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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
Journal Article
Nature communications, ISSN 2041-1723, 2019, Volume 10, Issue 1, pp. 1897 - 17
.... We found that early after mitogenic stimulation, RUNX3 binds to its target loci, where it opens chromatin structure by sequential recruitment of Trithorax group proteins and cellcycle regulators... 
UBIQUITINATION | AML1-ETO | ACETYLATION | MULTIDISCIPLINARY SCIENCES | TRANSCRIPTION | PROTEINS | QUANTITATIVE-ANALYSIS | POLYCOMB | CANCER | KINASES | FAMILY | Chromatin - metabolism | RNA, Small Interfering - genetics | Myeloid-Lymphoid Leukemia Protein - metabolism | TOR Serine-Threonine Kinases - metabolism | Core Binding Factor Alpha 3 Subunit - antagonists & inhibitors | Humans | Polycomb-Group Proteins - metabolism | TOR Serine-Threonine Kinases - genetics | Cell Cycle Checkpoints - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Cyclin-Dependent Kinase 4 - antagonists & inhibitors | Chromatin - chemistry | MAP Kinase Kinase 1 - antagonists & inhibitors | Butadienes - pharmacology | Signal Transduction | Epithelial Cells - pathology | MAP Kinase Kinase 1 - metabolism | Imidazoles - pharmacology | Cyclin-Dependent Kinase 4 - metabolism | Piperazines - pharmacology | Cell Cycle Checkpoints - drug effects | Polycomb-Group Proteins - genetics | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cell Line, Tumor | MAP Kinase Kinase 4 - genetics | RNA, Small Interfering - metabolism | ras Proteins - genetics | Core Binding Factor Alpha 3 Subunit - metabolism | Epithelial Cells - metabolism | Nitriles - pharmacology | Cyclin-Dependent Kinase 4 - genetics | Epithelial Cells - drug effects | ras Proteins - metabolism | Drosophila melanogaster - genetics | Chromatin Assembly and Disassembly - drug effects | Drosophila melanogaster - metabolism | MAP Kinase Kinase 1 - genetics | TOR Serine-Threonine Kinases - antagonists & inhibitors | MAP Kinase Kinase 4 - metabolism | HEK293 Cells | MAP Kinase Kinase 4 - antagonists & inhibitors | Chromatin - drug effects | Histone-Lysine N-Methyltransferase - genetics | Drosophila melanogaster - cytology | Gene Expression Regulation | p38 Mitogen-Activated Protein Kinases - genetics | Sirolimus - pharmacology | Animals | Histone-Lysine N-Methyltransferase - metabolism | Myeloid-Lymphoid Leukemia Protein - genetics | Core Binding Factor Alpha 3 Subunit - genetics | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Pyridines - pharmacology | Polycomb group proteins | Regulators | Molecular modelling | S phase | Genes | Cell cycle | Loci | Runx3 protein | Recruitment | Tumors | Chromatin remodeling
Journal Article
Nature chemical biology, ISSN 1552-4469, 2014, Volume 10, Issue 10, pp. 853 - 860
Activation of the ERK pathway is a hallmark of cancer, and targeting of upstream signaling partners led to the development of approved drugs. Recently,... 
ACTIVATION | MEK INHIBITION | DETERMINANTS | RAF | BIOCHEMISTRY & MOLECULAR BIOLOGY | DNA-DAMAGE | ACQUIRED-RESISTANCE | MAP KINASE ERK2 | BRAF | CONFORMATION | DEFICIENCY | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Gene Expression Regulation, Neoplastic | Intracellular Signaling Peptides and Proteins - metabolism | Piperazines - chemistry | Mitogen-Activated Protein Kinase 1 - chemistry | Enzyme Inhibitors - chemistry | Mitogen-Activated Protein Kinase 1 - genetics | Mitogen-Activated Protein Kinase 8 - genetics | Antineoplastic Agents - pharmacology | Mitogen-Activated Protein Kinase 3 - chemistry | Binding Sites | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Protein Structure, Tertiary | Recombinant Proteins - metabolism | Gene Expression | Indazoles - chemistry | Mitogen-Activated Protein Kinase 3 - genetics | Protein Structure, Secondary | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 8 - chemistry | Mitogen-Activated Protein Kinase 8 - metabolism | Enzyme Inhibitors - pharmacology | Protein-Serine-Threonine Kinases - genetics | Recombinant Proteins - chemistry | Recombinant Proteins - genetics | Antineoplastic Agents - chemistry | Piperazines - pharmacology | Indazoles - pharmacology | MAP Kinase Signaling System - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Intracellular Signaling Peptides and Proteins - chemistry | Cell Line, Tumor | Protein Binding | Protein-Serine-Threonine Kinases - chemistry | Kinetics | Mitogen-Activated Protein Kinase 1 - metabolism | Signal transduction | Binding sites | Pharmaceutical sciences | Cancer
Journal Article
PloS one, ISSN 1932-6203, 12/2016, Volume 11, Issue 12, p. e0167071
...) in podocytes, cDNAs and cell lysate of cultured human podocytes were used for the expression of nAChR mRNAs and proteins, respectively... 
