Search results for "nuclear protein"

showing 10 items of 337 documents

Genetic feminization of pheromones and its behavioral consequences in Drosophila males

1997

0036-8075 (Print) Journal Article Research Support, Non-U.S. Gov't; Pheromones are intraspecific chemical signals important for mate attraction and discrimination. In the fruit fly Drosophila melanogaster, hydrocarbons on the cuticular surface of the animal are sexually dimorphic in both their occurrence and their effects: Female-specific molecules stimulate male sexual excitation, whereas the predominant male-specific molecule tends to inhibit male excitation. Complete feminization of the pheromone mixture produced by males was induced by targeted expression of the transformer gene in adult oenocytes (subcuticular abdominal cells) or by ubiquitous expression during early imaginal life. The…

MaleSex CharacteristicsSex DifferentiationRecombinant Fusion ProteinsSexual BehaviorfungiHomosexualityNuclear Proteins/genetics/physiologyDrosophila melanogasterGene Expression RegulationAnimal/physiologyAnimalsSex Attractants/genetics/*physiologyFemaleDevelopmentalTransgenes
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Increase in Bcl-2 phosphorylation and reduced levels of BH3-only Bcl-2 family proteins in kainic acid-mediated neuronal death in the rat brain.

2003

Kainic acid induces excitotoxicity and nerve cell degeneration in vulnerable regions of rat brain, most markedly in hippocampus and amygdala. Part of the cell death following kainic acid is apoptotic as shown by caspase 3 activation and chromatin condensation. Here we have studied the regulation of pro- and anti-apoptotic proteins belonging to the Bcl-2 family in rat hippocampus and amygdala by kainic acid in relationship to ensuing neuronal death. The pro-apoptotic protein Bax was up-regulated in hippocampus 6 h after kainic acid administration. The increase in Bax was followed by the appearance of TdT-mediated dUTP nick end labelling-positive cells which were prominent at 24 h. Immunohist…

MaleTime FactorsExcitotoxicityCell Countmedicine.disease_causeSettore BIO/09 - Fisiologiachemistry.chemical_compoundPrecipitin TestExcitatory Amino Acid AgonistsSerinePhosphorylationCells CulturedNuclear Proteinbcl-2-Associated X ProteinNeuronsProto-Oncogene ProteinKainic AcidbiologyCell DeathImmunochemistryGeneral NeuroscienceBrainNuclear ProteinsImmunohistochemistryProto-Oncogene Proteins c-bcl-2Programmed cell deathKainic acidTime FactorNeuronal deathExcitatory Amino Acid AgonistBlotting WesternCaspase 3HippocampuBcl-2-associated X proteinProto-Oncogene ProteinsGlial Fibrillary Acidic ProteinmedicineIn Situ Nick-End LabelingAnimalsRats WistarProtein kinase AStaining and LabelingAnimalBcl-2 familyNeuronButylated HydroxytolueneEmbryo MammalianMolecular biologyPrecipitin Testsnervous system diseasesRatsnervous systemchemistrybiology.proteinRatNeuNBcl-2 proteinThe European journal of neuroscience
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Gain of MYCN region in a Wilms tumor-derived xenotransplanted cell line.

2010

Wilms tumor is one of the most common pediatric malignant tumors of the kidney. Although the WT1 gene, located at 11p13, has been proven to be implicated in the development of Wilms tumor, other genes such as MYCN are also involved. The purpose of this study is to genetically characterize a Wilms tumor metastasis xenotransplanted in nude mice. Immunogenotype evolution of the xenografts material was monitored for 29 months using molecular techniques, fluorescent in situ hybridization and multiplex ligation-dependent probe amplification, in addition to immunohistochemistry in tissue microarrays. Genetic alterations present in the original tumor and retained in the xenotransplanted tumor were …

MaleTransplantation HeterologousMice NudeIn situ hybridizationBiologyN-Myc Proto-Oncogene ProteinWilms TumorPathology and Forensic MedicineMetastasisExonMiceINDEL MutationmedicineAnimalsHumansneoplasmsMolecular BiologyIn Situ Hybridization FluorescenceOncogene ProteinsN-Myc Proto-Oncogene ProteinTissue microarrayNuclear ProteinsWilms' tumorCell BiologyNucleic acid amplification techniquemedicine.diseaseMolecular biologyImmunohistochemistryTransplantationChild PreschoolNucleic Acid Amplification TechniquesDiagnostic molecular pathology : the American journal of surgical pathology, part B
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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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Contribution of Large Genomic Rearrangements in Italian Lynch Syndrome Patients: Characterization of a Novel Alu-Mediated Deletion

