Search results for "DNA-BINDING PROTEIN"

showing 10 items of 449 documents

The transcription factor Zfh1 is involved in the regulation of neuropeptide expression and growth of larval neuromuscular junctions in Drosophila mel…

2008

AbstractDifferent aspects of neural development are tightly regulated and the underlying mechanisms have to be transcriptionally well controlled. Here we present evidence that the transcription factor Zfh1, the Drosophila member of the conserved zfh1 gene family, is important for different steps of neuronal differentiation. First, we show that late larval expression of the neuropeptide FMRFamide is dependent on correct levels of Zfh1 and that this regulation is presumably direct via a conserved zfh1 homeodomain binding site in the FMRFamide enhancer. Using MARCM analysis we additionally examined the requirement for Zfh1 during embryonic and larval stages of motoneuron development. We could …

Neuromuscular JunctionAxonal outgrowthAnimalsDrosophila ProteinsFMRFamideFMRFamideFRMFaEnhancerMolecular BiologyTranscription factorMotor NeuronsZfh1biologyEffectorfungiMARCMCell DifferentiationCell Biologybiology.organism_classificationSynapseMolecular biologyAxonsMotoneuronCell biologyDNA-Binding ProteinsRepressor ProteinsDrosophila melanogasternervous systemMARCMLarvaHomeoboxDrosophila melanogasterNeural developmentDevelopment NeurogenesisDevelopmental BiologyDevelopmental biology
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Sporogen, S14-95, and S-curvularin, three inhibitors of human inducible nitric-oxide synthase expression isolated from fungi.

2003

The induction of human inducible nitric-oxide synthase (iNOS) expression depends (among other factors) on activation of the signal transducer and activator of transcription 1 (STAT1) pathway. Therefore, the STAT1 pathway may be an appropriate target for the development of inhibitors of iNOS expression. HeLa S3 cells transiently transfected with a gamma-activated site (GAS)/interferon-stimulated response element-driven reporter gene construct were used as the primary screening system. Using this system, three novel inhibitors of interferon-gamma-dependent gene expression, namely, sporogen, S14-95, and S-curvularin, were isolated from different Penicillium species. These three compounds also …

Nitric Oxide Synthase Type IIINitric Oxide Synthase Type IIGene expressionHumansRNA MessengerEnzyme InhibitorsPromoter Regions GeneticCells CulturedNitritesPharmacologyRegulation of gene expressionReporter genebiologyPenicilliumNitric Oxide Synthase Type IIITransfectionCurvularinMolecular biologyNitric oxide synthaseDNA-Binding ProteinsSTAT1 Transcription FactorGene Expression Regulationbiology.proteinSTAT proteinTrans-ActivatorsMolecular MedicineEpoxy CompoundsZearalenoneNitric Oxide SynthaseCell DivisionMolecular pharmacology
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Involvement of PKC and NF-κB in Nitric Oxide Induced Apoptosis in Human Coronary Artery Smooth Muscle Cells

2001

Apoptosis of vascular smooth muscle cells is critically involved in progression of atherosclerosis and may prevent intimal hyperplasia in restenosis and vascular remodeling. Nitric oxide (NO) is known to induce apoptosis, but the signaling pathways still remain unclear. We investigated p53 accumulation, protein kinase C (PKC) activation and nuclear transcription factor (NF-kappaB) binding activity as possible signaling mechanisms of NO-induced apoptosis. Apoptosis was induced dose-dependently with the NO-donors sodiumnitroprusside (SNP: 232+/-48%) and SIN-1 (241+/-90% of actinomycin D induced apoptosis; means +/- SEM, *por =0.05 vs. control) in HSMC. Inhibition of PKC significantly attenuat…

