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Nature reviews. Cancer, ISSN 1474-1768, 2017, Volume 17, Issue 2, pp. 93 - 115
.... Proliferation depends on progression through four distinct phases of the cell cycle G0/G1, S, G2 and M which is regulated by several cyclin-dependent kinases (CDKs... 
INVESTIGATIONAL AURORA KINASE | PHASE-II TRIAL | POLO-LIKE-KINASE | EARLY EMBRYONIC-DEVELOPMENT | DINACICLIB SCH 727965 | ADVANCED SOLID TUMORS | ONCOLOGY | PREVENTS TUMOR-GROWTH | VOLASERTIB BI 6727 | DEPENDENT KINASE INHIBITOR | SMALL-MOLECULE INHIBITOR | Cyclin-Dependent Kinase 6 - antagonists & inhibitors | Humans | Checkpoint Kinase 1 - physiology | Aurora Kinase A - antagonists & inhibitors | Cyclin-Dependent Kinase 2 - physiology | Cell Cycle Proteins - antagonists & inhibitors | Protein-Tyrosine Kinases - physiology | Aurora Kinase A - physiology | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Proto-Oncogene Proteins - antagonists & inhibitors | Signal Transduction | Protein-Serine-Threonine Kinases - physiology | Checkpoint Kinase 1 - antagonists & inhibitors | Clinical Trials as Topic | Neoplasms - drug therapy | Animals | Cyclin-Dependent Kinase 4 - physiology | Nuclear Proteins - antagonists & inhibitors | Proto-Oncogene Proteins - physiology | Cyclin-Dependent Kinase 2 - antagonists & inhibitors | Cyclin-Dependent Kinase 6 - physiology | Nuclear Proteins - physiology | Cell Cycle Proteins - physiology | Protein-Tyrosine Kinases - antagonists & inhibitors | Proteins | Care and treatment | Usage | MicroRNA | Cell cycle | Research | Cancer
Journal Article
Cell death and differentiation, ISSN 1476-5403, 2014, Volume 21, Issue 10, pp. 1511 - 1521
Necroptosis is a form of programmed cell death that depends on the activation of receptor interacting protein kinase-1 (RIPK1) and RIPK3 by receptors such as... 
APOPTOSIS | RIPOPTOSOME | MLKL | MACROPHAGES | DOWNSTREAM | BIOCHEMISTRY & MOLECULAR BIOLOGY | MIXED LINEAGE KINASE | PROGRAMMED NECROSIS | DOMAIN-LIKE | CLEAVAGE | CELL-DEATH | CELL BIOLOGY | Protein Kinases - metabolism | Protein Structure, Tertiary | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Tumor Necrosis Factor-alpha - metabolism | Cell Line | Phosphorylation | Protein Kinases - genetics | Cell Survival | Humans | Protein Multimerization | Receptors, Tumor Necrosis Factor, Type I | Caspase 8 - metabolism | Imidazoles - pharmacology | Receptor-Interacting Protein Serine-Threonine Kinases - genetics | Necrosis - physiopathology | RNA Interference | Indoles - pharmacology | RNA, Small Interfering | Apoptosis - physiology | Enzyme Activation | Receptor-Interacting Protein Serine-Threonine Kinases - antagonists & inhibitors | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Receptor-Interacting Protein Serine-Threonine Kinases/genetics | Protein Kinases/genetics | Receptor-Interacting Protein Serine-Threonine Kinases/antagonists & inhibitors | Caspase 8/metabolism | Receptor-Interacting Protein Serine-Threonine Kinases/metabolism | Tumor Necrosis Factor-alpha/antagonists & inhibitors | Indoles/pharmacology | Life Sciences | Tumor Necrosis Factor-alpha/metabolism | Imidazoles/pharmacology | Immunology | Apoptosis/physiology | Protein Kinases/metabolism | Necrosis/physiopathology | Original Paper
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 05/2015, Volume 125, Issue 5, pp. 2123 - 2135
The G protein coupled estrogen receptor (GPER) mediates both the genomic and nongenomic effects of estrogen and has been implicated in breast cancer... 