2012

Lynch syndrome is associated with germ-line mutations in the DNA mismatch repair (MMR) genes, mainlyMLH1andMSH2. Most of the mutations reported in these genes to date are point mutations, small deletions, and insertions. Large genomic rearrangements in the MMR genes predisposing to Lynch syndrome also occur, but the frequency varies depending on the population studied on average from 5 to 20%. The aim of this study was to examine the contribution of large rearrangements in theMLH1andMSH2genes in a well-characterised series of 63 unrelated Southern Italian Lynch syndrome patients who were negative for pathogenic point mutations in theMLH1,MSH2, andMSH6genes. We identified a large novel delet…

Malecongenital hereditary and neonatal diseases and abnormalitiesgenomic rearragementArticle SubjectPopulationlcsh:MedicineSettore BIO/11 - Biologia MolecolareBiologyMLH1General Biochemistry Genetics and Molecular Biologynovel Alu-mediated deletionAlu ElementsmedicineHumanseducationneoplasmsAdaptor Proteins Signal TransducingSequence DeletionGene RearrangementGeneticseducation.field_of_studyGeneral Immunology and MicrobiologyPoint mutationlcsh:RNuclear ProteinsLynch syndrome; genomic rearragements; novel Alu-mediated deletionnutritional and metabolic diseasesGeneral MedicineGene rearrangementmedicine.diseaseColorectal Neoplasms Hereditary NonpolyposisMolecular biologyLynch syndromedigestive system diseasesDNA-Binding ProteinsMSH6Settore MED/18 - Chirurgia GeneraleLynch syndromeMutS Homolog 2 ProteinItalyMSH2FemaleDNA mismatch repairMutL Protein Homolog 1Research ArticleBioMed Research International
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2p15-p16.1 microdeletions encompassing and proximal to BCL11A are associated with elevated HbF in addition to neurologic impairment.

2015

Elevated fetal hemoglobin (HbF) ameliorates the clinical severity of hemoglobinopathies such as β-thalassemia and sickle cell anemia. Currently, the only curative approach for individuals under chronic transfusion/chelation support therapy is allogeneic stem cell transplantation. However, recent analyses of heritable variations in HbF levels have provided a new therapeutic target for HbF reactivation: the transcriptional repressor BCL11A. Erythroid-specific BCL11A abrogation is now actively being sought as a therapeutic avenue, but the specific impact of such disruption in humans remains to be determined. Although single nucleotide polymorphisms in BCL11A erythroid regulatory elements have …

Malecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyAdolescentImmunologyBiologyBiochemistrySettore MED/38 - Pediatria Generale E SpecialisticaRed Cells Iron and ErythropoiesisInternal medicinehemic and lymphatic diseasesFetal hemoglobinmedicineGene silencingHumansChildNervous System DiseaseFetal HemoglobinNuclear ProteinHematologyNuclear ProteinsCell BiologyHematologymedicine.diseasePhenotypeSickle cell anemiaUp-RegulationTransplantationRepressor ProteinsSettore MED/03 - Genetica MedicaChromosomes Human Pair 22p15-p16.1 microdeletions BCL11A HbF neurologicImmunologyFemaleStem cellChromosome DeletionNervous System DiseasesCarrier ProteinHaploinsufficiencyCarrier ProteinsHumanBlood
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Daily oscillation of gene expression in the retina is phase-advanced with respect to the pineal gland

2007

Abstract The photoreceptive retina and the non-photoreceptive pineal gland are components of the circadian and the melatonin forming system in mammals. To contribute to our understanding of the functional integrity of the circadian system and the melatonin forming system we have compared the daily oscillation of the two tissues under various seasonal lighting conditions. For this purpose, the 24-h profiles of the expression of the genes coding for arylalkylamine N-acetyltransferase (AA-NAT), nerve growth factor inducible gene-A (NGFI-A), nerve growth factor inducible gene-B (NGFI-B), retinoic acid related orphan receptor β (RORβ), dopamine D4 receptor, and period2 (Per2) have been simultane…

Maleendocrine systemmedicine.medical_specialtyGene ExpressionCell Cycle ProteinsBiologyArylalkylamine N-AcetyltransferasePineal GlandRetinaPinealocyteRats Sprague-DawleyMelatoninPineal glandInternal medicinemedicineAnimalsCircadian rhythmMolecular BiologyEarly Growth Response Protein 1RetinaSuprachiasmatic nucleusGeneral NeuroscienceReceptors Dopamine D4Nuclear ProteinsPeriod Circadian ProteinsMicroarray AnalysisCircadian RhythmRatsPER2Endocrinologymedicine.anatomical_structureFemaleNeurology (clinical)Developmental BiologyEndocrine glandmedicine.drugBrain Research
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Influence of photoperiodic history on clock genes and the circadian pacemaker in the rat retina

