Search results for "53"

showing 10 items of 2908 documents

Roles of TP53 in determining therapeutic sensitivity, growth, cellular senescence, invasion and metastasis.

2016

TP53 is a critical tumor suppressor gene that regulates cell cycle progression, apoptosis, cellular senescence and many other properties critical for control of normal cellular growth and death. Due to the pleiotropic effects that TP53 has on gene expression and cellular physiology, mutations at this tumor suppressor gene result in diverse physiological effects. T53 mutations are frequently detected in numerous cancers. The expression of TP53 can be induced by various agents used to treat cancer patients such as chemotherapeutic drugs and ionizing radiation. Radiation will induce Ataxia telangiectasia mutated (ATM) and other kinases that results in the phosphorylation and activation of TP53…

0301 basic medicineCancer Researchendocrine system diseasesMetastasimedicine.disease_causeMetastasisAntineoplastic AgentInvasionNeoplasmsTP53Neoplasm Metastasisbcl-2-Associated X ProteinAza CompoundProto-Oncogene ProteinApoptosis Regulatory ProteinbiologyCell CyclemiRMicroRNACell cycleCell biologyNeoplasm MetastasiGene Expression Regulation NeoplasticNutlin-3 chemosensitivityMdm2Molecular MedicineHumanSignal TransductionCyclin-Dependent Kinase Inhibitor p21Tumor suppressor genemiRsAntineoplastic AgentsCellular senescenceTP53; miRs; MDM2; Nutlin-3 chemosensitivity; Cellular senescence ; Invasion; Metastasis03 medical and health sciencesBcl-2-associated X proteinGeneticMDM2Proto-Oncogene ProteinsmicroRNAGeneticsmedicineHumansNeoplasm InvasivenessneoplasmsMolecular BiologyCell ProliferationNeoplasm InvasiveneAza CompoundsOncomirBridged Bicyclo Compounds HeterocyclicMicroRNAs030104 developmental biologyTumor progressionbiology.proteinNeoplasmTumor Suppressor Protein p53CarcinogenesisApoptosis Regulatory Proteins
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Signalling strength determines proapoptotic functions of STING

2017

Mammalian cells use cytosolic nucleic acid receptors to detect pathogens and other stress signals. In innate immune cells the presence of cytosolic DNA is sensed by the cGAS–STING signalling pathway, which initiates a gene expression programme linked to cellular activation and cytokine production. Whether the outcome of the STING response varies between distinct cell types remains largely unknown. Here we show that T cells exhibit an intensified STING response, which leads to the expression of a distinct set of genes and results in the induction of apoptosis. Of note, this proapoptotic STING response is still functional in cancerous T cells and delivery of small molecule STING agonists prev…

0301 basic medicineCell typeLeukemia T-CellTranscription Geneticmedicine.medical_treatmentScienceCellsT-LymphocytesGeneral Physics and AstronomyActivationApoptosisInnate Immune SensorBiologyCytosolic DnaCgasGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesCyclic Gmp-Amp[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologymedicineAnimalsReceptorlcsh:ScienceMultidisciplinaryInnate immune systemEffectorQ2nd-MessengerMembrane ProteinsGeneral ChemistryHedgehog signaling pathwayeye diseases3. Good healthCell biologyMice Inbred C57BLSting030104 developmental biologyCytokineDi-GmpImmunologylcsh:QInterferon Regulatory Factor-3Signal transductionTumor Suppressor Protein p53InfectionProtein BindingSignal TransductionNature Communications
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Study of interaction of antimutagenic 1,4-dihydropyridine AV-153-Na with DNA-damaging molecules and its impact on DNA repair activity

2018

Background1,4-dihydropyridines (1,4-DHP) possesses important biochemical and pharmacological properties, including antioxidant and antimutagenic activities. It was shown that the antimutagenic 1,4-dihydropyridine AV-153-Na interacts with DNA. The aim of the current study was to test the capability of the compound to scavenge peroxynitrite and hydroxyl radical, to test intracellular distribution of the compound, and to assess the ability of the compound to modify the activity of DNA repair enzymes and to protect the DNA in living cells against peroxynitrite-induced damage.MethodsPeroxynitrite decomposition was assayed by UV spectroscopy, hydroxyl radical scavenging—by EPR spectroscopy. DNA b…

