Search results for "Protein p53"

showing 10 items of 201 documents

p53 Involvement in the control of murine hair follicle regression.

2001

p53 is a transcription factor mediating a variety of biological responses including apoptotic cell death. p53 was recently shown to control apoptosis in the hair follicle induced by ionizing radiation and chemotherapy, but its role in the apoptosis-driven physiological hair follicle regression (catagen) remains to be elucidated. Here, we show that p53 protein is strongly expressed and co-localized with apoptotic markers in the regressing hair follicle compartments during catagen. In contrast to wild-type mice, p53 knockout mice show significant retardation of catagen accompanied by significant decrease in the number of apoptotic cells in the hair matrix. Furthermore, p53 null hair follicles…

medicine.medical_specialtyTumor suppressor genemedicine.medical_treatmentDown-RegulationApoptosisBiologyPathology and Forensic MedicineTelogen effluviumMiceBcl-2-associated X proteinDownregulation and upregulationInternal medicineProto-Oncogene ProteinsmedicineAnimalsbcl-2-Associated X ProteinMice Knockoutintegumentary systemGrowth factorAlopecia areatamedicine.diseaseHair follicleCell biologyUp-RegulationMice Inbred C57BLEndocrinologymedicine.anatomical_structureInsulin-Like Growth Factor Binding Protein 3Proto-Oncogene Proteins c-bcl-2Knockout mousebiology.proteinCommentaryFemaleTumor Suppressor Protein p53Hair FollicleThe American journal of pathology
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Generating p53-specific cytotoxic T lymphocytes by recombinant adenoviral vector-based vaccination in mice, but not man.

2002

Mutations and aberrant expression of the p53 tumor suppressor protein are the most frequent molecular alterations in human malignancy. Peptides derived from the wild-type (wt) p53 protein and presented by major histocompatibility complex (MHC) molecules for T lymphocyte recognition are believed to serve as universal tumor-associated antigens for cancer immunotherapy. We studied the immunogeneicity of a recombinant replication-defective adenoviral vector encoding human full-length wt p53 (rAd/hup53) in human leukocyte antigen (HLA)-A2K(b)-transgenic (Tg) mice and man. The generation of p53 epitope-specific cytotoxic T lymphocytes (CTLs) in p53-proficient and p53-deficient A2K(b)-Tg mice was …

medicine.medical_treatmentGenetic VectorsEpitopes T-LymphocyteMice TransgenicPilot ProjectsHuman leukocyte antigenBiologyMajor histocompatibility complexCancer VaccinesEpitopeAdenoviridaeMiceImmune systemCancer immunotherapyAntigenSpecies SpecificityNeoplasmsHLA-A2 AntigenGeneticsmedicineCytotoxic T cellAnimalsHumansTreatment FailureMolecular BiologyT lymphocyteGenetic TherapyGenes p53Self ToleranceImmunologybiology.proteinMolecular MedicineTumor Suppressor Protein p53T-Lymphocytes CytotoxicGene therapy
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Epigenetic siRNA and Chemical Screens Identify SETD8 Inhibition as a Therapeutic Strategy for p53 Activation in High-Risk Neuroblastoma

2017

Given the paucity of druggable mutations in high-risk neuroblastoma (NB), we undertook chromatin-focused small interfering RNA and chemical screens to uncover epigenetic regulators critical for the differentiation block in high-risk NB. High-content Opera imaging identified 53 genes whose loss of expression led to a decrease in NB cell proliferation and 16 also induced differentiation. From these, the secondary chemical screen identified SETD8, the H4K20me1 methyltransferase, as a druggable NB target. Functional studies revealed that SETD8 ablation rescued the pro-apoptotic and cell-cycle arrest functions of p53 by decreasing p53K382me1, leading to activation of the p53 canonical pathway. I…

p530301 basic medicineCancer ResearchSmall interfering RNAMethyltransferaseCellular differentiationDruggabilityBiologyArticleEpigenesis GeneticNeuroblastoma03 medical and health sciences0302 clinical medicineNeuroblastomamedicineHumansEpigeneticsRNA Small InterferingGeneCell ProliferationsiRNA screenCell growthQuinazolineCell DifferentiationdifferentiationHistone-Lysine N-Methyltransferasemedicine.diseaseSETD8030104 developmental biologyOncology030220 oncology & carcinogenesisQuinazolinesCancer researchdifferentiation; epigenetics; neuroblastoma; p53; SETD8; siRNA screen; Oncology; Cell Biology; Cancer ResearchTumor Suppressor Protein p53epigeneticHuman
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Expression of p63, p53 and ki-67 in patients with cervical intraepithelial neoplasia

