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1. Full Text IL-13-induced airway mucus production is attenuated by MAPK13 inhibition
by Alevy, Yael G and Patel, Anand C and Romero, Arthur G and Patel, Dhara A and Tucker, Jennifer and Roswit, William T and Miller, Chantel A and Heier, Richard F and Byers, Derek E and Brett, Tom J and Holtzman, Michael J
Journal of Clinical Investigation, ISSN 0021-9738, 12/2012, Volume 122, Issue 12, pp. 4555 - 4568
Increased mucus production is a common cause of morbidity and mortality in inflammatory airway diseases, including asthma, chronic obstructive pulmonary... 
MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATED PROTEIN-KINASE | BRONCHIAL EPITHELIAL-CELLS | MUCIN | P38-DELTA | MCLCA3 | P38 MAPK | INTERLEUKIN-13 | MEMBRANE-PROTEIN | VIRAL-INFECTION | RATIONAL DESIGN | Respiratory System - pathology | Interleukin-13 - physiology | Epithelial Cells - drug effects | Humans | Crystallography, X-Ray | Chloride Channels - genetics | Gene Knockdown Techniques | MAP Kinase Signaling System | Epithelial Cells - secretion | Pyrazoles - chemistry | Mitogen-Activated Protein Kinase 13 - antagonists & inhibitors | RNA Interference | Drug Design | Mitogen-Activated Protein Kinase 13 - chemistry | Mitogen-Activated Protein Kinase 13 - metabolism | Mucins - metabolism | Mitogen-Activated Protein Kinase 13 - genetics | Pulmonary Disease, Chronic Obstructive - metabolism | Binding Sites | Pyrazoles - pharmacology | Naphthalenes - chemistry | Cells, Cultured | Gene Expression Regulation | Models, Molecular | Mucus - secretion | Respiratory System - secretion | Naphthalenes - pharmacology | Chloride Channels - metabolism | Secretory Pathway - drug effects | Hydrogen Bonding | Protein Binding | Kinetics | Chloride Channels - physiology | Mucins - genetics | Respiratory mucosa | Interleukins | Genetic aspects | Research | Gene expression | Properties | Airway (Medicine) | Mitogen-activated protein kinases
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2. Full Text The p38 Mitogen-Activated Protein Kinase Critically Regulates Human Keratinocyte Inflammasome Activation
by Fenini, Gabriele and Grossi, Serena and Gehrke, Samuel and Beer, Hans-Dietmar and Satoh, Takashi K and Contassot, Emmanuel and French, Lars E
Journal of Investigative Dermatology, ISSN 0022-202X, 06/2018, Volume 138, Issue 6, pp. 1380 - 1390
Inflammasomes are key intracellular signaling platforms involved in innate immune responses to micro-organisms and danger signals. Extracellular... 
AIM2 INFLAMMASOME | ASC | DISEASES | INTERLEUKIN-1-BETA | FOS GENE-EXPRESSION | LESIONAL PSORIATIC SKIN | MAP-KINASES | K+ EFFLUX | NLRP3 INFLAMMASOME | NALP3 INFLAMMASOME | DERMATOLOGY | Phosphorylation | Inflammasomes - metabolism | Mitogen-Activated Protein Kinase 14 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 8 - antagonists & inhibitors | Humans | Protein Multimerization - immunology | Signal Transduction - immunology | CARD Signaling Adaptor Proteins - metabolism | Mitogen-Activated Protein Kinase 13 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 14 - metabolism | RNA Interference | Interleukin-1beta - metabolism | Myeloid Cells - immunology | Mitogen-Activated Protein Kinase 13 - metabolism | JNK Mitogen-Activated Protein Kinases | Mitogen-Activated Protein Kinase 8 - genetics | Mitogen-Activated Protein Kinase 13 - genetics | CARD Signaling Adaptor Proteins - immunology | Mitogen-Activated Protein Kinase 8 - metabolism | Cells, Cultured | Interleukin-1beta - immunology | Mitogen-Activated Protein Kinase 14 - genetics | CRISPR-Cas Systems - genetics | Keratinocytes - immunology | Keratinocytes - metabolism | Inflammasomes - immunology | Myeloid Cells - metabolism | Enzyme Activation | Primary Cell Culture | RNA, Small Interfering - metabolism
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3. Full Text BIRB796 Inhibits All p38 MAPK Isoforms in Vitro and in Vivo
by Yvonne Kuma and Guadalupe Sabio and Jenny Bain and Natalia Shpiro and Rodolfo Márquez and Ana Cuenda
Journal of Biological Chemistry, ISSN 0021-9258, 05/2005, Volume 280, Issue 20, pp. 19472 - 19479
The compound BIRB796 inhibits the stress-activated protein kinases p38α and p38β and is undergoing clinical trials for the treatment of inflammatory... 