0301 basic medicineCircular dichroismDNA repairDNA damageBiophysicsDNA repairlcsh:MedicineGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceschemistry.chemical_compoundAV-153-Na0302 clinical medicineFluorescence microscopeMolecular Biology14-dihydropyridineschemistry.chemical_classificationGeneral Neurosciencelcsh:RGeneral MedicineCell Biology030104 developmental biologyEnzymechemistry030220 oncology & carcinogenesisBiophysicsHydroxyl radicalGeneral Agricultural and Biological SciencesDNAPeroxynitritePeerJ
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Class I histone deacetylases regulate p53/NF-κB crosstalk in cancer cells

2016

The transcription factors NF-κB and p53 as well as their crosstalk determine the fate of tumor cells upon therapeutic interventions. Replicative stress and cytokines promote signaling cascades that lead to the co-regulation of p53 and NF-κB. Consequently, nuclear p53/NF-κB signaling complexes activate NF-κB-dependent survival genes. The 18 histone deacetylases (HDACs) are epigenetic modulators that fall into four classes (I-IV). Inhibitors of histone deacetylases (HDACi) become increasingly appreciated as anti-cancer agents. Based on their effects on p53 and NF-κB, we addressed whether clinically relevant HDACi affect the NF-κB/p53 crosstalk. The chemotherapeutics hydroxyurea, etoposide, an…

0301 basic medicineDNA damageApoptosisModels BiologicalHistone Deacetylases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorNeoplasmsHumansHydroxyureaEpigeneticsTranscription factorCellular SenescenceEtoposidebiologyNF-kappa BNF-κBCell Cycle CheckpointsDNA NeoplasmCell BiologyHDAC6Gene Expression Regulation NeoplasticHistone Deacetylase InhibitorsCrosstalk (biology)030104 developmental biologyHistonechemistry030220 oncology & carcinogenesisMutationCancer cellbiology.proteinCancer researchTumor Suppressor Protein p53VidarabineDNA DamageSignal TransductionCellular Signalling
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Contribution of allelic imbalance to colorectal cancer

2018

Point mutations in cancer have been extensively studied but chromosomal gains and losses have been more challenging to interpret due to their unspecific nature. Here we examine high-resolution allelic imbalance (AI) landscape in 1699 colorectal cancers, 256 of which have been whole-genome sequenced (WGSed). The imbalances pinpoint 38 genes as plausible AI targets based on previous knowledge. Unbiased CRISPR-Cas9 knockout and activation screens identified in total 79 genes within AI peaks regulating cell growth. Genetic and functional data implicate loss of TP53 as a sufficient driver of AI. The WGS highlights an influence of copy number aberrations on the rate of detected somatic point muta…

0301 basic medicineDenmarkLoss of HeterozygosityGeneral Physics and AstronomyAllelic ImbalanceLoss of heterozygosityGenotypeddc:576.5RNA Small Interferinglcsh:ScienceRNA Small Interfering/geneticsGeneticsMultidisciplinaryQGenomicsPhenotype3. Good healthGENOMEPhenotypesyöpägeenitAllelic ImbalanceTumor Suppressor Protein p53/geneticsColorectal NeoplasmsChromosomes Human Pair 8GENESDNA Copy Number VariationsGenotypeScienceTranscription Factors/geneticsGenomicscolorectal cancerBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyProto-Oncogene Proteins p21(ras)Proto-Oncogene Proteins p21(ras)/genetics03 medical and health sciencesmedicineHumansPoint MutationGenetic Predisposition to DiseaseGenepaksusuolisyöpäChromosome AberrationsWhole Genome SequencingHUMAN-COLONGene Expression ProfilingPoint mutationCancerGeneral Chemistrymedicine.diseaseColorectal Neoplasms/geneticsENHANCERS030104 developmental biologyCELLSlcsh:Q3111 BiomedicineTumor Suppressor Protein p53CRISPR-Cas SystemsmutaatiotTranscription FactorsMicrosatellite Repeats
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Inferring causation from time series in earth system sciences

2019

The heart of the scientific enterprise is a rational effort to understand the causes behind the phenomena we observe. In large-scale complex dynamical systems such as the Earth system, real experiments are rarely feasible. However, a rapidly increasing amount of observational and simulated data opens up the use of novel data-driven causal methods beyond the commonly adopted correlation techniques. Here, we give an overview of causal inference frameworks and identify promising generic application cases common in Earth system sciences and beyond. We discuss challenges and initiate the benchmark platform causeme.net to close the gap between method users and developers.

