Search results for "PROTEIN KINASE"

showing 10 items of 1188 documents

Effect of Methanolic Extract of Dandelion Roots on Cancer Cell Lines and AMP-Activated Protein Kinase Pathway

2017

Ethnomedicinal knowledge of plant-derived bioactives could help us in discovering new therapeutic compounds of great potential. Certainly, dandelion has been used in traditional ethno-medicinal systems (i.e., Chinese, Arabian, Indian, and Native American) to treat different types of cancer. Though, dandelion is highly vigorous, but the potential mode of action is still unclear. In the current study, the antiproliferative activity of methanolic extracts of dandelion root (MEDr) on cell viability of HepG2, MCF7, HCT116, and normal Hs27 was investigated. It was observed that MEDr (500 μg/mL) drastically decreased the growth of HepG2 cell line, while the effect on MCF7 and HCT116 cell lines was…

0301 basic medicineAMPKDandelionPharmacologytraditional medicine03 medical and health sciencesdandelion0302 clinical medicineAMP-activated protein kinasecancerPharmacology (medical)Viability assayCytotoxicityMode of actionOriginal ResearchPharmacologybiologyChemistrylcsh:RM1-950AMPKlcsh:Therapeutics. Pharmacology030104 developmental biologyCell cultureApoptosis030220 oncology & carcinogenesisbiology.proteincytotoxicityFrontiers in Pharmacology
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Synergistic activation of AMPK prevents from polyglutamine-inducedtoxicity inCaenorhabditis elegans

2020

11 páginas, 4 figuras. Supplementary material related to this article can be found, in the online version, at doi: https://doi.org/10.1016/j.phrs.2020.105105.

0301 basic medicineAMPKProtein subunitMutantEnzyme ActivatorsAMP-Activated Protein KinasesProtein Serine-Threonine KinasesProtein Aggregation PathologicalpolyQ toxicityArticleAnimals Genetically ModifiedProtein Aggregates03 medical and health sciences0302 clinical medicineRNA interferenceAutophagymedicineAnimalsAMPK Caenorhabditis elegans Metformin Salycilate Synergy polyQ toxicityCaenorhabditis elegans ProteinsCaenorhabditis elegansLoss functionCaenorhabditis elegansNeuronsPharmacologybiologyChemistrySalycilateAutophagyAMPKDrug Synergismbiology.organism_classificationSalicylatesMetforminCell biologyMetforminEnzyme ActivationSynergy030104 developmental biology030220 oncology & carcinogenesisMutationProteostasisPeptidesmedicine.drug
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Rosmarinic Acid Activates AMPK to Inhibit Metastasis of Colorectal Cancer

2018

Rosmarinic acid (RA) has been used as an anti-inflammatory, anti-diabetic, and anti-cancer agent. Although RA has also been shown to exert an anti-metastatic effect, the mechanism of this effect has not been reported to be associated with AMP-activated protein kinase (AMPK). The aim of this study was to elucidate whether RA could inhibit the metastatic properties of colorectal cancer (CRC) cells via the phosphorylation of AMPK. RA inhibited the proliferation of CRC cells through the induction of cell cycle arrest and apoptosis. In several metastatic phenotypes of CRC cells, RA regulated epithelial–mesenchymal transition (EMT) through the upregulation of an epithelial marker, E-cadherin, and…

0301 basic medicineAMPKrosmarinic acidCell cycle checkpointmatrix metalloproteinaseVimentincolorectal cancerMetastasis03 medical and health sciences0302 clinical medicineDownregulation and upregulationmedicinemetastasisPharmacology (medical)Protein kinase AOriginal ResearchPharmacologybiologyChemistryCell adhesion moleculelcsh:RM1-950EMTAMPKmedicine.disease030104 developmental biologylcsh:Therapeutics. PharmacologyApoptosis030220 oncology & carcinogenesisCancer researchbiology.proteinFrontiers in Pharmacology
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Retinoic Acid affects Lung Adenocarcinoma growth by inducing differentiation via GATA6 activation and EGFR and Wnt inhibition

