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Publication DateJournal of Medicinal Chemistry, ISSN 0022-2623, 01/2015, Volume 58, Issue 1, pp. 183 - 196
We developed a pharmacophore model for type II inhibitors that was used to guide the construction of a library of kinase inhibitors. Kinome-wide selectivity...
RESORCYLIC ACID LACTONE | INNATE | CHEMISTRY, MEDICINAL | OPTIMIZATION | MODEL | Small Molecule Libraries - pharmacology | Models, Chemical | Area Under Curve | Pyridines - chemistry | Humans | Pyridines - pharmacokinetics | Male | Structure-Activity Relationship | Proteome - chemistry | MAP Kinase Kinase Kinases - chemistry | Protein Kinase Inhibitors - chemistry | Drug Design | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Molecular Structure | Phosphorylation - drug effects | MAP Kinase Kinase Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - metabolism | Protein Kinase Inhibitors - pharmacokinetics | Protein Structure, Tertiary | Cell Line | Cell Survival - drug effects | Proteome - antagonists & inhibitors | Cells, Cultured | Models, Molecular | MAP Kinase Kinase Kinases - metabolism | Drug Discovery | Blotting, Western | Small Molecule Libraries - chemistry | Animals | Protein Binding | Mice | Protein Kinase Inhibitors - pharmacology | Protein-Serine-Threonine Kinases - chemistry | Pyridines - pharmacology | Small Molecule Libraries - pharmacokinetics | Proteome - metabolism | BASIC BIOLOGICAL SCIENCES | 60 APPLIED LIFE SCIENCES | INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CHEMISTRY
RESORCYLIC ACID LACTONE | INNATE | CHEMISTRY, MEDICINAL | OPTIMIZATION | MODEL | Small Molecule Libraries - pharmacology | Models, Chemical | Area Under Curve | Pyridines - chemistry | Humans | Pyridines - pharmacokinetics | Male | Structure-Activity Relationship | Proteome - chemistry | MAP Kinase Kinase Kinases - chemistry | Protein Kinase Inhibitors - chemistry | Drug Design | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Molecular Structure | Phosphorylation - drug effects | MAP Kinase Kinase Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - metabolism | Protein Kinase Inhibitors - pharmacokinetics | Protein Structure, Tertiary | Cell Line | Cell Survival - drug effects | Proteome - antagonists & inhibitors | Cells, Cultured | Models, Molecular | MAP Kinase Kinase Kinases - metabolism | Drug Discovery | Blotting, Western | Small Molecule Libraries - chemistry | Animals | Protein Binding | Mice | Protein Kinase Inhibitors - pharmacology | Protein-Serine-Threonine Kinases - chemistry | Pyridines - pharmacology | Small Molecule Libraries - pharmacokinetics | Proteome - metabolism | BASIC BIOLOGICAL SCIENCES | 60 APPLIED LIFE SCIENCES | INORGANIC, ORGANIC, PHYSICAL, AND ANALYTICAL CHEMISTRY
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Loading RightsCirculation, ISSN 0009-7322, 07/2019, Volume 140, Issue 3, pp. 207 - 224
BACKGROUND:More than 90% of individuals with Noonan syndrome (NS) with mutations clustered in the CR2 domain of RAF1 present with severe and often lethal...
hypertrophic | TRANSLOCATION | DEFECTS | CARDIAC & CARDIOVASCULAR SYSTEMS | signaling | MECHANISM | mitogen activated protein kinase kinase | MAP KINASE | clustered regularly interspaced short palindromic repeats | RASopathies | IDENTIFICATION | gene editing | extracellular regulated kinase | IN-VITRO | Noonan syndrome | PERIPHERAL VASCULAR DISEASE | induced pluripotent stem cells | SEPTATION | INHIBITORS | MUTATIONS | cardiomyopathy | RAF1 | Cardiomyopathy, Hypertrophic | Heart cells | Stem cells | Development and progression | Genetic aspects | Cellular signal transduction | Health aspects | Protein kinases
hypertrophic | TRANSLOCATION | DEFECTS | CARDIAC & CARDIOVASCULAR SYSTEMS | signaling | MECHANISM | mitogen activated protein kinase kinase | MAP KINASE | clustered regularly interspaced short palindromic repeats | RASopathies | IDENTIFICATION | gene editing | extracellular regulated kinase | IN-VITRO | Noonan syndrome | PERIPHERAL VASCULAR DISEASE | induced pluripotent stem cells | SEPTATION | INHIBITORS | MUTATIONS | cardiomyopathy | RAF1 | Cardiomyopathy, Hypertrophic | Heart cells | Stem cells | Development and progression | Genetic aspects | Cellular signal transduction | Health aspects | Protein kinases
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Loading RightsJournal of Biological Chemistry, ISSN 0021-9258, 01/2012, Volume 287, Issue 5, pp. 3381 - 3391
Mitogen-activated protein kinase kinase kinases (MAP3Ks) are activated by a wide spectrum of extracellular stimuli and are involved in various cellular events...