0301 basic medicineEarth scienceAquatic Ecology and Water Quality ManagementDynamical systems theoryComputer science530 PhysicsDatenmanagement und AnalyseSciencereviewGeneral Physics and Astronomyheart02 engineering and technologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesDatabasesLife ScienceCausationStatistical physics thermodynamics and nonlinear dynamicsintermethod comparisonlcsh:Scienceresearch workScientific enterpriseMultidisciplinaryWIMEKSeries (mathematics)QComputational sciencefeasibility study500General ChemistryAquatische Ecologie en Waterkwaliteitsbeheersimulation021001 nanoscience & nanotechnologyData sciencecausal inference climateEarth system scienceEnvironmental sciences030104 developmental biologytime series analysisCausal inferencePerspectiveBenchmark (computing)Observational studylcsh:Qconceptual frameworkdata management0210 nano-technologyClimate sciences
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Fatty Acids of Microbial Origin in the Perirenal Fat of Rats (Rattus norvegicus domestica) and Guinea Pigs (Cavia porcellus) Fed Various Diets.

2020

Guinea pigs are assumed to practice caecotrophy to a higher degree than rats. Studies from leporids suggest that through the practice of caecotrophy, hindgut fermenting species could build up microbial fatty acids (FA) in body tissues. We hypothesized that microbial FA would be detectable in the body tissue of guinea pigs and rats, and this to a higher degree in guinea pigs. Twenty-four rats and guinea pigs were fed with four different pelleted diets (lucerne-, meat-, meat-bone-, insect-based) in groups of six animals for 8 weeks. Perirenal adipose tissue differed in FA composition between the species in spite of the common diets. FA typically associated with microbial activity (saturated F…

0301 basic medicineFA10253 Department of Small Animals1303 BiochemistryRodentGuinea PigsCaviaAdipose tissuePerirenal fatBiochemistryGuinea pig1307 Cell Biology03 medical and health scienceschemistry.chemical_compoundAnimal scienceSpecies SpecificityRuminantbiology.animalCoprophagiaIsoAnimals2. Zero hunger030109 nutrition & dieteticsbiology630 AgricultureCaecotrophyalpha-Linolenic acidMicrobiotaOrganic ChemistryFatty AcidsHindgutCell BiologyRat.biology.organism_classificationGuinea pigAnimal FeedDietRats030104 developmental biologychemistryAdipose TissueDocosahexaenoic acidMicrobial fatty acids570 Life sciences; biology1605 Organic ChemistryLipidsReferences
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Hepatitis B Virus Exploits ERGIC-53 in Conjunction with COPII to Exit Cells.

2020

Several decades after its discovery, the hepatitis B virus (HBV) still displays one of the most successful pathogens in human populations worldwide. The identification and characterization of interactions between cellular and pathogenic components are essential for the development of antiviral treatments. Due to its small-sized genome, HBV highly depends on cellular functions to produce and export progeny particles. Deploying biochemical-silencing methods and molecular interaction studies in HBV-expressing liver cells, we herein identified the cellular ERGIC-53, a high-mannose-specific lectin, and distinct components of the endoplasmic reticulum (ER) export machinery COPII as crucial factor…