HUMAN ENDOTOXEMIA | SAP KINASES | ACTIVATED PROTEIN-KINASE | SPECIFICITIES | MECHANISM | PATHWAY | PHOSPHORYLATION | SUBSTRATE | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELLULAR STRESSES | IDENTIFICATION | Phosphorylation | Mitogen-Activated Protein Kinase 14 - antagonists & inhibitors | Humans | Substrate Specificity | Mitogen-Activated Protein Kinase 13 - antagonists & inhibitors | Pyrazoles - pharmacology | Amino Acid Sequence | Cell Line | Discs Large Homolog 1 Protein | Mitogen-Activated Protein Kinase 12 - antagonists & inhibitors | Rats | Mitogen-Activated Protein Kinase 11 - antagonists & inhibitors | Naphthalenes - pharmacology | Membrane Proteins | Proteins - genetics | Adaptor Proteins, Signal Transducing | Animals | Guanylate Kinases | Proteins - metabolism | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mice | Protein Kinase Inhibitors - pharmacology | HeLa Cells | Kinetics | Proteins - chemistry | In Vitro Techniques
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4. Full Text First comprehensive structural and biophysical analysis of MAPK13 inhibitors targeting DFG-in and DFG-out binding modes
by Yurtsever, Zeynep and Patel, Dhara A and Kober, Daniel L and Su, Alvin and Miller, Chantel A and Romero, Arthur G and Holtzman, Michael J and Brett, Tom J and Argonne National Lab. (ANL), Argonne, IL (United States). Advanced Photon Source (APS)
BBA - General Subjects, ISSN 0304-4165, 11/2016, Volume 1860, Issue 11, pp. 2335 - 2344
P38 MAP kinases are centrally involved in mediating extracellular signaling in various diseases. While much attention has previously been focused on the... 
p38 kinase | Structure-based drug design | Differential scanning fluorimetry | Chronic inflammatory lung disease | Kinase inhibitor | Inhibitor half-lives | ACTIVATED PROTEIN-KINASE | P38-GAMMA | P38-DELTA | BIOCHEMISTRY & MOLECULAR BIOLOGY | GLIDE | CYTOKINE PRODUCTION | BIOPHYSICS | ACCURATE DOCKING | PATHWAY | P38-ALPHA | SELECTIVITY | Protein Kinase Inhibitors - chemistry | Mitogen-Activated Protein Kinase 13 - antagonists & inhibitors | Humans | Mitogen-Activated Protein Kinase 13 - chemistry | Mitogen-Activated Protein Kinase 13 - metabolism | Protein Binding | Protein Kinase Inhibitors - pharmacology | Binding Sites | Quantitative Structure-Activity Relationship | Respiratory tract diseases | Analysis
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5. Full Text Novel Therapies to Inhibit Mucus Synthesis and Secretion in Airway Hypersecretory Diseases
by Ha, Emily V.S and Rogers, Duncan F
Pharmacology, ISSN 0031-7012, 01/2016, Volume 97, Issue 1-2, pp. 84 - 100
Background: In asthma and chronic obstructive pulmonary disease (COPD), airway mucus hypersecretion contributes to impaired mucociliary clearance, mucostasis... 
