Search results for "MAPK"

showing 10 items of 238 documents

Acquired BRAF inhibitor resistance: A multicenter meta-analysis of the spectrum and frequencies, clinical behaviour, and phenotypic associations of r…

2015

BackgroundAcquired resistance to BRAF inhibitors (BRAFi) is a near-universal phenomenon caused by numerous genetic and non-genetic alterations. In this study, we evaluated the spectrum, onset, pattern of progression, and subsequent clinical outcomes associated with specific mechanisms of resistance.MethodsWe compiled clinical and genetic data from 100 patients with 132 tissue samples obtained at progression on BRAFi therapy from 3 large, previously published studies of BRAFi resistance. These samples were subjected to whole-exome sequencing and/or polymerase chain reaction-based genetic testing.ResultsAmong 132 samples, putative resistance mechanisms were identified in 58%, including NRAS o…

OncologyNeuroblastoma RAS viral oncogene homologMaleCancer ResearchSkin NeoplasmsTime FactorsResistanceDNA Mutational AnalysisDrug ResistanceMedizinKaplan-Meier EstimateBioinformaticsmedicine.disease_causeRisk Factors2.1 Biological and endogenous factorsAetiologyVemurafenibMelanomaCancerMutationTumorDabrafenibMelanomaAcquiredMiddle AgedPhenotypeEuropePhenotypeTreatment OutcomeSpliceOncologyMeta-analysisPublic Health and Health ServicesDisease ProgressionFemalemedicine.drugSignal TransductionProto-Oncogene Proteins B-rafmedicine.medical_specialtyOncology and CarcinogenesisNRASAntineoplastic AgentsBiologyDisease-Free SurvivalArticleBRAFMEK1Clinical ResearchInternal medicineGeneticsmedicineBiomarkers TumorHumansGenetic Predisposition to DiseaseOncology & CarcinogenesisProtein Kinase InhibitorsProportional Hazards ModelsProportional hazards modelAustraliaDabrafenibmedicine.diseaseMAPKUnited StatesMeta-analysisVemurafenibDrug Resistance NeoplasmMutationNeoplasmBiomarkersEuropean journal of cancer (Oxford, England : 1990)
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Phospho-p38 MAPK expression in COPD patients and asthmatics and in challenged bronchial epithelium

2015

<b><i>Background:</i></b> The role of mitogen-activated protein kinases (MAPK) in regulating the inflammatory response in the airways of patients with chronic obstructive pulmonary disease (COPD) and asthmatic patients is unclear. <b><i>Objectives:</i></b> To investigate the expression of activated MAPK in lungs of COPD patients and in bronchial biopsies of asthmatic patients and to study MAPK expression in bronchial epithelial cells in response to oxidative and inflammatory stimuli. <b><i>Methods:</i></b> Immunohistochemical expression of phospho (p)-p38 MAPK, p-JNK1 and p-ERK1/2 was measured in bronchial mucosa in pat…

P38 MAPKMaleMAPK/ERK pathwayAsthma phenotypeSMOKERespiratory SystemMitogen-activated protein kinases; p65; Pathology of chronic obstructive pulmonary disease; Chronic obstructive pulmonary disease phenotypes; Asthma phenotypesPathology of chronic obstructive pulmonary diseasep38 Mitogen-Activated Protein KinasesChronic obstructive pulmonary disease phenotypePulmonary Disease Chronic ObstructiveOXIDATIVE STRESSMACROPHAGESRespiratory systemMitogen-activated protein kinasesChronic obstructive pulmonary disease phenotypesMitogen-activated protein kinases; p65; pathology of chronic obstructive pulmonary disease phenotypes; asthma phenotypesCOPDp65KinaseAsthma phenotypes; Chronic obstructive pulmonary disease phenotypes; Mitogen-activated protein kinases; p65; Pathology of chronic obstructive pulmonary disease; Pulmonary and Respiratory MedicineACTIVATED PROTEIN-KINASEInterleukinMiddle AgedImmunohistochemistrypathology of chronic obstructive pulmonary disease phenotypesAsthma phenotypesFemaleLife Sciences & BiomedicinePulmonary and Respiratory Medicinep38 mitogen-activated protein kinasesBlotting WesternINHIBITIONSocio-culturaleBronchiRespiratory MucosaOBSTRUCTIVE PULMONARY-DISEASE1102 Cardiovascular Medicine And HaematologyCell LinemedicineHumansLymphocyte CountInterleukin 8AgedAsthmaScience & Technologybusiness.industryInterleukin-8Transcription Factor RelAPATHWAYSMitogen-activated protein kinasemedicine.diseaseAsthmarespiratory tract diseasesSEVERITYCase-Control StudiesCELLSImmunologybusiness
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Traditional Chinese herbal medicine at the forefront battle against COVID-19: Clinical experience and scientific basis.

