Search results for "Protein p53"

showing 10 items of 201 documents

Effects of mutations in Wnt/β-catenin, hedgehog, Notch and PI3K pathways on GSK-3 activity—Diverse effects on cell growth, metabolism and cancer

2016

Glycogen synthase kinase-3 (GSK-3) is a serine/threonine kinase that participates in an array of critical cellular processes. GSK-3 was first characterized as an enzyme that phosphorylated and inactivated glycogen synthase. However, subsequent studies have revealed that this moon-lighting protein is involved in numerous signaling pathways that regulate not only metabolism but also have roles in: apoptosis, cell cycle progression, cell renewal, differentiation, embryogenesis, migration, regulation of gene transcription, stem cell biology and survival. In this review, we will discuss the roles that GSK-3 plays in various diseases as well as how this pivotal kinase interacts with multiple sign…

0301 basic medicineMAPK/ERK pathwaySettore MED/06 - Oncologia MedicaCellular differentiationPI3KTargeted therapyGlycogen Synthase Kinase 3Phosphatidylinositol 3-Kinases0302 clinical medicineGSK-3Neoplasmsbeta CateninGSK-3biologyReceptors NotchKinaseWnt signaling pathwayWnt/beta-cateninCell DifferentiationCell biologyGene Expression Regulation Neoplastic030220 oncology & carcinogenesismTORAkt; GSK-3; Hedgehog; Notch; PI3K; Targeted therapy; Therapy resistance; Wnt/beta-catenin; mTORSignal TransductionBeta-cateninNotchAkt GSK-3 Hedgehog mTOR Notch PI3K Targeted therapy Therapy resistance Wnt/beta-cateninCell Survivalmacromolecular substancesNO03 medical and health sciencesAkt; GSK-3 Hedgehog Notch PI3K Targeted therapy Therapy resistance Wnt/beta-catenin mTORAnimalsHumansHedgehog ProteinsProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayCell ProliferationAktTherapy resistanceAkt; GSK-3; Hedgehog; mTOR; Notch; PI3K; Targeted therapy; Therapy resistance; Wnt/beta-catenin; Molecular Biology; Cell BiologyCell BiologyWnt ProteinsMicroRNAs030104 developmental biologyMutationCancer researchbiology.proteinTumor Suppressor Protein p53Hedgehog
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The unbalanced p53/SIRT1 axis may impact lymphocyte homeostasis in COVID-19 patients

2021

Abstract Background/objectives A dysregulated inflammatory profile plays an important role in coronavirus disease-2019 (COVID-19) pathogenesis. Moreover, the depletion of lymphocytes is typically associated with an unfavourable disease course. We studied the role and impact of p53 and deacetylase Sirtuin 1 (SIRT1) on lymph-monocyte homeostasis and their possible effect on T and B cell signalling. Methods Gene expression analysis and flow cytometry were performed on peripheral blood mononuclear cells (PBMC) of 35 COVID-19 patients and 10 healthy donors (HD). Inflammatory cytokines, the frequency of Annexin+ cells among CD3+ T cells and CD19+ B cell subsets were quantified. Results PBMC from …

0301 basic medicineMicrobiology (medical)Male030106 microbiologyInflammationInfectious and parasitic diseasesRC109-216CD19ArticleProinflammatory cytokineBLNK Inflammation03 medical and health sciences0302 clinical medicineSirtuin 1Lymphocyte homeostasismedicineHomeostasisHumans030212 general & internal medicineLymphocytesInterleukin-7 receptorB cellAgedInflammationBLNKbiologySirtuin 1SARS-CoV-2COVID-19p53/SIRT1General MedicineIL-7RMiddle Agedmedicine.anatomical_structureInfectious DiseasesSettore MED/38 - PEDIATRIA GENERALE E SPECIALISTICABLNK; COVID-19; IL-7R; inflammation; p53/SIRT1ImmunologyB-cell linkerbiology.proteinCytokinesFemalemedicine.symptomTumor Suppressor Protein p53
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The EP300/TP53 pathway, a suppressor of the Hippo and canonical WNT pathways, is activated in human hearts with arrhythmogenic cardiomyopathy in the …