Review | Airways | MARCKS | Mucin | Macrolides | Bio-11006 | Chronic obstructive pulmonary disease | Mucus | Epidermal growth factor receptor | Asthma | CONTROLLED-TRIAL | RESPIRATORY-DISEASE | MUCIN EXPRESSION | EGFR INHIBITOR | OBSTRUCTIVE PULMONARY-DISEASE | EPITHELIAL-CELLS | MOUSE MODEL | ALLERGIC-ASTHMA | PHARMACOLOGY & PHARMACY | GOBLET CELL HYPERPLASIA | MACROLIDE ANTIBIOTICS | Ginkgolides - pharmacology | HSP70 Heat-Shock Proteins - antagonists & inhibitors | Myristoylated Alanine-Rich C Kinase Substrate | Humans | Mucus - drug effects | Intracellular Signaling Peptides and Proteins - metabolism | Pulmonary Disease, Chronic Obstructive - physiopathology | Lactones - pharmacology | Mitogen-Activated Protein Kinase 13 - antagonists & inhibitors | Inflammation Mediators - metabolism | Macrolides - pharmacology | Membrane Proteins - metabolism | Airway Remodeling - physiology | Ellagic Acid - pharmacology | Chloride Channels - antagonists & inhibitors | Asthma - physiopathology | Receptors, Purinergic P2Y | Mucus - secretion | Mucins - antagonists & inhibitors | Munc18 Proteins - antagonists & inhibitors | Mucins - biosynthesis | Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Hypoxia-Inducible Factor 1 - antagonists & inhibitors | GABA Antagonists | Protein-Tyrosine Kinases - antagonists & inhibitors | Body fluids | Signal transduction | Pharmacology | Epidermal growth factor
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6. Full Text p38α blocks brown adipose tissue thermogenesis through p38δ inhibition
by Matesanz, Nuria and Nikolic, Ivana and Leiva, Magdalena and Pulgarín-Alfaro, Marta and Santamans, Ayelén M and Bernardo, Edgar and Mora, Alfonso and Herrera-Melle, Leticia and Rodríguez, Elena and Beiroa, Daniel and Caballero, Ainoa and Martín-García, Elena and Acín-Pérez, Rebeca and Hernández-Cosido, Lourdes and Leiva-Vega, Luis and Torres, Jorge L and Centeno, Francisco and Nebreda, Angel R and Enríquez, José Antonio and Nogueiras, Rubén and Marcos, Miguel and Sabio, Guadalupe
PLoS Biology, ISSN 1544-9173, 07/2018, Volume 16, Issue 7, p. e2004455
Adipose tissue has emerged as an important regulator of whole-body metabolism, and its capacity to dissipate energy in the form of heat has acquired a special... 
ENERGY-BALANCE | STIMULATED GLUCOSE-UPTAKE | 3T3-L1 ADIPOGENESIS | WHITE FAT | ACTIVATED PROTEIN-KINASE | ADIPOCYTES | BEIGE FAT DEVELOPMENT | BIOCHEMISTRY & MOLECULAR BIOLOGY | BIOLOGY | UCP1 | ADULT HUMANS | P38 MAP KINASE | Body Mass Index | Diabetes Mellitus, Experimental - enzymology | Uncoupling Protein 1 - metabolism | Humans | Mice, Inbred C57BL | Adipose Tissue, Brown - physiology | Male | Adipose Tissue, Brown - enzymology | MAP Kinase Signaling System | Mice, Knockout | Animals | Diabetes Mellitus, Experimental - prevention & control | Mitogen-Activated Protein Kinase 13 - antagonists & inhibitors | Thermogenesis | Adipocytes, Brown - enzymology | Diet | Energy Metabolism | Mitogen-Activated Protein Kinase 14 - metabolism | Models, Biological | Obesity - prevention & control | Mitogen-Activated Protein Kinase 13 - metabolism | Adult | Obesity - enzymology | Enzyme Activation | Transformation | Adipose tissue | Body fat | Funding | Body weight | Medical services | Activation | Adipocytes | Kinases | High fat diet | Proteins | Body mass index | Energy | Animal tissues | Physiology | Inhibition | Adipose tissue (brown) | Supervision | Obesity | Internal medicine | Therapeutic applications | Body temperature | Medical treatment | Diabetes mellitus | Energy expenditure | Metabolism | Medicine | Body mass | Protein kinase | Body size | Insulin resistance | Skin | Mice | Gastrointestinal surgery | Diabetes
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7. Full Text p38δ mitogen-activated protein kinase regulates the expression of tight junction protein ZO-1 in differentiating human epidermal keratinocytes
by Siljamäki, Elina and Siljamäki, Elina and Raiko, Laura and Raiko, Laura and Toriseva, Mervi and Toriseva, Mervi and Nissinen, Liisa and Nissinen, Liisa and Näreoja, Tuomas and Näreoja, Tuomas and Peltonen, Juha and Peltonen, Juha and Kähäri, Veli-Matti and Kähäri, Veli-Matti and Peltonen, Sirkku and Peltonen, Sirkku
Archives of Dermatological Research, ISSN 0340-3696, 3/2014, Volume 306, Issue 2, pp. 131 - 141
Increasing evidence has recognized tight junctions (TJs) as the lower epidermal inside-out diffusion barrier located in granular cell layers of the epidermis.... 