2020

Abstract Background Throughout the 5000-year history of China, more than 300 epidemics were recorded. Traditional Chinese herbal medicine (TCM) has been used effectively to combat each of these epidemics’ infections, and saved many lives. To date, there are hundreds of herbal TCM formulae developed for the purpose of prevention and treatment during epidemic infections. When COVID-19 ravaged the Wuhan district in China in early January 2020, without a deep understanding about the nature of COVID-19, patients admitted to the TCM Hospital in Wuhan were immediately treated with TCM and reported later with >90% efficacy. Approach We conducted conduct a systematic survey of various TCM herbal pre…

PTGS2 Prostaglandin-endoperoxide synthase 2BattleAIV avian influenza virusCoV coronavirusPharmaceutical ScienceiNOS nitric oxide synthaseViral infection0302 clinical medicinePA patchouli alcoholSARS Severe Acute Respiratory SyndromeSMD Sheganmahuang decoctionDrug DiscoveryPandemicIL InterleukinMedicine Chinese TraditionalALI acute lung injuriesmedia_commonCOVID-19 coronavirus disease 2019MXSG Ma xing shi gan decoction0303 health sciencesTNF tumor necrosis factorClinical Trials as TopicCCL2 CC chemokine ligand 2FM1 FM1 coronavirusICU intensive care unitc-AMP cyclic adenosine phosphateHIV human immunodeficiency virus030220 oncology & carcinogenesisCOX-2 cyclooxygenase-2Molecular MedicineHerbal preparationsMedicinal herbsAbbreviations: ACE2 angiotensin-converting enzyme IITCM traditional Chinese medicineHSV-1 herpes simplex virus 1CASP3 caspase 3medicine.medical_specialtyChinaCoronavirus disease 2019 (COVID-19)Systematic surveymedia_common.quotation_subjectJEV Japanese encephalitis virusNF-κB nuclear factor kappa B cellsAntiviral AgentsArticleWHO World Health Organization03 medical and health sciencesIEC-6 rat intestinal epithelial cell line 6SOD superoxide dismutaseCDC Center for Disease Control and PreventionmedicineAVP arginine vasopressinPGE2 prostaglandin E2HumansIntensive care medicineLH Lianhuaqingwen capsule030304 developmental biologyPharmacologyMedicinal herbMDA malondialdehydeGCGJ Gancao ganjiang decoctionNO nitric oxidePlants Medicinalbusiness.industrySARS-CoV-2COVID-19CXCL C-X-C- motif chemokineMDCK Madin-Darby Canine Kidney cellsTLR-4 Toll-like receptor-4COVID-19 Drug TreatmentComplementary and alternative medicineViral infectionLPS lipopolysaccharidesRSV respiratory syncytial virusQFPD Qingfeipaidu decoctionbusinessLung congestionECMO extracorporeal membrane oxygenationMAPK mitogen-activated protein kinasePhytotherapyDrugs Chinese HerbalPhytomedicine : international journal of phytotherapy and phytopharmacology
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Shikonin reduces oedema induced by phorbol ester by interfering with IκBα degradation thus inhibiting translocation of NF-κB to the nucleus

2010

Background and purpose In the present paper we studied the effect of shikonin on ear oedema induced by 12-O-tetradecanoylphorbol-13-acetate (TPA), and determined the mechanisms through which shikonin might exert its topical anti-inflammatory action. Experimental approach Acute ear oedema was induced in mice by topical application of TPA. The in vitro assays used macrophages RAW 264.7 cells stimulated with lipopolysaccharide. Cyclooxygenase-2, inducible nitric oxide synthase, protein kinase Calpha, extracellular signal-regulated protein kinase (ERK), phosphorylated ERK (pERK), c-Jun N-terminal kinase (JNK), pJNK, p38, p-p38, p65, p-p65, inhibitor protein of nuclear factor-kappaB (NF-kappaB) …

PharmacologyMAPK/ERK pathwayIκBαKinasep38 mitogen-activated protein kinasesMitogen-activated protein kinasebiology.proteinElectrophoretic mobility shift assayBiologyNFKB1Protein kinase AMolecular biologyBritish Journal of Pharmacology
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Cucurbitacins as inducers of cell death and a rich source of potential anticancer compounds.