PATHWAYS | RESPONSES | COMPLEX | BIOCHEMISTRY & MOLECULAR BIOLOGY | INNATE | TRANSDUCTION | MAP KINASES | KAPPA-B | STRESS | PEROXIREDOXIN 6 | CELL-DEATH | MAP Kinase Signaling System - physiology | Oxidants - pharmacology | Apoptosis - drug effects | Transcription Factor AP-1 - genetics | Humans | NF-kappa B - metabolism | Transcription Factor AP-1 - metabolism | HEK293 Cells | MAP Kinase Kinase Kinase 5 - metabolism | Protein Structure, Tertiary | MAP Kinase Kinase Kinase 5 - genetics | MAP Kinase Kinase Kinases - genetics | Hydrogen Peroxide - pharmacology | MAP Kinase Kinase Kinases - metabolism | Enzyme Activation - drug effects | Mice, Knockout | Tumor Necrosis Factor-alpha - pharmacology | Animals | MAP Kinase Signaling System - drug effects | NF-kappa B - genetics | Adaptor Proteins, Signal Transducing - genetics | Mice | Apoptosis - physiology | Adaptor Proteins, Signal Transducing - metabolism | Enzyme Activation - genetics | MAP Kinases (MAPKs) | NF-κB | Activator Protein-1 (AP-1) | Transforming Growth Factor-β-activated kinase 1 (TAK1) | Signal Transduction | Tumor Necrosis Factor (TNF) | Apoptosis | Apoptosis Signal-regulating Kinase 1 (ASK1)
PATHWAYS | RESPONSES | COMPLEX | BIOCHEMISTRY & MOLECULAR BIOLOGY | INNATE | TRANSDUCTION | MAP KINASES | KAPPA-B | STRESS | PEROXIREDOXIN 6 | CELL-DEATH | MAP Kinase Signaling System - physiology | Oxidants - pharmacology | Apoptosis - drug effects | Transcription Factor AP-1 - genetics | Humans | NF-kappa B - metabolism | Transcription Factor AP-1 - metabolism | HEK293 Cells | MAP Kinase Kinase Kinase 5 - metabolism | Protein Structure, Tertiary | MAP Kinase Kinase Kinase 5 - genetics | MAP Kinase Kinase Kinases - genetics | Hydrogen Peroxide - pharmacology | MAP Kinase Kinase Kinases - metabolism | Enzyme Activation - drug effects | Mice, Knockout | Tumor Necrosis Factor-alpha - pharmacology | Animals | MAP Kinase Signaling System - drug effects | NF-kappa B - genetics | Adaptor Proteins, Signal Transducing - genetics | Mice | Apoptosis - physiology | Adaptor Proteins, Signal Transducing - metabolism | Enzyme Activation - genetics | MAP Kinases (MAPKs) | NF-κB | Activator Protein-1 (AP-1) | Transforming Growth Factor-β-activated kinase 1 (TAK1) | Signal Transduction | Tumor Necrosis Factor (TNF) | Apoptosis | Apoptosis Signal-regulating Kinase 1 (ASK1)
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Loading RightsProceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 03/2017, Volume 114, Issue 11, pp. E2096 - E2105
Apoptosis signal-regulating kinases (ASK1-3) are apical kinases of the p38 and JNK MAP kinase pathways. They are activated by diverse stress stimuli, including...
Signaling | MAP Kinase | Scaffolding | MKK6 | ASK1 | scaffolding | signaling | PROTEIN | CRYSTAL-STRUCTURE | MULTIDISCIPLINARY SCIENCES | MAP kinase | MODEL | SOMATIC MUTATIONS | THIOREDOXIN | DEPENDENT ACTIVATION | BINDING | SCATTERING | Amino Acid Sequence | Phosphorylation | MAP Kinase Kinase Kinase 5 - genetics | Signal Transduction | MAP Kinase Kinase Kinase 5 - chemistry | Humans | Models, Molecular | Substrate Specificity | Structure-Activity Relationship | MAP Kinase Kinase 6 - metabolism | MAP Kinase Kinase 6 - genetics | Models, Biological | Protein Binding | Protein Conformation | Protein Interaction Domains and Motifs | MAP Kinase Kinase Kinase 5 - metabolism | Mutation | MAP Kinase Kinase 6 - chemistry | Binding Sites | Physiological aspects | Observations | Apoptosis | Mitogen-activated protein kinases | Biological Sciences | PNAS Plus
Signaling | MAP Kinase | Scaffolding | MKK6 | ASK1 | scaffolding | signaling | PROTEIN | CRYSTAL-STRUCTURE | MULTIDISCIPLINARY SCIENCES | MAP kinase | MODEL | SOMATIC MUTATIONS | THIOREDOXIN | DEPENDENT ACTIVATION | BINDING | SCATTERING | Amino Acid Sequence | Phosphorylation | MAP Kinase Kinase Kinase 5 - genetics | Signal Transduction | MAP Kinase Kinase Kinase 5 - chemistry | Humans | Models, Molecular | Substrate Specificity | Structure-Activity Relationship | MAP Kinase Kinase 6 - metabolism | MAP Kinase Kinase 6 - genetics | Models, Biological | Protein Binding | Protein Conformation | Protein Interaction Domains and Motifs | MAP Kinase Kinase Kinase 5 - metabolism | Mutation | MAP Kinase Kinase 6 - chemistry | Binding Sites | Physiological aspects | Observations | Apoptosis | Mitogen-activated protein kinases | Biological Sciences | PNAS Plus
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Loading RightsNature Structural & Molecular Biology, ISSN 1545-9993, 12/2004, Volume 11, Issue 12, pp. 1192 - 1197
MEK1 and MEK2 are closely related, dual-specificity tyrosine/threonine protein kinases found in the Ras/Raf/MEK/ERK mitogen-activated protein kinase (MAPK)...