ZO-1 | Medicine & Public Health | p38 | Dermatology | MAPK kinase | Tight junction | Keratinocyte | Desmosome | BARRIER | RESOLUTION | COMPONENTS | DERMATOLOGY | IN-VITRO | INVASION | FLUORESCENCE MICROSCOPY | OCCLUDIN | GROWTH-FACTOR | SQUAMOUS CARCINOMA-CELLS | PSORIASIS | RNA, Small Interfering - genetics | Calcium - metabolism | Carcinoma, Squamous Cell - metabolism | Carcinoma, Squamous Cell - pathology | Humans | Middle Aged | Young Adult | Mitogen-Activated Protein Kinase 13 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 13 - metabolism | Adult | Female | Cell Differentiation | Mitogen-Activated Protein Kinase 13 - genetics | Zonula Occludens-1 Protein - metabolism | Tight Junctions - metabolism | Zonula Occludens-1 Protein - genetics | Signal Transduction | Gene Expression Regulation - genetics | Imidazoles - pharmacology | Gene Expression Regulation - drug effects | Keratinocytes - drug effects | Cell Line, Tumor | Aged | Pyridines - pharmacology | Keratinocytes - physiology
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8. Full Text Development of a p38δ mitogen activated protein kinase ELISA assay for the quantitative determination of inhibitor activity
by Goettert, Márcia and Shaalan, Nouran and Graeser, Ralph and Laufer, Stefan A
Journal of Pharmaceutical and Biomedical Analysis, ISSN 0731-7085, 07/2012, Volume 66, pp. 349 - 351
► Identification of inhibitors of p38δ MAPK by a direct ELISA assay based on a p38α assay for monitoring the phosphorylation of ATF-2. ► The assay is... 
p38δ | MAPK | Small-molecule inhibitors | ELISA | P38δ | RHEUMATOID-ARTHRITIS | PATHWAYS | CHEMISTRY, ANALYTICAL | p38 delta | ALPHA | PHARMACOLOGY & PHARMACY | P38-ALPHA | Enzyme-Linked Immunosorbent Assay - methods | Phosphorylation | Mitogen-Activated Protein Kinase 13 - antagonists & inhibitors | Arthritis, Rheumatoid - drug therapy | Protein Kinase Inhibitors - pharmacology | Activating Transcription Factor 2 - metabolism | Arthritis, Rheumatoid - physiopathology | Fibroblasts - metabolism
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9. MicroRNA-23a-5p regulates osteogenic differentiation of human bone marrow-derived mesenchymal stem cells by targeting mitogen-activated protein kinase-13
by Ren, Gang and Sun, Jing and Li, Meng-Meng and Zhang, Yong-Dong and Li, Rong-Hua and Li, Yu-Ming
Molecular medicine reports, 03/2018, Volume 17, Issue 3, p. 4554
The molecular mechanisms of osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) remain to be fully elucidated. MicroRNAs (miRs)... 