2011

Triterpenes have been reported to induce cell death. One relevant group of this family of compounds is cucurbitacins, which have been studied as inducers of apoptosis in various cancer cell lines. The most significant mechanisms with regard to the apoptotic effects of cucurbitacins are their ability to modify transcriptional activities via nuclear factors or genes and their capability to activate or inhibit pro- or anti-apoptotic proteins. Still, while the majority of studies on these compounds have dealt with their apoptotic effects on cancer cell lines, several research groups have also explored their anti-inflammatory activities. In general, cucurbitacins are considered to be selective i…

PharmacologyMAPK/ERK pathwayProgrammed cell deathCell CycleApoptosisCucurbitacinsCell cycleBiologyAntineoplastic Agents PhytogenicstatCell biologyCucurbitacinsApoptosisDrug Discoverybiology.proteinAnimalsHumansCyclin D3STAT3Signal TransductionCurrent pharmaceutical design
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The immunosuppressive activity of artemisinin‐type drugs towards inflammatory and autoimmune diseases

2021

The sesquiterpene lactone artemisinin from Artemisia annua L. is well established for malaria therapy, but its bioactivity spectrum is much broader. In this review, we give a comprehensive and timely overview of the literature regarding the immunosuppressive activity of artemisinin-type compounds toward inflammatory and autoimmune diseases. Numerous receptor-coupled signaling pathways are inhibited by artemisinins, including the receptors for interleukin-1 (IL-1), tumor necrosis factor-α (TNF-α), β3-integrin, or RANKL, toll-like receptors and growth factor receptors. Among the receptor-coupled signal transducers are extracellular signal-regulated protein kinase (ERK), c-Jun N-terminal kinas…

PharmacologyMAPK/ERK pathwaybiologybusiness.industryNF-kappa BArtemisinins570 Life sciencesAutoimmune DiseasesAP-1 transcription factorGrowth factor receptorRANKLDrug DiscoveryCancer researchbiology.proteinHumansMolecular MedicineMedicineSignal transductionbusinessProtein kinase AProtein kinase BImmunosuppressive AgentsPI3K/AKT/mTOR pathway570 BiowissenschaftenSignal TransductionMedicinal Research Reviews
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Symmetry Breaking and Establishment of Dorsal/Ventral Polarity in the Early Sea Urchin Embryo

2015

The mechanisms imposing the Dorsal/Ventral (DV) polarity of the early sea urchin embryo consist of a combination of inherited maternal information and inductive interactions among blastomeres. Old and recent studies suggest that a key molecular landmark of DV polarization is the expression of nodal on the future ventral side, in apparent contrast with other metazoan embryos, where nodal is expressed dorsally. A subtle maternally-inherited redox anisotropy, plus some maternal factors such as SoxB1, Univin, and p38-MAPK have been identified as inputs driving the spatially asymmetric transcription of nodal. However, all the mentioned factors are broadly distributed in the embryo as early as no…

Physics and Astronomy (miscellaneous)General MathematicsRepressorNodalSettore BIO/11 - Biologia MolecolareBiologyp38 MAPKsymmetry breakingWntTranscription (biology)Computer Science (miscellaneous)dorsal/ventral axiGenePsychological repressionsea urchin embryodorsal/ventral axishypoxialcsh:Mathematicsdorsal/ventral axis; redox gradient; hypoxia; symmetry breaking; organizing centre; Nodal; Hbox12 transcription repressor; p38 MAPK; Wnt; sea urchin embryoWnt signaling pathwayEmbryoBlastomerelcsh:QA1-939Cell biologyorganizing centreChemistry (miscellaneous)Hbox12 transcription repressorredox gradientNODAL
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Calcitonin gene-related peptide partly protects cultured smooth muscle cells from apoptosis induced by an oxidative stress via activation of ERK1/2 M…

2003

Abstract Oxidative stress induced by a glucose/glucose oxidase (G/GO) generator system dose-dependently decreased the viability of cultured vascular smooth muscle cells (VSMC) as estimated by MTT assay. Cell death was induced in 40% of cells exposed to 0.2 IU/ml of the free radical generating mixture. Annexin-V labeling, Hoechst staining together with DNA laddering demonstrated that apoptosis was responsible for this cell loss. Pretreatment of the cells with 10−8 M calcitonin gene-related peptide (CGRP) significantly attenuated the damaging effect of the oxidative stress. Indeed, cell viability was estimated to be 80% in CGRP-treated group, instead of 60% in absence of CGRP treatment. This …

