Search results for " Transformed"

showing 10 items of 77 documents

Benzo[a]pyrene represses DNA repair through altered E2F1/E2F4 function marking an early event in DNA damage-induced cellular senescence

2020

AbstractTranscriptional regulation of DNA repair is of outmost importance for the restoration of DNA integrity upon genotoxic stress. Here we report that the potent environmental carcinogen benzo[a]pyrene (B[a]P) activates a cellular DNA damage response resulting in transcriptional repression of mismatch repair (MMR) genes (MSH2, MSH6, EXO1) and of RAD51, the central homologous recombination repair (HR) component, ultimately leading to downregulation of MMR and HR. B[a]P-induced gene repression is caused by abrogated E2F1 signalling. This occurs through proteasomal degradation of E2F1 in G2-arrested cells and downregulation of E2F1 mRNA expression in G1-arrested cells. Repression of E2F1-me…

Cyclin-Dependent Kinase Inhibitor p21SenescenceAcademicSubjects/SCI00010DNA repairDNA damageRAD51E2F4 Transcription FactorBiologyDNA Mismatch Repair03 medical and health sciences0302 clinical medicineCell Line TumorBenzo(a)pyreneGeneticsHumansCellular SenescenceCell Line Transformed030304 developmental biology0303 health sciencesGene regulation Chromatin and EpigeneticsRecombinational DNA RepairEpithelial CellsKv Channel-Interacting ProteinsCell Cycle CheckpointsDNAFibroblastsCell biologyDNA-Binding ProteinsRepressor ProteinsMSH6DNA Repair EnzymesExodeoxyribonucleasesMutS Homolog 2 ProteinGamma RaysMSH2030220 oncology & carcinogenesisCarcinogensMCF-7 CellsDNA mismatch repairRad51 RecombinaseCell agingE2F1 Transcription FactorDNA DamageSignal TransductionNucleic Acids Research
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Transcriptional repression of Bmp2 by p21(Waf1/Cip1) links quiescence to neural stem cell maintenance.

2013

Relative quiescence and self renewal are defining features of adult stem cells, but their potential coordination remains unclear. Subependymal neural stem cells (NSCs) lacking cyclin-dependent kinase (CDK) inhibitor (CKI) 1a (p21) exhibit rapid expansion that is followed by their permanent loss later in life. Here we demonstrate that transcription of the gene encoding bone morphogenetic protein 2 (Bmp2) in NSCs is under the direct negative control of p21 through actions that are independent of CDK. Loss of p21 in NSCs results in increased levels of secreted BMP2, which induce premature terminal differentiation of multipotent NSCs into mature non-neurogenic astrocytes in an autocrine and/or …

Cyclin-Dependent Kinase Inhibitor p21Time FactorsCellular differentiationBone Morphogenetic Protein 2Nerve Tissue ProteinsBiologyTransfectionParacrine signallingMiceNeural Stem CellsCyclin-dependent kinaseTransduction GeneticSubependymal zoneAnimalsCell Line TransformedRegulation of gene expressionMice KnockoutGeneral NeuroscienceNeurogenesisCell CycleAge FactorsCell DifferentiationNeural stem cellCell biologyKi-67 AntigenBromodeoxyuridineGene Expression RegulationMutagenesisCulture Media Conditionedbiology.proteinNeoplastic Stem CellsCarrier ProteinsNeuroscienceAdult stem cellSubcellular FractionsNature neuroscience
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Immunosurveillance of lung melanoma metastasis in EBI-3-deficient mice mediated by CD8+ T cells.

2008

Abstract EBV-induced gene 3 (EBI-3) codes for a soluble type I receptor homologous to the p40 subunit of IL-12 that is expressed by APCs following activation. In this study, we assessed the role of EBI-3 in a model of lung melanoma metastasis. Intravenous injection of the B16-F10 cell line resulted in a significant reduction of lung tumor metastasis in EBI-3−/− recipient mice compared with wild-type mice. The immunological finding accompanying this effect was the expansion of a newly described cell subset called IFN-γ producing killer dendritic cells associated with CD8+ T cell responses in the lung of EBI-3−/− mice including IFN-γ release and TNF-α-induced programmed tumor cell death. Depl…

Cytotoxicity ImmunologicAdoptive cell transferLung NeoplasmsT cellImmunologyMelanoma ExperimentalBiologyCD8-Positive T-LymphocytesArticleMetastasisMinor Histocompatibility AntigensGene Knockout TechniquesMiceCell Line TumormedicineImmunology and AllergyCytotoxic T cellAnimalsLung MelanomaReceptors CytokineImmunologic SurveillanceCell Line TransformedMice KnockoutMelanomamedicine.diseaseImmunosurveillanceMice Inbred C57BLmedicine.anatomical_structureCell Transformation NeoplasticImmunologyInjections IntravenousAnimals; CD8-Positive T-Lymphocytes; Cell Line Transformed; Cell Line Tumor; Cell Transformation Neoplastic; Cytotoxicity Immunologic; Gene Knockout Techniques; Immunologic Surveillance; Injections Intravenous; Lung Neoplasms; Melanoma Experimental; Mice; Mice Inbred C57BL; Mice Knockout; Neoplasm Transplantation; Receptors Cytokine; T-Box Domain ProteinsCancer researchT-Box Domain ProteinsCD8Neoplasm Transplantation
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Consequences of antigen self-presentation by tumor-specific cytotoxic T cells.