Osteopontin - genetics | MicroRNAs - antagonists & inhibitors | Humans | Alkaline Phosphatase - metabolism | Male | MicroRNAs - metabolism | Osteopontin - metabolism | Core Binding Factor Alpha 1 Subunit - metabolism | Mesenchymal Stromal Cells - cytology | Mitogen-Activated Protein Kinase 13 - antagonists & inhibitors | RNA Interference | Mitogen-Activated Protein Kinase 13 - metabolism | Adult | Female | Cell Differentiation | Mitogen-Activated Protein Kinase 13 - genetics | 3' Untranslated Regions | Alkaline Phosphatase - genetics | Bone Marrow Cells - cytology | Cells, Cultured | Mesenchymal Stromal Cells - metabolism | MicroRNAs - genetics | Antagomirs - metabolism | Core Binding Factor Alpha 1 Subunit - genetics | Osteogenesis | RNA, Small Interfering - metabolism
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10. Full Text Isoforms of p38MAPK gamma and delta contribute to differentiation of human AML cells induced by 1,25-dihydroxyvitamin D
by Zhang, Jing and Harrison, Jonathan S and Studzinski, George P
Experimental cell research, 01/2011, Volume 317, Issue 1, p. 117
Inhibition of p38MAPK alpha/beta is known to enhance 1,25-dihydroxyvitamin (1,25D)-induced monocytic differentiation, but the detailed mechanism of this effect... 
Gene Expression Regulation, Enzymologic - drug effects | Humans | Leukemia, Myeloid, Acute - metabolism | Monocytes - metabolism | Mitogen-Activated Protein Kinase 12 - genetics | Dose-Response Relationship, Drug | Cell Differentiation - genetics | Mitogen-Activated Protein Kinase 12 - metabolism | Mitogen-Activated Protein Kinase 13 - antagonists & inhibitors | Time Factors | Isoenzymes - metabolism | U937 Cells | Mitogen-Activated Protein Kinase 13 - metabolism | Antigens, Differentiation - metabolism | Mitogen-Activated Protein Kinase 13 - genetics | Mitogen-Activated Protein Kinase 13 - physiology | Gene Expression Regulation, Neoplastic - drug effects | Mitogen-Activated Protein Kinase 12 - physiology | Monocytes - physiology | Isoenzymes - physiology | Mitogen-Activated Protein Kinase 12 - antagonists & inhibitors | Isoenzymes - genetics | Leukemia, Myeloid, Acute - pathology | Imidazoles - pharmacology | Monocytes - drug effects | Cell Differentiation - drug effects | Calcitriol - pharmacology | HL-60 Cells | Antigens, Differentiation - genetics | Protein Kinase Inhibitors - pharmacology | Pyridines - pharmacology | Leukemia, Myeloid, Acute - genetics
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11. Full Text The P38alpha and P38delta MAP kinases may be gene therapy targets in the future treatment of severe burns
by Wang, Shuyun and Huang, Qiaobing and Guo, Xiaohua and Brunk, Ulf T and Han, Jiahuai and Zhao, Keseng and Zhao, Ming
Shock (Augusta, Ga.), 08/2010, Volume 34, Issue 2, p. 176
Microvascular barrier damage, induced by thermal injury, imposes life-threatening problems owing to the pathophysiological consequences of plasma loss and... 
Mitogen-Activated Protein Kinase 14 - antagonists & inhibitors | Burns - blood | Humans | Actins - metabolism | Cells, Cultured | Enzyme Inhibitors - pharmacology | Capillary Permeability - drug effects | Protein Kinase C - antagonists & inhibitors | Animals | MAP Kinase Signaling System - drug effects | Mitogen-Activated Protein Kinase 13 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 14 - metabolism | Mitogen-Activated Protein Kinase 13 - metabolism | Burns - therapy | Imidazoles - therapeutic use | Genetic Therapy - methods | Pyridines - therapeutic use | Tight Junctions - drug effects
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12. Full Text MKP-1 inhibits high NaCl-induced activation of p38 but does not inhibit the activation of TonEBP/OREBP: opposite roles of p38alpha and p38delta
by Zhou, Xiaoming and Ferraris, Joan D and Dmitrieva, Natalia I and Liu, Yusen and Burg, Maurice B
Proceedings of the National Academy of Sciences of the United States of America, 04/2008, Volume 105, Issue 14, p. 5620
High NaCl rapidly activates p38 MAPK by phosphorylating it, the phosphorylation presumably being regulated by a balance of kinases and phosphatases. Kinases... 