MIGRATION | MEDICINE, RESEARCH & EXPERIMENTAL | DRUG-THERAPY | ACTIVATION | PATHWAY | GROWTH | GPR30 | PROTEIN-COUPLED RECEPTORS | SIZE-CONTROL | TAZ | 17-BETA-ESTRADIOL | Carcinoma, Ductal, Breast - genetics | Neoplasms, Hormone-Dependent - metabolism | Protein-Serine-Threonine Kinases - analysis | Phosphorylation | Estrogens - pharmacology | Humans | Neoplasm Proteins - physiology | Gene Expression Regulation, Neoplastic | Neoplasms, Hormone-Dependent - physiopathology | Breast Neoplasms - physiopathology | Breast Neoplasms - metabolism | Neoplasms, Hormone-Dependent - genetics | RNA Interference | Phospholipase C beta - physiology | Cell Division | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Female | Transcription, Genetic | Phosphoproteins - physiology | Receptors, G-Protein-Coupled - drug effects | Carcinoma, Ductal, Breast - metabolism | Protein-Serine-Threonine Kinases - metabolism | Receptors, G-Protein-Coupled - physiology | Estrogens - physiology | GTP-Binding Protein alpha Subunits, Gq-G11 - genetics | rho-Associated Kinases - physiology | Transcription Factors - physiology | Protein Kinase C - physiology | Carcinoma, Ductal, Breast - physiopathology | Protein-Serine-Threonine Kinases - physiology | GTP-Binding Protein alpha Subunits, Gq-G11 - antagonists & inhibitors | GTP-Binding Protein alpha Subunits, Gq-G11 - physiology | Tumor Suppressor Proteins - physiology | Adaptor Proteins, Signal Transducing - physiology | Receptors, Estrogen - drug effects | Animals | Breast Neoplasms - genetics | Cell Transformation, Neoplastic | Signal Transduction - physiology | Mice | Mice, Inbred BALB C | Protein Processing, Post-Translational | Cell Movement | Receptors, Estrogen - physiology | Tumor Suppressor Proteins - analysis | Cell receptors | Estrogen | Physiological aspects | Development and progression | Breast cancer | Cellular signal transduction | Research | Studies | Kinases | Rodents | Oncology
Journal Article
Circulation research, ISSN 1524-4571, 2007, Volume 100, Issue 3, pp. 328 - 341
The AMP-activated protein kinase (AMPK) system acts as a sensor of cellular energy status that is conserved in all eukaryotic cells... 
Calcium signaling | Signaling pathways | Diabetes | Metabolism | Insulin | RAT-LIVER | CARDIAC & CARDIOVASCULAR SYSTEMS | insulin | 5-AMINOIMIDAZOLE-4-CARBOXAMIDE RIBONUCLEOSIDE | STIMULATED GLUCOSE-TRANSPORT | calcium signaling | ACETYL-COA CARBOXYLASE | COENZYME-A CARBOXYLASE | SKELETAL-MUSCLE | signaling pathways | FATTY-ACID OXIDATION | ENDOTHELIAL-CELLS | CELL-PERMEABLE ACTIVATOR | PANCREATIC BETA-CELLS | PERIPHERAL VASCULAR DISEASE | metabolism | HEMATOLOGY | diabetes | Consensus Sequence | Protein Subunits | Protein-Serine-Threonine Kinases - deficiency | Insulin - physiology | Obesity - drug therapy | Humans | Muscle Cells - drug effects | Adipocytes - drug effects | AMP-Activated Protein Kinases | Aminoimidazole Carboxamide - pharmacology | Multienzyme Complexes - deficiency | Calcium - physiology | Adenosine Triphosphate - metabolism | Energy Metabolism - physiology | Binding Sites | Peptide Hormones - physiology | Hypoglycemic Agents - therapeutic use | Amino Acid Sequence | Diabetes Mellitus - drug therapy | Models, Molecular | Rats | Hypoglycemic Agents - pharmacology | Mice, Knockout | Calcium-Calmodulin-Dependent Protein Kinase Kinase | Carbohydrate Metabolism - physiology | Aminoimidazole Carboxamide - analogs & derivatives | Diabetes Mellitus - therapy | Protein-Serine-Threonine Kinases - drug effects | Mice | Protein-Serine-Threonine Kinases - chemistry | Cell Cycle - drug effects | Energy Metabolism - drug effects | Lipid Metabolism - physiology | Multienzyme Complexes - drug effects | Carbohydrate Metabolism - drug effects | Phosphorylation | Metformin - therapeutic use | Molecular Sequence Data | Hepatocytes - metabolism | Ribonucleotides - pharmacology | Hepatocytes - drug effects | Adenosine Monophosphate - metabolism | Protein-Serine-Threonine Kinases - physiology | Metformin - pharmacology | Muscle Cells - metabolism | Protein-Serine-Threonine Kinases - genetics | Diabetes Mellitus - metabolism | Neoplasms - enzymology | Multienzyme Complexes - genetics | Enzyme Activation - drug effects | Protein Processing, Post-Translational - physiology | Multienzyme Complexes - chemistry | Obesity - metabolism | Sequence Homology, Amino Acid | Sequence Alignment | Animals | Oxygen Consumption - drug effects | Adipocytes - metabolism | Multienzyme Complexes - physiology | Lipid Metabolism - drug effects | Cell Cycle - physiology | Neoplasms - pathology
Journal Article
BMC genomics, ISSN 1471-2164, 2015, Volume 16, Issue 1, p. 386
Background: The mitogen-activated protein kinase (MAPK) cascade consists of three types of reversibly phosphorylated kinases, namely, MAPK, MAPK kinase (MAPKK/MEK... 
MAPKKK | Abiotic stress | MAPKK | Biotic stress | Cucumis sativus | MAPK | Plant hormones | PROTEIN-KINASE GENE | ARABIDOPSIS-THALIANA | SATIVUS | CASCADE | PLANT-RESISTANCE | SIGNALING PATHWAY | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | SEQUENCE | GENETICS & HEREDITY | BRASSICA-NAPUS L | EXPRESSION | RICE | Gene Duplication | Mitogen-Activated Protein Kinase Kinases - genetics | Genomics | Molecular Sequence Data | Cucumis sativus - genetics | Gene Expression Profiling | Cucumis sativus - physiology | Phylogeny | Promoter Regions, Genetic - genetics | Mitogen-Activated Protein Kinases - chemistry | MAP Kinase Kinase Kinases - chemistry | Mitogen-Activated Protein Kinase Kinases - metabolism | MAP Kinase Signaling System - genetics | Conserved Sequence | Transcription, Genetic | Protein-Serine-Threonine Kinases - metabolism | Multigene Family - genetics | Protein Structure, Tertiary | Amino Acid Sequence | Genome, Plant - genetics | MAP Kinase Kinase Kinases - genetics | Stress, Physiological - genetics | Protein-Serine-Threonine Kinases - genetics | Chromosome Mapping | MAP Kinase Kinase Kinases - metabolism | Cucumis sativus - growth & development | Amino Acid Motifs | Mitogen-Activated Protein Kinase Kinases - chemistry | Sequence Alignment | MAP Kinase Signaling System - drug effects | Cucumis sativus - cytology | Mitogen-Activated Protein Kinases - genetics | Protein-Serine-Threonine Kinases - chemistry | Plant Growth Regulators - pharmacology | Evolution, Molecular | Mitogen-Activated Protein Kinases - metabolism | Amino acids | Mitogens | Protein kinases
Journal Article