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Journal Article
Biochemical journal, ISSN 1470-8728, 2009, Volume 420, Issue 3, pp. 345 - 361
RTKs (receptor tyrosine kinases) play important roles in cellular proliferation and differentiation... 
Extracellular-signal-regulated kinase (ERK) | Pleiotrophin | Anaplastic large cell lymphoma (ALCL) | Neuroblastoma | Non-small cell lung cancer (NSLCL) | Midkine | Anaplastic lymphoma kinase (ALK) | Inflammatory myofibroblastic tumour (IMT) | ALK PROTEIN EXPRESSION | inflammatory myofibroblastic tumour (IMT) | NPM-ALK | HEPARIN-BINDING | GROWTH-FACTOR PLEIOTROPHIN | non-small cell lung cancer (NSLCL) | BIOCHEMISTRY & MOLECULAR BIOLOGY | anaplastic lymphoma kinase (ALK) | EML4-ALK FUSION GENE | neuroblastoma | LARGE-CELL LYMPHOMA | extracellular-signal-regulated kinase (ERK) | pleiotrophin | NEUROTROPHIC FACTOR HBNF | INFLAMMATORY MYOFIBROBLASTIC TUMOR | NON-HODGKINS-LYMPHOMA | midkine | anaplastic large cell lymphoma (ALCL) | RECEPTOR TYROSINE KINASE | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Oncogene Proteins, Fusion - metabolism | Signal Transduction | Carcinoma, Non-Small-Cell Lung - genetics | Protein-Tyrosine Kinases - metabolism | Humans | Lung Neoplasms - metabolism | Neuroblastoma - genetics | Carcinoma, Non-Small-Cell Lung - metabolism | Lung Neoplasms - pathology | Nuclear Proteins - metabolism | Receptor Protein-Tyrosine Kinases | Protein-Tyrosine Kinases - genetics | Models, Biological | Oncogene Proteins, Fusion - genetics | Lymphoma, Large-Cell, Anaplastic - pathology | Neuroblastoma - metabolism | Nuclear Proteins - genetics | Lymphoma, Large-Cell, Anaplastic - metabolism | Neuroblastoma - pathology | Lymphoma, Large-Cell, Anaplastic - genetics | ALK, anaplastic lymphoma kinase | LTK, leucocyte tyrosine kinase | MUC-1, mucin-1 | IRS-1, IR substrate-1 | PTN, pleiotrophin | TGFβ, transforming growth factor β | ERK, extracellular-signal-regulated kinase | PKB, protein kinase B | Shc, Src homology and collagen homology | TPM, tropomyosin | IMP cyclohydrolase | MK, midkine | MYH9, non-muscle myosin heavy chain | MAM, meprin, A5 protein and receptor protein tyrosine phosphatase mu | NPM, nucleophosmin | mTOR, mammalian target of rapamycin | NIPA, nuclear interacting partner of ALK | RPTP, receptor protein tyrosine phosphatase | DLBCL, diffuse large B-cell lymphoma | FOXO3a, forkhead box O 3a | NF-κB, nuclear factor κB | Shp1, SH2 domain-containing phosphatase 1 | RANBP2, Ran-binding protein 2 | ALCL, anaplastic large cell lymphoma | Dpp, decapentaplegic | FRS2, fibroblast growth factor receptor substrate 2 | LDLa, low-density lipoprotein class A | EGFR, epidermal growth factor receptor | SEC31L1, SEC31 homologue A | GIST, gastrointestinal stromal tumour | RTK, receptor tyrosine kinase | SH2, Src homology 2 | TFG, TRK-fused gene | ATIC, 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase | CLTC, clathrin heavy chain | MAPK, mitogen-activated protein