2000

Abstract CDS-positive cytotoxic T cells (CTL) recognize antigenic peptides in combination with major histocompatibility complex (MHC) class I molecules on the surface of syngeneic antigen presenting cells (APC). In the present paper we show that cells from tumor antigen-specific CTL clones present their cognate antigenic peptide to other CTL from the same clone. Inter-CTL peptide presentation resulted in activation of the cells of one CTL clone to MHC-unrestricted lysis of bystander cells. In contrast to the behaviour of this clone, another CTL clone did not lyse bystander cells after incubation with the cognate peptide, but was activated to self-destruction. The human herpes virus Epstein-…

Cytotoxicity ImmunologicAntigen PresentationbiologyT cellImmunologyAntigen presentationchemical and pharmacologic phenomenaHematologyMHC restrictionMajor histocompatibility complexMolecular biologyCTL*medicine.anatomical_structureAntigenHLA-A2 Antigenbiology.proteinmedicineTumor Cells CulturedImmunology and AllergyCytotoxic T cellHumansAntigen-presenting cellCell Line TransformedT-Lymphocytes CytotoxicImmunobiology
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A tyrosinase peptide presented by HLA-B35 is recognized on a human melanoma by autologous cytotoxic T lymphocytes

1999

We previously described different cytotoxic T lymphocyte (CTL) clones isolated from the blood lymphocytes of a melanoma patient after in vitro stimulation with autologous tumor cells. These CTL clones recognized at least 2 distinct antigens on the melanoma cells. Here, we show that one of them consists of a peptide derived from tyrosinase and presented by HLA-B35. The peptide is 9 amino acids long and has the sequence LPSSADVEF. It can be presented by the 2 major B35 allelic subtypes, B*3501 and B*3503. As HLA-B35 is one of the most frequent HLA-B specificities, being present in about 20% of Caucasian individuals, it may be a useful target for peptide-based immunotherapy of melanoma.

Cytotoxicity ImmunologicHerpesvirus 4 HumanCancer Researchmedicine.medical_treatmentAntigen presentationTyrosinase PeptideBiologyTransfectionAntigenTumor Cells CulturedmedicineAnimalsHumansCytotoxic T cellAmino Acid SequenceMelanomaPeptide sequenceAllelesCell Line TransformedB-LymphocytesMonophenol MonooxygenaseMelanomaImmunotherapymedicine.diseasePeptide FragmentsRecombinant ProteinsCTL*OncologyCOS CellsImmunologyCancer researchHLA-B35 AntigenT-Lymphocytes CytotoxicInternational Journal of Cancer
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Poly(ADP-ribosyl)ation accelerates DNA repair in a pathway dependent on Cockayne syndrome B protein

2003

Activation of poly(ADP-ribose)polymerases 1 and 2 (PARP-1 and PARP-2) is one of the earliest responses of mammalian cells to DNA damage by numerous genotoxic agents. We have analysed the influence of PARP inhibition, either achieved by over-expression of the DNA binding domain of PARP-1 or by treatment with 3,4-dihydro-5-[4-(1-piperidinyl)butoxyl]-1(2H)-isoquinolinone, on the repair of single-strand breaks (SSB), pyrimidine dimers and oxidative base modifications sensitive to Fpg protein (mostly 8-hydroxyguanine) in mammalian cells at very low, non-cytotoxic levels of DNA damage. The data show that the repair rates of all three types of DNA damage are significantly lower in PARP-inhibited c…

DNA RepairDNA damageDNA repairPoly ADP ribose polymerase[SDV]Life Sciences [q-bio]Pyrimidine dimerBiologyPoly(ADP-ribose) Polymerase InhibitorsPoly (ADP-Ribose) Polymerase InhibitorCockayne syndromeDexamethasone03 medical and health sciencesMice0302 clinical medicinePiperidinesCricetinaeGeneticsmedicineAnimalsPoly-ADP-Ribose Binding ProteinsComputingMilieux_MISCELLANEOUS030304 developmental biologyCell Line TransformedMice Knockout0303 health sciencesDNA HelicasesArticlesDNADNA repair protein XRCC4Fibroblastsmedicine.diseaseIsoquinolinesMolecular biology3. Good healthDNA Repair Enzymes030220 oncology & carcinogenesisPoly(ADP-ribose) PolymerasesNucleotide excision repairDNA DamageSignal Transduction
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Nucleotide excision repair of abasic DNA lesions

2019

AbstractApurinic/apyrimidinic (AP) sites are a class of highly mutagenic and toxic DNA lesions arising in the genome from a number of exogenous and endogenous sources. Repair of AP lesions takes place predominantly by the base excision pathway (BER). However, among chemically heterogeneous AP lesions formed in DNA, some are resistant to the endonuclease APE1 and thus refractory to BER. Here, we employed two types of reporter constructs accommodating synthetic APE1-resistant AP lesions to investigate the auxiliary repair mechanisms in human cells. By combined analyses of recovery of the transcription rate and suppression of transcriptional mutagenesis at specifically positioned AP lesions, w…