2006

The influence of seasonal lighting conditions on expression of clock genes and the circadian pacemaker was investigated in the rat retina. For this purpose, the 24-h profiles of nine clock genes (bmal1, clock, per1, per2, per3, dec1, dec2, cry1 and cry 2) and the arylalkylamine N-acetyltransferase gene as an indicator of the circadian pacemaker output were compared between light-dark periods of 8 : 16 and 16 : 8 h. The photoperiod influenced the daily patterns of the amount of transcript for per1, per3, dec2 and arylalkylamine N-acetyltransferase. This indicates that photoperiodic information modulates clock gene expression in addition to the circadian pacemaker of the retina. Under constan…

Maleendocrine systemmedicine.medical_specialtyTime FactorsPhotoperiodGene ExpressionBiologyRetinaRats Sprague-DawleyInternal medicinemedicineAnimalsRNA MessengerEye ProteinsOscillating genephotoperiodismAnalysis of VarianceReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceNuclear ProteinsCircadian RhythmRatsPER2CLOCKDEC1PER3EndocrinologyGene Expression RegulationArylalkylamineFemalesense organshormones hormone substitutes and hormone antagonistsPER1European Journal of Neuroscience
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Genetic Instability and Intratumoral Heterogeneity in Neuroblastoma with MYCN Amplification Plus 11q Deletion

2013

Background/Aim Genetic analysis in neuroblastoma has identified the profound influence of MYCN amplification and 11q deletion in patients’ prognosis. These two features of high-risk neuroblastoma usually occur as mutually exclusive genetic markers, although in rare cases both are present in the same tumor. The purpose of this study was to characterize the genetic profile of these uncommon neuroblastomas harboring both these high-risk features. Methods We selected 18 neuroblastomas with MNA plus 11q loss detected by FISH. Chromosomal aberrations were analyzed using Multiplex Ligation-dependent Probe Amplification and Single Nucleotide Polymorphism array techniques. Results and Conclusion Thi…

Malelcsh:MedicineMutually exclusive eventsGenetic analysisPediatricsGenetic profileChromosome BreakpointsNeuroblastomaGene duplicationPathologylcsh:ScienceChildGeneticsOncogene ProteinsN-Myc Proto-Oncogene ProteinMultidisciplinaryNuclear ProteinsOncologyChild PreschoolCytogenetic AnalysisMedicineFemaleChromosome DeletionResearch ArticleGenetic MarkersBiologyPolymorphism Single NucleotideCytogeneticsDiagnostic MedicineNeuroblastomamedicineGeneticsCancer GeneticsHumansIn patientGenetic Predisposition to DiseaseneoplasmsBiologyClinical GeneticsChromosomes Human Pair 11lcsh:RGene AmplificationInfantmedicine.diseaseGenetic markerPediatric OncologyMycn amplificationCancer researchlcsh:QBiomarkersGeneral PathologyPLoS ONE
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SPANX-B and SPANX-C (Xq27 region) gene dosage analysis in Down’s syndrome subjects with undescended testes

2009

Down’s syndrome (DS) is one of the most common numer- ical chromosomal aberrations, usually caused by trisomy of chromosome 21, and is frequently complicated with congen- ital heart defects, duodenal obs truction and other conditions including undescended testis (UDT) (Fonkalsrud 1970). The incidence of undescended testes in DS was reported to be 6.52% (Chew and Hutson 2004) while the incidence of UDT in the first year is approximately 0.2%–0.8% in the nor- mal population (Benson et al . 1991; Ichiyanagi et al . 1998). Rapley et al . (2000) provided evidence for a testicular germ- cell tumours (TGCT) predisposition locus at Xq27; the au- thors obtained an hlod score of 4.7 from families wit…

Malemedicine.medical_specialtyAdolescentPopulationGene DosageBiologyGene dosageYoung AdultSettore MED/38 - Pediatria Generale E SpecialisticaInternal medicineCryptorchidismGeneticsmedicineHumansChildeducationGynecologyeducation.field_of_studyS syndromeIncidence (epidemiology)Genetic VariationNuclear Proteinsmedicine.diseaseNeoplasm ProteinsSPANX-B and SPANX-C (Xq27 region) gene dosage analysis in Down's syndrome subjects with undescended testes.EndocrinologyChild PreschoolDown SyndromeTrisomyJournal of Genetics
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