2017

Objective: Cervical intraepithelial neoplasia (CIN) is a dysplastic process in cervical squamous epithelium and carries a risk of progression to cervical cancer. The aim of this study was to compare expression of three biomarkers named p53, p63 and Ki-67 in patients with various grades of cervical intraepithelial neoplasia and in a control group. Material and Method: 58 patients were enrolled in the study. Each patient underwent a colposcopy-guided biopsy of the cervix. Immunostaining for markers (p53, p63 and Ki-67) was performed on tissue samples of normal cases (n=10), CIN I (n=20), CIN II (n=14), and CIN III (n=14). Results: Our study showed a significant increase of the expression of t…

p530301 basic medicineUterine Cervical Neoplasmsurologic and male genital diseasesGastroenterology0302 clinical medicineYoung adultCervical cancerp63medicine.diagnostic_testbiologyvirus diseasesMiddle AgedImmunohistochemistryfemale genital diseases and pregnancy complicationsKoilocytesurgical procedures operativemedicine.anatomical_structure030220 oncology & carcinogenesisKi-67Disease ProgressionKi-67ImmunohistochemistryFemalelcsh:RB1-214Adultmedicine.medical_specialtyAdolescentCervical intraepithelial neoplasiaPathology and Forensic MedicineYoung Adult03 medical and health sciencesInternal medicineBiopsyBiomarkers Tumorlcsh:PathologymedicineHumansneoplasmsCervixCervical intraepithelial neoplasiabusiness.industryMembrane ProteinsUterine Cervical Dysplasiamedicine.diseaseKi-67 Antigen030104 developmental biologybiology.proteinTumor Suppressor Protein p53businessTurkish Journal of Pathology
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p73 deficiency results in impaired self renewal and premature neuronal differentiation of mouse neural progenitors independently of p53

2010

10 p.-5 fig.

p53Cancer ResearchGenotypeCellular differentiationImmunologyPopulationp73RegulatorBiologyCellular and Molecular NeuroscienceMiceNeurosphereAnimalsProgenitor celleducationCell ProliferationNeuronsNeural stem cellseducation.field_of_studyCell growthTumor Suppressor ProteinsNuclear ProteinsCell DifferentiationNeurodegenerative DiseasesTumor Protein p73Cell BiologyEmbryonic stem cellasymmetric divisionNeural stem cellCell biologyDNA-Binding ProteinsDifferentiationSelf-renewalOriginal ArticleTumor Suppressor Protein p53
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Apollon gene silencing induces apoptosis in breast cancer cells via p53 stabilisation and caspase-3 activation

2009

We analysed the effects of small interfering RNA (siRNA)-mediated silencing of Apollon, a member of the inhibitors of apoptosis protein family, on the proliferative potential and ability of human breast cancer cell lines to undergo apoptosis. In wild-type p53 ZR75.1 cells, Apollon knockdown resulted in a marked, time-dependent decline of cell growth and an increased rate of apoptosis, which was associated with p53 stabilisation and activation of the mitochondrial-dependent apoptotic pathway. Pre-incubation of cells with a p53-specific siRNA resulted in a partial rescue of cell growth inhibition, as well as in a marked reduction of the apoptotic response, indicating p53 as a major player in …

p53Cancer ResearchSmall interfering RNAProgrammed cell deathcaspase-3ApollonCaspase 3Breast NeoplasmsApollon gene apoptosisBiologyModels BiologicalInhibitor of Apoptosis ProteinsRNA interferenceTumor Cells CulturedGene silencingHumansGene SilencingRNA Small InterferingCell Proliferationhuman breast cancerGene knockdownCell growthCaspase 3Protein StabilityapoptosisEnzyme ActivationOncologyApoptosissiRNACancer researchSettore BIO/14 - FarmacologiaFemaleTumor Suppressor Protein p53Translational Therapeutics
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Endoderm development requires centrioles to restrain p53-mediated apoptosis in the absence of ERK activity

2021

Centrioles comprise the heart of centrosomes, microtubule-organizing centers. To study the function of centrioles in lung and gut development, we genetically disrupted centrioles throughout the mouse endoderm. Surprisingly, removing centrioles from the endoderm did not disrupt intestinal growth or development but blocked lung branching. In the lung, acentriolar SOX2-expressing airway epithelial cells apoptosed. Loss of centrioles activated p53, and removing p53 restored survival of SOX2-expressing cells, lung branching, and mouse viability. To investigate how endodermal p53 activation specifically killed acentriolar SOX2-expressing cells, we assessed ERK, a prosurvival cue. ERK was active t…

p53Cell SurvivalApoptosisInbred C57BLMedical and Health SciencesArticleGeneral Biochemistry Genetics and Molecular BiologyMiceMorphogenesis2.1 Biological and endogenous factorsAnimalscentrioleintestine developmentAetiologyExtracellular Signal-Regulated MAP KinasesendodermLungMolecular BiologyCentriolesSOXB1 Transcription FactorsStem CellsEndodermapoptosisEpithelial CellsCell BiologyBiological SciencesIntestinesMice Inbred C57BLlung branchingERKembryonic structuresTumor Suppressor Protein p53Microtubule-Associated ProteinsDevelopmental BiologyDevelopmental Cell
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Heterogeneity within and between primary colorectal carcinomas and matched metastases as revealed by analysis of Ki-ras and p53 mutations