kinase | Hen-1, hesitation-1 | MEK, MAPK | PI3K, phosphoinositide 3-kinase | HEK, human embryonic kidney | SCD-2, suppressor of constitutive dauer 2 | Review | EBPβ, CCAAT | CARS, cysteinyl-tRNA synthetase | JNK, c-Jun N-terminal kinase | ERK kinase | Grb2, growthfactor-receptor-bound protein 2 | SCC, squamous cell carcinoma | EML4, echinoderm microtubule-associated protein like 4 | SHH, sonic hedghog | BCR-Abl, breakpoint cluster region-Abl | IR, insulin receptor | ALO17, ALK lymphoma oligomerization partner on chromosome 17 | enhancer-binding protein β | PLCγ, phospholipase Cγ | NSCLC, non-small cell lung cancer | UCN-01, unco-ordinated 1 | Cdc42, cell division cycle 42 | STAT, signal transducer and activator of transcription | DRG, dorsal root ganglia | MSN, moesin | dALK, Drosophila ALK | IL-3, interleukin-3 | CNS, central nervous system | JAK, Janus kinase | CML, chronic myeloid leukaemia | Jeb, jelly belly | IMT, inflammatory myofibroblastic tumour
Journal Article
Blood, ISSN 0006-4971, 10/2012, Volume 120, Issue 17, pp. 3510 - 3518
CRLF2 rearrangements, JAK1/2 point mutations, and JAK2 fusion genes have been identified in Philadelphia chromosome (Ph)-like acute lymphoblastic leukemia... 
MAMMALIAN TARGET | RAPAMYCIN | IN-VITRO | ABERRANT STAT5 | RECEPTOR | OF-FUNCTION MUTATIONS | HEMATOLOGY | B-PROGENITOR | GENETIC ALTERATIONS | STAT5 ACTIVATION | CRLF2 | Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - metabolism | TOR Serine-Threonine Kinases - metabolism | Humans | Immunoglobulins - genetics | Molecular Targeted Therapy | Immunoglobulins - metabolism | TOR Serine-Threonine Kinases - antagonists & inhibitors | Janus Kinase 1 - metabolism | STAT5 Transcription Factor - genetics | STAT5 Transcription Factor - metabolism | Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - drug therapy | TOR Serine-Threonine Kinases - genetics | Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - mortality | Janus Kinase 1 - genetics | Janus Kinase 2 - metabolism | Antineoplastic Agents - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Receptors, Cytokine - metabolism | Drug Evaluation, Preclinical | Child | Philadelphia Chromosome | Receptors, Cytokine - genetics | Janus Kinase 2 - antagonists & inhibitors | Disease Models, Animal | Pyrazoles - pharmacology | Acute Disease | Janus Kinase 2 - genetics | Survival Rate | Signal Transduction - genetics | Janus Kinase 1 - antagonists & inhibitors | Sirolimus - pharmacology | Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - genetics | Xenograft Model Antitumor Assays | Animals | Signal Transduction - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Lymphoid Neoplasia
Journal Article
Journal Article
Arteriosclerosis, thrombosis, and vascular biology, ISSN 1079-5642, 05/2005, Volume 25, Issue 5, pp. 950 - 956
OBJECTIVE—Reactive oxygen species (ROS) integrate cellular signaling pathways involved in aortic smooth muscle cell (SMC) proliferation and migration... 