Cell Line | Dual Specificity Phosphatase 1 - genetics | Mitogen-Activated Protein Kinase 14 - antagonists & inhibitors | Dual Specificity Phosphatase 1 - physiology | Sodium Chloride - pharmacology | Dual Specificity Phosphatase 1 - antagonists & inhibitors | Humans | NFATC Transcription Factors - metabolism | Enzyme Activation - drug effects | Transcription Factors - metabolism | Mitogen-Activated Protein Kinase 13 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 14 - metabolism | Mitogen-Activated Protein Kinase 13 - metabolism | Phosphorylation - drug effects
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13. New drugs offer a lifeline for COPD and other respiratory diseases. Mucus-blocking medications could save countless lives
DukeMedicine healthnews, ISSN 2153-8387, 02/2013, Volume 19, Issue 2, p. 3
Mitogen-Activated Protein Kinase 13 - antagonists & inhibitors | Humans | Mucus - metabolism | Respiratory Tract Diseases - physiopathology | Pulmonary Disease, Chronic Obstructive - physiopathology | Respiratory Tract Diseases - drug therapy | Pulmonary Disease, Chronic Obstructive - drug therapy
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14. Full Text Interleukin (IL)‐4 and IL‐13 up‐regulate monocyte chemoattractant protein‐1 expression in human bronchial epithelial cells: involvement of p38 mitogen‐activated protein kinase, extracellular signal‐regulated kinase 1/2 and Janus kinase‐2 but not c‐Jun NH2‐terminal kinase 1/2 signalling pathways
by Ip, W. K and Wong, C. K and Lam, C. W. K
Clinical & Experimental Immunology, ISSN 0009-9104, 07/2006, Volume 145, Issue 1, pp. 162 - 172
Summary The Th2 cytokines interleukin (IL)‐4 and IL‐13 and chemokine monocyte chemoattractant protein‐1 (MCP‐1) are significantly involved in bronchial... 
chemokines/monokines | allergy | epithelial cells | cytokines/interleukins | signalling/signal transduction | Allergy | Cytokines/interleukins | Epithelial cells | Chemokines/monokines | Signalling/signal transduction | ALLERGIC INFLAMMATION | CYTOKINES | CHEMOKINES | KAPPA-B | RELEASE | IMMUNOLOGY | HUMAN EOSINOPHILS | EOTAXIN-2 | ASTHMA PATHOGENESIS | ALVEOLAR MACROPHAGES | AIRWAY HYPERRESPONSIVENESS | Up-Regulation | Epithelial Cells - metabolism | Gene Expression - drug effects | Protein-Tyrosine Kinases - metabolism | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | JNK Mitogen-Activated Protein Kinases - metabolism | Interleukins - metabolism | MAP Kinase Signaling System | Dose-Response Relationship, Drug | Janus Kinase 2 | Bronchi - metabolism | Chemokine CCL2 - metabolism | Flavonoids - pharmacology | p38 Mitogen-Activated Protein Kinases - metabolism | Proto-Oncogene Proteins - metabolism | Cell Survival - drug effects | Proto-Oncogene Proteins - antagonists & inhibitors | JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors | Interleukin-4 - metabolism | Imidazoles - pharmacology | Tyrphostins - pharmacology | Interleukin-13 - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Mitogen-Activated Protein Kinase 3 - metabolism | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Pyridines - pharmacology | Enzyme Activation | Cell Line, Transformed | Protein-Tyrosine Kinases - antagonists & inhibitors | Proteins | Mutual fund industry | Protein kinases | signal transduction | monokines | cytokines | Basic Immunology | chemokines | signalling | interleukins
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15. Full Text c-Jun N-terminal kinase is required for metalloproteinase expression and joint destruction in inflammatory arthritis
by Han, Z and Boyle, D.L and Chang, L and Bennett, B and Karin, M and Yang, L and Manning, A.M and Firestein, G.S
Journal of Clinical Investigation, ISSN 0021-9738, 2001, Volume 108, Issue 1, pp. 73 - 81
Mitogen-activated protein kinase (MAPK) cascades are involved in inflammation and tissue destruction in rheumatoid arthritis (RA). In particular, c-Jun... 
