Search results for "Proto-Oncogene Proteins c-mdm2"

showing 10 items of 21 documents

The MDM2-p53 pathway is involved in preconditioning-induced neuronal tolerance to ischemia

2018

Brain preconditioning (PC) refers to a state of transient tolerance against a lethal insult that can be evoked by a prior mild event. It is thought that PC may induce different pathways responsible for neuroprotection, which may involve the attenuation of cell damage pathways, including the apoptotic cell death. In this context, p53 is a stress sensor that accumulates during brain ischemia leading to neuronal death. The murine double minute 2 gene (MDM2), a p53-specific E3 ubiquitin ligase, is the main cellular antagonist of p53, mediating its degradation by the proteasome. Here, we study the role of MDM2-p53 pathway on PC-induced neuroprotection both in cultured neurons (in vitro) and rat …

Cell death0301 basic medicineProgrammed cell deathCell SurvivalNeuronalScience2415 Biología MolecularIschemiaNeuroprotectionArticleBrain ischemiaMiceBrain ischemia03 medical and health sciences0302 clinical medicineIschemiaXarxes neuronals (Neurobiologia)medicineAnimalsIschemic PreconditioningCell damageCells CulturedBrain preconditioningNeuronsMultidisciplinarybiologyChemistryQRBrainProto-Oncogene Proteins c-mdm2MDM2-p53medicine.diseaseNeuroprotectionRatsCell biologyUbiquitin ligaseDisease Models Animal030104 developmental biology2490 Neurocienciasbiology.proteinMedicineIschemic preconditioningMdm2Tumor Suppressor Protein p53030217 neurology & neurosurgerySignal Transduction
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Molecular modeling approaches in the discovery of new drugs for anti-cancer therapy: the investigation of p53-MDM2 interaction and its inhibition by …

2010

The mdm2 oncogene product, MDM2, is an ubiquitin protein ligase that inhibits the transcriptional activity of the tumor suppressor p53 and promotes its degradation. About 50% of all human cancers present mutations or deletions in the TP53 gene. In the remaining half of all human neoplasias that express the wild-type protein, aberrations of p53 regula- tors, such as MDM2, account for p53 inhibition. For this reason, designing small-molecule inhibitors of the p53-MDM2 protein-protein interaction is a promising strategy for the treatment of cancers retaining wild-type p53. The development of inhibitors has been challenging. Although many small-molecule MDM2 inhibitors have shown potent in vitr…

IndolesTumor suppressor geneAntineoplastic AgentsMolecular Dynamics SimulationBioinformaticsBiochemistryGene productNeoplasmsDrug DiscoverymedicineHumansImidazolinesMolecular Modeling New Drugs for Anti-Cancer Therapy p53-MDM2 InteractionPharmacologyBenzodiazepinonesbiologyOncogeneOrganic ChemistryCancerProto-Oncogene Proteins c-mdm2medicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaSmall moleculeUbiquitin ligaseOxindolesProtein Structure TertiaryDrug Designbiology.proteinCancer researchMolecular MedicineMdm2PharmacophoreTumor Suppressor Protein p53Current medicinal chemistry
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Novel isatin-derived molecules activate p53 via interference with Mdm2 to promote apoptosis

2018

International audience; The p53 protein is a key tumor suppressor in mammals. In response to various forms of genotoxic stress p53 stimulates expression of genes whose products induce cell cycle arrest and/or apoptosis. An E3-ubiquitin ligase, Mdm2 (mouse-double-minute 2) and its human ortholog Hdm2, physically interact with the amino-terminus of p53 to mediate its ubiquitin-mediated degradation via the proteasome. Thus, pharmacological inhibition of the p53-Mdm2 interaction leads to overall stabilization of p53 and stimulation of its anti-tumorigenic activity. In this study we characterize the biological effects of a novel class of non-genotoxic isatin Schiff and Mannich base derivatives (…