MECHANISM | RECOGNITION | SPECIFICITY | CRYSTAL-STRUCTURE | TYROSINE KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CASCADE | IDENTIFICATION | CELL BIOLOGY | BIOPHYSICS | PATHWAY | GROWTH | ACTIVATED PROTEIN-KINASES | MAP Kinase Kinase 1 - antagonists & inhibitors | Humans | Enzyme Inhibitors - pharmacology | Models, Molecular | MAP Kinase Kinase 1 - metabolism | MAP Kinase Kinase 2 - metabolism | MAP Kinase Kinase 2 - chemistry | MAP Kinase Kinase 1 - chemistry | MAP Kinase Kinase 2 - antagonists & inhibitors | Enzyme Inhibitors - chemistry | Protein Structure, Quaternary | Conserved Sequence | Molecular Structure | Structural Homology, Protein | Binding Sites | Dimerization | Physiological aspects | Cellular signal transduction | Research | Structure | Protein kinases
MECHANISM | RECOGNITION | SPECIFICITY | CRYSTAL-STRUCTURE | TYROSINE KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CASCADE | IDENTIFICATION | CELL BIOLOGY | BIOPHYSICS | PATHWAY | GROWTH | ACTIVATED PROTEIN-KINASES | MAP Kinase Kinase 1 - antagonists & inhibitors | Humans | Enzyme Inhibitors - pharmacology | Models, Molecular | MAP Kinase Kinase 1 - metabolism | MAP Kinase Kinase 2 - metabolism | MAP Kinase Kinase 2 - chemistry | MAP Kinase Kinase 1 - chemistry | MAP Kinase Kinase 2 - antagonists & inhibitors | Enzyme Inhibitors - chemistry | Protein Structure, Quaternary | Conserved Sequence | Molecular Structure | Structural Homology, Protein | Binding Sites | Dimerization | Physiological aspects | Cellular signal transduction | Research | Structure | Protein kinases
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Loading RightsThe Plant Cell, ISSN 1040-4651, 5/2012, Volume 24, Issue 5, pp. 2225 - 2236
In Arabidopsis thaliana, the MEKK1-MKK1/MKK2-MPK4 mitogen-activated protein (MAP) kinase cascade represses cell death and immune responses. In mekk1, mkk1...
Proteins | Pathogens | Phenotypes | Cell death | Gene expression regulation | Genetic mutation | Immunity | Transgenic plants | Plant cells | Seedlings | OF-FUNCTION MUTATION | DEFENSE RESPONSES | MEKK1 | CONSTITUTIVE ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | SYSTEMIC ACQUIRED-RESISTANCE | CELL-DEATH | PLANT SCIENCES | CELL BIOLOGY | THALIANA | MPK4 ACTIVATION | DISEASE RESISTANCE | INNATE IMMUNITY | MAP Kinase Kinase Kinase 1 - metabolism | Arabidopsis Proteins - genetics | Mitogen-Activated Protein Kinase Kinases - genetics | Phosphorylation | Arabidopsis - enzymology | Plant Immunity - genetics | MAP Kinase Kinase Kinases - genetics | Arabidopsis - immunology | MAP Kinase Kinase 1 - metabolism | MAP Kinase Kinase Kinases - metabolism | Plant Immunity - physiology | Arabidopsis - genetics | Arabidopsis Proteins - metabolism | MAP Kinase Kinase 1 - genetics | Mitogen-Activated Protein Kinase Kinases - metabolism | Mitogen-Activated Protein Kinases - genetics | MAP Kinase Kinase Kinase 1 - genetics | Mitogen-Activated Protein Kinases - metabolism | Arabidopsis thaliana | Genetic aspects | Research | Nucleotide sequencing | Protein kinases | DNA sequencing
Proteins | Pathogens | Phenotypes | Cell death | Gene expression regulation | Genetic mutation | Immunity | Transgenic plants | Plant cells | Seedlings | OF-FUNCTION MUTATION | DEFENSE RESPONSES | MEKK1 | CONSTITUTIVE ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | SYSTEMIC ACQUIRED-RESISTANCE | CELL-DEATH | PLANT SCIENCES | CELL BIOLOGY | THALIANA | MPK4 ACTIVATION | DISEASE RESISTANCE | INNATE IMMUNITY | MAP Kinase Kinase Kinase 1 - metabolism | Arabidopsis Proteins - genetics | Mitogen-Activated Protein Kinase Kinases - genetics | Phosphorylation | Arabidopsis - enzymology | Plant Immunity - genetics | MAP Kinase Kinase Kinases - genetics | Arabidopsis - immunology | MAP Kinase Kinase 1 - metabolism | MAP Kinase Kinase Kinases - metabolism | Plant Immunity - physiology | Arabidopsis - genetics | Arabidopsis Proteins - metabolism | MAP Kinase Kinase 1 - genetics | Mitogen-Activated Protein Kinase Kinases - metabolism | Mitogen-Activated Protein Kinases - genetics | MAP Kinase Kinase Kinase 1 - genetics | Mitogen-Activated Protein Kinases - metabolism | Arabidopsis thaliana | Genetic aspects | Research | Nucleotide sequencing | Protein kinases | DNA sequencing
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Loading RightsMolecular and Cellular Biology, ISSN 0270-7306, 02/2001, Volume 21, Issue 3, pp. 893 - 901
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley...
