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Apoptosis, ISSN 1360-8185, 3/2008, Volume 13, Issue 3, pp. 343 - 353
... (mitogen-activated protein kinases) pathways, which modulate the activity of transcription factors by phosphorylation... 
Biochemistry, general | Kinases inhibitors | Retinal pigment epithelium cells | Biomedicine | MAP kinases | Oncology | Cancer Research | Ultra violet | AP-1 | Virology | Cell Biology | Apoptosis | OXIDATIVE STRESS | ACTIVATED PROTEIN-KINASE | PHOSPHORYLATION | JNK | BIOCHEMISTRY & MOLECULAR BIOLOGY | INVOLVEMENT | retinal pigment epithelium cells | apoptosis | FOS | kinases inhibitors | ultra violet | CELL BIOLOGY | GENE-EXPRESSION | INHIBITORS | C-JUN | Retina - radiation effects | Cell Line | MAP Kinase Signaling System - physiology | Mitogen-Activated Protein Kinase 8 - antagonists & inhibitors | Apoptosis - radiation effects | Mitogen-Activated Protein Kinase 9 - metabolism | Humans | Mitogen-Activated Protein Kinase 8 - metabolism | Mitogen-Activated Protein Kinase 9 - radiation effects | Pigment Epithelium of Eye - physiopathology | Proto-Oncogene Proteins c-fos - metabolism | p38 Mitogen-Activated Protein Kinases - radiation effects | Transcription Factor AP-1 - metabolism | MAP Kinase Kinase 4 - metabolism | Ultraviolet Rays | Retina - enzymology | Mitogen-Activated Protein Kinase 9 - antagonists & inhibitors | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mitogen-Activated Protein Kinase 8 - radiation effects | p38 Mitogen-Activated Protein Kinases - metabolism | Apoptosis - physiology | Pigment Epithelium of Eye - cytology | Mitogen-Activated Protein Kinase 1 - metabolism | Epithelium | Protein kinases
Journal Article
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
Biochemical journal, ISSN 1470-8728, 2007, Volume 408, Issue 3, pp. 297 - 315
The specificities of 65 compounds reported to be relatively specific inhibitors of protein kinases have been profiled against a panel of 70-80 protein kinases... 
Drug discovery | Kinase profiling | Protein kinase | Anti-cancer drugs | Inhibitor specificity | RHO-ASSOCIATED KINASE | TUMOR PROGRESSION | FAMILY-MEMBERS | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELL-PROLIFERATION | protein kinase | P38 MAP KINASE | CYCLIN-DEPENDENT KINASES | RECEPTOR TYROSINE KINASES | drug discovery | kinase profiling | SB 203580 | anti-cancer drugs | ISOFORMS IN-VITRO | P90 RSK | inhibitor specificity | Amino Acid Sequence | Cell Line | Phosphorylation | Recombinant Proteins - antagonists & inhibitors | Animals | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Humans | Drug Design | Protein Kinase Inhibitors - pharmacology | Enzyme Activation | Mitogen-Activated Protein Kinases - metabolism | Spodoptera | Yes1, Yamaguchi sarcoma viral oncogene homologue 1 | CSK, C-terminal Src kinase | Lck, lymphocyte cell-specific protein-tyrosine kinase | EGF, epidermal growth factor | FGF-R, fibroblast-growth-factor receptor | PAK, p21-activated protein kinase | PDK, 3-phosphoinositide-dependent protein kinase | PI3K, phosphatidylinositol (phosphoinositide) 3-kinase | NEK, NIMA (never in mitosis in Aspergillus nidulans)-related kinase | RSK, p90 ribosomal S6 kinase | HEK-293 cells, human embryonic kidney-293 cells | VEGF, vascular endothelial growth factor (vasoendothelial growth factor) | EF2K, elongation-factor-2 kinase | CK, casein kinase | PTEN, phosphatase and tensin homologue deleted on chromosome 10 | ERK, extracellular-signal-regulated kinase | ATM, ataxia telangiectasia mutated | SRPK, serine-arginine protein kinase | IL-1, interleukin 1 | MNK, MAPK-integrating protein kinase | ROCK, Rho-dependent protein kinase | CaMKK, CaMK kinase | GST, glutathione transferase | MKK1, MAPK kinase-1 (also called MEK1, MAPK or ERK kinase 1) | GAK, cyclin G-associated kinase | FMK, fluoromethylketone | MST, mammalian