Nitroprussidemedicine.medical_specialtyVascular smooth muscleIntimal hyperplasiaPhysiologyApoptosisDNA FragmentationNaphthalenesNitric OxideMuscle Smooth VascularNitric oxidechemistry.chemical_compoundNF-KappaB Inhibitor alphaRestenosisInternal medicinemedicineHumansNitric Oxide DonorsEnzyme InhibitorsCells CulturedProtein Kinase CProtein kinase CCell Nucleusbusiness.industryNF-kappa BNF-κBStaurosporinemedicine.diseaseCoronary VesselsDNA-Binding Proteinsmedicine.anatomical_structurechemistryApoptosisMolsidomineCancer researchCardiologyI-kappa B ProteinsTumor Suppressor Protein p53businessArteryCellular Physiology and Biochemistry
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Effects of p63 expression on survival in oral squamous cell carcinoma

2007

BACKGROUND: P63 is the protein codified by p63 gene, a p53 gene homolog, known for its pivotal role in cell cycle regulation, and involved in the tumor differentiation. Aims of the present study were to assess the frequency and pattern of p63 protein expression in oral squamous cell carcinoma (OSCC) in relation to the main tumour characteristics and to verify whether p63 can be considered a marker of prognosis in patients with OSCC. MATERIAL AND METHODS: In a retrospective study, a cohort of 64 OSCC patients was investigated for p63 protein expression and its cellular localization by immunohistochemistry (monoclonal mouse anti-human p63 protein-clone 4A4). After grouping by p63 expression, …

OncologyAdultMaleCancer Researchmedicine.medical_specialtyPathologySurvival rateBiologyOSCCInternal medicinemedicineBiomarkers TumorCox regression analysisHumansGrading (tumors)GeneSurvival rateCellular localizationAgedNeoplasm StagingCox regression analysis; OSCC; p53 family; p63; Survival rate;p63integumentary systemTumor Suppressor ProteinsRetrospective cohort studyGeneral MedicineMiddle AgedPrognosisSurvival Analysisp63 p53 family OSCC Survival rate Cox regression analysisDNA-Binding Proteinsstomatognathic diseasesOncologyCohortMonoclonalCarcinoma Squamous CellTrans-ActivatorsImmunohistochemistryFemaleMouth NeoplasmsOSCCsense organsp53 familyp53 familyCox regressionTranscription Factors
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Excision repair cross-complementation group 1 protein overexpression as a predictor of poor survival for high-grade serous ovarian adenocarcinoma.

2010

Abstract Objective The excision repair cross-complementation group 1 (ERCC1) expression is a predictor of survival after surgical treatment for several malignancies. Its overexpression has been reported as a marker of platinum resistance in lung cancer. However, the relevance of ERCC1 expression in ovarian cancer (OC) is the subject of controversy, both as a predictive parameter for platinum resistance and because of its association with poor prognosis. Therefore, we performed a retrospective study investigating ERCC1 expression and its correlation with patients' survival in OC. Methods We analyzed the ERCC1 protein expression using four different ERCC1 antibodies (clone 8F1) with different…

OncologyAdultmedicine.medical_specialtyNeoplasm Residualmedicine.medical_treatmentERCC1 Protein ExpressionPredictive Value of TestsInternal medicineOvarian carcinomamedicineHumansLung cancerSurvival rateAgedNeoplasm StagingRetrospective StudiesAged 80 and overOvarian NeoplasmsChemotherapybusiness.industryAge FactorsObstetrics and GynecologyMiddle Agedmedicine.diseaseEndonucleasesImmunohistochemistryCystadenocarcinoma SerousDNA-Binding ProteinsSerous fluidOncologyFemaleERCC1businessOvarian cancerGynecologic oncology
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Identification of a genetic signature enriching for response to ibrutinib in relapsed/refractory follicular lymphoma in the DAWN phase 2 trial.

2021

Abstract Background The single‐arm DAWN trial (NCT01779791) of ibrutinib monotherapy in patients with relapsed/refractory follicular lymphoma (FL) showed an overall response rate (ORR) of 20.9% and a median response duration of 19.4 months. This biomarker analysis of the DAWN dataset sought to determine genetic classifiers for prediction of response to ibrutinib treatment. Methods Whole exome sequencing was performed on baseline tumor samples. Potential germline variants were excluded; a custom set of 1216 cancer‐related genes was examined. Responder‐ versus nonresponder‐associated variants were identified using Fisher's exact test. Classifiers with increasing numbers of genes were created …