0301 basic medicineHepatitis B virusSec24AEndosomeHBV assemblyVesicular Transport ProteinsN-glycosylationBiologymedicine.disease_causeEndoplasmic ReticulumTransfectionGenomeESCRTArticle03 medical and health sciencesN-linked glycosylationViral life cycleCell Line TumormedicineHBVHumansCOPIICOPIIlcsh:QH301-705.5Hepatitis B virus030102 biochemistry & molecular biologyEndosomal Sorting Complexes Required for TransportEndoplasmic reticulumVirionMembrane ProteinsGeneral MedicineHepatitis BHBV egressERGIC-53Cell biologyProtein Transport030104 developmental biologyMannose-Binding Lectinslcsh:Biology (General)HepatocytesLMAN-1COP-Coated VesiclesCells
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Phenolic extract from oleaster (Olea europaea var. Sylvestris) leaves reduces colon cancer growth and induces caspase-dependent apoptosis in colon ca…

2017

Erratum inCorrection: Phenolic extract from oleaster (Olea europaea var. Sylvestris) leaves reduces colon cancer growth and induces caspase-dependent apoptosis in colon cancer cells via the mitochondrial apoptotic pathway. [PLoS One. 2017]; International audience; Dietary polyphenols, derived from natural products, have received a great interest for their chemopreventive properties against cancer. In this study, we investigated the effects of phenolic extract of the oleaster leaves (PEOL) on tumor growth in mouse model and on cell death in colon cancer cell lines. We assessed the effect of oleaster leaf infusion on HCT116 (human colon cancer cell line) xenograft growth in athymic nude mice.…

0301 basic medicineLeavesCarcinoma Cellslcsh:MedicineApoptosisPlant ScienceMitochondrionEndoplasmic ReticulumBiochemistry[ SDV.CAN ] Life Sciences [q-bio]/Cancer0302 clinical medicineMedicine and Health SciencesMitochondrial calcium uptakeDiseaselcsh:ScienceEnergy-Producing OrganellesStainingchemistry.chemical_classificationSecretory PathwayMultidisciplinaryCell DeathPlant AnatomyCytochrome cCell StainingAnimal ModelsMitochondriaOlive Leaf ExtractChemistryOncologyExperimental Organism SystemsBiochemistryCell Processes030220 oncology & carcinogenesisPhysical SciencesCellular Structures and OrganellesResearch ArticleProgrammed cell deathActivationMouse Models[SDV.CAN]Life Sciences [q-bio]/CancerBioenergeticsBiologyResearch and Analysis MethodsColorectal-CancerCaspase-Dependent Apoptosis03 medical and health sciencesModel OrganismsPhenolsCytochrome-CColorectal CancerReactive oxygen speciesP53Cell growthProteinlcsh:RChemical CompoundsBiology and Life SciencesCancers and NeoplasmsPolyphenolsCell BiologyMolecular biology030104 developmental biologychemistrySpecimen Preparation and TreatmentApoptosisbiology.proteinCalciumlcsh:QPLoS ONE
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RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1 and TP53 pathways and regulatory miRs as therapeutic targets in hepatocellular carcinoma

2019

Introduction: Hepatocellular carcinoma (HCC) is a significant problem globally because of viral infections and the increasing incidence of obesity and fatty liver disease. However, it is difficult to treat because its inherent genetic heterogeneity results in activation of numerous signaling pathways. Kinases have been targeted for decades with varying results, but the development of therapeutic resistance is a major challenge. Areas covered: The key roles of the RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1, TP53 microRNAs (miRs) as therapeutic targets are discussed and we suggests novel approaches for targeting miRs or their downstream targets to combat HCC. We performed literature searches using…

0301 basic medicineMAPK/ERK pathwayCarcinoma HepatocellularHepatocellular carcinmamedicine.medical_treatmentClinical BiochemistryAntineoplastic AgentsmTORC1signal transduction inhibitorsTargeted therapy03 medical and health sciences0302 clinical medicineDrug DiscoverymicroRNAmedicinePTENAnimalsHumanscancerMolecular Targeted TherapyTP53HCCRAS/RAF/MEK/ERKProtein kinase BPI3K/AKT/mTOR pathwaymiRNAPharmacologybiologybusiness.industryKinaseLiver NeoplasmsMirhepatocellular carcinomatargeted therapyGene Expression Regulation NeoplasticMicroRNAssignal transduction inhibitor030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisbiology.proteinCancer researchMolecular MedicinePI3K/PTEN/AKTbusinessSignal Transduction
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