Isatin0301 basic medicineProgrammed cell deathCell cycle checkpointAntineoplastic AgentsApoptosis[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyPiperazinesHistonesMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineNutlinCell Line TumorProto-Oncogene ProteinsAnimalsHumansMolecular Biologychemistry.chemical_classificationDNA ligaseIsatinImidazolesISMBDsProto-Oncogene Proteins c-mdm2Cell BiologyNutlinp53-activating moleculesCell biology030104 developmental biologychemistryProteasomeApoptosis030220 oncology & carcinogenesisbiology.proteinMdm2PumaTumor Suppressor Protein p53Apoptosis Regulatory Proteinsautomated microscopy system OperettaResearch PaperDevelopmental BiologyCell Cycle
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Anaplastic Wilms' tumour, a subtype displaying poor prognosis, harbours p53 gene mutations

1994

The genetics of Wilms' tumour (WT), a paediatric malignancy of the kidney, is complex. Inactivation of the tumour suppressor gene, WT1, is associated with tumour aetiology in approximately 10-15% of WTs. Chromosome 17p changes have been noted in cytogenetic studies of WTs, prompting us to screen 140 WTs for p53 mutations. When histopathology reports were available, p53 mutations were present in eight of eleven anaplastic WTs, a tumour subtype associated with poor prognosis. Amplification of MDM2, a gene whose product binds and sequesters p53, was excluded. Our results indicate that p53 alterations provide a molecular marker for anaplastic WTs.

MaleTumor suppressor geneDNA Mutational AnalysisMolecular Sequence DataGene mutationBiologyMalignancymedicine.disease_causePolymerase Chain ReactionWilms TumorProto-Oncogene ProteinsGeneticsmedicineHumansAmino Acid SequenceGeneAllelesMutationBase SequencefungiNuclear ProteinsCell DifferentiationProto-Oncogene Proteins c-mdm2Wilms' tumorGenes p53Prognosismedicine.diseaseKidney NeoplasmsNeoplasm ProteinsGene Expression Regulation Neoplasticbody regionsGenetic markerbiology.proteinCancer researchMdm2FemaleTumor Suppressor Protein p53Nature Genetics
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Effects of the MDM2 inhibitor Nutlin-3a on sensitivity of pancreatic cancer cells to berberine and modified berberines in the presence and absence of…

2021

Abstract Approaches to improve pancreatic cancer therapy are essential as this disease has a very bleak outcome. Approximately 80% of pancreatic cancers are pancreatic ductal adenocarcinomas (PDAC). A key regulatory gene frequently mutated (∼75%) in PDAC is the TP53 tumor suppressor gene which controls the transcription of multiple genes involved in cell cycle progression, apoptosis, cancer progression and other growth regulatory processes. The mouse double minute 2 homolog (MDM2) gene product is a nuclear-localized E3 ubiquitin ligase and negatively regulates the TP53 protein which results in its proteasomal degradation. Various MDM2 inhibitors have been isolated and examined in clinical t…

Nutlin-3aCancer ResearchBerberineendocrine system diseasesTumor suppressor geneNAX compoundsApoptosisPiperazinesTargeted therapyGene productCell Line TumorPancreatic cancerGeneticsmedicineHumansTP53neoplasmsMolecular BiologyRegulator geneNAX compundsbiologyChemistryImidazolesPDACCancerProto-Oncogene Proteins c-mdm2PDCAmedicine.diseaseUbiquitin ligasePancreatic NeoplasmsCell culturebiology.proteinCancer researchNAX compoundMolecular MedicineMdm2Tumor Suppressor Protein p53Signal TransductionAdvances in Biological Regulation
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Molecular and immunohistochemical analysis of the prognostic value of cell-cycle regulators in urothelial neoplasms of the bladder.

