Search results for "Protein p53"

showing 10 items of 201 documents

Transcription, apoptosis and p53: catch-22

2005

The tumor suppressor p53 is a transcription factor and is activated in response to DNA damage or oncogenic transformation through modification of its interaction with regulatory proteins. The transcription factor activity of p53 is thought to mediate its primary functions of cell-cycle arrest and apoptosis through the gene expression it regulates, and evidence to support this interpretation continues to accumulate. However, reports of transcription-independent activities of p53, especially in the induction of apoptosis, persist. In particular, recent studies suggest that cytosolic p53 directly interacts with members of the BCL-2 family of apoptosis regulators, thereby triggering mitochondri…

Transcription GeneticTumor suppressor geneDNA damageApoptosisBiologylaw.inventionTranscription (biology)ApoptosislawGene expressionGeneticsCancer researchAnimalsHumansSuppressorE2F1Tumor Suppressor Protein p53Transcription factorTrends in Genetics
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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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Direct Activation of Bax by p53 Mediates Mitochondrial Membrane Permeabilization and Apoptosis

2004

The tumor suppressor p53 exerts its anti-neoplastic activity primarily through the induction of apoptosis. We found that cytosolic localization of endogenous wild-type or trans-activation–deficient p53 was necessary and sufficient for apoptosis. p53 directly activated the proapoptotic Bcl-2protein Bax in the absence of other proteins to permeabilize mitochondria and engage the apoptotic program. p53 also released both proapoptotic multidomain proteins and BH3-only proteins [Proapoptotic Bcl-2family proteins that share only the third Bcl-2homology domain (BH3)] that were sequestered by Bcl-xL. The transcription-independent activation of Bax by p53 occurred with similar kinetics and concentra…

Tumor suppressor geneProtein ConformationUltraviolet RaysWheat Germ AgglutininsRecombinant Fusion Proteinsbcl-X ProteinApoptosisEndogenyMitochondrionBiologyPermeabilityHomology (biology)law.inventionMiceCytosollawProto-Oncogene ProteinsMitochondrial membrane permeabilizationAnimalsHumansCells CulturedCell Line Transformedbcl-2-Associated X ProteinCell NucleusMultidisciplinaryCytochromes cIntracellular MembranesGenes p53MitochondriaCell biologyCytosolGene Expression RegulationProto-Oncogene Proteins c-bcl-2ApoptosisLiposomesMutationSuppressorTumor Suppressor Protein p53biological phenomena cell phenomena and immunityCarrier ProteinsBH3 Interacting Domain Death Agonist ProteinHeLa CellsScience
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Human Papilloma Virus-Dependent HMGA1 Expression Is a Relevant Step in Cervical Carcinogenesis

2008

HMGA1 is a member of a small family of architectural transcription factors involved in the coordinate assembly of multiprotein complexes referred to as enhanceosomes. In addition to their role in cell proliferation, differentiation, and development, high-mobility group proteins of the A type (HMGA) family members behave as transforming protoncogenes either in vitro or in animal models. Recent reports indicated that HMGA1 might counteract p53 pathway and provided an interesting hint on the mechanisms determining HMGA's transforming potential. HMGA1 expression is deregulated in a very large array of human tumors, including cervical cancer, but very limited information is available on the mole…

Uterine Cervical NeoplasmCancer ResearchDNA-Binding ProteinBiologyHeLa Celllcsh:RC254-282DNA-binding proteinRNA interferenceCell Line TumorHMGA1a ProteinRNA MessengerReceptor Notch1PapillomaviridaePapillomavirus InfectionPsychological repressionTranscription factorCell ProliferationReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingHMGAOncogene Proteins ViralCell Transformation Virallcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensHMGA1Gene Expression Regulation NeoplasticGene expression profilingCancer cellCancer researchbiology.proteinFemaleTumor Suppressor Protein p53HumanNeoplasia
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Wee1 inhibition potentiates Wip1-dependent p53-negative tumor cell death during chemotherapy

2016

AbstractInactivation of p53 found in more than half of human cancers is often associated with increased tumor resistance to anti-cancer therapy. We have previously shown that overexpression of the phosphatase Wip1 in p53-negative tumors sensitizes them to chemotherapeutic agents, while protecting normal tissues from the side effects of anti-cancer treatment. In this study, we decided to search for kinases that prevent Wip1-mediated sensitization of cancer cells, thereby interfering with efficacy of genotoxic anti-cancer drugs. To this end, we performed a flow cytometry-based screening in order to identify kinases that regulated the levels of γH2AX, which were used as readout. Another criter…

