Search results for "PROTEIN KINASE"

showing 10 items of 1188 documents

Dynamics of Ca2+ and guanosine 5'-[gamma-thio]triphosphate action on insulin secretion from alpha-toxin-permeabilized HIT-T15 cells.

1994

The time course of Ca2+ and GTP-analogue effects on insulin secretion was investigated in HIT-T15 cells permeabilized with Staphylococcus alpha-toxin. These cells responded to Ca2+ in the range 0.1-10 microM and could be used in a dynamic perifusion system because of the minimal run-down of the secretory response. High Ca2+ (10 microM) elicited a monophasic ATP-dependent stimulation of insulin secretion that reached a peak within 5 min (approximately 20-fold increase) and rapidly decreased during the subsequent 15 min to a plateau remaining above basal rates (0.1 microM Ca2+). The decrease in Ca(2+)-induced insulin secretion with time could not be attributed to decreased capacity to respond…

Cell Membrane PermeabilityGTP'medicine.medical_treatmentStimulationCalcium-Calmodulin-Dependent Protein Kinases - antagonists & inhibitorsBiochemistryPiperazinesAdenosine TriphosphateDesensitization (telecommunications)1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineInsulin SecretionGuanosine 5'-O-(3-Thiotriphosphate) - pharmacologyStaphylococcus aureus alpha-toxinInsulinGuanosine Triphosphate - pharmacologyGuanylyl ImidodiphosphateKinasePiperazines - pharmacologyInsulin secretionAdenosine Triphosphate - pharmacologyPermeabilized cellsGuanosine TriphosphateResearch Articlemedicine.medical_specialtyStaphylococcus aureuschemistry.chemical_elementBiologyCalciumGuanylyl Imidodiphosphate - pharmacologyExocytosisCell LineInsulin - secretionInternal medicinemedicine1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivativesSecretionMolecular BiologyInsulinCell BiologyIsoquinolinesATPKineticsEndocrinologyCalcium - pharmacologychemistryIsoquinolines - pharmacologyGuanosine 5'-O-(3-Thiotriphosphate)Type C PhospholipasesCalcium-Calmodulin-Dependent Protein KinasesCalciumType C Phospholipases - pharmacologyGTP
researchProduct

Mitogenic effects of phospholipase D and phosphatidic acid in transiently permeabilized astrocytes: effects of ethanol.

2003

Investigations of lipid-mediated signalling pathways are often limited by a lack of methods for the intracellular delivery of lipid messengers. We established a procedure for the transient permeabilization of astrocytes by an oxygen-insensitive mutant of streptolysin-O (SLO) to investigate the participation of the phospholipase D (PLD) signalling pathway in astroglial cell proliferation. Exogenous PLD, when incubated in the presence of SLO, caused an increase in DNA synthesis (measured by thymidine incorporation) which was completely suppressed by ethanol (0.3%, v/v). In parallel experiments, phosphatidic acid also induced a dose-dependent mitogenic response which, however, was not affected…

Cell Membrane PermeabilityIndolesmedicine.drug_classPhosphatidic AcidsBiologyBiochemistryDiglyceridesCellular and Molecular Neurosciencechemistry.chemical_compoundBacterial ProteinsmedicinePhospholipase DAnimalsEnzyme InhibitorsProtein kinase ACells CulturedDiacylglycerol kinaseDNA synthesisDose-Response Relationship DrugEthanolPhospholipase DPhosphatidic acidDNAProtein kinase inhibitorRatschemistryBiochemistryAstrocytesStreptolysinslipids (amino acids peptides and proteins)Signal transductionMitogensIntracellularCell DivisionSignal TransductionJournal of neurochemistry
researchProduct

Quinoline-Based Molecules Targeting c-Met, EGF, and VEGF Receptors and the Proteins Involved in Related Carcinogenic Pathways