ACETYLCHOLINE-RECEPTORS | CIGARETTE-SMOKING | NMDA RECEPTORS | RISK-FACTOR | MULTIDISCIPLINARY SCIENCES | RENAL-FUNCTION | INJURY | DIABETIC-NEPHROPATHY | CHRONIC KIDNEY-DISEASE | CARDIOVASCULAR MORBIDITY | ROS PRODUCTION | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Apoptosis - genetics | Male | Nicotinic Antagonists - pharmacology | Spin Labels | Reactive Oxygen Species - agonists | Nicotine - pharmacology | MAP Kinase Kinase 4 - metabolism | Cyclic N-Oxides - pharmacology | Mitogen-Activated Protein Kinase 1 - genetics | Female | MAP Kinase Kinase 4 - antagonists & inhibitors | Membrane Proteins - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Receptors, Nicotinic - metabolism | Podocytes - metabolism | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | Membrane Proteins - genetics | Tissue Culture Techniques | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Gene Expression Regulation | p38 Mitogen-Activated Protein Kinases - genetics | Nicotine - antagonists & inhibitors | Podocytes - cytology | Reactive Oxygen Species - antagonists & inhibitors | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Podocytes - drug effects | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Acetylcysteine - pharmacology | MAP Kinase Kinase 4 - genetics | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Oxidative Stress - drug effects | Receptors, Nicotinic - genetics | Cell Line, Transformed | Mitogen-Activated Protein Kinase 1 - metabolism | Oxidative stress | Physiological aspects | Research | Health aspects | Health/Alcohol and other Drugs/Information/Nicotine and Tobacco | Nicotine | Smoking | Apoptosis | Cell proliferation | Reactive oxygen species | Phosphorylation | Laboratories | Syngeneic grafts | Downstream effects | Tempol | Acetylcysteine | Superoxide dismutase | mRNA | Medical schools | Antioxidants | Proteins | Receptors | Rodents | Mesangial cells | Localization | Medical research | Oxygen | Extracellular signal-regulated kinase | JNK protein | Permeability | Gene expression | Cigarette smoking | Signaling | Molecular modelling | Inhibitors | Acetylcholine receptors (nicotinic) | In vivo methods and tests | Kidney diseases | Diabetes | Kidney transplantation
Journal Article
American journal of physiology. Heart and circulatory physiology, ISSN 1522-1539, 2005, Volume 288, Issue 2, pp. H971 - H976
Pharmacological activation of the prosurvival kinases Akt and ERK-1/2 at reperfusion, after a period of lethal ischemia, protects the heart against ischemia-reperfusion injury... 
Myocardial infarction | Phosphatidylinositol 3-kinase-Akt | Reperfusion injury | Mitogen-activated protein kinases | MITOCHONDRIAL PERMEABILITY TRANSITION | OXIDATIVE STRESS | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | phosphatidylinositol 3-kinase-Akt | mitogen-activated protein kinases | myocardial infarction | PORE | INJURY | PERIPHERAL VASCULAR DISEASE | reperfusion injury | Phosphorylation | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Male | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Myocardial Reperfusion Injury - pathology | Myocardial Infarction - pathology | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Survival - physiology | Protein-Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins - metabolism | MAP Kinase Kinase 1 - antagonists & inhibitors | Proto-Oncogene Proteins - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Enzyme Inhibitors - pharmacology | Rats | MAP Kinase Kinase 1 - metabolism | Myocardium - pathology | MAP Kinase Kinase 2 - metabolism | Myocardial Infarction - metabolism | Rats, Sprague-Dawley | Proto-Oncogene Proteins c-akt | Myocardial Reperfusion Injury - metabolism | Myocardium - enzymology | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Ischemic Preconditioning, Myocardial | MAP Kinase Kinase 2 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - metabolism
Journal Article
Journal of cell science, ISSN 0021-9533, 2013, Volume 126, Issue 17, pp. 3990 - 3999
.... Here, we use MCF10A cells, which fail to form tight junctions and express very little endogenous Crumbs3, to show that inducing expression of the polarity protein Scribble is sufficient to promote... 