2021

Aim Arrhythmogenic cardiomyopathy (ACM) is a primary myocardial disease that typically manifests with cardiac arrhythmias, progressive heart failure and sudden cardiac death (SCD). ACM is mainly caused by mutations in genes encoding desmosome proteins. Desmosomes are cell-cell adhesion structures and hubs for mechanosensing and mechanotransduction. The objective was to identify the dysregulated molecular and biological pathways in human ACM in the absence of overt heart failure. Methods and results Transcriptomes in the right ventricular endomyocardial biopsy samples from three independent individuals carrying truncating mutations in the DSP gene and 5 control samples were analyzed by RNA-S…

0301 basic medicinePhysiologyCardiomyopathy030204 cardiovascular system & hematologyBiologyMechanotransduction CellularBiological pathway03 medical and health sciences0302 clinical medicinePhysiology (medical)medicineHumansMechanotransductionEP300Wnt Signaling PathwayArrhythmogenic Right Ventricular DysplasiaHeart FailureHippo signaling pathwayWnt signaling pathwayArrhythmias CardiacOriginal Articlesmedicine.diseaseCell biologyDeath Sudden Cardiac030104 developmental biologyCardiomyopathy Gene expression Hippo pathway RNA-Sequencing TP53 WNT pathwayHeart failureTumor Suppressor Protein p53Signal transductionCardiomyopathiesCardiology and Cardiovascular MedicineE1A-Associated p300 ProteinCardiovascular Research
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Enzymatic Spermine Metabolites Induce Apoptosis Associated with Increase of p53, caspase-3 and miR-34a in Both Neuroblastoma Cells, SJNKP and the N-M…

2021

Neuroblastoma (NB) is a common malignant solid tumor in children and accounts for 15% of childhood cancer mortality. Amplification of the N-Myc oncogene is a well-established poor prognostic marker in NB patients and strongly correlates with higher tumor aggression and resistance to treatment. New therapies for patients with N-Myc-amplified NB need to be developed. After treating NB cells with BSAO/SPM, the detection of apoptosis was determined after annexin V-FITC labeling and DNA staining with propidium iodide. The mitochondrial membrane potential activity was checked, labeling cells with the probe JC-1 dye. We analyzed, by real-time RT-PCR, the transcript of genes involved in the apoptot…

0301 basic medicinePolyamine; neuroblastoma; apoptosis; microRNA; mitochondria; reactive oxygen species; oncotherapychemistry.chemical_compound0302 clinical medicineAnnexinpolyamineSettore BIO/10 - BiochimicaAntineoplastic Combined Chemotherapy ProtocolsCytotoxic T cellSettore BIO/06 - Anatomia Comparata E CitologiaBiology (General)Membrane Potential Mitochondrialreactive oxygen speciesN-Myc Proto-Oncogene ProteinmicroRNAChemistryCaspase 3apoptosisGeneral MedicineBlotGene Expression Regulation Neoplasticmitochondria030220 oncology & carcinogenesisAmine Oxidase (Copper-Containing)Signal TransductiononcotherapyQH301-705.5Caspase 3apoptosis; microRNA; mitochondria; neuroblastoma; oncotherapy; polyamine; reactive oxygen species.ArticleNO03 medical and health sciencesneuroblastomaNeuroblastomaCell Line TumormedicineAnimalsHumansPropidium iodideRats WistarCell ProliferationOncogeneGene Amplificationmedicine.diseaseapoptosis; microRNA; mitochondria; neuroblastoma; oncotherapy; polyamine; reactive oxygen speciesMolecular biologyMicroRNAs030104 developmental biologyApoptosisSpermineTumor Suppressor Protein p53
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p53 and p53-related mediators PAI-1 and IGFBP-3 are downregulated in peripheral blood mononuclear cells of HIV-patients exposed to non-nucleoside rev…

2019

The improved effectiveness and safety of the combined antiretroviral therapy (cART) has largely diminished mortality and AIDS-defining morbidity of HIV-patients. Nevertheless, chronic age-related diseases in these individuals are more common and their underlying pathogenic mechanisms of these actions seem to involve accelerated aging and enhanced inflammation. The present study explores markers of these processes in a heterogenous Spanish HIV cohort using peripheral blood samples of HIV-patients and matched uninfected controls. We isolated periheral blood mononuclear cells (PBMCs) and i) compared the expression of a panel of 14 genes related to inflammation and senescence in PBMCs of HIV-pa…

