Search results for "PROTEIN KINASE"

showing 10 items of 1188 documents

Estrogen Receptor Signaling and the PI3K/Akt Pathway Are Involved in Betulinic Acid-Induced eNOS Activation

2016

Betulinic acid (BA) is a naturally occurring pentacyclic triterpenoid with anti-inflammatory, antiviral and anti-cancer properties. Beneficial cardiovascular effects such as increased nitric oxide (NO) production through enhancement of endothelial NO synthase (eNOS) activity and upregulation of eNOS expression have been demonstrated for this compound. In the present study, immortalized human EA.hy 926 endothelial cells were incubated for up to 1 h with 1–100 µM BA and with the phosphatidylinositol-3-kinase (PI3K) inhibitors LY294002 and wortmannin, or the estrogen receptor (ER) antagonist ICI 182,780. Phosphorylation status of eNOS and total eNOS protein were analyzed by Western blotting us…

0301 basic medicinePharmaceutical ScienceEstrogen receptorPI3KAnalytical ChemistryWortmanninchemistry.chemical_compound0302 clinical medicineEnosDrug DiscoveryLY294002PhosphorylationFulvestrantLungbiologyEstradiolendothelial cellsReceptors EstrogenChemistry (miscellaneous)030220 oncology & carcinogenesisMolecular MedicinePhosphorylationSignal transductionPentacyclic TriterpenesWortmanninSignal Transductionestrogen receptormedicine.medical_specialtyNitric Oxide Synthase Type IIIMorpholinesArticleCell Linelcsh:QD241-44103 medical and health sciencesbetulinic acidlcsh:Organic chemistryInternal medicinemedicineAnimalsHumansPhysical and Theoretical ChemistryProtein kinase BPI3K/AKT/mTOR pathwayendothelial nitric oxide synthaseAktOrganic ChemistryFibroblastsbiology.organism_classificationMolecular biologyTriterpenesbetulinic acid; endothelial nitric oxide synthase; endothelial cells; estrogen receptor; PI3K; AktRatsAndrostadienes030104 developmental biologyEndocrinologychemistryGene Expression RegulationChromonesPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktMolecules
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Target Identification of Active Constituents of Shen Qi Wan to Treat Kidney Yang Deficiency Using Computational Target Fishing and Network Pharmacolo…

2019

Background: Kidney yang deficiency syndrome (KYDS) is one of the most common syndromes treated with traditional Chinese medicine (TCM) among elderly patients. Shen Qi Wan (SQW) has been effectively used in treating various diseases associated with KYDS for hundreds of years. However, due to the complex composition of SQW, the mechanism of action remains unknown. Purpose: To identify the mechanism of the SQW in the treatment of KYDS and determine the molecular targets of SQW. Methods: The potential targets of active ingredients in SQW were predicted using PharmMapper. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were carried out using the …

0301 basic medicinePharmacology03 medical and health scienceschemistry.chemical_compoundtraditional Chinese medicinetranscriptomics0302 clinical medicinemedicinenetwork pharmacologyPharmacology (medical)HRASKEGGBlood urea nitrogenMAPK14Original ResearchPharmacologyCreatinineKidneylcsh:RM1-950phytotherapy030104 developmental biologymedicine.anatomical_structurelcsh:Therapeutics. PharmacologychemistryMechanism of action030220 oncology & carcinogenesisgene ontologypotential targetsmedicine.symptomProto-oncogene tyrosine-protein kinase SrcFrontiers in Pharmacology
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Curcumin at Low Doses Potentiates and at High Doses Inhibits ABT-737-Induced Platelet Apoptosis

2021

Curcumin is a natural bioactive component derived from the turmeric plant Curcuma longa, which exhibits a range of beneficial activities on human cells. Previously, an inhibitory effect of curcumin on platelets was demonstrated. However, it is unknown whether this inhibitory effect is due to platelet apoptosis or procoagulant platelet formation. In this study, curcumin did not activate caspase 3-dependent apoptosis of human platelets, but rather induced the formation of procoagulant platelets. Interestingly, curcumin at low concentration (5 µM) potentiated, and at high concentration (50 µM) inhibited ABT-737-induced platelet apoptosis, which was accompanied by inhibition of ABT-737-mediated…

0301 basic medicinePharmacologyPiperazinesNitrophenolschemistry.chemical_compound0302 clinical medicinePlateletBiology (General)SpectroscopyCaspaseSulfonamidesbiologyKinaseapoptosisGeneral MedicinethrombinDrug Resistance Multipleprocoagulant activityComputer Science ApplicationsChemistry030220 oncology & carcinogenesisplateletsmedicine.drugBlood PlateletsAdenosine monophosphateautophagyCurcuminQH301-705.5ArticleCatalysisInorganic Chemistry03 medical and health sciencesCurcumaThrombinmedicineHumansATP Binding Cassette Transporter Subfamily B Member 1Physical and Theoretical ChemistryQD1-999Molecular BiologyProtein kinase BPlant ExtractsBiphenyl CompoundsOrganic ChemistryAdenosine Monophosphate030104 developmental biologychemistryApoptosisbiology.proteinCurcuminProto-Oncogene Proteins c-aktPlatelet Aggregation InhibitorsInternational Journal of Molecular Sciences
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N-Desmethyldauricine Induces Autophagic Cell Death in Apoptosis-Defective Cells via Ca2+ Mobilization