OncologyCancer ResearchFollicular lymphomaBiochemistrychemistry.chemical_compoundGenetic signaturePiperidinesRecurrenceMedicineExomeLymphoma FollicularExome sequencingRC254-282Research ArticlesNeoplasms. Tumors. Oncology. Including cancer and carcinogensHematologyDNA-Binding ProteinsExact testOncologyIbrutinibRefractory Follicular LymphomaClin oncolResearch ArticleGenetic Markersmedicine.medical_specialtyImmunologyAntineoplastic AgentslymphomaBiologyGermline mutationInternal medicinePartial responseExome SequencingHumansRadiology Nuclear Medicine and imagingIn patientbusiness.industryAdeninegenetic variantsClinical Cancer ResearchbiomarkersCell Biologymedicine.diseasemutationsFANCAMutational analysisCARD Signaling Adaptor ProteinschemistryGuanylate CyclaseFamily medicineRelapsed refractoryMutationbusinessCancer medicine
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germline mutations in women with familial breast cancer and a relative with haematological malignancy

2009

Biallelic inactivation of the ATM gene causes ataxia-telangiectasia (A-T), a complex neurological disease associated with a high risk of leukaemias and lymphomas. Mothers of A-T children, obligate ATM heterozygote mutation carriers, have a breast cancer (BC) relative risk of about 3. The frequency of ATM carriers in BC women with a BC family history has been estimated to be 2.70%. To further our clinical understanding of familial BC and examine whether haematological malignancies are predictive of ATM germline mutation, we estimated the frequency of heterozygote mutation carriers in a series of 122 BC women with a family history of both BC and haematological malignancy and without BRCA1/2 m…

OncologyCancer ResearchLymphomaDNA Mutational AnalysisCell Cycle ProteinsAtaxia Telangiectasia Mutated Proteins0302 clinical medicineBreast cancerGene FrequencyRisk FactorsMissense mutationGenetics0303 health scienceseducation.field_of_studyLeukemiafamilial breast cancerAtaxia–telangiectasiaPedigreeDNA-Binding ProteinsOncology030220 oncology & carcinogenesisMutation (genetic algorithm)EMMAFemaleAdultHeterozygotemedicine.medical_specialtyMolecular Sequence DataPopulationBreast NeoplasmsProtein Serine-Threonine KinasesBiologyRisk Assessment03 medical and health sciencesGermline mutationBreast cancerPredictive Value of TestsInternal medicinemedicineHumansGenetic Predisposition to DiseaseGenetic TestingeducationAllele frequencyGerm-Line Mutation030304 developmental biologyBase SequenceTumor Suppressor ProteinsHeterozygote advantagemedicine.diseaseAtaxia-telangiectasia
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Correction:Cancer risks by gene, age, and gender in 6350 carriers of pathogenic mismatch repair variants: findings from the Prospective Lynch Syndrom…

2020

Lynch syndrome (LS) results from pathogenic variants in the mismatch repair (MMR) genes and is the most common hereditary cancer syndrome, affecting an estimated 1 in 300 individuals. Pathogenic variants in each of the MMR genes path_MLH1, path_MSH2, path_MSH6, and path_PMS2 result in different risks for cancers in organs including the colorectum, endometrium, ovaries, stomach, small bowel, bile duct, pancreas, and upper urinary tract. Accurate estimates of these risks are essential for planning appropriate approaches to the prevention or early diagnosis of cancers but the robustness of previous studies has been limited by factors including retrospective design,1,2 lack of validation in ind…