PROMOTES CELL-SURVIVAL | ACTIVATED PROTEIN-KINASE | PHOSPHATIDYLINOSITOL 3-KINASE | ASK1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | GLYCOGEN-SYNTHASE KINASE-3 | N-TERMINAL KINASE | DEATH | KAPPA-B | TRANSCRIPTION FACTOR | TRANSDUCTION PATHWAY | CELL BIOLOGY | Proto-Oncogene Proteins - metabolism | Amino Acid Sequence | Cell Line | Phosphorylation | Signal Transduction | Cell Survival | MAP Kinase Kinase Kinases - genetics | Humans | Protein-Serine-Threonine Kinases | Substrate Specificity | MAP Kinase Kinase Kinases - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Serine - chemistry | MAP Kinase Kinase Kinases - chemistry | Proto-Oncogene Proteins c-akt | JNK Mitogen-Activated Protein Kinases | MAP Kinase Kinase Kinase 5 | HeLa Cells | Apoptosis | Mitogen-Activated Protein Kinases - metabolism | Cell Growth and Development
PROMOTES CELL-SURVIVAL | ACTIVATED PROTEIN-KINASE | PHOSPHATIDYLINOSITOL 3-KINASE | ASK1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | GLYCOGEN-SYNTHASE KINASE-3 | N-TERMINAL KINASE | DEATH | KAPPA-B | TRANSCRIPTION FACTOR | TRANSDUCTION PATHWAY | CELL BIOLOGY | Proto-Oncogene Proteins - metabolism | Amino Acid Sequence | Cell Line | Phosphorylation | Signal Transduction | Cell Survival | MAP Kinase Kinase Kinases - genetics | Humans | Protein-Serine-Threonine Kinases | Substrate Specificity | MAP Kinase Kinase Kinases - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Serine - chemistry | MAP Kinase Kinase Kinases - chemistry | Proto-Oncogene Proteins c-akt | JNK Mitogen-Activated Protein Kinases | MAP Kinase Kinase Kinase 5 | HeLa Cells | Apoptosis | Mitogen-Activated Protein Kinases - metabolism | Cell Growth and Development
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Loading RightsGastroenterology, ISSN 0016-5085, 2008, Volume 135, Issue 4, pp. 1311 - 1321
Background & Aims: Acetaminophen (APAP) overdose is the most frequent cause of drug-induced liver failure. C-jun N-terminal kinase (JNK) is thought to play a...
Gastroenterology and Hepatology | JNK ACTIVATION | APOPTOSIS | GAMMA-RADIATION | PROTEIN-KINASE | MAP KINASES | TNF-ALPHA | STRESS | GASTROENTEROLOGY & HEPATOLOGY | ISOLATED MOUSE HEPATOCYTES | CELL-DEATH | INDUCED HEPATOTOXICITY | Drug Overdose - metabolism | Hepatocytes - pathology | JNK Mitogen-Activated Protein Kinases - metabolism | Male | Mitogen-Activated Protein Kinase 9 - genetics | Drug Overdose - pathology | Acetaminophen - poisoning | Mitogen-Activated Protein Kinase 8 - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | JNK Mitogen-Activated Protein Kinases - genetics | MAP Kinase Kinase Kinase 5 - metabolism | Chemical and Drug Induced Liver Injury - pathology | Disease Models, Animal | Drug Overdose - physiopathology | MAP Kinase Kinase Kinase 5 - genetics | Mitogen-Activated Protein Kinase 9 - metabolism | Mice, Inbred C57BL | Mitogen-Activated Protein Kinase 8 - metabolism | p38 Mitogen-Activated Protein Kinases - genetics | Chemical and Drug Induced Liver Injury - physiopathology | Mice, Knockout | Gene Expression Regulation, Enzymologic | Animals | Signal Transduction - drug effects | Chemical and Drug Induced Liver Injury - metabolism | Signal Transduction - physiology | Mice | Analgesics, Non-Narcotic - poisoning | Hepatocytes - enzymology | Liver diseases | Protein kinases | Liver | Glutathione | Apoptosis | Index Medicus | Abridged Index Medicus
Gastroenterology and Hepatology | JNK ACTIVATION | APOPTOSIS | GAMMA-RADIATION | PROTEIN-KINASE | MAP KINASES | TNF-ALPHA | STRESS | GASTROENTEROLOGY & HEPATOLOGY | ISOLATED MOUSE HEPATOCYTES | CELL-DEATH | INDUCED HEPATOTOXICITY | Drug Overdose - metabolism | Hepatocytes - pathology | JNK Mitogen-Activated Protein Kinases - metabolism | Male | Mitogen-Activated Protein Kinase 9 - genetics | Drug Overdose - pathology | Acetaminophen - poisoning | Mitogen-Activated Protein Kinase 8 - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | JNK Mitogen-Activated Protein Kinases - genetics | MAP Kinase Kinase Kinase 5 - metabolism | Chemical and Drug Induced Liver Injury - pathology | Disease Models, Animal | Drug Overdose - physiopathology | MAP Kinase Kinase Kinase 5 - genetics | Mitogen-Activated Protein Kinase 9 - metabolism | Mice, Inbred C57BL | Mitogen-Activated Protein Kinase 8 - metabolism | p38 Mitogen-Activated Protein Kinases - genetics | Chemical and Drug Induced Liver Injury - physiopathology | Mice, Knockout | Gene Expression Regulation, Enzymologic | Animals | Signal Transduction - drug effects | Chemical and Drug Induced Liver Injury - metabolism | Signal Transduction - physiology | Mice | Analgesics, Non-Narcotic - poisoning | Hepatocytes - enzymology | Liver diseases | Protein kinases | Liver | Glutathione | Apoptosis | Index Medicus | Abridged Index Medicus