Scribble | Polarity | Tight junctions | Mammary epithelium | EMT | ERK | CELL-CELL JUNCTIONS | PROTEIN-KINASE-C | BARRIER FUNCTION | E-CADHERIN | MAMMALIAN EPITHELIAL-CELLS | BETA-CATENIN | MESENCHYMAL TRANSITION | TIGHT JUNCTION | CELL BIOLOGY | MALIGNANT PROGRESSION | TUMOR-SUPPRESSOR SCRIBBLE | MAP Kinase Signaling System - physiology | Phosphorylation | Epithelial-Mesenchymal Transition - physiology | Homeodomain Proteins - metabolism | Humans | Membrane Glycoproteins - biosynthesis | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Transcriptional Activation | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | RNA Interference | Mitogen-Activated Protein Kinase 1 - genetics | HEK293 Cells | Transcription, Genetic | Flavonoids - pharmacology | Membrane Proteins - metabolism | Chromones - pharmacology | Tight Junctions - metabolism | MAP Kinase Kinase 1 - antagonists & inhibitors | Tumor Suppressor Proteins - metabolism | Homeodomain Proteins - biosynthesis | JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - genetics | Down-Regulation | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Morpholines - pharmacology | Transcription Factors - antagonists & inhibitors | Transcription Factors - biosynthesis | Anthracenes - pharmacology | Transcription Factors - metabolism | Membrane Proteins - biosynthesis | MAP Kinase Signaling System - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Homeodomain Proteins - antagonists & inhibitors | Protein Kinase Inhibitors - pharmacology | RNA, Small Interfering | Tumor Suppressor Proteins - biosynthesis | Mitogen-Activated Protein Kinase 1 - metabolism | Zinc Finger E-box-Binding Homeobox 1
Journal Article
Journal of Allergy and Clinical Immunology, The, ISSN 0091-6749, 2008, Volume 121, Issue 4, pp. 893 - 902.e2
.... Objectives We sought to study the activation of the mitogen-activated protein kinase (MAPK) signaling pathway in airway cells... 
Allergy and Immunology | mitogen-activated protein kinase | chemokines | epithelial function | bronchial biopsy | Asthma | LUNG | BRONCHIAL EPITHELIAL-CELLS | MAP KINASE | asthma | PROLIFERATION | IMMUNOLOGY | ALLERGY | GM-CSF | PATHWAY | INFLAMMATION | SMOOTH-MUSCLE-CELLS | DIFFERENTIATION | EXPRESSION | Phosphorylation | Bronchi - enzymology | Humans | Middle Aged | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | JNK Mitogen-Activated Protein Kinases - metabolism | Male | Enzyme Induction - immunology | MAP Kinase Signaling System - immunology | Enzyme Activation - immunology | Respiratory Mucosa - pathology | Chemokines - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - biosynthesis | Adult | Female | p38 Mitogen-Activated Protein Kinases - metabolism | Bronchi - pathology | Respiratory Mucosa - secretion | Chemokines - biosynthesis | Chemokines - secretion | Mitogen-Activated Protein Kinase 1 - physiology | p38 Mitogen-Activated Protein Kinases - physiology | Asthma - enzymology | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Respiratory Mucosa - enzymology | Mitogen-Activated Protein Kinase 3 - physiology | Mitogen-Activated Protein Kinase 1 - biosynthesis | Mitogen-Activated Protein Kinase 3 - metabolism | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mitogen-Activated Protein Kinases - physiology | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Asthma - pathology | Mitogen-Activated Protein Kinase 1 - metabolism | Mitogen-Activated Protein Kinases - metabolism | Protein kinases | Proteins | Studies | Signal transduction | Cell culture | Rodents | Cloning | Smooth muscle | Kinases
Journal Article
PloS one, ISSN 1932-6203, 04/2015, Volume 10, Issue 4, p. e0124007
Cell invasion is a crucial mechanism of cancer metastasis and malignancy. Matrix metallo-proteinase-9 (MMP-9) is an important proteolytic enzyme involved in... 