OncologyMaleColorectal cancer*Lynch syndromePenetranceDNA Mismatch Repair0302 clinical medicineDatabases GeneticMalalties hereditàriesProspective StudiesCàncer*PMS2Genetics (clinical)Mismatch Repair Endonuclease PMS2Cancer0303 health sciencesSex CharacteristicsFactors de risc en les malalties1184 Genetics developmental biology physiologyMLH1Middle Aged16. Peace & justiceLynch syndrome3. Good healthDNA-Binding ProteinsMutS Homolog 2 Proteinsyöpägeenit*MSH2030220 oncology & carcinogenesis*MSH6030211 gastroenterology & hepatologyDNA mismatch repairFemalegeneettiset tekijätMutL Protein Homolog 1Genetic diseasesAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesRisk factors in diseasessuolistosyövätMUTATION CARRIERSMLH1Risk AssessmentArticlesukupuoliAge and gender03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseLynchin oireyhtymäGene030304 developmental biologyAgedbusiness.industryEndometrial cancerCorrectionnutritional and metabolic diseasesCancer*MLH1MSH6medicine.diseaseColorectal Neoplasms Hereditary NonpolyposisSurvival Analysisdigestive system diseasesMSH2MSH6Lynch syndromePMS2MSH2Mutation3111 BiomedicineikäbusinessOvarian cancer
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Prognostic role and implications of mutation status of tumor suppressor gene ARID1A in cancer: A systematic review and meta-analysis

2015

Loss of the tumor suppressor gene AT-rich interactive domain-containing protein 1A (ARID1A) has been demonstrated in several cancers, but its prognostic role is unknown. We aimed to investigate the risk associated with loss of ARID1A (ARID1A-) for all-cause mortality, cancer-specific mortality and recurrence of disease in subjects with cancer. PubMed and SCOPUS search from database inception until 01/31/2015 without language restriction was conducted, contacting authors for unpublished data. Eligible were prospective studies reporting data on prognostic parameters in subjects with cancer, comparing participants with presence of ARID1A (ARID1A+) vs. ARID1A-, assessed either via immunohistoch…

OncologyMalemedicine.medical_specialtyBioinformaticsARID1A SWI/SNF chromatin remodeling targeted therapy tumor suppressor genechromatin remodelingCohort StudiesARID1A; Chromatin remodeling; SWI/SNF; Targeted therapy; Tumor suppressor gene; OncologyInternal medicineNeoplasmsMedicineHumansARID1A; SWI/SNF; chromatin remodeling; targeted therapy; tumor suppressor geneGenes Tumor Suppressortumor suppressor geneProspective cohort studybusiness.industryConfoundingHazard ratioCancerNuclear ProteinsMiddle Agedmedicine.diseasePrognosistargeted therapyARID1AConfidence intervalDNA-Binding ProteinsSWI/SNFOncologyRelative riskMeta-analysisMutationFemalebusinessCohort studyResearch PaperTranscription Factors
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Confirmation of TNIP1 but not RHOB and PSORS1C1 as systemic sclerosis risk factors in a large independent replication study

2012

Item does not contain fulltext INTRODUCTION: A recent genome-wide association study in European systemic sclerosis (SSc) patients identified three loci (PSORS1C1, TNIP1 and RHOB) as novel genetic risk factors for the disease. The aim of this study was to replicate the previously mentioned findings in a large multicentre independent SSc cohort of Caucasian ancestry. METHODS: 4389 SSc patients and 7611 healthy controls from different European countries and the USA were included in the study. Six single nucleotide polymorphisms (SNP): rs342070, rs13021401 (RHOB), rs2233287, rs4958881, rs3792783 (TNIP1) and rs3130573 (PSORS1C1) were analysed. Overall significance was calculated by pooled analys…

Oncologymedicine.medical_specialtysystemic sclerosisRHOBImmunologyGenome-wide association studySingle-nucleotide polymorphismBioinformaticsPolymorphism Single NucleotideGeneral Biochemistry Genetics and Molecular BiologyArticleWhite PeopleRheumatologyRisk FactorsInternal medicineRhoB GTP-Binding Proteinsystemic sclerosis; genome wide screening; genetic risk factorsmedicinegenetic risk factorsImmunology and AllergySNPHumansGenetic Predisposition to DiseaseAllelerhoB GTP-Binding ProteinRheumatology and AutoimmunityScleroderma Systemicbusiness.industryHaplotypeProteinsgenome wide screeningDNA-Binding ProteinsEuropeHaplotypesCohortEvaluation of complex medical interventions Auto-immunity transplantation and immunotherapy [NCEBP 2]businessGenome-Wide Association Study
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