2016

AbstractA fundamental task in cancer research aims at the identification of new pharmacological therapies that can affect tumor growth. Differentiation therapy might exploit this function not only for hematological diseases, such as acute promyelocytic leukemia (APML) but also for epithelial tumors, including lung cancer. Here we show that Retinoic Acid (RA) arrests in vitro and in vivo the growth of Tyrosine Kinase Inhibitors (TKI) resistant Non Small Cell Lung Cancer (NSCLC). In particular, we found that RA induces G0/G1 cell cycle arrest in TKI resistant NSCLC cells and activates terminal differentiation programs by modulating the expression of GATA6, a key transcription factor involved …

0301 basic medicineAcute promyelocytic leukemiaScienceEGFRRetinoic acidMice NudeTretinoinBiologyArticle03 medical and health scienceschemistry.chemical_compoundDifferentiation therapySettore BIO/13 - Biologia ApplicataCarcinoma Non-Small-Cell LungCell Line TumorGATA6 Transcription FactormedicineRetinoic acidAnimalsHumansLung cancerProtein Kinase InhibitorsWnt Signaling PathwayTranscription factorCell ProliferationMultidisciplinaryQRWnt signaling pathwayCell Differentiationmedicine.diseaseG1 Phase Cell Cycle CheckpointsXenograft Model Antitumor Assaysrespiratory tract diseasesErbB Receptorslung cancerAnimals; Carcinoma Non-Small-Cell Lung; Cell Differentiation; Cell Line Tumor; Cell Proliferation; Drug Resistance Neoplasm; ErbB Receptors; G1 Phase Cell Cycle Checkpoints; GATA6 Transcription Factor; Humans; Mice Nude; Protein Kinase Inhibitors; Signal Transduction; Tretinoin; Wnt Signaling Pathway; Xenograft Model Antitumor Assays030104 developmental biologychemistryDrug Resistance NeoplasmImmunologyCancer researchMedicineAdenocarcinomaEngineering sciences. TechnologyTyrosine kinaseSignal Transduction
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TLR1 and PRKAA1 Gene Polymorphisms in the Development of Atrophic Gastritis and Gastric Cancer.

2018

Background & Aims: Previous genome-wide association studies showed that genetic polymorphisms in toll-like receptor 1 (TLR1) and protein kinase AMP-activated alpha 1 catalytic subunit (PRKAA1) genes were associated with gastric cancer (GC) or increased Helicobacter pylori (H. pylori) infection susceptibility. The aim of this study was to evaluate the association between TLR1 and PRKAA1 genes polymorphisms and H.pylori infection, atrophic gastritis (AG) or GC in the European population.Methods: Single-nucleotide polymorphisms (SNPs) were analysed in 511 controls, 340 AG patients and 327 GC patients. TLR1 C>T (rs4833095) and PRKAA1 C>T (rs13361707) were genotyped by the real-time po…

0301 basic medicineAdultGastritis AtrophicMalemedicine.medical_specialtyAtrophic gastritisSingle-nucleotide polymorphismAMP-Activated Protein KinasesGastroenterologyPolymorphism Single NucleotideWhite Peoplelaw.inventionHelicobacter Infections03 medical and health sciences0302 clinical medicineGene FrequencylawRisk FactorsStomach NeoplasmsInternal medicineGenotypemedicineSNPHumansGenetic Predisposition to DiseaseAllelePolymerase chain reactionGenetic Association StudiesGenetic associationAgedbiologyHelicobacter pyloribusiness.industryGastroenterologyHelicobacter pyloriMiddle Agedbiology.organism_classificationmedicine.diseaseToll-Like Receptor 1Europe030104 developmental biologyPhenotype030220 oncology & carcinogenesisCase-Control StudiesFemalebusinessJournal of gastrointestinal and liver diseases : JGLD
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Selective p38α MAP kinase/MAPK14 inhibition in enzymatically modified LDL-stimulated human monocytes: implications for atherosclerosis.

