447, Issue 7147, pp. 1017 - 1020
AMP-activated protein kinase (AMPK, also known as SNF1A) has been primarily studied as a metabolic regulator that is activated in response to energy deprivation... 
CYTOKINESIS | MUTANTS | ROLES | DISC | MULTIDISCIPLINARY SCIENCES | LIGHT-CHAIN | MYOSIN-II | NONMUSCLE MYOSIN | Protein Kinases - metabolism | Cell Polarity | Protein-Serine-Threonine Kinases - deficiency | Phosphorylation | Protein Kinases - genetics | Mitosis | Humans | Multienzyme Complexes - metabolism | Male | Drosophila Proteins - metabolism | Drosophila melanogaster - genetics | AMP-Activated Protein Kinases | Multienzyme Complexes - deficiency | Female | Protein Kinases - deficiency | Protein-Serine-Threonine Kinases - metabolism | Cell Line | Drosophila melanogaster - cytology | Protein-Serine-Threonine Kinases - genetics | Multienzyme Complexes - genetics | Phenotype | Animals | Energy Metabolism | Drosophila Proteins - deficiency | Drosophila melanogaster - enzymology | Drosophila melanogaster - growth & development | Myosin Light Chains - metabolism | Drosophila Proteins - genetics | Physiological aspects | Usage | Cell physiology | Research | Protein kinases | Drosophila | Chemistry | Biochemistry | Cellular biology | Kinases | Proteins | Control | Deprivation | Polarity | Mathematical models | Activation energy | Drosophila Proteins | Multienzyme Complexes | Protein-Serine-Threonine Kinases | Biochemistry, Molecular Biology | Cellular Biology | Life Sciences | Protein Kinases | Myosin Light Chains | Drosophila melanogaster
Journal Article
Nature (London), ISSN 1476-4687, 2016, Volume 534, Issue 7605, pp. 55 - 62
...), and SKP1 loss also to increased SRC tyrosine kinase. Global proteomic data confirmed a stromal... 
PATHWAYS | HETEROGENEITY | PIK3CA MUTATIONS | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | GENES | BIOLOGY | RECEPTOR | EXPRESSION | SIGNATURE | REVEALS | Protein Kinases - metabolism | Focal Adhesion Kinase 1 - genetics | Receptor, Epidermal Growth Factor - genetics | Protein Kinases - genetics | Cyclin-Dependent Kinases - metabolism | Receptor, ErbB-2 - genetics | Receptors, G-Protein-Coupled - metabolism | Genomics | Humans | Gene Expression Regulation, Neoplastic | Receptor, ErbB-2 - metabolism | Phosphoproteins - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - genetics | Tumor Suppressor Protein p53 - genetics | Breast Neoplasms - metabolism | Receptor-Interacting Protein Serine-Threonine Kinase 2 - metabolism | Breast Neoplasms - enzymology | Receptor, Epidermal Growth Factor - metabolism | Phosphoproteins - analysis | Mass Spectrometry | src-Family Kinases - metabolism | Female | Cyclin-Dependent Kinases - genetics | Focal Adhesion Kinase 1 - metabolism | Chromosomes, Human, Pair 5 - genetics | Breast Neoplasms - classification | Chromosome Deletion | p21-Activated Kinases - genetics | Signal Transduction | Molecular Sequence Annotation | Calcium-Binding Proteins - deficiency | Phosphoproteins - genetics | Mutation - genetics | S-Phase Kinase-Associated Proteins - metabolism | p21-Activated Kinases - metabolism | Phosphatidylinositol 3-Kinases - genetics | Breast Neoplasms - genetics | Class I Phosphatidylinositol 3-Kinases | Proteomics | S-Phase Kinase-Associated Proteins - genetics | Receptors, G-Protein-Coupled - genetics | src-Family Kinases - genetics | Calcium-Binding Proteins - genetics | Breast cancer | Genetic aspects | Research | Oncology, Experimental | Cancer | Physiological aspects | Methods | Mutation (Biology) | Proteins | Gene amplification | Peptides | Protein expression | Genomes | Mutation | Kinases | Deoxyribonucleic acid--DNA | Tumors
Journal Article
Nature (London), ISSN 1476-4687, 2010, Volume 468, Issue 7324, pp. 653 - 658
.... We studied the Lkb1 tumour suppressor and its substrate AMP-activated protein kinase (AMPK), kinases that coordinate metabolism with cell growth... 