2017

Resistance of cancer cells to chemotherapy remains a significant problem in oncology. Mechanisms regulating programmed cell death, including apoptosis, autophagy or necrosis, in the treatment of cancers have been extensively investigated over the last few decades. Autophagy is now emerging as an important pathway in regulating cell death or survival in cancer therapy. Recent studies demonstrated variety of natural small-molecules could induce autophagic cell death in apoptosis-resistant cancer cells, therefore, discovery of novel autophagic enhancers from natural products could be a promising strategy for treatment of chemotherapy-resistant cancer. By computational virtual docking analysis,…

0301 basic medicinePharmacologyProgrammed cell deathautophagyKinaseDrug discoveryAutophagylcsh:RM1-950BiologyCell biology03 medical and health sciences030104 developmental biologylcsh:Therapeutics. PharmacologyApoptosisautophagic cell deathN-desmethyldauricineSERCACancer cellCytotoxic T cellPharmacology (medical)apoptosis-resistantProtein kinase AOriginal ResearchFrontiers in Pharmacology
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Tetrandrine, an Activator of Autophagy, Induces Autophagic Cell Death via PKC-α Inhibition and mTOR-Dependent Mechanisms

2017

Emerging evidence suggests the therapeutic role of autophagic modulators in cancer therapy. This study aims to identify novel traditional Chinese medicinal herbs as potential anti-tumor agents through autophagic induction, which finally lead to autophagy mediated-cell death in apoptosis-resistant cancer cells. Using bioactivity-guided purification, we identified tetrandrine (Tet) from herbal plant, Radix stephaniae tetrandrae, as an inducer of autophagy. Across a number of cancer cell lines, we found that breast cancer cells treated with tetrandrine show an increase autophagic flux and formation of autophagosomes. In addition, tetrandrine induces cell death in a panel of apoptosis-resistant…

0301 basic medicinePharmacologyProgrammed cell deathautophagylcsh:RM1-950AutophagyCaspase 3BiologytetrandrineCaspase 7Cell biologyTetrandrine03 medical and health scienceschemistry.chemical_compoundlcsh:Therapeutics. Pharmacology030104 developmental biologychemistryCancer cellmTORPharmacology (medical)apoptosis-resistantPKC-αProtein kinase API3K/AKT/mTOR pathwayOriginal ResearchFrontiers in Pharmacology
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Activation of microglia synergistically enhances neurodegeneration caused by MPP+ in human SH-SY5Y cells

2019

While MPP+ may not directly activate microglia, the initial neuronal damage inflicted by the toxin may trigger microglia, possibly leading to synergistic pro-apoptotic interaction between neuro-inflammation and toxin-induced neurotoxicity, which may further aggravate neurodegeneration. However, what molecular targets are synergistically up or downregulated during this interaction is not well understood. Here, we addressed this by co-culturing fully differentiated human SH-SY5Y cells treated with parkinsonian toxin 1-Methyl-4-phenylpyridinium (MPP+), with endotoxin-activated microglial cell line EOC 20 to determine how this interaction affects pro-apoptotic (p38, JNK, and bax:bcl2 ratios) an…

0301 basic medicinePharmacologySH-SY5YMicrogliaChemistryp38 mitogen-activated protein kinasesNeurodegenerationNeurotoxicityInflammationmedicine.diseaseCell biology03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structureApoptosismedicineViability assaymedicine.symptom030217 neurology & neurosurgeryEuropean Journal of Pharmacology
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Chemoresistance and chemosensitization in cholangiocarcinoma

2017

One of the main difficulties in the management of patients with advanced cholangiocarcinoma (CCA) is their poor response to available chemotherapy. This is the result of powerful mechanisms of chemoresistance (MOC) of quite diverse nature that usually act synergistically. The problem is often worsened by altered MOC gene expression in response to pharmacological treatment. Since CCA includes a heterogeneous group of cancers their genetic signature coding for MOC genes is also diverse; however, several shared traits have been defined. Some of these characteristics are shared with other types of liver cancer, namely hepatocellular carcinoma and hepatoblastoma. An important goal in modern onco…