RHEUMATOID-ARTHRITIS | TRANSCRIPTION FACTORS | SIGNAL-TRANSDUCTION | PATHWAYS | MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATED PROTEIN-KINASE | KAPPA-B REGULATION | P38 | COLLAGENASE | GENE-EXPRESSION | JNK2 | Rats, Inbred Lew | MAP Kinase Signaling System | Arthritis, Experimental - pathology | Protein-Tyrosine Kinases - physiology | RNA, Messenger - biosynthesis | Protein-Tyrosine Kinases - genetics | Transcription Factor AP-1 - deficiency | Protein Processing, Post-Translational - drug effects | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Enzyme Induction - drug effects | Flavonoids - pharmacology | Interleukin-1 - antagonists & inhibitors | Phosphorylation - drug effects | p38 Mitogen-Activated Protein Kinases | Isoenzymes - physiology | Cells, Cultured - drug effects | Collagenases - genetics | Collagenases - biosynthesis | Isoenzymes - genetics | Enzyme Inhibitors - pharmacology | Rats | Anthracenes - pharmacology | Cells, Cultured - enzymology | Interleukin-1 - pharmacology | Matrix Metalloproteinase 13 | Mice, Knockout | Transcription Factors - metabolism | Animals | Mitogen-Activated Protein Kinase 10 | Mitogen-Activated Protein Kinase 8 | Mitogen-Activated Protein Kinase 9 | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mitogen-Activated Protein Kinases - physiology | Proto-Oncogene Proteins c-jun - metabolism | Activating Transcription Factor 2 | Transcription Factor AP-1 - physiology | Cyclic AMP Response Element-Binding Protein - metabolism | Mitogen-Activated Protein Kinases - genetics | Mice | Arthritis, Experimental - enzymology | Isoenzymes - antagonists & inhibitors | MAP Kinase Kinase Kinase 1 | Mitogen-Activated Protein Kinase 3 | Synovial Membrane - cytology | Protein-Tyrosine Kinases - antagonists & inhibitors
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16. Full Text Ischemic Postconditioning in Pigs: No Causal Role for Risk Activation
by Skyschally, Andreas and van Caster, Patrick and Boengler, Kerstin and Gres, Petra and Musiolik, Judith and Schilawa, Dustin and Schulz, Rainer and Heusch, Gerd
Circulation Research, ISSN 0009-7330, 01/2009, Volume 104, Issue 1, pp. 15 - 18
Ischemic postconditioning (IPoC) reduces infarct size following ischemia/reperfusion. Whether or not phosphorylation of RISK (reperfusion injury salvage... 