MAINTENANCE | ACTIVATED PROTEIN-KINASE | DROSOPHILA LKB1 | GENE | SERINE-THREONINE KINASE | PATHWAY | PEUTZ-JEGHERS-SYNDROME | MULTIDISCIPLINARY SCIENCES | MICE | TRANSCRIPTION FACTOR | DEFICIENCY | Protein-Serine-Threonine Kinases - deficiency | AMP-Activated Protein Kinases - metabolism | TOR Serine-Threonine Kinases - metabolism | Multiprotein Complexes | Hematopoietic Stem Cells - pathology | Aneuploidy | Male | AMP-Activated Protein Kinases - deficiency | Mechanistic Target of Rapamycin Complex 1 | Cell Division | Gene Deletion | Cell Death | Female | Energy Metabolism - physiology | Protein-Serine-Threonine Kinases - metabolism | Hematopoietic Stem Cells - drug effects | Signal Transduction | Cell Survival | Mice, Inbred C57BL | Catalytic Domain - genetics | Protein-Serine-Threonine Kinases - genetics | Spindle Apparatus - pathology | Hematopoietic Stem Cells - metabolism | Mitochondria - metabolism | Mitochondria - pathology | Sirolimus - pharmacology | AMP-Activated Protein Kinases - chemistry | Regeneration | Animals | Proteins - metabolism | Centrosome - pathology | Hematopoietic Stem Cells - cytology | Cell Cycle - physiology | Mice | Enzyme Activation | Pancytopenia - genetics | AMP-Activated Protein Kinases - genetics | Energy metabolism | Bioenergetics | Cell cycle | Tumor suppressor genes | Research | Properties | Hematopoietic stem cells | Kinases | Metabolism | Stem cells | Tumors
Journal Article
The Journal of clinical investigation, ISSN 1558-8238, 2017, Volume 128, Issue 1, pp. 402 - 414
Journal Article
Molecular cell, ISSN 1097-2765, 2010, Volume 40, Issue 1, pp. 75 - 86
.... This response is mediated by a conserved pathway involving the nuclear ATM kinase and cytoplasmic IκB kinase (IKK... 
PROTEIN | POLYUBIQUITIN | ISOFORMS | PATHWAY | BIOCHEMISTRY & MOLECULAR BIOLOGY | NF-KAPPA-B | BINDING | CELL BIOLOGY | Protein-Serine-Threonine Kinases - deficiency | Humans | Male | NF-kappa B - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Ubiquitination | RNA Interference | Time Factors | Tumor Suppressor Proteins - deficiency | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor Proteins - metabolism | MAP Kinase Kinase Kinases - genetics | Cell Cycle Proteins - metabolism | Etoposide - pharmacology | Ubiquitin-Conjugating Enzymes - genetics | MAP Kinase Kinase Kinases - metabolism | Ataxia Telangiectasia Mutated Proteins | Signal Transduction - drug effects | Ubiquitin-Conjugating Enzymes - metabolism | Mice | DNA Damage | Enzyme Activation | Mutation | Tumor Necrosis Factor-alpha - metabolism | Phosphorylation | Pyrones - pharmacology | DNA-Binding Proteins - deficiency | DNA-Binding Proteins - metabolism | Transfection | I-kappa B Kinase - metabolism | MAP Kinase Kinase Kinases - deficiency | Mice, Mutant Strains | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | Cell Line | Mice, Inbred C57BL | Protein-Serine-Threonine Kinases - genetics | Morpholines - pharmacology | I-kappa B Kinase - genetics | DNA-Binding Proteins - genetics | Nerve Tissue Proteins - genetics | X-Linked Inhibitor of Apoptosis Protein - genetics | Nerve Tissue Proteins - metabolism | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Adaptor Proteins, Signal Transducing - genetics | X-Linked Inhibitor of Apoptosis Protein - metabolism | Protein Binding | Adaptor Proteins, Signal Transducing - metabolism | Camptothecin - pharmacology | Ubiquitin | Ligases | Lysine | Oncology, Experimental | Automated teller machines | Research | Glutamate | Cancer
Journal Article