2020

The quinoline ring system has long been known as a versatile nucleus in the design and synthesis of biologically active compounds. Currently, more than one hundred quinoline compounds have been approved in therapy as antimicrobial, local anaesthetic, antipsychotic, and anticancer drugs. In drug discovery, indeed, over the last few years, an increase in the publication of papers and patents about quinoline derivatives possessing antiproliferative properties has been observed. This trend can be justified by the versatility and accessibility of the quinoline scaffold, from which new derivatives can be easily designed and synthesized. Within the numerous quinoline small molecules developed as a…

Cell SurvivalAngiogenesisPharmaceutical ScienceAntineoplastic AgentsReviewMolecular Dynamics SimulationAnalytical Chemistrylcsh:QD241-441Structure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicinelcsh:Organic chemistryEpidermal growth factorquinolineDrug DiscoverySAR studieHumansPhysical and Theoretical Chemistrycarcinogenic pathwaysProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesantiproliferative compoundChemistryDrug discoveryOrganic ChemistryQuinolineBiological activityProto-Oncogene Proteins c-metantiproliferative compoundstargeted therapySettore CHIM/08 - Chimica FarmaceuticaSmall moleculeErbB Receptorscarcinogenic pathwayReceptors Vascular Endothelial Growth FactorSAR studiesChemistry (miscellaneous)030220 oncology & carcinogenesisQuinolinesCancer researchMolecular Medicinekinases modulatorkinases modulatorsbiological dataSignal TransductionMolecules
researchProduct

Recent advances in the development of cyclin-dependent kinase 7 inhibitors.

2019

Abstract Cyclin dependent kinase 7 (CDK7) plays a double role as it activates several other cyclin dependent kinases and participates to the initiation of transcription. This kinase is overexpressed in various types of tumors. Relatively few selective CDK7 inhibitors have been up to now disclosed. Most of these inhibitors belong to two chemical families: pyrazolopyrimidines and pyrazolotriazines on one side and pyrimidines on another side. They also differ by their molecular mechanism of action. Some are acting as competitive inhibitors and some others are covalent inhibitors. With these tools, the understanding of the potential therapeutic interest of CDK7 inhibitors in cancer is rapidly g…

Cell SurvivalAntineoplastic Agents01 natural sciences03 medical and health sciencesDrug DevelopmentCyclin-dependent kinaseTranscription (biology)Cell Line TumorDrug DiscoverymedicineAnimalsHumansIC50Protein Kinase Inhibitors030304 developmental biologyPharmacology0303 health sciencesbiology010405 organic chemistryChemistryKinaseTriazinesOrganic ChemistryGeneral Medicinemedicine.diseaseCyclin-Dependent Kinases0104 chemical sciencesLeukemiaPyrimidinesbiology.proteinCancer researchMolecular mechanismCyclin-dependent kinase 7Cyclin-Dependent Kinase-Activating KinaseEuropean journal of medicinal chemistry
researchProduct

Galantamine modulates nicotinic receptor and blocks Aβ-enhanced glutamate toxicity

2004

Galantamine is a plant alkaloid that is used in the treatment of Alzheimer's disease. We have studied the effects of galantamine on beta-amyloid-enhanced glutamate toxicity using primary rat cultured cortical neurons. Nicotine and galantamine alone, and in combination, protected neurons against this neurotoxicity. The protection was not blocked by alpha4beta2 nicotinic acetylcholine receptor (nAChR) antagonists, but was partially blocked by alpha7 nAChR antagonists. Galantamine induced phosphorylation of Akt, an effector of phosphatidylinositol 3-kinase (PI3K), while PI3K inhibitors blocked the protective effect and Akt phosphorylation. The antibody FK1, which selectively blocks the alloste…

Cell SurvivalBiophysicsGlutamic AcidReceptors NicotinicPharmacologycomplex mixturesBiochemistryNeuroprotectionmedicineGalantamineAnimalsDrug InteractionsMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCerebral CortexNeuronsAmyloid beta-PeptidesDose-Response Relationship DrugGalantamineChemistryGlutamate receptorNeurotoxicityCell Biologymedicine.diseaseRatsNeuroprotective AgentsNicotinic agonistnervous systemPhosphorylationmedicine.drugBiochemical and Biophysical Research Communications
researchProduct

