Search results for "PROTEIN KINASE"

showing 10 items of 1188 documents

Deregulation of the EGFR/PI3K/PTEN/Akt/mTORC1 pathway in breast cancer: possibilities for therapeutic intervention

2014

// Nicole M. Davis 1 , Melissa Sokolosky 1 , Kristin Stadelman 1 , Stephen L. Abrams 1 , Massimo Libra 2 , Saverio Candido 2 , Ferdinando Nicoletti 2 , Jerry Polesel 3 , Roberta Maestro 4 , Antonino D’Assoro 5 , Lyudmyla Drobot 6 , Dariusz Rakus 7 , Agnieszka Gizak 7 , Piotr Laidler 8 , Joanna Dulinska-Litewka 8 , Joerg Basecke 9 , Sanja Mijatovic 10 , Danijela Maksimovic-Ivanic 10 , Giuseppe Montalto 11,12 , Melchiorre Cervello 12 , Timothy L. Fitzgerald 13 , Zoya N. Demidenko 14 , Alberto M. Martelli 15 , Lucio Cocco 15 , Linda S. Steelman 1 and James A. McCubrey 1 1 Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University Greenville, NC 27858 USA 2 …

Oncologymedicine.medical_specialtytherapy resistanceClass I Phosphatidylinositol 3-Kinasesmedicine.medical_treatmentBreast NeoplasmsReviewBiologyMechanistic Target of Rapamycin Complex 1PI3KMetastasisTargeted therapyPhosphatidylinositol 3-KinasesBreast cancerTARGETED THERAPYInternal medicinemedicinePTENHumansTargeted Therapy Therapy Resistance Mutations PI3K mTOR rapamycinskin and connective tissue diseasesProtein kinase BneoplasmsPI3K/AKT/mTOR pathwayRoswell Park Cancer InstituterapamycinTOR Serine-Threonine KinasesMTORPTEN PhosphohydrolaseCancerTargeted TherapyTherapy Resistancemedicine.diseaseTargeted Therapy; Therapy Resistance; Mutations; PI3K; mTOR; rapamycin3. Good healthErbB ReceptorsGene Expression Regulation NeoplasticOncologyMultiprotein ComplexesCancer researchbiology.proteinFemaleReceptor Epidermal Growth FactormutationRAPAMYCINProto-Oncogene Proteins c-aktMutationsSignal Transduction
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Regulation of tartrate metabolism by TtdR and relation to the DcuS–DcuR-regulated C4-dicarboxylate metabolism of Escherichia coli

2009

Escherichia coli catabolizes l-tartrate under anaerobic conditions to oxaloacetate by the use of l-tartrate/succinate antiporter TtdT and l-tartrate dehydratase TtdAB. Subsequently, l-malate is channelled into fumarate respiration and degraded to succinate by the use of fumarase FumB and fumarate reductase FrdABCD. The genes encoding the latter pathway (dcuB, fumB and frdABCD) are transcriptionally activated by the DcuS–DcuR two-component system. Expression of the l-tartrate-specific ttdABT operon encoding TtdAB and TtdT was stimulated by the LysR-type gene regulator TtdR in the presence of l- and meso-tartrate, and repressed by O2 and nitrate. Anaerobic expression required a functional fn…

OperonBiologymedicine.disease_causeMicrobiologyAntiportersSubstrate SpecificityOperonEscherichia colimedicinePromoter Regions GeneticTartratesEscherichia coliPsychological repressionHydro-LyasesRegulator geneNitratesEscherichia coli ProteinsPromoterGene Expression Regulation BacterialFumarate reductaseDNA-Binding ProteinsOxygenGlucoseBiochemistryDehydrataseFumaraseProtein KinasesTranscription FactorsMicrobiology
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Nonsense-mediated mRNA decay controls the changes in yeast ribosomal protein pre-mRNAs levels upon osmotic stress.