homologue Ste20-like kinase | PKA, cAMP-dependent protein kinase | FKBP, FK506-binding protein | PPAR, peroxisome-proliferator-activated receptor | IKK, inhibitory κB kinase | PH, pleckstrin homology | MBP, myelin basic protein | AICAR, aminoimidazole-4-carboxamide-1-β-D-ribofuranoside | MAPKAP-K, MAPK-activated protein kinase | Sf21, Spodoptera frugiperda (fall armyworm) 21 | MARK, microtubule-affinity-regulating kinase | PIM, provirus integration site for Moloney murine leukaemia virus | LPS, lipopolysaccharide | MSK, mitogen- and stress-activated protein kinase | MAPK, mitogen-activated protein kinase | MELK, maternal embryonic leucine-zipper kinase | His6, hexahistidine | CAK, cyclin-dependent kinase-activating kinase | Eph-A2, Ephrin A2 receptor | PLK, polo-like kinase | ATF2, activating transcription factor 2 | PKD, protein kinase D | Src, sarcoma kinase | AMPK, AMP-activated protein kinase | MMS, methyl methanesulfonate | CHK, checkpoint kinase | JNK, c-Jun N-terminal kinase | TORC1, mTOR (mammalian target of rapamycin)–raptor (regulatory associated protein of mTOR) complex | BRSK, brain-specific kinase | RIP2, receptor-interacting protein 2 | IGF-1, insulin-like growth factor-1 | S6K1, S6 kinase 1 | DYRK, dual-specificity tyrosine-phosphorylated and -regulated kinase | HIPK, homeodomain-interacting protein kinase | ZMP, aminoimidazole-4-carboxamide-1-β-D-ribofuranoside monophosphate | PRAK, p38-regulated activated kinase | PKC, protein kinase C | Src-I1, Src inhibitor 1 | TANK, TRAF (tumour-necrosis-factor-receptor-associated factor)-family-member-associated nuclear factor κB activator | NFAT, nuclear factor for activated T-cells | PHK, phosphorylase kinase | GSK3, glycogen synthase kinase 3 | PKB, protein kinase B (also called Akt) | CaMK, calmodulin-dependent kinase | CDK, cyclin-dependent protein kinase | NDRG, N-myc downstream-regulated gene | SmMLCK, smooth-muscle myosin light-chain kinase | TBK1, TANK-binding kinase 1 | PRK, protein kinase C-related kinase | SGK, serum- and glucocorticoid-induced kinase
Journal Article
Cancer research (Chicago, Ill.), ISSN 0008-5472, 10/2004, Volume 64, Issue 19, pp. 7099 - 7109
.... In addition, BAY 43-9006 demonstrated significant activity against several receptor tyrosine kinases involved in neovascularization and tumor progression, including vascular endothelial growth factor receptor (VEGFR... 
CELLS | ACTIVATION | GENE | ONCOLOGY | SIGNALING PATHWAY | PROTEIN-KINASE | MAP KINASE | B-RAF | INHIBITORS | CANCER | ENDOTHELIAL GROWTH-FACTOR | Niacinamide - analogs & derivatives | Humans | Phenylurea Compounds | Neovascularization, Pathologic - enzymology | Benzenesulfonates - pharmacology | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Receptors, Vascular Endothelial Growth Factor - antagonists & inhibitors | Female | MAP Kinase Kinase Kinases - antagonists & inhibitors | Administration, Oral | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Neoplasms - enzymology | Neoplasms - blood supply | MAP Kinase Kinase Kinases - metabolism | Receptor Protein-Tyrosine Kinases - metabolism | Disease Progression | Proto-Oncogene Proteins c-raf - metabolism | Neoplasms - drug therapy | Xenograft Model Antitumor Assays | Animals | MAP Kinase Signaling System - drug effects | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mice, Nude | Neovascularization, Pathologic - drug therapy | Cell Line, Tumor | Mice | Proto-Oncogene Proteins c-raf - antagonists & inhibitors | Pyridines - pharmacology | MAP Kinase Kinase Kinase 1 | Mitogen-Activated Protein Kinase 3 | Mitogen-Activated Protein Kinase 1 - metabolism | Mitogen-Activated Protein Kinases - metabolism
Journal Article
Cancer cell, ISSN 1535-6108, 2010, Volume 17, Issue 6, pp. 547 - 559
In mice, Lkb1 deletion and activation of Kras G12D results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these... 