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Loading RightsJournal of Clinical Oncology, ISSN 0732-183X, 05/2008, Volume 26, Issue 13, pp. 2139 - 2146
Purpose To assess the tolerability, pharmacokinetics (PKs), and pharmacodynamics (PDs) of the mitogenactivated protein kinase kinase (MEK) 1/2 inhibitor...
MEK INHIBITOR | POTENT | VIVO | ONCOLOGY | PATHWAY | GROWTH | COLON | TUMORS | ras Proteins - genetics | Phosphorylation | Proto-Oncogene Proteins p21(ras) | Humans | Middle Aged | Melanoma - enzymology | Male | Antineoplastic Agents - administration & dosage | Extracellular Signal-Regulated MAP Kinases - metabolism | Protein Kinase Inhibitors - adverse effects | Dose-Response Relationship, Drug | Benzimidazoles - administration & dosage | Neoplasms - genetics | Antineoplastic Agents - adverse effects | DNA Mutational Analysis | Melanoma - genetics | Aged, 80 and over | Adult | Female | Antineoplastic Agents - pharmacokinetics | Benzimidazoles - adverse effects | Protein Kinase Inhibitors - pharmacokinetics | MAP Kinase Kinase 1 - antagonists & inhibitors | Leukocytes, Mononuclear - drug effects | Drug Administration Schedule | Administration, Oral | Benzimidazoles - pharmacokinetics | Neoplasms - enzymology | MAP Kinase Kinase 1 - metabolism | Proto-Oncogene Proteins - genetics | Treatment Outcome | MAP Kinase Kinase 2 - metabolism | Melanoma - pathology | Neoplasms - drug therapy | Protein Kinase Inhibitors - administration & dosage | Maximum Tolerated Dose | Ki-67 Antigen - analysis | MAP Kinase Kinase 2 - antagonists & inhibitors | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Leukocytes, Mononuclear - enzymology | Aged | Cell Proliferation - drug effects | Mutation | Neoplasm Staging | Neoplasms - pathology | Index Medicus
MEK INHIBITOR | POTENT | VIVO | ONCOLOGY | PATHWAY | GROWTH | COLON | TUMORS | ras Proteins - genetics | Phosphorylation | Proto-Oncogene Proteins p21(ras) | Humans | Middle Aged | Melanoma - enzymology | Male | Antineoplastic Agents - administration & dosage | Extracellular Signal-Regulated MAP Kinases - metabolism | Protein Kinase Inhibitors - adverse effects | Dose-Response Relationship, Drug | Benzimidazoles - administration & dosage | Neoplasms - genetics | Antineoplastic Agents - adverse effects | DNA Mutational Analysis | Melanoma - genetics | Aged, 80 and over | Adult | Female | Antineoplastic Agents - pharmacokinetics | Benzimidazoles - adverse effects | Protein Kinase Inhibitors - pharmacokinetics | MAP Kinase Kinase 1 - antagonists & inhibitors | Leukocytes, Mononuclear - drug effects | Drug Administration Schedule | Administration, Oral | Benzimidazoles - pharmacokinetics | Neoplasms - enzymology | MAP Kinase Kinase 1 - metabolism | Proto-Oncogene Proteins - genetics | Treatment Outcome | MAP Kinase Kinase 2 - metabolism | Melanoma - pathology | Neoplasms - drug therapy | Protein Kinase Inhibitors - administration & dosage | Maximum Tolerated Dose | Ki-67 Antigen - analysis | MAP Kinase Kinase 2 - antagonists & inhibitors | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Leukocytes, Mononuclear - enzymology | Aged | Cell Proliferation - drug effects | Mutation | Neoplasm Staging | Neoplasms - pathology | Index Medicus
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Loading RightsJournal of Biological Chemistry, ISSN 0021-9258, 12/2013, Volume 288, Issue 52, pp. 37332 - 37342
Non-visual arrestins scaffold mitogen-activated protein kinase (MAPK) cascades. The c-Jun N-terminal kinases (JNKs) are members of MAPK family. Arrestin-3 has...