2013

The expression of ribosomal protein (RP) genes requires a substantial part of cellular transcription, processing and translation resources. Thus, the RP expression must be tightly regulated in response to conditions that compromise cell survival. In Saccharomyces cerevisiae cells, regulation of the RP gene expression at the transcriptional, mature mRNA stability and translational levels during the response to osmotic stress has been reported. Reprogramming global protein synthesis upon osmotic shock includes the movement of ribosomes from RP transcripts to stress-induced mRNAs. Using tiling arrays, we show that osmotic stress yields a drop in the levels of RP pre-mRNAs in S. cerevisiae cell…

OsmosisTranscription GeneticNonsense-mediated decaylcsh:MedicineYeast and Fungal ModelsMolecular cell biologyGene Expression Regulation FungalGene expressionProtein biosynthesisRNA PrecursorsRNA Processing Post-Transcriptionallcsh:ScienceOligonucleotide Array Sequence AnalysisCellular Stress ResponsesRegulation of gene expressionMultidisciplinarybiologyProtein translationExonsGenomicsCell biologyFunctional GenomicsMitogen-activated protein kinaseResearch ArticleRibosomal ProteinsSaccharomyces cerevisiae ProteinsOsmotic shockEstrès oxidatiuSaccharomyces cerevisiaeGenes FungalDNA transcriptionSaccharomyces cerevisiaeModels BiologicalGenètica molecularSaccharomycesModel OrganismsRibosomal proteinStress PhysiologicalBiologylcsh:RRNA stabilitybiology.organism_classificationMolecular biologyIntronsNonsense Mediated mRNA DecayKineticsRNA processingbiology.proteinlcsh:QGene expressionGenome Expression AnalysisProteïnesPloS one
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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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The cytoplasmic PASC domain of the sensor kinase DcuS of Escherichia coli : role in signal transduction, dimer formation, and DctA interaction

2013

The cytoplasmic PAS(C) domain of the fumarate responsive sensor kinase DcuS of Escherichia coli links the transmembrane to the kinase domain. PAS(C) is also required for interaction with the transporter DctA serving as a cosensor of DcuS. Earlier studies suggested that PAS(C) functions as a hinge and transmits the signal to the kinase. Reorganizing the PAS(C) dimer interaction and, independently, removal of DctA, converts DcuS to the constitutive ON state (active without fumarate stimulation). ON mutants were categorized with respect to these two biophysical interactions and the functional state of DcuS: type I-ON mutations grossly reorganize the homodimer, and decrease interaction with Dct…

PAS domainDicarboxylic Acid TransportersModels MolecularfumarateProtein ConformationEscherichia coli ProteinsDNA Mutational AnalysisDctAModels Biological570 Life sciencessignal transduction.Escherichia coliProtein Interaction Domains and MotifsProtein MultimerizationDcuS sensor kinaseProtein KinasesOriginal ResearchSignal Transduction570 Biowissenschaften
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MCC1019, a selective inhibitor of the Polo-box domain of Polo-like kinase 1 as novel, potent anticancer candidate

2019

Polo-like kinase (PLK1) has been identified as a potential target for cancer treatment. Although a number of small molecules have been investigated as PLK1 inhibitors, many of which showed limited selectivity. PLK1 harbors a regulatory domain, the Polo box domain (PBD), which has a key regulatory function for kinase activity and substrate recognition. We report on 3-bromomethyl-benzofuran-2-carboxylic acid ethyl ester (designated: MCC1019) as selective PLK1 inhibitor targeting PLK1 PBD. Cytotoxicity and fluorescence polarization-based screening were applied to a library of 1162 drug-like compounds to identify potential inhibitors of PLK1 PBD. The activity of compound MC1019 against the PLK1…

PBD Polo box domainMTD maximal tolerance doseCDC25 cell division cycle 25HIF-1α hypoxia-inducible factor 1 αMST microscale thermophoresisIC50 50% inhibition concentrationMFP M phase promoting factorPARP-1 poly(ADP-ribose) polymerase-10302 clinical medicineFOXO forkhead box ONec-1 necrostatin 1CDC2 cell division cycle protein 2 homologGeneral Pharmacology Toxicology and PharmaceuticsMitotic catastropheCDK cyclin-dependent kinase0303 health sciencesChemistryPolo-like kinaseMono-targeted therapyCell cycleBUBR1 budding uninhibited by benzimidazole-related 1Polo box domain030220 oncology & carcinogenesisPLK1 Polo-like kinaseNecroptosisSpindle damagePLK1IHC immunohistochemistryOriginal articleNecroptosisCell cyclePLK1APC/C anaphase-promoting complex/cyclosomePLK3ABC avidin-biotin complexPI propidium iodide03 medical and health sciencesFBS fetal bovine serumPDB Protein Data BankKd the dissociation constantKinase activity030304 developmental biologyAkt/PKB signaling pathwayCell growthlcsh:RM1-950LC3 light chain 3lcsh:Therapeutics. PharmacologyCancer researchDAPKs death-associated protein kinase3-MA 3-methyladenineDAPI 4′6-diamidino-2-phenylindoleSAC spindle assembly checkpointActa Pharmaceutica Sinica B
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Between Scylla and Charibdis: eIF2α kinases as targets for cancer chemotherapy

