Search results for "GPI-Linked Protein"

showing 9 items of 19 documents

Differential inhibition of TRAIL-mediated DR5-DISC formation by decoy receptors 1 and 2.

2006

International audience; Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family that induces cancer cell death by apoptosis with some selectivity. TRAIL-induced apoptosis is mediated by the transmembrane receptors death receptor 4 (DR4) (also known as TRAIL-R1) and DR5 (TRAIL-R2). TRAIL can also bind decoy receptor 1 (DcR1) (TRAIL-R3) and DcR2 (TRAIL-R4) that fail to induce apoptosis since they lack and have a truncated cytoplasmic death domain, respectively. In addition, DcR1 and DcR2 inhibit DR4- and DR5-mediated, TRAIL-induced apoptosis and we demonstrate here that this occurs through distinct mechanisms. While DcR1 prevents the assembly of the…

MESH : Hela CellsMESH: Membrane GlycoproteinsMESH: Membrane MicrodomainsDecoy Receptor 1ApoptosisMESH : Membrane GlycoproteinsReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandJurkat Cells0302 clinical medicineMESH : Tumor Necrosis Factor Decoy ReceptorsMESH: Jurkat CellsDecoy receptorsReceptorCells CulturedMESH : Jurkat CellsMESH : Tumor Necrosis Factor-alpha0303 health sciencesMembrane GlycoproteinsMESH : Protein BindingArticlesMESH : Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsTumor Necrosis Factor Receptor-Associated Peptides and ProteinsCell biology030220 oncology & carcinogenesisCaspasesDeath-inducing signaling complexApoptosis/drug effects; Apoptosis Regulatory Proteins/antagonists & inhibitors; Apoptosis Regulatory Proteins/pharmacology; Caspases/metabolism; Cells Cultured; Death Domain Receptor Signaling Adaptor Proteins; Enzyme Activation/drug effects; GPI-Linked Proteins; HeLa Cells; Humans; Jurkat Cells; Membrane Glycoproteins/antagonists & inhibitors; Membrane Glycoproteins/pharmacology; Membrane Microdomains/drug effects; Protein Binding/drug effects; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor/metabolism; TNF-Related Apoptosis-Inducing Ligand; Tumor Necrosis Factor Decoy Receptors; Tumor Necrosis Factor Receptor-Associated Peptides and Proteins/metabolism; Tumor Necrosis Factor-alpha/antagonists & inhibitors; Tumor Necrosis Factor-alpha/pharmacologyMESH : Apoptosis Regulatory ProteinsMESH: TNF-Related Apoptosis-Inducing LigandProtein BindingMESH: Cells CulturedDeath Domain Receptor Signaling Adaptor ProteinsMESH: Enzyme ActivationBiologyMESH: Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsGPI-Linked Proteins03 medical and health sciencesMembrane MicrodomainsCell surface receptorMESH : Cells Cultured[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyReceptors Tumor Necrosis Factor Member 10cHumansMESH: Protein Binding[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing LigandMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyDeath domainMESH: CaspasesMESH: HumansTumor Necrosis Factor-alphaMESH: Apoptosis Regulatory ProteinsMESH: ApoptosisMESH : HumansCell BiologyMESH: Receptors Tumor Necrosis FactorMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : Receptors Tumor Necrosis FactorEnzyme ActivationMESH: Hela CellsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsApoptosisMESH: Tumor Necrosis Factor-alphaMESH : Membrane MicrodomainsMESH : CaspasesApoptosis Regulatory ProteinsMESH : Enzyme ActivationMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy ReceptorsHeLa CellsMESH: Death Domain Receptor Signaling Adaptor Proteins
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Evidence for PTGER4 ,PSCA, and MBOAT7 as risk genes for gastric cancer on the genome and transcriptome level

2018

Genetic associations between variants on chromosome 5p13 and 8q24 and gastric cancer (GC) have been previously reported in the Asian population. We aimed to replicate these findings and to characterize the associations at the genome and transcriptome level. We performed a fine-mapping association study in 1926 GC patients and 2012 controls of European descent using high dense SNP marker sets on both chromosomal regions. Next, we performed expression quantitative trait locus (eQTL) analyses using gastric transcriptome data from 143 individuals focusing on the GC associated variants. On chromosome 5p13 the strongest association was observed at rs6872282 (P = 2.53 x 10(-04)) and on chromosome …