Wip1ApoptosisCell Cycle ProteinsPharmacologyMESH: G2 Phase Cell Cycle CheckpointsHistonesMESH : PhosphorylationMiceMESH : Cell Cycle ProteinsMESH: AnimalsMESH: Tumor Suppressor Protein p53MESH: HistonesKinaseTp53 mutationsMESH : Mice Transgenic3. Good healthProtein Phosphatase 2CSurvival RateMESH : Antineoplastic AgentsH2ax phosphorylationP53 activationMESH: Protein Phosphatase 2CRNA InterferenceMESH : Colorectal NeoplasmsMESH : Carrier ProteinsHistone H2axMESH: MitochondriaImmunologyHuman fibroblastsMESH: Carrier ProteinsAntineoplastic AgentsMESH: Protein-Tyrosine KinasesMESH: Protein-Serine-Threonine KinasesMESH : Cisplatin03 medical and health sciencesMESH: Cell Cycle ProteinsGenotoxic stressMESH : Protein-Tyrosine KinasesHumansMESH : HistonesAnticancer TherapyMESH: DNA DamageCisplatinMESH: HumansMESH: Phosphorylation[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMESH : HumansMESH : Nuclear Proteins030104 developmental biologyCancer cellMESH: Antineoplastic AgentsCisplatinCarrier ProteinsMESH: Nuclear ProteinsMESH : ApoptosisDna-damage response0301 basic medicineCancer ResearchMESH: Caspase 3MESH : Caspase 3PhosphorylationCytotoxicityMESH : DNA DamageSensitizationmedicine.diagnostic_testCaspase 3Nuclear ProteinsProtein-Tyrosine KinasesMESH : Survival RateMitochondriaG2 Phase Cell Cycle CheckpointsWee1medicine.anatomical_structureMESH : Protein Phosphatase 2COriginal ArticleMESH : MitochondriaColorectal Neoplasmsmedicine.drugMESH : Protein-Serine-Threonine KinasesMESH: Cell Line TumorMESH: Survival RateMESH: Mice TransgenicMESH: RNA InterferencePhosphataseMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesFlow cytometryCellular and Molecular NeuroscienceCell Line TumorMESH : MicemedicineAnimalsMESH: MiceMESH : Cell Line TumorMESH: ApoptosisCell BiologyMESH : Tumor Suppressor Protein p53MESH: CisplatinCancer researchbiology.proteinMESH : AnimalsMESH : G2 Phase Cell Cycle CheckpointsMESH : RNA InterferenceTumor Suppressor Protein p53MESH: Colorectal NeoplasmsDNA DamageCell Death & Disease
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Apoptosis and cell cycle aberrations in epithelial odontogenic lesions : an evidence by the expression of p53, Bcl-2 and Bax

2017

Background Ameloblastoma (AMB), odontogenic keratocyst (OKC) and adenomatoid odontogenic tumor (AOT) are epithelial odontogenic lesions with diverse biologic profiles. Defects in regulation of apoptosis and cell cycle may be involved in the development and progression of those lesions, therefore we aimed to investigate the expression of Bcl-2, Bax and p53 to better understand the possible role of these proteins in AMBs, OKCs and AOTs. Material and Methods The studied sample consisted of 20 AMBs, 20 OKCs and 20 AOTs. Immunohistochemistry technique was performed for the antibodies p53, Bcl-2 and Bax. Immunoreactivity was observed in the epithelial component and positive cells were counted in …

bcl-X ProteinApoptosisAmeloblastoma03 medical and health sciences0302 clinical medicinemedicineHumansKeratocystCell Cycle ProteinAmeloblastomaGeneral Dentistrybcl-2-Associated X ProteinOral Medicine and PathologybiologyAdenomatoid odontogenic tumorResearchCell Cycle030206 dentistryCell cyclemedicine.disease:CIENCIAS MÉDICAS [UNESCO]ImmunohistochemistryJaw NeoplasmsOtorhinolaryngologyApoptosis030220 oncology & carcinogenesisUNESCO::CIENCIAS MÉDICASOdontogenic Cystsbiology.proteinCancer researchImmunohistochemistryOdontogenesisSurgerymedicine.symptomAntibodyTumor Suppressor Protein p53
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Potential role of p53 protein as a novel biomarker of sperm quality, able to predict the success of ART techniques. EcoFoodFertility Project

2018

Introduction: Protein p53 is well known as “The guardian of genome”; it changes its concentration in human spermatozoa DNAin relation to the damage of the latter. It has been suggested thatthe role of the p53 ancestral gene was to ensure the integrity ofthe genomic germline and the fidelity of the evelopment process.The aim of this study is to evaluate if different concentrations of p53 protein in human spermatozoa could influence embryo quality and pregnancy rate and possibly representing a potential predictive marker of sperm quality for successful fertilization .Methods: From July 2013 to June 2017 we have examinatedretrospectively 79 couples with 2-5 years of infertility history.Males had…

business.industryProtein p53 human spermatozoa biomarker of sperm quality.P53 proteinBiomarker (medicine)MedicineComputational biologySettore BIO/06 - Anatomia Comparata E CitologiaSperm qualityToxicologybusinessReproductive Toxicology
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Sequence-specific and DNA structure-dependent interactions of Escherichia coli MutS and human p53 with DNA