Signal Transduction | INDUCED APOPTOSIS | MAP-KINASE | NONVISUAL ARRESTINS | BIOCHEMISTRY & MOLECULAR BIOLOGY | Scaffold Proteins | PROTEIN-COUPLED RECEPTORS | Arrestin | DEATH | Protein Phosphorylation | SIGNAL-TRANSDUCTION | MAP Kinases (MAPKs) | INOSITOL HEXAKISPHOSPHATE | CORTICAL-NEURONS | PATHWAY | BETA-ARRESTINS | Jun N-terminal Kinase (JNK) | MAP Kinase Kinase 7 - genetics | Phosphorylation - physiology | MAP Kinase Signaling System - physiology | Cell Proliferation | MAP Kinase Kinase Kinase 5 - genetics | Isoenzymes - genetics | Mitogen-Activated Protein Kinase 9 - metabolism | Mitogen-Activated Protein Kinase 8 - metabolism | Cercopithecus aethiops | Arrestins - genetics | Mitogen-Activated Protein Kinase 9 - genetics | Arrestins - metabolism | Mice, Knockout | MAP Kinase Kinase 7 - metabolism | Animals | Isoenzymes - metabolism | Mitogen-Activated Protein Kinase 8 - genetics | Mice | MAP Kinase Kinase Kinase 5 - metabolism | COS Cells | Enzyme Activation - physiology | Cell Survival - physiology | Protein Binding - physiology
Signal Transduction | INDUCED APOPTOSIS | MAP-KINASE | NONVISUAL ARRESTINS | BIOCHEMISTRY & MOLECULAR BIOLOGY | Scaffold Proteins | PROTEIN-COUPLED RECEPTORS | Arrestin | DEATH | Protein Phosphorylation | SIGNAL-TRANSDUCTION | MAP Kinases (MAPKs) | INOSITOL HEXAKISPHOSPHATE | CORTICAL-NEURONS | PATHWAY | BETA-ARRESTINS | Jun N-terminal Kinase (JNK) | MAP Kinase Kinase 7 - genetics | Phosphorylation - physiology | MAP Kinase Signaling System - physiology | Cell Proliferation | MAP Kinase Kinase Kinase 5 - genetics | Isoenzymes - genetics | Mitogen-Activated Protein Kinase 9 - metabolism | Mitogen-Activated Protein Kinase 8 - metabolism | Cercopithecus aethiops | Arrestins - genetics | Mitogen-Activated Protein Kinase 9 - genetics | Arrestins - metabolism | Mice, Knockout | MAP Kinase Kinase 7 - metabolism | Animals | Isoenzymes - metabolism | Mitogen-Activated Protein Kinase 8 - genetics | Mice | MAP Kinase Kinase Kinase 5 - metabolism | COS Cells | Enzyme Activation - physiology | Cell Survival - physiology | Protein Binding - physiology
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11.
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TAK1-mediated autophagy and fatty acid oxidation prevent hepatosteatosis and tumorigenesis
Journal of Clinical Investigation, ISSN 0021-9738, 08/2014, Volume 124, Issue 8, pp. 3566 - 3578
The MAP kinase kinase kinase TGF beta-activated kinase 1 (TAK1) is activated by TLRs, IL-1, TNF, and TGF beta and in turn activates IKK-NF-kappa beta and JNK,...