Male0301 basic medicineCancer ResearchGenotypeQuantitative Trait LocieQTL studyBiologyGPI-Linked ProteinsPolymorphism Single NucleotideGenomeTranscriptome03 medical and health sciencesAntigens NeoplasmStomach NeoplasmsGene expressionmedicineHumansSNPGenetic Predisposition to DiseaseRadiology Nuclear Medicine and imagingGeneGenetic Association StudiesOriginal ResearchCancer BiologyGeneticsGene Expression ProfilingChromosome MappingMembrane ProteinsChromosomeCancermedicine.diseaseNeoplasm ProteinsGene Expression Regulation Neoplastic030104 developmental biologyOncologygenetic association studyCase-Control StudiesExpression quantitative trait locigene expressionChromosomes Human Pair 5FemaleReceptors Prostaglandin E EP4 SubtypeAcyltransferasesChromosomes Human Pair 8Cancer Medicine
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Neuroprotective potential of antihyperglycemic drug metformin in streptozocin-induced rat model of sporadic Alzheimer's disease.

2020

Abstract The earliest hallmarks of sporadic Alzheimer's disease (sAD) are impaired glucose metabolism, chronic neuroinflammation, diminished synaptic plasticity and subsequent cognitive decline. The safest antidiabetic drug metformin has shown both glucose metabolism-improving and cognition-enhancing action in type 2 diabetes patients and diabetic model animals. However, metformin has not been previously studied in intracerebroventricular streptozocin (STZ)-induced model of sAD. Therefore, our aim was to assess the preventive action of metformin in sAD model-rats. Firstly, the actions of metformin (75 and 100 mg/kg) on cognitive functions and sociability were examined. Secondly, we wanted t…

0301 basic medicineMaleendocrine system diseasesNerve Tissue ProteinsType 2 diabetesPharmacologyGPI-Linked ProteinsNeuroprotectionStreptozocin03 medical and health sciencesGlycogen Synthase Kinase 30302 clinical medicineCognitionAlzheimer DiseaseMorris Water Maze TestMedicineAnimalsHypoglycemic AgentsCognitive declineRats WistarSocial BehaviorNeuroinflammationInjections IntraventricularPharmacologyGlucose Transporter Type 1Behavior AnimalGlucose Transporter Type 3business.industrydigestive oral and skin physiologyGlucose transporternutritional and metabolic diseasesBrainmedicine.diseaseMetforminMetforminAstrogliosisDisease Models Animal030104 developmental biologyGlucoseNeuroprotective AgentsSynaptic plasticityAcetylcholinesterasebusinessNeuroglia030217 neurology & neurosurgerymedicine.drugEuropean journal of pharmacology
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Carnitine congener mildronate protects against stress- and haloperidol-induced impairment in memory and brain protein expression in rats.

2014

The present study investigates the efficacy of mildronate, a carnitine congener, to protect stress and haloperidol-induced impairment of memory in rats and the expression of brain protein biomarkers involved in synaptic plasticity, such as brain-derived neurotrophic factor (BDNF), acetylcholine esterase and glutamate decarboxylase 67 (GAD67). Two amnesia models were used: 2h immobilization stress and 3-week haloperidol treatment. Stress caused memory impairment in the passive avoidance test and induced a significant 2-fold BDNF elevation in hippocampal and striatal tissues that was completely inhibited by mildronate. Mildronate decreased the level of GAD67 (but not acetylcholine esterase) e…

Malemedicine.medical_specialtyGlutamate decarboxylaseAmnesiaNerve Tissue ProteinsHippocampal formationGPI-Linked ProteinsNeurotrophic factorsMemoryStress PhysiologicalInternal medicineCarnitinemedicineHaloperidolAvoidance LearningMemory impairmentAnimalsCarnitineRats WistarMaze LearningPharmacologyChemistryGlutamate DecarboxylaseBrain-Derived Neurotrophic FactorBrainRatsEndocrinologyNeuroprotective AgentsSynaptic plasticityAcetylcholinesteraseHaloperidolmedicine.symptomNeuroscienceBiomarkersmedicine.drugMethylhydrazinesEuropean journal of pharmacology
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Prognostic impact of CD73 expression and its relationship to PD-L1 in patients with radically treated pancreatic cancer

2020

AbstractImmune suppressing molecule CD73 is overexpressed in various cancers and associated with poor survival. Little is so far known about the predictive value of CD73 in pancreatic ductal adenocarcinoma (PDAC). The purpose of this study was to investigate the prognostic significance of CD73 in PDAC. The study material consisted of 110 radically treated patients for PDAC. Tissue microarray blocks were constructed and stained immunohistochemically using CD73 antibody. Staining intensity and numbers of stained tumour cells, inflammatory cells, stroma, and blood vessels were assessed. High-level CD73 expression in tumour cells was positively associated with PD-L1 expression, perineural invas…