PERMEABILITY TRANSITION PORE | CARDIAC & CARDIOVASCULAR SYSTEMS | PROTECTION | REPERFUSION | reperfusion injury | NECROSIS-FACTOR-ALPHA | ADENOSINE RECEPTORS | infarct size | INHIBITION | MYOCARDIAL INFARCT SIZE | cardioprotection | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | MOUSE HEARTS | SIGNAL TRANSDUCER | Glycogen Synthase Kinase 3 - physiology | MAP Kinase Kinase 2 - physiology | Nitriles - pharmacology | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Glycogen Synthase Kinase 3 beta | Ribosomal Protein S6 Kinases, 70-kDa - physiology | MAP Kinase Kinase 1 - physiology | Myocardial Reperfusion Injury - enzymology | Ribosomal Protein S6 Kinases, 70-kDa - biosynthesis | Protein Processing, Post-Translational - drug effects | Swine | Mitogen-Activated Protein Kinase 3 - biosynthesis | Myocardial Infarction - pathology | Swine, Miniature | Phosphorylation - drug effects | Myocardial Infarction - enzymology | MAP Kinase Kinase 1 - antagonists & inhibitors | Butadienes - pharmacology | Glycogen Synthase Kinase 3 - biosynthesis | Mitogen-Activated Protein Kinase 1 - physiology | Glycogen Synthase Kinase 3 - antagonists & inhibitors | Ribosomal Protein S6 Kinases, 70-kDa - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Coronary Occlusion - enzymology | Enzyme Induction | Proto-Oncogene Proteins c-akt - physiology | Enzyme Activation - drug effects | Mitogen-Activated Protein Kinase 3 - physiology | Mitogen-Activated Protein Kinase 1 - biosynthesis | Proto-Oncogene Proteins c-akt - biosynthesis | Animals | Androstadienes - pharmacology | Myocardial Reperfusion | MAP Kinase Kinase 2 - antagonists & inhibitors | Coronary Occlusion - pathology | Phosphatidylinositol 3-Kinases - physiology | Protein Kinase Inhibitors - pharmacology | Myocardial Reperfusion Injury - prevention & control | Proto-Oncogene Proteins c-akt - antagonists & inhibitors
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17. Full Text COT drives resistance to RAF inhibition through MAP kinase pathway reactivation
by Johannessen, Cory M and Boehm, Jesse S and Kim, So Young and Thomas, Sapana R and Wardwell, Leslie and Johnson, Laura A and Emery, Caroline M and Stransky, Nicolas and Cogdill, Alexandria P and Barretina, Jordi and Caponigro, Giordano and Hieronymus, Haley and Murray, Ryan R and Salehi-Ashtiani, Kourosh and Hill, David E and Vidal, Marc and Zhao, Jean J and Yang, Xiaoping and Alkan, Ozan and Kim, Sungjoon and Harris, Jennifer L and Wilson, Christopher J and Myer, Vic E and Finan, Peter M and Root, David E and Roberts, Thomas M and Golub, Todd and Flaherty, Keith T and Dummer, Reinhard and Weber, Barbara L and Sellers, William R and Schlegel, Robert and Wargo, Jennifer A and Hahn, William C and Garraway, Levi A
Nature, ISSN 0028-0836, 12/2010, Volume 468, Issue 7326, pp. 968 - 972
Oncogenic mutations in the serine/threonine kinase B-RAF (also known as BRAF) are found in 50-70% of malignant melanomas(1). Pre-clinical studies have... 
TRANSFORMATION | CELLS | ACTIVATION | TUMOR PROGRESSION | GENE | SIGNALING PATHWAY | MULTIDISCIPLINARY SCIENCES | SENSITIVITY | BRAF | MUTATIONS | CANCER | Allosteric Regulation | Humans | Gene Expression Regulation, Neoplastic | Melanoma - enzymology | Gene Expression Profiling | MAP Kinase Signaling System | Mitogen-Activated Protein Kinase Kinases - metabolism | Melanoma - genetics | Indoles - pharmacology | Proto-Oncogene Proteins B-raf - metabolism | Proto-Oncogene Proteins B-raf - chemistry | Melanoma - metabolism | Proto-Oncogene Proteins - metabolism | Gene Library | Proto-Oncogene Proteins c-raf - genetics | MAP Kinase Kinase Kinases - genetics | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Proto-Oncogene Proteins - genetics | Clinical Trials as Topic | MAP Kinase Kinase Kinases - metabolism | Enzyme Activation - drug effects | Open Reading Frames - genetics | Sulfonamides - pharmacology | Proto-Oncogene Proteins c-raf - metabolism | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Drug Resistance, Neoplasm - genetics | Sulfonamides - therapeutic use | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Cell Line, Tumor | Indoles - therapeutic use | Protein Kinase Inhibitors - pharmacology | Drug Resistance, Neoplasm - drug effects | Mitogen-Activated Protein Kinases - metabolism | Protein research | Research | Properties | Protein kinases | Cancer cells | Cell lines | Biochemistry | Mutation | Kinases | Genes | Cancer
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