2006

Abstract Objective To evaluate the prognostic and predictive value of molecular and immunohistochemical markers related to cell-cycle control in terms of recurrence, progression, and survival in urothelial neoplasms of the bladder (UNB). Patients and Methods Clinical and pathological findings of 84 patients with UNB were assessed. Homozygous deletion (HD) and promoter methylation of p14 ARF , p15 INK4B , p16 INK4A , loss of heterozygosity of the locus 9p21, p53 mutations, and immunohistochemical expression of p53, p16, p14, p21, p27, pRb, Ki67, MDM2, and cyclin D1 proteins were evaluated in relation to overall survival (OS), recurrence-free survival (RFS), and progression-free survival (PFS…

OncologyMalemedicine.medical_specialtyUrologyCell Cycle ProteinsLoss of heterozygosityCyclin D1p14arfPredictive Value of TestsInternal medicineTumor Suppressor Protein p14ARFmedicineBiomarkers TumorHumansCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p15Univariate analysisBladder cancerbusiness.industryCarcinomaRetinoblastomaAnatomical pathologyProto-Oncogene Proteins c-mdm2Cell cyclemedicine.diseasePrognosisImmunohistochemistrySurvival AnalysisKi-67 AntigenMolecular Diagnostic TechniquesUrinary Bladder NeoplasmsCancer researchDisease ProgressionImmunohistochemistryFemaleNeoplasm Recurrence LocalTumor Suppressor Protein p53UrotheliumbusinessCyclin-Dependent Kinase Inhibitor p27European urology
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Molecular dynamics studies on Mdm2 complexes: An analysis of the inhibitor influence

2012

p53 is a powerful anti-tumoral molecule frequently inactivated by mutations or deletions in cancer. However, half of all human tumors expresses wild-type p53, and its activation, by antagonizing its negative regulator Mdm2, might offer a new strategy for therapeutic protocol. In this work, we present a molecular dynamics study on Mdm2 structure bound to two different known inhibitors with the aim to investigate the structural transitions between apo-Mdm2 and Mdm2-inhibitor complexes. We tried to gain information about conformational changes binding a benzodiazepine derivative inhibitor with respect the known nutlin and the apo form. The conformational changes alter the size of the cleft and…

Protein ConformationBiophysicsMolecular Dynamics SimulationMdm2 p53 nutlin benzodiazepine Molecular DynamicsBiochemistryNegative regulatorBenzodiazepineschemistry.chemical_compoundMolecular dynamicsHumansMoleculeEnzyme InhibitorsMolecular BiologyBinding SitesbiologyChemistryProto-Oncogene Proteins c-mdm2Cell BiologyNutlinSettore CHIM/08 - Chimica FarmaceuticaBiochemistryDrug DesignBiophysicsbiology.proteinMdm2LinkerBiochemical and Biophysical Research Communications
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Parthenolide sensitizes hepatocellular carcinoma cells to trail by inducing the expression of death receptors through inhibition of STAT3 activation

2011

This article shows that HepG2, Hep3B, and SK-Hep1 cells, three lines of human hepatocellular carcinoma (HCC) cells, are resistant to apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Parthenolide, a sesquiterpene lactone found in European feverfew, has been shown to exert both anti-inflammatory and anti-cancer activities. This article demonstrates that co-treatment with parthenolide and TRAIL-induced apoptosis with synergistic interactions in the three lines of HCC cells. In order to explain these effects we ascertained that parthenolide increased either at protein or mRNA level the total content of death receptors TRAIL-R1 and -R2 as well as their surfac…

STAT3 Transcription FactorCarcinoma HepatocellularPhysiologyClinical BiochemistryCellDown-RegulationTRAILApoptosisPharmacologyParthenolideSTAT3TNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundSettore BIO/10 - BiochimicamedicineHumansParthenolidePhosphorylationReceptorSTAT3CaspaseJanus KinasesbiologyLiver NeoplasmsProto-Oncogene Proteins c-mdm2Hep G2 CellsReceptors Death DomainCell BiologyapoptosiEnzyme ActivationGene Expression Regulation Neoplasticmedicine.anatomical_structurechemistryCell cultureApoptosisCaspasesbiology.proteinSTAT proteinDrug Screening Assays AntitumorTumor Suppressor Protein p53SesquiterpenesJournal of Cellular Physiology
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Paclitaxel and beta-lapachone synergistically induce apoptosis in human retinoblastoma Y79 cells by downregulating the levels of phospho-Akt.