2011

[EN] The eIF2 alpha kinases integrate translation initiation rates with nutrient availability, thus allowing cells to adapt to nutrient scarcity. Recent evidence has uncovered new functions of these kinases in tumour cell biology, ranging from regulation of cell cycle progression, maintenance of genome stability, control of apoptosis, and cell survival under nutrient stress and hypoxia. Accordingly, active eIF2 alpha kinases modulate the antineoplasic activity of several antitumour drugs, either by exacerbating their cytotoxic effect or by promoting chemoresistance. Understanding of eIF2 alpha kinases molecular roles may provide mechanistic insights into how tumour cells sense and adapt to …

PERKBioquímicaTranslationBiologiaCancer ResearchCancer chemotherapyEukaryotic Initiation Factor-2Antineoplastic AgentsBiologyBioinformaticsNeoplasmsBIOQUIMICA Y BIOLOGIA MOLECULARHumansCytotoxic T cellCell survivalGenome stabilityKinaseNutrient stressPKRGeneral MedicineProtein kinase ROncologyApoptosiseIF2 alpha phosphorylationCancer researchGCN2Clinical and Translational Oncology
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The dark side of the moon: The PI3K/PTEN/AKT pathway in colorectal carcinoma

2009

Wild-type KRAS status is required but not sufficient to confer sensitivity to anti-epidermal growth factor receptor (EGFR) monoclonal antibodies (mAbs) in colorectal cancer patients. As a consequence, one of the major challenges is to identify, in non-mutant KRAS patients, other markers that can predict lack of response to this therapy. Small series have investigated the clinical effect of PIK3CA mutations on resistance to anti-EGFR mAbs and discrepant results have been observed. Furthermore, PTEN loss in metastases may be predictive of resistance to anti-EGFR mAbs, even if PTEN determination is far from an immediate clinical application. The introduction of modulators of the PI3K/AKT/mTOR …

PTENCancer ResearchClass I Phosphatidylinositol 3-KinasesPrognosiSettore MED/06 - Oncologia MedicaColorectal cancerCetuximabColorectal NeoplasmPhosphoinositide 3-kinasemedicine.disease_causePhosphatidylinositol 3-KinasesAntineoplastic Combined Chemotherapy ProtocolsBiomarkers TumormedicineHumansPTENPanitumumabEpidermal growth factor receptorProtein kinase BPI3K/AKT/mTOR pathwayClass I Phosphatidylinositol 3-KinaseAntineoplastic Combined Chemotherapy ProtocolbiologyCetuximabAKTMTORPanitumumabPTEN PhosphohydrolaseAntibodies MonoclonalGeneral MedicinePrognosismedicine.diseaseErbB ReceptorsOncologyMutationbiology.proteinCancer researchReceptor Epidermal Growth FactorKRASPhosphatidylinositol 3-KinaseColorectal NeoplasmsProto-Oncogene Proteins c-aktHumanSignal Transductionmedicine.drug
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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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Modulation of voltage-gated K(+) channels Kv11 and Kv1 4 by forskolin.

2002

Forskolin (FSK) affects voltage-gated K + (Kv) currents in different cell types, but it is not known which of the various subunits form FSK-sensitive Kv channels. We compared the effect of the compound at Kv1.1 and Kv1.4 channels ectopically expressed in HEK 293 cells. Low FSK concentrations induced a phosphorylation-dependent potentiation of Kv1.1 currents. At higher concentrations, this effect was superimposed by a fast, cAMP-independent channel block. Kv1.4 currents were inhibited with lower potency by FSK but were not modified by phosphorylation. The variable effect of the compound might help to distinguish between Kv subunits expressed by native cells.  2002 Elsevier Science Ltd. All …

Patch-Clamp TechniquesPotassium ChannelsStereochemistryBiologyMembrane PotentialsCellular and Molecular Neurosciencechemistry.chemical_compoundmedicineCyclic AMPHumansPatch clampPhosphorylationProtein kinase ACells CulturedPharmacologyFrequency-shift keyingForskolinDose-Response Relationship DrugHEK 293 cellsColforsinCyclic AMP-Dependent Protein KinasesElectrophysiologyElectrophysiologyKineticsMechanism of actionchemistryPotassium Channels Voltage-GatedBiophysicsPhosphorylationKv1.4 Potassium Channelmedicine.symptomKv1.1 Potassium ChannelIon Channel GatingAlgorithmsNeuropharmacology
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