0301 basic medicineSenescenceAdultMaleAnti-HIV Agents030106 microbiologyDown-RegulationInflammationHIV InfectionsCCL2Peripheral blood mononuclear cell03 medical and health sciencesVirologyAntiretroviral Therapy Highly ActivePlasminogen Activator Inhibitor 1medicineCXCL10HumansCellular SenescencePharmacologyInflammationbusiness.industryInterleukin-6Interleukin-18virus diseasesMiddle AgedCCL20Chemokine CXCL10030104 developmental biologyInsulin-Like Growth Factor Binding Protein 3ImmunologyLeukocytes MononuclearReverse Transcriptase InhibitorsInterleukin 18Tumor necrosis factor alphaFemalemedicine.symptomTumor Suppressor Protein p53businessAntiviral research
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Telomeres and Telomerase During Human Papillomavirus-Induced Carcinogenesis

2018

Human papillomaviruses (HPVs) belong to a small spherical virus family and are transmitted through direct contact, most often through sexual behavior. More than 200 types of HPV are known, a dozen or so of which are classified as high-risk viruses (HR HPV) and may contribute to the development of cervical cancer. HPV is a small virus with a capsid composed of L1 and L2 proteins, which are crucial for entry to the cell. The infection begins at the basal cell layer and progresses to involve cells from higher layers of the cervical epithelium. E6 and E7 viral proteins are involved in the process of carcinogenesis. They interact with suppressors of oncogenesis, including p53 and Rb proteins. Th…

0301 basic medicineTelomeraseOncogene ProteinsCarcinogenesisCellReview ArticleBiologymedicine.disease_causeRetinoblastoma ProteinVirus03 medical and health sciences0302 clinical medicineGeneticsmedicineHumansTelomerase reverse transcriptasePapillomaviridaeTelomeraseTelomere ShorteningPharmacologyPapillomavirus InfectionsDNA replicationGeneral MedicineOncogene Proteins ViralVirus InternalizationCell Transformation ViralTelomere030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisCancer researchDisease ProgressionMolecular MedicineRNAFemaleTumor Suppressor Protein p53CarcinogenesisMolecular Diagnosis & Therapy
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Acute depletion of telomerase components DKC1 and NOP10 induces oxidative stress and disrupts ribosomal biogenesis via NPM1 and activation of the P53…

2020

Mutations in DKC1, NOP10, and TINF2 genes, coding for proteins in telomerase and shelterin complexes, are responsible for diverse diseases known as telomeropathies and ribosomopathies, including dyskeratosis congenita (DC, ORPHA 1775). These genes contribute to the DC phenotype through mechanisms that are not completely understood. We previously demonstrated in models of DC that oxidative stress is an early and independent event that occurs prior to telomere shortening. To clarify the mechanisms that induce oxidative stress, we silenced genes DKC1, NOP10, and TINF2 with siRNA technology. With RNA array hybridisation, we found several altered pathways for each siRNA model. Afterwards, we ide…

0301 basic medicineTelomeraseTelomere-Binding ProteinsCell Cycle ProteinsShelterin ComplexCell LineAdherens junction03 medical and health sciences0302 clinical medicineRibonucleoproteins Small NucleolarmedicineRNA Small InterferingMolecular BiologyTelomeraseTelomere ShorteningRibonucleoproteinChemistryRNANuclear ProteinsCell BiologyTelomereShelterinmedicine.diseaseCell biologyTelomereOxidative Stress030104 developmental biology030220 oncology & carcinogenesisMutationTumor Suppressor Protein p53NucleophosminRibosomesDyskeratosis congenitaBiogenesisBiochimica et biophysica acta. Molecular cell research
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Genotoxicity and Epigenotoxicity of Carbazole-Derived Molecules on MCF-7 Breast Cancer Cells

2021

The carbazole compounds PK9320 (1-(9-ethyl-7-(furan-2-yl)-9H-carbazol-3-yl)-N-methylmethanamine) and PK9323 (1-(9-ethyl-7-(thiazol-4-yl)-9H-carbazol-3-yl)-N-methylmethanamine), second-generation analogues of PK083 (1-(9-ethyl-9H-carbazol-3-yl)-N-methylmethanamine), restore p53 signaling in Y220C p53-mutated cancer cells by binding to a mutation-induced surface crevice and acting as molecular chaperones. In the present paper, these three molecules have been tested for mutant p53-independent genotoxic and epigenomic effects on wild-type p53 MCF-7 breast adenocarcinoma cells, employing a combination of Western blot for phospho-γH2AX histone, Comet assay and methylation-sensitive arbitrarily pr…