MEDICINE, RESEARCH & EXPERIMENTAL | CELLS | HEPATOCELLULAR-CARCINOMA | ACTIVATED PROTEIN-KINASE | LIPID-METABOLISM | TAK1 | INSULIN-RESISTANCE | IN-VIVO | NF-KAPPA-B | CANCER | HEPATOCYTE-SPECIFIC DELETION | AMP-Activated Protein Kinases - metabolism | TOR Serine-Threonine Kinases - metabolism | Autophagy - physiology | Hepatocytes - metabolism | Liver Neoplasms, Experimental - prevention & control | Autophagy - drug effects | Mechanistic Target of Rapamycin Complex 1 | Multiprotein Complexes - antagonists & inhibitors | TOR Serine-Threonine Kinases - antagonists & inhibitors | Liver Neoplasms, Experimental - metabolism | Multiprotein Complexes - metabolism | Hepatocytes - cytology | MAP Kinase Kinase Kinases - deficiency | Liver Neoplasms, Experimental - genetics | Fatty Acids - metabolism | Hepatocytes - drug effects | Fatty Liver - genetics | Fatty Liver - metabolism | Oxidation-Reduction | MAP Kinase Kinase Kinases - genetics | Mice, Inbred C57BL | Fatty Liver - prevention & control | Mice, Transgenic | MAP Kinase Kinase Kinases - metabolism | Sirolimus - pharmacology | Mice, Knockout | Animals | Mice | PPAR alpha - metabolism | Prevention | Autophagy (Cytology) | Liver diseases | Physiological aspects | Biological oxidation (Metabolism) | Research | Protein kinases | Studies | Phosphorylation | Rodents | Liver | Lipids | Biosynthesis | Tumorigenesis | Kinases | Laboratory animals | Gene expression | Autophagy
MEDICINE, RESEARCH & EXPERIMENTAL | CELLS | HEPATOCELLULAR-CARCINOMA | ACTIVATED PROTEIN-KINASE | LIPID-METABOLISM | TAK1 | INSULIN-RESISTANCE | IN-VIVO | NF-KAPPA-B | CANCER | HEPATOCYTE-SPECIFIC DELETION | AMP-Activated Protein Kinases - metabolism | TOR Serine-Threonine Kinases - metabolism | Autophagy - physiology | Hepatocytes - metabolism | Liver Neoplasms, Experimental - prevention & control | Autophagy - drug effects | Mechanistic Target of Rapamycin Complex 1 | Multiprotein Complexes - antagonists & inhibitors | TOR Serine-Threonine Kinases - antagonists & inhibitors | Liver Neoplasms, Experimental - metabolism | Multiprotein Complexes - metabolism | Hepatocytes - cytology | MAP Kinase Kinase Kinases - deficiency | Liver Neoplasms, Experimental - genetics | Fatty Acids - metabolism | Hepatocytes - drug effects | Fatty Liver - genetics | Fatty Liver - metabolism | Oxidation-Reduction | MAP Kinase Kinase Kinases - genetics | Mice, Inbred C57BL | Fatty Liver - prevention & control | Mice, Transgenic | MAP Kinase Kinase Kinases - metabolism | Sirolimus - pharmacology | Mice, Knockout | Animals | Mice | PPAR alpha - metabolism | Prevention | Autophagy (Cytology) | Liver diseases | Physiological aspects | Biological oxidation (Metabolism) | Research | Protein kinases | Studies | Phosphorylation | Rodents | Liver | Lipids | Biosynthesis | Tumorigenesis | Kinases | Laboratory animals | Gene expression | Autophagy
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Loading RightsJournal of Diabetes Investigation, ISSN 2040-1116, 07/2017, Volume 8, Issue 4, pp. 434 - 445
Aims/Introduction Angiotensin‐(1–7) (Ang‐[1–7]), recognized as a new bioactive peptide in the renin–angiotensin system, shows biological and pharmacological...
Cardiomyocytes | Angiotensin‐(1–7) | High glucose | Angiotensin-(1–7) | APOPTOSIS | OXIDATIVE STRESS | Angiotensin-(1-7) | DIABETIC CARDIOMYOPATHY | EXOGENOUS HYDROGEN-SULFIDE | NARINGIN | HEART | P38 MAPK PATHWAY | HYPERGLYCEMIA | EPITHELIAL-CELLS | ENDOCRINOLOGY & METABOLISM | Leptin - antagonists & inhibitors | Anthracenes | Cell Line | Glucose - adverse effects | Pyridines | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Leptin - metabolism | Acetylcysteine | Rats | Peptide Fragments - pharmacology | Membrane Potential, Mitochondrial - drug effects | Animals | Imidazoles | MAP Kinase Signaling System - drug effects | Myocytes, Cardiac - drug effects | Myocytes, Cardiac - metabolism | Angiotensin I - pharmacology | Leptin | Analysis | Heart cells | Angiotensin | Glucose | Mitogens | Protein kinases | Dextrose | Transcription factors | Oxygen | Diabetes mellitus | c-Jun protein | Extracellular signal-regulated kinase | MAP kinase | Kinases | Proteins | Mitochondria | Renin | Protein kinase | Membrane potential | Cardiovascular diseases | Species | Injuries | Apoptosis | Original
Cardiomyocytes | Angiotensin‐(1–7) | High glucose | Angiotensin-(1–7) | APOPTOSIS | OXIDATIVE STRESS | Angiotensin-(1-7) | DIABETIC CARDIOMYOPATHY | EXOGENOUS HYDROGEN-SULFIDE | NARINGIN | HEART | P38 MAPK PATHWAY | HYPERGLYCEMIA | EPITHELIAL-CELLS | ENDOCRINOLOGY & METABOLISM | Leptin - antagonists & inhibitors | Anthracenes | Cell Line | Glucose - adverse effects | Pyridines | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Leptin - metabolism | Acetylcysteine | Rats | Peptide Fragments - pharmacology | Membrane Potential, Mitochondrial - drug effects | Animals | Imidazoles | MAP Kinase Signaling System - drug effects | Myocytes, Cardiac - drug effects | Myocytes, Cardiac - metabolism | Angiotensin I - pharmacology | Leptin | Analysis | Heart cells | Angiotensin | Glucose | Mitogens | Protein kinases | Dextrose | Transcription factors | Oxygen | Diabetes mellitus | c-Jun protein | Extracellular signal-regulated kinase | MAP kinase | Kinases | Proteins | Mitochondria | Renin | Protein kinase | Membrane potential | Cardiovascular diseases | Species | Injuries | Apoptosis | Original
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Loading RightsJournal of Biological Chemistry, ISSN 0021-9258, 08/2015, Volume 290, Issue 32, pp. 19900 - 19909
Accumulating evidence suggests that activation of mitogen-activated protein kinases (MAPKs) and nuclear factor NF-kappa B exacerbates early brain injury (EBI)...
