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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
Oncogene, ISSN 1476-5594, 2007, Volume 26, Issue 22, pp. 3227 - 3239
The Ras-dependent extracellular signal-regulated kinase (ERK) 1/2 mitogen-activated protein (MAP... 
Signal transduction | MAP kinase | ERK1/2 | Cell cycle | G1 phase | SIGNAL-TRANSDUCTION PATHWAYS | signal transduction | cell cycle | EARLY GENE-PRODUCTS | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELL-CYCLE ARREST | INITIATION-FACTOR 4E | DNA-SYNTHESIS | CELL BIOLOGY | NIH 3T3 CELLS | DEPENDENT KINASE | ONCOLOGY | GENETICS & HEREDITY | SMOOTH-MUSCLE-CELLS | MESSENGER-RNA TRANSPORT | MAP Kinase Signaling System - physiology | Cell Proliferation | Mitogen-Activated Protein Kinase 1 - physiology | Mitogen-Activated Protein Kinase 3 - genetics | Humans | Mitogen-Activated Protein Kinase 1 - deficiency | G1 Phase - physiology | S Phase - genetics | Mitogen-Activated Protein Kinase 3 - physiology | Animals | MAP Kinase Signaling System - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Mitogen-Activated Protein Kinase 1 - genetics | S Phase - physiology | Mitogen-Activated Protein Kinase 3 - deficiency | G1 Phase - genetics | Enzyme Activation - genetics | Enzyme Activation - physiology | Mitogen-Activated Protein Kinase 1 - metabolism | Control | Physiological aspects | Cellular signal transduction | Genetic aspects | Research | Protein kinases | Genetics | Kinases | Mammals | Cancer | Life Sciences | G1 Phase | S Phase | Biochemistry, Molecular Biology | Enzyme Activation | Mitogen-Activated Protein Kinase 1 | Mitogen-Activated Protein Kinase 3 | MAP Kinase Signaling System
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
Molecular and Cellular Biology, ISSN 0270-7306, 10/2001, Volume 21, Issue 19, pp. 6706 - 6717
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley... 
SIGNAL-TRANSDUCTION | ACTIVATED PROTEIN-KINASE | ONCOGENIC RAS | INDUCED APOPTOSIS | PHOSPHATIDYLINOSITOL 3-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | B-RAF | GROWTH-FACTOR | CELL-CYCLE PROGRESSION | INDEPENDENT PATHWAYS | SERINE/THREONINE KINASE | CELL BIOLOGY | MAP Kinase Kinase 1 | MAP Kinase Signaling System | Mitogen-Activated Protein Kinase Kinases - metabolism | Cell Nucleus - metabolism | Extracellular Matrix - physiology | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | rho GTP-Binding Proteins - genetics | Cells, Cultured | Tumor Suppressor Protein p53 - metabolism | Proto-Oncogene Proteins - genetics | cdc42 GTP-Binding Protein - physiology | rho GTP-Binding Proteins - physiology | Proto-Oncogene Proteins c-raf - metabolism | Proto-Oncogene Proteins c-akt | Animals | rac1 GTP-Binding Protein - physiology | cdc42 GTP-Binding Protein - genetics | Proto-Oncogene Proteins - physiology | Anoikis | Fibroblasts - cytology | Mice | Mutation | Mitogen-Activated Protein Kinase 3 | Apoptosis | Mitogen-Activated Protein Kinase 1 - metabolism | Mitogen-Activated Protein Kinases - metabolism | rac1 GTP-Binding Protein - genetics | Protein-Serine-Threonine Kinases | Biodiversity | Cellular Biology | Embryology and Organogenesis | Life Sciences | Mitogen-Activated Protein Kinase Kinases | Fibroblasts | Proto-Oncogene Proteins | Subcellular Processes | Mitogen-Activated Protein Kinases | Proto-Oncogene Proteins c-raf | Extracellular Matrix | Biochemistry, Molecular Biology | Systematics, Phylogenetics and taxonomy | Tumor Suppressor Protein p53 | cdc42 GTP-Binding Protein | Development Biology | rac1 GTP-Binding Protein | Mitogen-Activated Protein Kinase 1 | Molecular biology | rho GTP-Binding Proteins | Cell Nucleus | Cancer | Cell Growth and Development
Journal Article
PloS one, ISSN 1932-6203, 05/2012, Volume 7, Issue 5, p. e36964
Articular cartilage is physiologically exposed to repeated loads. The mechanical properties of cartilage are due to its extracellular matrix, and homeostasis... 
ADHESION | SHEAR | TGF-BETA | PROTEIN | BOVINE ARTICULAR CHONDROCYTES | MULTIDISCIPLINARY SCIENCES | ENDOTHELIAL-CELLS | KINASE | MECHANICAL STIMULATION | FLOW | PRIMARY CILIA | Chondrocytes - cytology | Phosphorylation | Transcription Factor AP-1 - genetics | Stress, Mechanical | Transcription Factor AP-1 - metabolism | Cartilage, Articular - physiology | MAP Kinase Signaling System - genetics | Chondrocytes - physiology | Cartilage, Articular - metabolism | Early Growth Response Protein 1 - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Mechanotransduction, Cellular - genetics | Chondrocytes - metabolism | Extracellular Matrix Proteins - metabolism | Hydrogel, Polyethylene Glycol Dimethacrylate - metabolism | Signal Transduction | Cartilage, Articular - cytology | Down-Regulation | Extracellular Matrix Proteins - genetics | p38 Mitogen-Activated Protein Kinases - genetics | Smad Proteins - genetics | Sepharose - metabolism | Animals | Transforming Growth Factor beta - genetics | Mitogen-Activated Protein Kinases - genetics | Mice | Smad Proteins - metabolism | Transforming Growth Factor beta - metabolism | Early Growth Response Protein 1 - metabolism | Mitogen-Activated Protein Kinases - metabolism | DNA microarrays | Analysis | Genes | Physiological aspects | Mechanical properties | Bone morphogenetic proteins | Transforming growth factors | Gene expression | Mitogens | Protein kinases | Compression | Transcription factors | Hydrogels | Genomics | Transforming growth factor-a | Homeostasis | Genomes | Shear stresses | Kinases | Western blotting | Proteins | Cartilage | Signal transduction | Pathways | Smad2 protein | Atherosclerosis | Extracellular matrix | Data analysis | Extracellular signal-regulated kinase | MAP kinase | Cartilage (articular) | Metabolism | Signaling | Embedded systems | Protein kinase | Collagen | Chondrocytes | Mitogen-Activated Protein Kinases | Sepharose | Biochemistry, Molecular Biology | Cartilage, Articular/physiology | Cartilage, Articular/cytology | Transcription Factor AP-1 | MAP Kinase Signaling System | Life Sciences | Mechanotransduction, Cellular | Hydrogel, Polyethylene Glycol Dimethacrylate | Extracellular Matrix Proteins | Smad Proteins | Early Growth Response Protein 1 | p38 Mitogen-Activated Protein Kinases | Transforming Growth Factor beta | Cartilage, Articular/metabolism
Journal Article
Oncogene, ISSN 1476-5594, 2007, Volume 26, Issue 22, pp. 3291 - 3310
Journal Article