0301 basic medicinemedicine.disease_causeEpigenesis GeneticHistoneslcsh:Chemistry0302 clinical medicineSettore BIO/06 - Anatomia Comparata E Citologialcsh:QH301-705.5SpectroscopyEpigenomicsDNA methylationbiologyChemistryGeneral Medicine3. Good healthComputer Science Applicationscarbazole derivativeHistone030220 oncology & carcinogenesisDNA methylationMCF-7 CellsFemaleepigeneticSignal TransductionCarbazolesAntineoplastic AgentsBreast NeoplasmsArticleCatalysisInorganic Chemistry03 medical and health sciencesbreast cancermedicineHumansEpigeneticsPhysical and Theoretical ChemistryMolecular BiologyepigeneticsOrganic Chemistrygenomic instabilityComet assaySettore BIO/18 - Genetica030104 developmental biologylcsh:Biology (General)lcsh:QD1-999MCF-7carbazole derivativesCancer cellbiology.proteinCancer researchTumor Suppressor Protein p53GenotoxicityDNA DamageMutagensInternational Journal of Molecular Sciences
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CHK1-targeted therapy to deplete DNA replication-stressed, p53-deficient, hyperdiploid colorectal cancer stem cells.

2017

ObjectiveCancer stem cells (CSCs) are responsible for tumour formation and spreading, and their targeting is required for tumour eradication. There are limited therapeutic options for advanced colorectal cancer (CRC), particularly for tumours carrying RAS-activating mutations. The aim of this study was to identify novel CSC-targeting strategies.DesignTo discover potential therapeutics to be clinically investigated as single agent, we performed a screening with a panel of FDA-approved or investigational drugs on primary CRC cells enriched for CSCs (CRC-SCs) isolated from 27 patients. Candidate predictive biomarkers of efficacy were identified by integrating genomic, reverse-phase protein mic…

0301 basic medicinep53DNA ReplicationCELL CYCLE CONTROLDNA damageColorectal cancerColonmedicine.medical_treatmentAntineoplastic AgentsBiologyBioinformaticsmedicine.disease_causeDNA DAMAGETargeted therapy03 medical and health sciencesCancer stem cellCell Line TumormedicineHumansCHEK11506DRUG DEVELOPMENTOligonucleotide Array Sequence AnalysisMutationCOLORECTAL CANCERSettore MED/06 - ONCOLOGIA MEDICAGastroenterologyCHEMOTHERAPYmedicine.diseaseImmunohistochemistryPrexasertib030104 developmental biologyPyrazinesCheckpoint Kinase 1MutationCancer researchNeoplastic Stem CellsPyrazolesStem cellTumor Suppressor Protein p53Colorectal NeoplasmsGut
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Wip1 phosphatase: between p53 and MAPK kinases pathways.

2016

IF 5.008; International audience; Cells undergoing oncogenic transformation frequently inactivate tumor suppressor pathways that could prevent their uncontrolled growth. Among those pathways p53 and p38MAPK pathways play a critical role in regulation of cell cycle, senescence and cell death in response to activation of oncogenes, stress and DNA damage. Consequently, these two pathways are important in determining the sensitivity of tumor cells to anti-cancer treatment. Wild type p53-induced phosphatase, Wip1, is involved in governance of both pathways. Recently, strategies directed to manipulation with Wip1 activity proposed to advance current day anticancer treatment and novel chemical com…

0301 basic medicinep53Programmed cell deathDNA damagetumor suppressorPhosphatase[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyReviewPyruvate dehydrogenase phosphataseBiologyBioinformaticsmedicine.disease_causechemotherapyp38 Mitogen-Activated Protein Kinases[ SDV.CAN ] Life Sciences [q-bio]/Cancerphosphatase03 medical and health sciencesmedicineAnimalsHumansGenetically modified animal[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyCell CycleCell cycleCell biologyProtein Phosphatase 2C030104 developmental biologyCell Transformation NeoplasticOncologyMutationSignal transductionTumor Suppressor Protein p53CarcinogenesisDNA DamageSignal TransductionOncotarget
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