SIGNALING PATHWAYS | VASOSPASM | LEARNING-DEFICITS | PHOSPHORYLATION | INFLAMMATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | GROWTH | MECHANISMS | NF-KAPPA-B | EXPRESSION | PROTECTS | Neurons - pathology | Phosphorylation | Transcription Factor RelA - antagonists & inhibitors | Apoptosis - drug effects | Injections, Intraventricular | Male | Cerebrovascular Trauma - metabolism | I-kappa B Proteins - metabolism | I-kappa B Proteins - genetics | Transcription Factor RelA - genetics | Anti-Inflammatory Agents, Non-Steroidal - pharmacology | MAP Kinase Kinase 4 - metabolism | Neuroprotective Agents - pharmacology | I-kappa B Proteins - antagonists & inhibitors | MAP Kinase Kinase 4 - antagonists & inhibitors | Neurons - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | MAP Kinase Kinase Kinases - antagonists & inhibitors | Neurons - drug effects | Subarachnoid Hemorrhage - drug therapy | Disease Models, Animal | NF-KappaB Inhibitor alpha | Signal Transduction | MAP Kinase Kinase Kinases - genetics | Gene Expression Regulation | Rats | p38 Mitogen-Activated Protein Kinases - genetics | Zearalenone - analogs & derivatives | MAP Kinase Kinase Kinases - metabolism | Subarachnoid Hemorrhage - genetics | Subarachnoid Hemorrhage - pathology | Rats, Sprague-Dawley | Stereotaxic Techniques | Subarachnoid Hemorrhage - metabolism | Animals | Transcription Factor RelA - metabolism | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cerebrovascular Trauma - pathology | MAP Kinase Kinase 4 - genetics | Cerebrovascular Trauma - prevention & control | Protein Kinase Inhibitors - pharmacology | Cerebrovascular Trauma - genetics | Zearalenone - pharmacology | TAK1 | neuroprotection | 5Z-7-oxozeaenol | subarachnoid hemorrhage | Neurobiology | mitogen-activated protein kinase (MAPK) | apoptosis | brain | NF-κB (NF-KB)
SIGNALING PATHWAYS | VASOSPASM | LEARNING-DEFICITS | PHOSPHORYLATION | INFLAMMATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | GROWTH | MECHANISMS | NF-KAPPA-B | EXPRESSION | PROTECTS | Neurons - pathology | Phosphorylation | Transcription Factor RelA - antagonists & inhibitors | Apoptosis - drug effects | Injections, Intraventricular | Male | Cerebrovascular Trauma - metabolism | I-kappa B Proteins - metabolism | I-kappa B Proteins - genetics | Transcription Factor RelA - genetics | Anti-Inflammatory Agents, Non-Steroidal - pharmacology | MAP Kinase Kinase 4 - metabolism | Neuroprotective Agents - pharmacology | I-kappa B Proteins - antagonists & inhibitors | MAP Kinase Kinase 4 - antagonists & inhibitors | Neurons - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | MAP Kinase Kinase Kinases - antagonists & inhibitors | Neurons - drug effects | Subarachnoid Hemorrhage - drug therapy | Disease Models, Animal | NF-KappaB Inhibitor alpha | Signal Transduction | MAP Kinase Kinase Kinases - genetics | Gene Expression Regulation | Rats | p38 Mitogen-Activated Protein Kinases - genetics | Zearalenone - analogs & derivatives | MAP Kinase Kinase Kinases - metabolism | Subarachnoid Hemorrhage - genetics | Subarachnoid Hemorrhage - pathology | Rats, Sprague-Dawley | Stereotaxic Techniques | Subarachnoid Hemorrhage - metabolism | Animals | Transcription Factor RelA - metabolism | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cerebrovascular Trauma - pathology | MAP Kinase Kinase 4 - genetics | Cerebrovascular Trauma - prevention & control | Protein Kinase Inhibitors - pharmacology | Cerebrovascular Trauma - genetics | Zearalenone - pharmacology | TAK1 | neuroprotection | 5Z-7-oxozeaenol | subarachnoid hemorrhage | Neurobiology | mitogen-activated protein kinase (MAPK) | apoptosis | brain | NF-κB (NF-KB)
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