0301 basic medicinePharmacologybile ductschemotherapydrug delivery systems0302 clinical medicineChemosensitizationantineoplastic agentsmolecular biologyReceptorhumansreceptor protein-tyrosine kinasesmedia_commonapoptosisgene expression regulationbile duct neoplasmsDrug Resistance Multipletargeted therapiesGene Expression Regulation Neoplasticmultiplebiliary cancer; chemotherapy; liver cancer; multidrug resistance; targeted therapies; antineoplastic agents; apoptosis; bile duct neoplasms; bile ducts; cell survival; cholangiocarcinoma; drug delivery systems; drug resistance multiple; drug resistance; neoplasm; epithelial cells; gene expression regulation neoplastic; genetic therapy; humans; protein kinase inhibitors; receptor protein-tyrosine kinases; signal transduction; treatment outcome; molecular medicine; molecular biology030220 oncology & carcinogenesisHepatocellular carcinomabiliary cancerLiver cancercholangiocarcinomaTyrosine kinasesignal transductionDrugHepatoblastomamedia_common.quotation_subjectcell survivalPharmacological treatmentliver cancer03 medical and health sciencesmultidrug resistancemedicinemolecular medicinedrug resistancebusiness.industrymedicine.diseaseepithelial cellsneoplasticprotein kinase inhibitors030104 developmental biologyDrug Resistance NeoplasmCancer researchtreatment outcomebusinessneoplasmgenetic therapy
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Silencing of C3G increases cardiomyocyte survival inhibition and apoptosis via regulation of p-ERK1/2 and Bax.

2018

Experimental studies have shown that overexpression of Rap guanine nucleotide exchange factor 1 (C3G) plays pro-survival and anti-apoptotic roles through molecule phosphorylated extracellular signal-regulated kinase1/2 (p-ERK1/2) in cardiomyocytes. However, it is still unclear if silencing of C3G may increase cell survival inhibition and apoptosis in cardiomyocytes, and whether C3G silence induced injuries are reduced by the overexpression of C3G through regulation of p-ERK1/2 and pro-apoptotic molecule Bax. In this study, the rat-derived H9C2 cardiomyocytes were infected with C3G small hairpin RNA interference recombinant lentiviruses, which silenced the endogenous C3G expression in the ca…

0301 basic medicinePhysiologyCell SurvivalEndogenyApoptosisCell LineSmall hairpin RNA03 medical and health sciences0302 clinical medicinePhysiology (medical)ExtracellularmedicineGene silencingAnimalsMyocytes CardiacGene SilencingGuanine Nucleotide-Releasing Factor 2Cell Proliferationbcl-2-Associated X ProteinPharmacologyMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Cell growthChemistryHypoxia (medical)PhosphoproteinsCell biologyRats030104 developmental biologyApoptosis030220 oncology & carcinogenesisPhosphorylationmedicine.symptomClinical and experimental pharmacologyphysiology
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Comparative Proteomics Unveils LRRFIP1 as a New Player in the DAPK1 Interactome of Neurons Exposed to Oxygen and Glucose Deprivation

2020

Altres ajuts: The group has received funding from 'la Caixa Foundation' CI15-00009, from the European Institute of Innovation and Technology (EIT) PoC-2016-SPAIN-04, which receives support from the European Union's Horizon 2020 research and innovation program, and from the 'Fundación para la Innovación y la Prospectiva en Salud en España (FIPSE)' program 3594-18. Death-associated protein kinase 1 (DAPK1) is a pleiotropic hub of a number of networked distributed intracellular processes. Among them, DAPK1 is known to interact with the excitotoxicity driver NMDA receptor (NMDAR), and in sudden pathophysiological conditions of the brain, e.g., stroke, several lines of evidence link DAPK1 with t…

0301 basic medicinePhysiologyClinical BiochemistryExcitotoxicitymedicine.disease_causeProteomicsBiochemistryInteractomeNeuroprotectionArticle03 medical and health sciences0302 clinical medicinemedicineDAPK1Protein kinase AMolecular Biologychemistry.chemical_classificationReactive oxygen specieslcsh:RM1-950OGDROSCell BiologyneuronferroptosisCell biology030104 developmental biologymedicine.anatomical_structurelcsh:Therapeutics. Pharmacologychemistrynervous systemNMDANeuronLRRFIP1MCAO030217 neurology & neurosurgeryIntracellularAntioxidants
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Cytotoxicity ofSalvia miltiorrhizaAgainst Multidrug-Resistant Cancer Cells

2016

Salvia miltiorrhiza Bunge (Lamiaceae) is a well-known Chinese herb that possesses numerous therapeutic activities, including anticancer effects. In this study, the cytotoxicity and the biological mechanisms of S. miltiorrhiza (SM) root extract on diverse resistant and sensitive cancer cell lines were investigated. CEM/ADR5000 cells were 1.68-fold resistant to CCRF-CEM cells, while HCT116 (p53[Formula: see text] and U87.MG[Formula: see text]EGFR cells were hypersensitive (collateral sensitive) compared to their parental cells. SM root extract stimulated ROS generation, cell cycle S phase arrest and apoptosis. The induction of the intrinsic apoptotic pathway was validated by increased cleavag…

0301 basic medicinePoly ADP ribose polymerasep38 mitogen-activated protein kinasesApoptosisSalvia miltiorrhizaCaspase 3PharmacologyBiologySalvia miltiorrhiza03 medical and health sciences0302 clinical medicineCell Line TumorNeoplasmsHumansCytotoxicityCell Cycle CheckpointsGeneral MedicineCell cycleAntineoplastic Agents PhytogenicMolecular biology030104 developmental biologyComplementary and alternative medicineDrug Resistance NeoplasmApoptosisCaspases030220 oncology & carcinogenesisCancer cellReactive Oxygen SpeciesDrugs Chinese HerbalThe American Journal of Chinese Medicine
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