Programmed cell deathVascular smooth musclep38 mitogen-activated protein kinasesCalcitonin Gene-Related PeptideMyocytes Smooth MuscleApoptosisBiologyDNA ladderingCalcitonin gene-related peptidemedicine.disease_causeProtective AgentsMuscle Smooth VascularmedicineAnimalsHumansCGRPViability assayRats WistarMolecular BiologyCells CulturedMitogen-Activated Protein Kinase 3integumentary systemSAPKCell BiologyHydrogen PeroxideMAPKMolecular biologyRatsUp-RegulationNeuropeptideOxidative StressMitogen-activated protein kinaseVascular smooth muscle cellbiology.proteinMitogen-Activated Protein KinasesOxidative stressReceptors Calcitonin Gene-Related PeptideSignal TransductionBiochimica et biophysica acta
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ErbB-3 activation by NRG-1β sustains growth and promotes vemurafenib resistance in BRAF-V600E colon cancer stem cells (CSCs)

2015

Approximately 5-10% of metastatic colorectal cancers harbor a BRAF-V600E mutation, which is correlated with resistance to EGFR-targeted therapies and worse clinical outcome. Vice versa, targeted inhibition of BRAF-V600E with the selective inhibitor PLX 4032 (Vemurafenib) is severely limited due to feedback re-activation of EGFR in these tumors. Mounting evidence indicates that upregulation of the ErbB-3 signaling axis may occur in response to several targeted therapeutics, including Vemurafenib, and NRG-1β-dependent re-activation of the PI3K/AKT survival pathway has been associated with therapy resistance. Here we show that colon CSCs express, next to EGFR and ErbB-2, also significant amoun…

Proto-Oncogene Proteins B-rafMAPK/ERK pathwayIndolesReceptor ErbB-3Colorectal cancerNeuregulin-1colon cancer stem cellsMice NudeAntineoplastic AgentsMiceErbBErbB-3medicineAnimalsHumansNeuregulin 1VemurafenibClonogenic assayskin and connective tissue diseasesProtein kinase BneoplasmsPI3K/AKT/mTOR pathwayCell ProliferationOligonucleotide Array Sequence AnalysisNRG-1βSulfonamidesbiologyReverse Transcriptase Polymerase Chain Reactionbusiness.industryFlow Cytometrymedicine.diseaseImmunohistochemistryXenograft Model Antitumor AssaysVemurafenibOncologyDrug Resistance NeoplasmColonic NeoplasmsImmunologyNeoplastic Stem CellsCancer researchbiology.proteinbusinessPriority Research Papermedicine.drug
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B-Raf Acts via the ROCKII/LIMK/Cofilin Pathway To Maintain Actin Stress Fibers in Fibroblasts

2004

Members of the Raf family of serine/threonine protein kinases have been well studied in a variety of organisms ranging from Drosophila to humans. Three raf homologues (raf-1, B-raf, and A-raf) exist in mammals, while a single prototypic homologue exists in lower organisms. A wealth of genetic and biochemical data have indicated that Raf family members are signaling kinases that are integral components of the conserved Ras/Raf/MEK/ERK signaling cascade. Following activation by Ras-dependent mechanisms, Raf protein kinases act as mitogen-activated protein (MAP) kinase kinase kinases, which phosphorylate and activate the type 1/2 MAP kinase kinases, also known as MEK1/2. These dual-specificity…

Proto-Oncogene Proteins B-rafMAPK/ERK pathwaymacromolecular substancesProtein Serine-Threonine KinasesTransfectionCell LineProto-Oncogene Proteins B-rafLim kinaseMiceCell MovementStress FibersAnimalsHumansPhosphorylationKinase activityCell Growth and DevelopmentMolecular BiologyRho-associated protein kinaseCytoskeletonrho-Associated KinasesbiologyKinaseMicrofilament ProteinsIntracellular Signaling Peptides and ProteinsLim KinasesCell BiologyFibroblastsMolecular biologyActinsCell biologyProto-Oncogene Proteins c-rafActin Depolymerizing FactorsMitogen-activated protein kinasebiology.proteinProto-Oncogene Proteins c-rafMitogen-Activated Protein KinasesProtein KinasesSignal TransductionMolecular and Cellular Biology
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