Male0301 basic medicinePathologyentsyymitDatabases Factualpancreatic cancerPerineural invasionB7-H1 Antigen0302 clinical medicineRisk FactorsTumor MicroenvironmentMedicine5'-NucleotidasehaimasyöpäAged 80 and overTissue microarraybiologyGeneral MedicineMiddle AgedPrognosisTreatment OutcomesyöpäsolutChemotherapy AdjuvantimmuunijärjestelmäLymphatic Metastasis030220 oncology & carcinogenesisOriginal ArticleFemaleAntibodyCarcinoma Pancreatic DuctalPD-L1Cell typemedicine.medical_specialtyMicroenvironmentGPI-Linked ProteinsRisk AssessmentPancreaticoduodenectomyPathology and Forensic Medicine03 medical and health sciencesLymphocytes Tumor-InfiltratingPancreatectomyImmune systemStromaPancreatic cancerPD-L1Biomarkers TumorHumansMolecular BiologyAgedNeoplasm Stagingbusiness.industryennusteetPancreatic cancerCell Biologymedicine.disease3126 Surgery anesthesiology intensive care radiologymicroenvironmentPancreatic Neoplasms030104 developmental biologybiology.proteinCD73prognosisNeoplasm Gradingbusiness
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Characterization of neutrophil subsets in healthy human pregnancies

2014

We have previously shown that in successful pregnancies increased arginase activity is a mechanism that contributes to the suppression of the maternal immune system. We identified the main type of arginase-expressing cells as a population of activated low-density granulocytes (LDGs) in peripheral blood mononuclear cells and in term placentae. In the present study, we analyzed the phenotype of LDGs and compared it to the phenotype of normal density granulocytes (NDGs) in maternal peripheral blood, placental biopsies and cord blood. Our data reveal that only LDGs but no NDGs could be detected in placental biopsies. Phenotypically, NDGs and LDGs from both maternal and cord blood expressed diff…

NeutrophilsPlacentaEnzyme Metabolismlcsh:MedicineGene ExpressionBiochemistryCell DegranulationNeutrophil ActivationImmune toleranceLeukocyte Count0302 clinical medicineImmunophenotypingPregnancyMolecular Cell BiologySUPPRESSOR-CELLSlcsh:Science0303 health scienceseducation.field_of_studyMultidisciplinaryL-ARGININEObstetrics and GynecologyFetal BloodInnate Immunity3. Good healthEnzymesmedicine.anatomical_structurePhenotypeARGINASE ACTIVITYCord bloodMedicineScience & Technology - Other TopicsFemaleBiological MarkersTHERAPEUTIC PERSPECTIVESResearch ArticleEXPRESSIONAdultCordGeneral Science & TechnologyImmune CellsPopulationImmunologyBiologyMETABOLISMGRANULOCYTESGPI-Linked ProteinsPeripheral blood mononuclear cellMECHANISMSImmunophenotyping03 medical and health sciencesImmune systemAntigens CDPlacentaMD MultidisciplinarymedicineImmune ToleranceHumansCell LineageeducationBiology030304 developmental biologyScience & TechnologyArginaseMULTIDISCIPLINARY SCIENCESlcsh:RImmunityOXIDANT RELEASEImmunologyWomen's Healthlcsh:QClinical ImmunologyIMMUNE-SYSTEMCell Adhesion MoleculesCytometryBiomarkers030215 immunology
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Growth Arrest Specific 1 (Gas1) Gene Overexpression in Liver Reduces the In Vivo Progression of Murine Hepatocellular Carcinoma and Partially Restore…

2015

The prognosis of hepatocellular carcinoma patients is usually poor, the size of tumors being a limiting factor for surgical treatments. Present results suggest that the overexpression of Gas1 (growth arrest specific 1) gene reduces the size, proliferating activity and malignancy of liver tumors. Mice developing diethylnitrosamine-induced hepatocellular carcinoma were subjected to hydrodynamic gene delivery to overexpress Gas1 in liver. This treatment significantly (p < 0.05) reduced the number of large tumors, while the difference in the total number of lesions was not significant. Moreover, the number of carcinoma foci in the liver and the number of lung metastases were reduced. These resu…

MaleCarcinoma Hepatocellularlcsh:MedicineCell Cycle ProteinsGene deliveryBiologyGPI-Linked ProteinsReal-Time Polymerase Chain ReactionTransfectionMiceCell Line TumorGene expressionCarcinomamedicineAnimalslcsh:ScienceLungCell ProliferationRegulation of gene expressionMultidisciplinaryMicroarray analysis techniquesLiver Neoplasmslcsh:RCell cyclemedicine.diseaseMolecular biologyHedgehog signaling pathwayGene Expression Regulation NeoplasticLiverHepatocellular carcinomaDisease ProgressionHydrodynamicslcsh:QResearch ArticlePLoS ONE
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Epigenetic Transcriptional Regulation of the Growth Arrest-Specific gene 1 (Gas1) in Hepatic Cell Proliferation at Mononucleosomal Resolution