2016

The first ATP-competitive p38α MAPK/MAPK14 inhibitor with excellent in vivo efficacy and selectivity, skepinone-L, is now available. We investigated the impact of selective p38α MAPK/MAPK14 inhibition on enzymatically modified LDL (eLDL) stimulated human monocytes with its implications for atherosclerosis. Among the different p38 MAPK isoforms, p38α/MAPK14 was the predominantly expressed and activated isoform in isolated human peripheral blood monocytes. Moreover, eLDL colocalized with macrophages positive for p38α MAPK/MAPK14 in human carotid endarterectomy specimens. Using the human leukemia cell line THP-1 and/or primary monocyte-derived macrophages, skepinone-L inhibited eLDL-induced ac…

0301 basic medicineAdultMaleChemokineMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesCD36CCL4Dibenzocycloheptenes030204 cardiovascular system & hematologyBiochemistryGene Expression Regulation EnzymologicMonocytesMitogen-Activated Protein Kinase 1403 medical and health sciences0302 clinical medicineCell Line TumorGeneticsHumansInterleukin 8Molecular BiologyFoam cellMAPK14AgedAged 80 and overCaspase 7biologyChemistryCaspase 3Cholesterol LDLAtherosclerosisMolecular biology030104 developmental biologyBiochemistryMitogen-activated protein kinasebiology.proteinFemaleBiotechnologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Mechanisms of action of metformin in type 2 diabetes: Effects on mitochondria and leukocyte-endothelium interactions.

2020

Type 2 diabetes (T2D) is a very prevalent, multisystemic, chronic metabolic disorder closely related to atherosclerosis and cardiovascular diseases. It is characterised by mitochondrial dysfunction and the presence of oxidative stress. Metformin is one of the safest and most effective anti-hyperglycaemic agents currently employed as first-line oral therapy for T2D. It has demonstrated additional beneficial effects, unrelated to its hypoglycaemic action, on weight loss and several diseases, such as cancer, cardiovascular disorders and metabolic diseases, including thyroid diseases. Despite the vast clinical experience gained over several decades of use, the mechanism of action of metformin i…

0301 basic medicineAdvanced glycation end product (AGE)AMP-activated protein kinase (AMPK)endocrine system diseasesglycerol 3-phosphate dehydrogenase (GPD)Clinical Biochemistrytype 1 diabetes (T1D)Type 2 diabetesmTORC1Review Articleelectron transport chain (ETC)PharmacologyMitochondrionmedicine.disease_causeBiochemistry0302 clinical medicineLeukocytesCREB-binding protein (CBP)inner mitochondrial membrane (IMM)lcsh:QH301-705.5lcsh:R5-920cAMP response element-binding (CREB)glucagon-like peptide 1 (GLP-1)type 2 diabetes (T2D)Type 2 diabetesMetforminMetforminMitochondriamedicine.anatomical_structurereactive nitrogen species (RNS)reactive oxygen species (ROS)sirtuin (SIRT)medicine.symptomlcsh:Medicine (General)cardiovascular diseases (CVD)medicine.drugEndotheliumnitric oxide synthase (NOS)polycystic ovary syndrome (PCOS)Pathophysiologyinsulin resistance (IR)superoxide dismutase (SOD)03 medical and health sciencesglycated haemoglobin (HbA1c)medicineorganic cation transporter (OCT)HumansEndotheliumintercellular adhesion molecule-1 (ICAM-1)business.industryoxidative phosphorylation (OXPHOS)Organic Chemistryperoxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)AMPKmedicine.diseaseAtherosclerosisvascular cell adhesion molecule-1 (VCAM-1)Treatment030104 developmental biologylcsh:Biology (General)Mechanism of actionDiabetes Mellitus Type 2Oxidative stressbusinessinsulin receptor substrate (IRS)030217 neurology & neurosurgeryOxidative stress
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IGF-1 Haploinsufficiency Causes Age-Related Chronic Cochlear Inflammation and Increases Noise-Induced Hearing Loss

2021

This article belongs to the Collection Insulin-Like Growth Factors in Development, Cancers and Aging.