Computational Evaluation and In Vitro Validation of New Epidermal Growth Factor Receptor Inhibitors

2020

Background:The Epidermal Growth Factor Receptor (EGFR) is a transmembrane protein that acts as a receptor of extracellular protein ligands of the epidermal growth factor (EGF/ErbB) family. It has been shown that EGFR is overexpressed by many tumours and correlates with poor prognosis. Therefore, EGFR can be considered as a very interesting therapeutic target for the treatment of a large variety of cancers such as lung, ovarian, endometrial, gastric, bladder and breast cancers, cervical adenocarcinoma, malignant melanoma and glioblastoma.Methods:We have followed a structure-based virtual screening (SBVS) procedure with a library composed of several commercial collections of chemicals (615,46…

Cell SurvivalDrug Evaluation PreclinicalAntineoplastic Agents01 natural sciencesReceptor tyrosine kinaseStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicineErbBEpidermal growth factorCell Line TumorDrug DiscoverymedicineHumansEpidermal growth factor receptorPropidium iodideProtein Kinase InhibitorsCell ProliferationEGFR inhibitorsDose-Response Relationship DrugMolecular StructurebiologyCell growthChemistryGeneral Medicine0104 chemical sciencesErbB ReceptorsMolecular Docking Simulation010404 medicinal & biomolecular chemistry030220 oncology & carcinogenesisbiology.proteinCancer researchErlotinibDrug Screening Assays Antitumormedicine.drugCurrent Topics in Medicinal Chemistry
researchProduct

Inhibitors of Rho-kinase modulate amyloid-β (Aβ) secretion but lack selectivity for Aβ42

2005

Certain non-steroidal anti-inflammatory drugs (NSAIDs) preferentially inhibit production of the amyloidogenic Abeta42 peptide, presumably by direct modulation of gamma-secretase activity. A recent report indicated that NSAIDs could reduce Abeta42 by inhibition of the small GTPase Rho, and a single inhibitor of Rho kinase (ROCK) mimicked the effects of Abeta42-lowering NSAIDs. To investigate whether Abeta42 reduction is a common property of ROCK inhibitors, we tested commercially available compounds in cell lines that were previously used to demonstrate the Abeta42-lowering activity of NSAIDs. Surprisingly, we found that two ROCK inhibitors reduced total Abeta secretion in a dose-dependent m…

Cell SurvivalMutantPeptideCHO CellsProtein Serine-Threonine KinasesPharmacologyBiochemistryAmyloid beta-Protein PrecursorCellular and Molecular NeuroscienceCricetulusCricetinaeEndopeptidasesmental disordersAmyloid precursor proteinAnimalsAspartic Acid EndopeptidasesSecretionSmall GTPaseEnzyme InhibitorsRho-associated protein kinasechemistry.chemical_classificationrho-Associated KinasesAmyloid beta-PeptidesbiologyAnti-Inflammatory Agents Non-SteroidalIntracellular Signaling Peptides and ProteinsIn vitro toxicologyProtein-Tyrosine KinasesPeptide Fragmentsnervous system diseasesBiochemistrychemistrybiology.proteinAmyloid Precursor Protein SecretasesSelectivityProtein Processing Post-TranslationalJournal of Neurochemistry
researchProduct

The yeast mitogen-activated protein kinase Slt2 is involved in the cellular response to genotoxic stress

2012

Abstract Background The maintenance of genomic integrity is essential for cell viability. Complex signalling pathways (DNA integrity checkpoints) mediate the response to genotoxic stresses. Identifying new functions involved in the cellular response to DNA-damage is crucial. The Saccharomyces cerevisiae SLT2 gene encodes a member of the mitogen-activated protein kinase (MAPK) cascade whose main function is the maintenance of the cell wall integrity. However, different observations suggest that SLT2 may also have a role related to DNA metabolism. Results This work consisted in a comprehensive study to connect the Slt2 protein to genome integrity maintenance in response to genotoxic stresses.…