CELLCYCLE | SIGNALING | INACTIVATION | SUPPRESSOR | SIGNATURES | ONCOLOGY | SRC | ADENOCARCINOMA | SENSITIVITY | MUTATIONS | LKB1/STK11 | EXPRESSION | TUMORIGENESIS | CELL BIOLOGY | Lung Neoplasms - drug therapy | Protein-Serine-Threonine Kinases - deficiency | Protein-Tyrosine Kinases - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Genomics | Humans | Lung Neoplasms - metabolism | Gene Expression Profiling | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Cell Movement - genetics | Phosphorylation - genetics | RNA Interference | Gene Expression Regulation, Neoplastic - genetics | MAP Kinase Kinase 1 - antagonists & inhibitors | Carcinoma, Non-Small-Cell Lung - metabolism | Signal Transduction - genetics | Enzyme Inhibitors - therapeutic use | Focal Adhesion Protein-Tyrosine Kinases - antagonists & inhibitors | Focal Adhesion Protein-Tyrosine Kinases - genetics | Focal Adhesions - genetics | Signal Transduction - drug effects | Mice, Nude | Cell Line, Tumor | Mice | TOR Serine-Threonine Kinases | src-Family Kinases - genetics | Protein-Tyrosine Kinases - antagonists & inhibitors | ras Proteins - genetics | Lung Neoplasms - pathology | Cell Transdifferentiation - genetics | Protein-Tyrosine Kinases - genetics | Neoplasm Metastasis - drug therapy | Mice, Mutant Strains | Protein-Serine-Threonine Kinases - antagonists & inhibitors | src-Family Kinases - metabolism | Female | Drug Therapy, Combination | Lung Neoplasms - genetics | Cell Adhesion - genetics | Carcinoma, Non-Small-Cell Lung - genetics | Focal Adhesion Protein-Tyrosine Kinases - metabolism | Intracellular Signaling Peptides and Proteins - antagonists & inhibitors | src-Family Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - genetics | Proto-Oncogene Proteins - genetics | Up-Regulation - genetics | Xenograft Model Antitumor Assays | Neoplasm Metastasis - genetics | Animals | MAP Kinase Kinase 2 - antagonists & inhibitors | Protein Kinase Inhibitors - therapeutic use | Focal Adhesions - metabolism | Proteomics | Protein Kinase Inhibitors - pharmacology | Oncology, Experimental | Analysis | Lung cancer | Development and progression | Metastasis | Research | Cancer
Journal Article
Leukemia, ISSN 1476-5551, 2011, Volume 25, Issue 7, pp. 1080 - 1094
The Ras/Raf/mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK... 
targeted therapy | Ras | therapeutic sensitivity | Raf | resistance | ERK | ABROGATE CYTOKINE DEPENDENCY | INITIATION-FACTOR 4E | ACUTE MYELOID-LEUKEMIA | KINASE INHIBITOR PROTEIN | DRUG-INDUCED APOPTOSIS | BONE-MARROW MICROENVIRONMENT | ONCOLOGY | ACUTE LYMPHOBLASTIC-LEUKEMIA | CHRONIC LYMPHOCYTIC-LEUKEMIA | MURINE HEMATOPOIETIC-CELLS | HEMATOLOGY | SIGNAL-REGULATED KINASE | ras Proteins - genetics | MAP Kinase Signaling System - physiology | Mitogen-Activated Protein Kinase Kinases - genetics | Apoptosis - drug effects | raf Kinases - antagonists & inhibitors | Humans | Neoplasm Proteins - physiology | Mitogen-Activated Protein Kinase Kinases - physiology | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Neoplasm Proteins - antagonists & inhibitors | Antineoplastic Agents - therapeutic use | Molecular Targeted Therapy | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Extracellular Signal-Regulated MAP Kinases - genetics | Gene Expression Regulation, Leukemic - genetics | raf Kinases - physiology | MAP Kinase Signaling System - genetics | Drug Design | Antineoplastic Agents - pharmacology | Extracellular Signal-Regulated MAP Kinases - physiology | Neoplasm Proteins - genetics | raf Kinases - genetics | ras Proteins - physiology | Cell Division - genetics | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | ras Proteins - antagonists & inhibitors | Gene Expression Regulation, Leukemic - drug effects | Leukemia - drug therapy | Cell Division - drug effects | Phosphatidylinositol 3-Kinases - genetics | Drug Resistance, Neoplasm - genetics | MAP Kinase Signaling System - drug effects | Models, Biological | Phosphatidylinositol 3-Kinases - physiology | Apoptosis - physiology | Drug Resistance, Neoplasm - physiology | Drug Resistance, Neoplasm - drug effects | Chemotherapy | Extracellular signal-regulated kinases | Leukemia | Physiological aspects | Genetic aspects | Research | Drug therapy | Health aspects | Mitogen-activated protein kinases | Cancer
Journal Article