SMC | SOD | Thrombin | Cell signaling | ROS | OXIDATIVE STRESS | thrombin | NITRIC-OXIDE SYNTHASE | KINASE | TRANSDUCER | HEAT-SHOCK | P47(PHOX) | cell signaling | GROWTH | PERIPHERAL VASCULAR DISEASE | DYSFUNCTION | HEMATOLOGY | OXIDANTS | MAP Kinase Signaling System - physiology | Superoxide Dismutase - genetics | Reactive Oxygen Species - metabolism | Protein-Tyrosine Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Extracellular Signal-Regulated MAP Kinases - metabolism | Janus Kinase 2 | Mice, Mutant Strains | p38 Mitogen-Activated Protein Kinases - metabolism | Aorta - enzymology | STAT3 Transcription Factor - metabolism | Superoxide Dismutase - metabolism | Proto-Oncogene Proteins - metabolism | Proto-Oncogene Proteins - antagonists & inhibitors | Atherosclerosis - pathology | Mice, Inbred C57BL | Cells, Cultured | Enzyme Inhibitors - pharmacology | Atherosclerosis - metabolism | Cell Division - drug effects | Aorta - pathology | Cell Compartmentation - physiology | Cell Division - physiology | Gene Expression Regulation, Enzymologic | Muscle, Smooth, Vascular - pathology | Animals | MAP Kinase Signaling System - drug effects | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mice | Superoxide Dismutase-1 | Muscle, Smooth, Vascular - enzymology | Hypertrophy | Protein-Tyrosine Kinases - antagonists & inhibitors
Journal Article
PloS one, ISSN 1932-6203, 2012, Volume 7, Issue 8, p. e42507
Remodelling of the extracellular matrix (ECM) and cell surface by matrix metalloproteinases (MMPs) is an important function of monocytes and macrophages.... 
CELLS | MONOCYTE | INTERFERON-GAMMA | INFLAMMATION | MODULATORS | MULTIDISCIPLINARY SCIENCES | GENES | INHIBITOR | ARTHRITIS | EXPRESSION | MOLECULES | Gene Expression Regulation, Enzymologic - drug effects | Matrix Metalloproteinases - genetics | Monocytes - cytology | Humans | NF-kappa B - metabolism | Phosphatidylinositol 3-Kinases - metabolism | RNA, Messenger - metabolism | Receptors, IgG - metabolism | Tissue Inhibitor of Metalloproteinases - genetics | Atherosclerosis - enzymology | STAT1 Transcription Factor - metabolism | Janus Kinase 2 - metabolism | Chromones - pharmacology | Janus Kinase 2 - antagonists & inhibitors | Atherosclerosis - pathology | RNA, Messenger - genetics | Morpholines - pharmacology | Thiophenes - pharmacology | Macrophages - cytology | Cell Adhesion - drug effects | Enzyme Activation - drug effects | Reverse Transcriptase Polymerase Chain Reaction | Tissue Inhibitor of Metalloproteinases - metabolism | Interleukin-1 - pharmacology | Macrophages - enzymology | Monocytes - drug effects | Up-Regulation - drug effects | Tumor Necrosis Factor-alpha - pharmacology | Phenotype | Lipopolysaccharides - pharmacology | Macrophages - drug effects | Mitogen-Activated Protein Kinases - genetics | Matrix Metalloproteinases - metabolism | Macrophage Activation - drug effects | Interferon-gamma - pharmacology | Mitogen-Activated Protein Kinases - metabolism | Heart | Matrix metalloproteinases | Activation | Arthritis | Tissue inhibitor of metalloproteinase 3 | mRNA | Matrix metalloproteinase | Kinases | Macrophages | Cell surface | Proteins | Ethics | Signal transduction | Cell activation | Rodents | Atherosclerosis | Interleukin 1 | Janus kinase | Extracellular matrix | Plaques | Interstitial collagenase | Enzymes | Cytokines | Blood & organ donations | Research & development--R&D | Inflammation | Collagenase | Tumor necrosis factor-α | Gene expression | Steady state | Gelatinase A | Signaling | Monocytes | CD16 antigen | Arteriosclerosis | Collagen | Research & development | R&D
Journal Article
The Journal of pharmacology and experimental therapeutics, ISSN 0022-3565, 06/2003, Volume 305, Issue 3, pp. 1222 - 1232
Journal Article
Annual review of biochemistry, ISSN 0066-4154, 2006, Volume 75, Issue 1, pp. 93 - 109
.... In spite of the conservation among protein tyrosine kinases (PTKs), one can develop small molecules that block the activity of a narrow spectrum of PTKs and that exhibitmuch less toxicity than the currently used chemotherapeutic agents... 