2004

Analysis of the genetic status of Ki-ras and p53 in primary colorectal carcinomas and matched colorectal liver metastasis from 30 patients reveals an overall heterogeneity both within and between the two tumoral tissues. Both genes were found mutated with a similar frequency in both tissues; however, identical mutations in primary tumor and matched metastasis were found less frequently in the case of the Ki-ras than the p53 gene. Only in three cases the same p53 and Ki-ras mutations found in the primary tumor were found also in the metastasis. In several metastatic specimens the DNA bearing a mutation detected also in the primary tumor appears significantly less abundant than the wild-type …

p53Colorectal cancerDNA Mutational AnalysisStatistics as TopicBiophysicsKi-raBiologyOncogene Protein p21(ras)medicine.disease_causeBiochemistryMetastasisMetastasischemistry.chemical_compoundSequence Homology Nucleic AcidmedicineHumansMolecular BiologyGeneRegulation of gene expressionMutationGene Expression ProfilingCarcinomaLiver NeoplasmsCell BiologySequence Analysis DNAmedicine.diseasePrimary tumorGene expression profilingGene Expression Regulation NeoplasticColorectal carcinomaGenes raschemistryMutationCancer researchTumor Suppressor Protein p53Colorectal NeoplasmsDNA
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UV-B exposure causes DNA damage and changes in protein expression in northern pike (Esox lucius) posthatched embryos.

2012

The ongoing anthropogenically caused ozone depletion and climate change has increased the amount of biologically harmful UV-B radiation, which is detrimental to fish in embryonal stages. The effects of UV-B radiation on the levels and locations of DNA damage manifested as cyclobutane pyrimidine dimers (CPDs), heat shock protein 70 (HSP70) and p53 protein in newly hatched embryos of pike were examined. Pike larvae were exposed in the laboratory to current and enhanced doses of UV-B radiation. UV-B exposure caused the formation of CPDs in a fluence rate-dependent manner, and the CPDs were found deeper in the tissues with increasing fluence rates. UV-B radiation induced HSP70 in epidermis, and…

p53Embryo NonmammalianDNA damagehaukiUltraviolet RaysBlotting WesternNorthern pikeGene ExpressionPyrimidine dimerBiologyEyeBiochemistryProtein expressionultravioletti-B-säteilyDNA-vauriotAnimalsHSP70 Heat-Shock ProteinsPhysical and Theoretical ChemistryEsoxHSP70kalan alkiopoikasetPikecomputer.programming_languageEpidermis (botany)BrainEmbryoGeneral MedicineAnatomybiology.organism_classificationMolecular biologyultraviolet-BImmunohistochemistryfish embryosHsp70Pyrimidine DimersEsocidaeDNA damageEpidermisTumor Suppressor Protein p53computerDNA DamagePhotochemistry and photobiology
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Predictive value of p53, Ki67 and TLR5 in neoplastic progression of Barrett’s esophagus: a matched case–control study

2022

Abstract Barrett’s esophagus progresses to high-grade dysplasia or cancer along the well-established metaplasia-dysplasia-adenocarcinoma sequence. The aim of this study was to evaluate the value of p53, Ki67, and toll-like receptor 5 (TLR5) in prediction of malignant progression of Barrett’s metaplasia and low-grade dysplasia. This was a retrospective matched case–control study based on Northern and Central Finland population. Patients diagnosed with esophageal high-grade dysplasia or adenocarcinoma were included. From these patients, all previous endoscopy samples were obtained along with original diagnostic HE-slides and clinical data. Age- and sex-matched patients with non-progressing Ba…

p53Esophageal NeoplasmsbiomarkkeritAdenocarcinomaPathology and Forensic MedicineimmunohistokemiaBarrett EsophagusHumansBarrett’s esophagusTLR5Molecular BiologyRetrospective StudiesMetaplasiaSurveillanceCell BiologyGeneral MedicineImmunohistochemistrydigestive system diseasesToll-Like Receptor 5antigeenitKi-67 AntigenDysplasia markerCase-Control StudiesproteiinitEsophageal adenocarcinomatarkkailuTumor Suppressor Protein p53ruokatorvisyöpäKi67Virchows Archiv
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