MATRIX METALLOPROTEINASES | ANGIOGENESIS | NUCLEAR-FACTOR | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | INDUCED MATRIX-METALLOPROTEINASE-9 EXPRESSION | CYCLOOXYGENASE-2 EXPRESSION | PROLIFERATION | FOS | C-JUN | NF-KAPPA-B | Phosphorylation | Epithelial Cells - metabolism | Tetradecanoylphorbol Acetate - pharmacology | Mitogen-Activated Protein Kinase 8 - antagonists & inhibitors | Transcription Factor AP-1 - genetics | Epithelial Cells - drug effects | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Gene Expression Regulation, Neoplastic | Gastric Mucosa - metabolism | Mitogen-Activated Protein Kinase 9 - genetics | Tetradecanoylphorbol Acetate - antagonists & inhibitors | Transcription Factor AP-1 - metabolism | Dose-Response Relationship, Drug | Matrix Metalloproteinase 9 - metabolism | Matrix Metalloproteinase 9 - genetics | Oligodeoxyribonucleotides - genetics | Mitogen-Activated Protein Kinase 1 - genetics | Mitogen-Activated Protein Kinase 8 - genetics | Flavonoids - pharmacology | Stomach - drug effects | Oligodeoxyribonucleotides - metabolism | Stomach - pathology | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | Mitogen-Activated Protein Kinase 9 - metabolism | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 8 - metabolism | Proto-Oncogene Proteins c-fos - metabolism | Epithelial Cells - pathology | Antibodies - pharmacology | Cell Movement - drug effects | Transcription Factor AP-1 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - metabolism | Mitogen-Activated Protein Kinase 9 - antagonists & inhibitors | Cell Line, Tumor | Proto-Oncogene Proteins c-fos - genetics | Antineoplastic Agents, Phytogenic - pharmacology | Mitogen-Activated Protein Kinase 1 - metabolism | Enzymes | Care and treatment | Oligodeoxynucleotides | Stomach cancer | Cancer cells | Cancer | Transcription factors | Oligonucleotides | Malignancy | Metastasis | Matrix metalloproteinase | Kinases | Cancer therapies | Medical schools | Western blotting | Metastases | Anticancer properties | Angiogenesis | Signal transduction | Pathways | Fos protein | Proteolysis | Metalloproteinase | c-Fos protein | Gastric cancer | Invasiveness | Extracellular signal-regulated kinase | c-Jun protein | Blocking | Breast cancer | Gene expression | Gelatinase B | Polymerase chain reaction | Signaling | Acetic acid
Journal Article
Arteriosclerosis, thrombosis, and vascular biology, ISSN 1524-4636, 2016, Volume 36, Issue 6, pp. 1122 - 1131
OBJECTIVE—The c-Jun NH2-terminal kinases (JNK) are regulated by a wide variety of cellular stresses and have been implicated in apoptotic signaling... 
atherosclerosis | apoptosis | macrophages | MAP kinase signaling system | endoplasmic reticulum stress | SURVIVAL | ACTIVATION | PHOSPHORYLATION | BAD | SIGNAL-TRANSDUCTION | OBESITY | NH2-TERMINAL KINASE (JNK)1 | INSULIN-RESISTANCE | INFLAMMATION | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | REQUIREMENT | Mitogen-Activated Protein Kinase 8 - antagonists & inhibitors | Apoptosis - drug effects | Bone Marrow Cells - enzymology | Atherosclerosis - genetics | Mitogen-Activated Protein Kinase 9 - genetics | PTEN Phosphohydrolase - antagonists & inhibitors | Atherosclerosis - enzymology | Hypercholesterolemia - enzymology | Diet, High-Fat | Bone Marrow Transplantation | Receptors, LDL - deficiency | bcl-Associated Death Protein - metabolism | Bone Marrow Cells - drug effects | Mitogen-Activated Protein Kinase 8 - genetics | Aortic Diseases - enzymology | Proto-Oncogene Proteins c-akt - metabolism | Aorta - enzymology | Aortic Diseases - pathology | Disease Models, Animal | Receptors, LDL - genetics | Atherosclerosis - pathology | Genetic Predisposition to Disease | Macrophages - pathology | Signal Transduction | Cell Survival | Aorta - drug effects | Mice, Inbred C57BL | Bone Marrow Cells - pathology | Cells, Cultured | PTEN Phosphohydrolase - metabolism | Plaque, Atherosclerotic | Mitogen-Activated Protein Kinase 9 - deficiency | Macrophages - enzymology | Mice, Knockout | Aorta - pathology | Mitogen-Activated Protein Kinase 8 - deficiency | Aortic Diseases - genetics | Phenotype | Animals | Endoplasmic Reticulum Stress | Mitogen-Activated Protein Kinase 9 - antagonists & inhibitors | Macrophages - drug effects | Protein Kinase Inhibitors - pharmacology | Hypercholesterolemia - genetics
Journal Article