0301 basic medicineAgingApoptosisHaploinsufficiencyMice0302 clinical medicineBiology (General)Insulin-Like Growth Factor ICell DeathapoptosisGeneral Medicine3. Good healthCochleaCytokinesmedicine.symptomHaploinsufficiencyNoise-induced hearing lossmedicine.medical_specialtyHeterozygoteHearing lossQH301-705.5InflammationArticleARHLProinflammatory cytokine03 medical and health sciencesInternal medicinemedicineotorhinolaryngologic diseasesAnimalsRNA MessengerProtein kinase BCochleaInflammationbusiness.industryGene Expression ProfilingAKTTGFβ1Auditory Thresholdmedicine.diseaseOxidative Stress030104 developmental biologyEndocrinologyGene Expression RegulationHearing Loss Noise-InducedAgeingSynapsesIL1βJNKbusinessNoise030217 neurology & neurosurgeryBiomarkersNIHL
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Homocysteine Induces Apoptosis of Human Umbilical Vein Endothelial Cells via Mitochondrial Dysfunction and Endoplasmic Reticulum Stress

2017

Homocysteine- (Hcy-) induced endothelial cell apoptosis has been suggested as a cause of Hcy-dependent vascular injury, while the proposed molecular pathways underlying this process are unclear. In this study, we investigated the adverse effects of Hcy on human umbilical vein endothelial cells (HUVEC) and the underlying mechanisms. Our results demonstrated that moderate-dose Hcy treatment induced HUVEC apoptosis in a time-dependent manner. Furthermore, prolonged Hcy treatment increased the expression of NOX4 and the production of intracellular ROS but decreased the ratio of Bcl-2/Bax and mitochondrial membrane potential (MMP), resulting in the leakage of cytochrome c and activation of caspa…

0301 basic medicineAgingArticle SubjectApoptosis030204 cardiovascular system & hematologyTransfectionBiochemistryUmbilical vein03 medical and health sciences0302 clinical medicineRisk FactorsHuman Umbilical Vein Endothelial CellsHumanslcsh:QH573-671Protein kinase AEndoplasmic Reticulum Chaperone BiPHomocysteinebiologylcsh:CytologyKinaseEndoplasmic reticulumCytochrome cCell BiologyGeneral MedicineEndoplasmic Reticulum StressMitochondriaCell biology030104 developmental biologyApoptosiscardiovascular systemUnfolded protein responsebiology.proteinPhosphorylationResearch ArticleOxidative Medicine and Cellular Longevity
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Intensified mitophagy in skeletal muscle with aging is downregulated by PGC-1alpha overexpression in vivo.

2018

Mitochondrial dysfunction plays an important role in the etiology of age-related muscle atrophy known as sarcopenia. PGC-1α is positioned at the center of crosstalk in regulating mitochondrial quality control, but its role in mitophagy in aged skeletal muscle is currently unclear. The present study investigated the effects of aging and PGC-1α overexpression via in vivo DNA transfection on key mitophagy protein markers, as well as mitochondrial dynamics related proteins, metabolic function and antioxidant capacity in mouse muscle. C57BL/6J mice at the age of 2 mo (young, Y; N = 14) and 24 mo (old, O; N = 14) were transfected in vivo with either PGC-1α DNA (OE, N = 7) or GFP (N = 7) into the …

0301 basic medicineAgingUbiquitin-Protein LigasesPINK1MitochondrionBiochemistryMitochondrial DynamicsGTP Phosphohydrolases03 medical and health sciencesMice0302 clinical medicineIn vivoPhysiology (medical)MitophagymedicineAnimalsMuscle SkeletalChemistryMitophagySkeletal muscleTransfectionmedicine.diseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMuscle atrophyCell biologyMitochondriaOxidative Stress030104 developmental biologymedicine.anatomical_structureGene Expression RegulationSarcopeniaBeclin-1medicine.symptomProtein Kinases030217 neurology & neurosurgeryFree radical biologymedicine
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