Cell cycle checkpoint<it>Saccharomyces cerevisiae</it>DNA damageSaccharomyces cerevisiaeGenotoxic StressSaccharomyces cerevisiaeBiologyBiochemistrylcsh:RC254-282checkpointlcsh:QH573-671Protein kinase AMolecular BiologyGeneticsDNA integrity checkpointKinaselcsh:CytologyResearchCell BiologyCell cyclebiology.organism_classificationlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensgenotoxic stressCell biologyDNA damageSlt2
researchProduct

Synthesis and antiproliferative activity of substituted 3[2-(1H-indol-3-yl)-1,3-thiazol-4-yl]-1H-pyrrolo[3,2-b]pyridines, marine alkaloid nortopsenti…

2014

A large number of indolyl-4-azaindolyl thiazoles, nortopsentin analogues, were conveniently synthesized. The antiproliferative activity of the new derivatives was examined against four human tumor cell lines with different histologic origin. Seven derivatives consistently reduced the growth of the experimental models independently of TP53 gene status and exhibited the highest activity against the malignant peritoneal mesothelioma (STO) cell line. The most active compound of this series acts as a CDK1 inhibitor, and was found to cause cell cycle arrest at G 2 /M phase, to induce apoptosis by preventing the phosphorylation of survivin in Thr 34 and to increase the cytotoxic activity of paclit…

Cell cycle checkpointCDK1 InhibitorsAntiproliferative Activity CDK1 Inhibitors Diffuse Malignant Peritoneal Mesothelioma Nortopsentin Analogues SurvivinPyridinesStereochemistrySurvivinDiffuse Malignant Peritoneal MesotheliomaAntineoplastic AgentsApoptosisAntiproliferative Activity; CDK1 Inhibitors; Diffuse Malignant Peritoneal Mesothelioma; Nortopsentin Analogues; SurvivinBiochemistryCell LineAntiproliferative ActivityStructure-Activity Relationshipchemistry.chemical_compoundDrug DiscoverySurvivinHumansCytotoxic T cellProtein Kinase InhibitorsCell ProliferationPharmacologyCyclin-dependent kinase 1AlkaloidOrganic ChemistrySettore CHIM/08 - Chimica FarmaceuticaPaclitaxelchemistryCell cultureApoptosisNortopsentin AnaloguesMolecular Medicine
researchProduct

Cisplatin sensitivity is related to late DNA damage processing and checkpoint control rather than to the early DNA damage response

2008

The present study aimed at elucidating mechanisms dictating cell death triggered by cisplatin-induced DNA damage. We show that CL-V5B hamster mutant cells, a derivative of V79B, are hypersensitive to cisplatin-induced apoptotic death. CL-V5B cells are characterized by attenuated cisplatin-induced early (2-6 h) stress response, such as phosphorylation of stress-activated protein kinases (SAPK/JNK), ATM and Rad3-related (ATR) protein kinase, histone H2AX and checkpoint kinase-1 (Chk-1). Human FANCC cells also showed a reduced phosphorylation of H2AX and SAPK/JNK at early time point after cisplatin treatment. This was not the case for BRCA2-defective VC-8 hamster cells, indicating that the FA …

Cell cycle checkpointCisplatin-DNA adducts ; DNA repair ; Interstrand cross links ; DNA damage response ; Cell cycle checkpoint ; Cell deathDNA damageDNA repairHealth Toxicology and MutagenesisApoptosisCell LineHistonesDNA AdductsCricetinaeGeneticsmedicineAnimalsHumansCHEK1PhosphorylationMolecular BiologyChromosome AberrationsCisplatinbiologyJNK Mitogen-Activated Protein KinasesDNA replicationG2-M DNA damage checkpointMolecular biologyCell biologyHistonebiology.proteinCisplatinDNA DamageMutagensmedicine.drug
researchProduct