2013

Many proteins involved in DNA repair systems interact with DNA that has structure altered from the typical B-form helix. Using magnetic beads to immobilize DNAs containing various types of structures, we evaluated the in vitro binding activities of two well-characterized DNA repair proteins, Escherichia coli MutS and human p53. E. coli MutS bound to double-stranded DNAs, with higher affinity for a G/T mismatch compared to a G/A mismatch and highest affinity for larger non-B-DNA structures. E. coli MutS bound best to DNA between pH 6 and 9. Experiments discriminated between modes of p53-DNA binding, and increasing ionic strength reduced p53 binding to nonspecific double-stranded DNA, but had…

chemistry.chemical_classificationDNA ligaseDNA clampHMG-boxBase pairEscherichia coli ProteinsOsmolar ConcentrationBiophysicsDNACell BiologyBiologyBiochemistryMutS DNA Mismatch-Binding ProteinDNA binding siteBiochemistrychemistryMutS-1Escherichia coliHumansNucleic Acid ConformationProtein–DNA interactionAmino Acid SequenceTumor Suppressor Protein p53Molecular BiologyReplication protein AAnalytical Biochemistry
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Progenitor death drives retinal dysplasia and neuronal degeneration in a mouse model of Atrip-Seckel syndrome

2020

ABSTRACT Seckel syndrome is a type of microcephalic primordial dwarfism (MPD) that is characterized by growth retardation and neurodevelopmental defects, including reports of retinopathy. Mutations in key mediators of the replication stress response, the mutually dependent partners ATR and ATRIP, are among the known causes of Seckel syndrome. However, it remains unclear how their deficiency disrupts the development and function of the central nervous system (CNS). Here, we investigated the cellular and molecular consequences of ATRIP deficiency in different cell populations of the developing murine neural retina. We discovered that conditional inactivation of Atrip in photoreceptor neurons …

lcsh:MedicineMedicine (miscellaneous)315BlindnessMicechemistry.chemical_compoundImmunology and Microbiology (miscellaneous)Cell DeathneurodevelopmentStem CellsNeurodegenerationapoptosisneurodegenerationSyndromeCell biologyDNA-Binding Proteinsdna damage responsemedicine.anatomical_structurePhotoreceptor Cells VertebrateResearch Articlelcsh:RB1-214NeurogenesisNeuroscience (miscellaneous)Embryonic DevelopmentBiologyRetinaGeneral Biochemistry Genetics and Molecular Biologylcsh:PathologymedicineAnimalsAbnormalities MultipleProgenitor cellVision OcularAdaptor Proteins Signal TransducingCell ProliferationProgenitorRetinalcsh:RRetinalEmbryo Mammalianmedicine.diseasephotoreceptorDisease Models AnimalSeckel syndromechemistryvisual system developmentNerve DegenerationRetinal dysplasiaRetinal DysplasiaTumor Suppressor Protein p53Primordial dwarfismDNA DamageDisease Models & Mechanisms
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Synergistic cytotoxic interactions between sodium butyrate, MG132 and camptothecin in human retinoblastoma Y79 cells.

2000

This paper studies the effects caused in human retinoblastoma Y79 cells by treatment with combinations of sodium butyrate, the inhibitor of topoisomerase I camptothecin and the inhibitor of 26S proteasome MG132. The combination of sodium butyrate and camptothecin resulted in a strong synergistic cytotoxicity, as revealed by combination indices of 0.77 and 0.52 calculated at IC(50) and IC(75). Synergistic interactions were also demonstrated for combinations of sodium butyrate and MG132, camptothecin and MG132 and for a combination of all three compounds. The cytotoxic effects observed after the combined treatments can be considered a consequence of apoptosis, as suggested by the appearance o…

medicine.drug_classCell SurvivalLeupeptinsSodiumchemistry.chemical_elementApoptosisButyrateBiologyCysteine Proteinase Inhibitorschemistry.chemical_compoundMG132Antineoplastic Combined Chemotherapy ProtocolsmedicineTumor Cells CulturedHumansheterocyclic compoundsEnzyme InhibitorsRetinoblastomaCaspase 3TopoisomeraseRetinoblastomaSodium butyrateDrug SynergismGeneral Medicinemedicine.diseaseeye diseasesEnzyme ActivationButyrateschemistryBiochemistryProto-Oncogene Proteins c-bcl-2CaspasesCancer researchbiology.proteinCamptothecinTopoisomerase I InhibitorsTumor Suppressor Protein p53CamptothecinTopoisomerase inhibitormedicine.drugTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
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