Signal transduction | Tyrphostin | Tyrosine phosphorylation | Cancer therapy | IRREVERSIBLE INHIBITORS | SIGNAL-TRANSDUCTION THERAPY | GROWTH-FACTOR-RECEPTOR | signal transduction | ANTIPROLIFERATIVE AGENTS | BIOCHEMISTRY & MOLECULAR BIOLOGY | BCR-ABL | CHRONIC MYELOID-LEUKEMIA | CELL LUNG-CANCER | cancer therapy | SELECTIVE INHIBITOR | IN-VITRO | tyrphostin | tyrosine phosphorylation | TUMOR-GROWTH | Erlotinib Hydrochloride | Protein-Tyrosine Kinases - metabolism | Humans | Graft Occlusion, Vascular - prevention & control | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Piperazines - metabolism | Antineoplastic Agents - therapeutic use | Piperazines - chemistry | Pyrimidines - chemistry | Pyrimidines - metabolism | Antineoplastic Agents - metabolism | Janus Kinase 3 - antagonists & inhibitors | Protein Kinase Inhibitors - chemistry | Fusion Proteins, bcr-abl | Quinazolines - metabolism | Adenosine Triphosphate - metabolism | Janus Kinase 2 - metabolism | Receptors, Vascular Endothelial Growth Factor - antagonists & inhibitors | Molecular Structure | Janus Kinase 3 - metabolism | Tyrphostins - chemistry | Quinazolines - chemistry | Janus Kinase 2 - antagonists & inhibitors | Receptors, Platelet-Derived Growth Factor - antagonists & inhibitors | Piperazines - therapeutic use | Antineoplastic Agents - chemistry | Imatinib Mesylate | Tyrphostins - therapeutic use | Protein Kinase Inhibitors - therapeutic use | Pyrimidines - therapeutic use | Quinazolines - therapeutic use | Receptors, Platelet-Derived Growth Factor - metabolism | Tyrphostins - metabolism | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Signal Transduction - physiology | Benzamides | Adenosine Triphosphate - chemistry | Protein Kinase Inhibitors - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2012, Volume 109, Issue 11, pp. 4257 - 4262
Noonan syndrome (NS), a genetic disease caused in half of cases by activating mutations of the tyrosine phosphatase SHP2 (PTPN11), is characterized by... 
Phosphorylation | Phenotypes | Animal models | Phosphatases | Noonan syndrome | Growth hormones | Mice | Genetic mutation | Growth retardation | Binding sites | SIGNALING PATHWAYS | DEFECTS | signaling | ACTIVATED PROTEIN-KINASE | MULTIDISCIPLINARY SCIENCES | TYROSINE-PHOSPHATASE SHP2 | HEIGHT | DELETION | PTPN11 SHP2 | growth hormone insensitivity | MALFORMATIONS | MOUSE MODEL | MUTATIONS | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism | Noonan Syndrome - enzymology | ras Proteins - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Phosphoproteins - metabolism | Noonan Syndrome - blood | Insulin-Like Growth Factor I - secretion | Mitogen-Activated Protein Kinase Kinases - metabolism | STAT5 Transcription Factor - metabolism | Janus Kinase 2 - metabolism | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Binding Sites | Animals, Newborn | Insulin-Like Growth Factor I - biosynthesis | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Rats | Growth Hormone - pharmacology | Enzyme Activation - drug effects | Mutation - genetics | Noonan Syndrome - genetics | Biometry | Animals | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics | Gene mutations | Physiological aspects | Development and progression | Genetic aspects | Research | Growth factors | Health aspects | Phosphotransferases | Life Sciences | Biological Sciences
Journal Article
Drug metabolism and disposition, ISSN 1521-009X, 2014, Volume 42, Issue 4, pp. 759 - 773
Journal Article