2009

Paclitaxel (PTX) and beta-lapachone (LPC) are naturally occurring compounds that have shown a large spectrum of anticancer activity. In this article we show for the first time that PTX/LPC combination induces potent synergistic apoptotic effects in human retinoblastoma Y79 cells. Combination of suboptimal doses of PTX (0.3 nM) and LPC (1.5 microM) caused biochemical and morphological signs of apoptosis at 48 h of treatment. These effects were accompanied by potent lowering in inhibitor of apoptosis proteins and by activation of Bid and caspases 3 and 6 with lamin B and PARP breakdown. PTX/LPC combination acted by favoring p53 stabilization through a lowering in p-Akt levels and in ps166-MDM…

Time FactorsPhysiologyClinical BiochemistryApoptosisInhibitor of Apoptosis ProteinsWortmanninchemistry.chemical_compoundSettore BIO/10 - BiochimicaAntineoplastic Combined Chemotherapy ProtocolsPhosphorylationCaspasebiologyCaspase 6Lamin Type BCaspase 3Protein StabilityRetinoblastomaDrug SynergismProto-Oncogene Proteins c-mdm2TransfectionBiochemistrylipids (amino acids peptides and proteins)Poly(ADP-ribose) PolymerasesWortmanninBH3 Interacting Domain Death Agonist Proteinretinoblastoma survival factors apoptosisPaclitaxelCell SurvivalPoly ADP ribose polymeraseActive Transport Cell NucleusDown-RegulationInhibitor of apoptosisTransfectionCell Line TumorHumansProtein kinase BProtein Kinase InhibitorsCell NucleusDose-Response Relationship DrugCell BiologyAntineoplastic Agents PhytogenicAndrostadieneschemistryCell cultureApoptosisbiology.proteinCancer researchTumor Suppressor Protein p53Proto-Oncogene Proteins c-aktNaphthoquinonesJournal of cellular physiology
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Analysis of p53 and mdm2 proteins in malignant fibrous histiocytoma in absence of gene alteration: prognostic significance.

2000

TP53 and MDM2 genes and their protein expression were evaluated in frozen and paraffin-embedded tissue from 27 patients with malignant fibrous histiocytoma to elucidate the relationship between them, their implication in tumor progression mechanisms and their possible diagnostic-prognostic value in malignant fibrous histiocytoma. Single-strand conformation polymorphism analysis and direct sequencing of polymerase chain reaction-amplified DNA were used to establish two TP53 mutations (7.4%): a point mutation and a 63-bp duplication. Amplification of the MDM2 gene was observed in two tumors (7.4%) by means of Southern-blot analysis, one of them also carrying the TP53 point mutation. Immunohis…

Tumor suppressor geneBlotting WesternSoft Tissue NeoplasmsBiologyPolymerase Chain ReactionPathology and Forensic MedicineImmunoenzyme TechniquesMiceProto-Oncogene ProteinsGene duplicationGene expressionAnimalsHumansneoplasmsMolecular BiologyGeneTP53 Gene MutationPolymorphism Single-Stranded ConformationalCell NucleusMice Inbred BALB CHistiocytoma Benign FibrousPoint mutationNuclear ProteinsSingle-strand conformation polymorphismProto-Oncogene Proteins c-mdm2Cell BiologyGeneral MedicineDNA NeoplasmMolecular biologyNeoplasm ProteinsSurvival RateBlotting SouthernTumor progressionMutationCancer researchNeoplasm Recurrence LocalTumor Suppressor Protein p53Virchows Archiv : an international journal of pathology
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