DNA RepairTranscription GeneticDNA damageDNA repairGenome Integrity Repair and ReplicationGene Knockout Techniques03 medical and health sciencesEndonucleasechemistry.chemical_compoundTranscription (biology)CRISPR-Associated Protein 9DNA-(Apurinic or Apyrimidinic Site) LyaseGeneticsHumansAP siteCell Line TransformedSkin030304 developmental biologyGene Editing0303 health sciencesBase SequencebiologyGenome Human030302 biochemistry & molecular biologyDNABase excision repairFibroblastsMolecular biologyXeroderma Pigmentosum Group A ProteinDNA-Binding ProteinschemistryMutationbiology.proteinCRISPR-Cas SystemsDNADNA DamageProtein BindingNucleotide excision repairNucleic Acids Research
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The human p53 gene mutated at position 249per se is not sufficient to immortalize human liver cells

1999

A particular point mutation of the tumor suppressor gene p53, namely a G→T transversion at the third base of codon 249, is frequently detected in primary hepatocellular carcinomas from patients living in areas where the levels of dietary exposure to aflatoxin B 1 and the rates of infection with the hepatitis B virus are very high. Very recently, a nontumorigenic liver epithelial cell line (HACL-1) with a finite life-span and expressing a number of hepatocyte-specific markers was established from a human hepatocellular adenoma in our laboratory. To analyze the role of mutated p53 in the immortalization of human liver cells, we transfected HACL-1 cells with an expression vector containing a h…

DNA ComplementaryTumor suppressor geneMutantBiologyTransfectionmedicine.disease_causemedicineHumansCodonCell Line TransformedMutationExpression vectorBase SequenceHepatologyPoint mutationGene Transfer TechniquesDrug Resistance MicrobialTransfectionHepatocellular adenomaGenes p53medicine.diseaseMolecular biologyLiverCell cultureMutationCell DivisionHepatology
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The cyclopentenone-type prostaglandin 15-deoxy-delta12,14-prostaglandin J2 inhibits CD95 ligand gene expression in T lymphocytes: interference with p…

2003

Abstract 15-Deoxy-Δ12,14-PGJ2 (15d-PGJ2) is a cyclopentenone-type PG endowed with anti-inflammatory properties and produced by different cells, including those of the immune system. 15d-PGJ2 is a natural ligand of the peroxisome proliferator-activated receptor (PPAR)-γ nuclear receptor, but relevant PPARγ-independent actions mediated by this prostanoid have been described. Fas (APO-1/CD95) and its ligand (Fas-L) are cell surface proteins whose interaction activates apoptosis of Fas-expressing targets. In T cells, the Fas-Fas-L system regulates activation-induced cell death and has been implicated in diseases in which lymphocyte homeostasis is compromised. Moreover, several studies have desc…

Fas Ligand ProteinNerve growth factor IBT-LymphocytesImmunologyPeroxisome proliferator-activated receptorReceptors Cytoplasmic and NuclearApoptosisCyclopentanesBiologyLigandsLymphocyte ActivationJurkat cellsImmediate-Early ProteinsTransactivationchemistry.chemical_compoundJurkat CellsMiceHeat Shock Transcription FactorsPeroxisomesImmunology and AllergyAnimalsHumansHSP70 Heat-Shock ProteinsGene Silencingfas ReceptorReceptorPromoter Regions GeneticCell Line TransformedEarly Growth Response Protein 1chemistry.chemical_classificationHybridomasMembrane GlycoproteinsProstaglandin D2Fas receptorMolecular biologyDNA-Binding ProteinschemistryNuclear receptorlipids (amino acids peptides and proteins)Prostaglandin D2Transcription Factors
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Development and characterization of a 293 cell line with regulatable expression of the hepatitis B virus large envelope protein

2004

During the life cycle of hepatitis B virus (HBV) the large L envelope protein plays a pivotal role that is related to its peculiar dual transmembrane topology. To study the complex structure and diverse functions of L under regulated conditions of production, a human 293 cell line stably expressing L under the control of the ecdysone-inducible promoter was generated. Cells demonstrated stringent dose- and time-dependent kinetics of induction with undetectable background expression in the absence of the inducer. Temporal control of L expression allowed to trace (i) its posttranslational reorientation resulting in the mixed topology; (ii) its spatial redistribution from the endoplasmic reticu…

Gene Expression Regulation ViralHepatitis B virusEcdysoneProtein ConformationEndoplasmic reticulumLiver cellCell MembraneCellGolgi ApparatusBiologyEndoplasmic Reticulummedicine.disease_causebiology.organism_classificationMolecular biologymedicine.anatomical_structureViral Envelope ProteinsHepadnaviridaeCell cultureVirologyMembrane topologymedicineHumansSecretionPromoter Regions GeneticCell Line TransformedJournal of Virological Methods
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