2011

Background Gas1 (growth arrest-specific 1) gene is known to inhibit cell proliferation in a variety of models, but its possible implication in regulating quiescence in adult tissues has not been examined to date. The knowledge of how Gas1 is regulated in quiescence may contribute to understand the deregulation occurring in neoplastic diseases. Methodology/Principal Findings Gas1 expression has been studied in quiescent murine liver and during the naturally synchronized cell proliferation after partial hepatectomy. Chromatin immunoprecipitation at nucleosomal resolution (Nuc-ChIP) has been used to carry out the study preserving the in vivo conditions. Transcription has been assessed at real …

Chromatin ImmunoprecipitationTranscription GeneticGene Expressionlcsh:MedicineCell Cycle ProteinsRNA polymerase IIBiologyGPI-Linked ProteinsMethylationHistone DeacetylasesChromatin remodelingEpigenesis GeneticS PhaseHistonesMiceMolecular Cell BiologyTranscriptional regulationAnimalsHepatectomyEpigeneticsPromoter Regions Geneticlcsh:ScienceBiologyCell ProliferationHistone AcetyltransferasesRegulation of gene expressionMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionGene Expression Profilinglcsh:RG1 PhaseAcetylationHistone ModificationImmunohistochemistryMolecular biologyChromatinNucleosomesChromatinHistoneGene Expression RegulationLiverbiology.proteinlcsh:QTranscription Initiation SiteChromatin immunoprecipitationProtein BindingResearch ArticlePLoS ONE
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Dynamic regulation of the cancer stem cell compartment by Cripto-1 in colorectal cancer.

2015

Stemness was recently depicted as a dynamic condition in normal and tumor cells. We found that the embryonic protein Cripto-1 (CR1) was expressed by normal stem cells at the bottom of colonic crypts and by cancer stem cells (CSCs) in colorectal tumor tissues. CR1-positive populations isolated from patient-derived tumor spheroids exhibited increased clonogenic capacity and expression of stem-cell-related genes. CR1 expression in tumor spheroids was variable over time, being subject to a complex regulation of the intracellular, surface and secreted protein, which was related to changes of the clonogenic capacity at the population level. CR1 silencing induced CSC growth arrest in vitro with a …

Colorectal cancerColorectal NeoplasmCriptoMiceIntercellular Signaling Peptides and ProteinTumor Cells CulturedRegulation of gene expressionCulturedstem cell; CRIPTO 1GPI-Linked ProteinCell biologyNeoplasm ProteinsTumor CellsGene Expression Regulation NeoplasticGenes srcNeoplastic Stem CellsIntercellular Signaling Peptides and ProteinsFemaleStem cellColorectal NeoplasmsHumanSignal Transductioncolorectal cancerBiologyGPI-Linked ProteinsAnimals; Colorectal Neoplasms; Female; GPI-Linked Proteins; Gene Expression Regulation Neoplastic; Genes src; Humans; Intercellular Signaling Peptides and Proteins; Mice; Neoplasm Proteins; Neoplastic Stem Cells; Proto-Oncogene Proteins c-akt; Signal Transduction; Spheroids Cellular; Tumor Cells Cultured; Cell Biology; Molecular BiologyNeoplasm ProteinCancer stem cellSettore MED/04 - PATOLOGIA GENERALESpheroids CellularmedicineGene silencingAnimalsHumansClonogenic assayProtein kinase BMolecular BiologysrcOriginal PaperNeoplasticAnimalCell Biologymedicine.diseaseGene Expression RegulationGenesNeoplastic Stem CellCellularSpheroidsanimals; colorectal neoplasms; female; GPI-linked proteins; gene expression regulation; neoplastic; genes src; humans; intercellular signaling peptides and proteins; mice; neoplasm proteins; neoplastic stem cells; proto-oncogene proteins c-akt; signal transduction; spheroids; cellular; tumor cells; culturedAnimals; Colorectal Neoplasms; Female; GPI-Linked Proteins; Gene Expression Regulation Neoplastic; Genes src; Humans; Intercellular Signaling Peptides and Proteins; Mice; Neoplasm Proteins; Neoplastic Stem Cells; Proto-Oncogene Proteins c-akt; Signal Transduction; Spheroids Cellular; Tumor Cells Cultured; Molecular Biology; Cell BiologyProto-Oncogene Proteins c-akt
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