Search results for "oncogen"

showing 10 items of 1031 documents

Induction of c-fos gene expression by the selective sigma receptor ligand EMD 57445 in rat brain.

1996

Based on animal studies it has been reasoned that ligands to sigma binding sites might be effective in the treatment of schizophrenic disorders and may also be used to investigate this largely elusive disorder on a molecular level. Expression patterns of c-fos in rat brain were studied following treatment with single doses of the sigma ligand EMD 57445 (0.3, 1, 3, 30 mg/kg s.c.). Specific c-fos gene expression was detected at all concentrations tested in various cortical areas. The signals observed were dose-dependent with the highest intensities in the piriform cortex. Strong signals were also detected in hippocampal areas CA 1,2,3 and the gyrus dentatus, as well as in the medial habenula …

medicine.medical_specialtyMammillary bodyNucleus accumbensHippocampal formationc-FosHippocampusRats Sprague-DawleyPiperidinesPiriform cortexInternal medicinemedicineAnimalsReceptors sigmaPharmacology (medical)OxazolesBiological PsychiatryIn Situ HybridizationPharmacologybiologyDose-Response Relationship DrugChemistryOlfactory tubercleBrainRatsPsychiatry and Mental healthEndocrinologyNeurologyHypothalamusIslands of Callejabiology.proteinFemaleNeurology (clinical)Proto-Oncogene Proteins c-fosAntipsychotic AgentsEuropean neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology
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Embryonic and foetal Islet-1 positive cells in human hearts are also positive to c-Kit.

2011

During embryogenesis, the mammalian heart develops from a primitive heart tube originating from two bilateral primary heart fields located in the lateral plate mesoderm. Cells belongings to the pre-cardiac mesoderm will differentiate into early cardiac progenitors, which express early transcription factors which are also common to the Isl-1 positive cardiac progenitor cells isolated from the developing pharyngeal mesoderm and the foetal and post-natal mice hearts. A second population of cardiac progenitor cells positive to c-Kit has been abundantly isolated from adult hearts. Until now, these two populations have been considered two different sets of progenitor cells present in the heart in…

medicine.medical_specialtyMesodermHistologyTime FactorsPopulationLIM-Homeodomain ProteinsBiophysicsembryoReceptors Cell SurfaceBiologyIsl-1; c-Kit; human heart; embryo; foetusAndrologyFetusfoetus.Antigens CDPregnancyInternal medicinec-Kitmental disordersmedicineHumansMyocytes CardiacProgenitor celleducationlcsh:QH301-705.5Fetuseducation.field_of_studyOriginal PaperLateral plate mesodermMyocardiumEmbryogenesisEndoglinInfant NewbornEmbryoHeartCell BiologyEmbryonic stem cellImmunohistochemistryfoetusProto-Oncogene Proteins c-kitEndocrinologymedicine.anatomical_structureIsl-1 c-Kit human heart embryo foetuslcsh:Biology (General)Isl-1Femalehuman heartpsychological phenomena and processesTranscription FactorsEuropean journal of histochemistry : EJH
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PPARγ as an indicator of vascular function in an experimental model of metabolic syndrome in rabbits

2021

Abstract Background and aims Underlying mechanisms associated with vascular dysfunction in metabolic syndrome (MetS) remain unclear and can even vary from one vascular bed to another. Methods In this study, MetS was induced by a high-fat, high-sucrose diet, and after 28 weeks, aorta and renal arteries were removed and used for isometric recording of tension in organ baths, protein expression by Western blot, and histological analysis to assess the presence of atherosclerosis. Results MetS induced a mild hypertension, pre-diabetes, central obesity and dyslipidaemia. Our results indicated that MetS did not change the contractile response in either the aorta or renal artery. Conversely, vasodi…

medicine.medical_specialtyNitric Oxide Synthase Type IIIVasodilationmedicine.disease_causeEnosmedicine.arteryInternal medicineAnimalsMedicineRenal arteryProtein kinase BSistema cardiovascularMetabolic SyndromeAortaDiabetisbiologybusiness.industryModels Theoreticalmedicine.diseasebiology.organism_classificationPPAR gammaVasodilationEndocrinologyEndothelium VascularRabbitsSodium nitroprussideMetabolic syndromeCardiology and Cardiovascular MedicinebusinessProto-Oncogene Proteins c-aktOxidative stressmedicine.drugAtherosclerosis
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Aberrant copy numbers of ALK gene is a frequent genetic alteration in neuroblastomas.

2009

A total of 50 neuroblastomas were assessed for frequency of ALK gene copy number aberrations by interphase fluorescence in situ hybridization using a break-apart fluorescence in situ hybridization probe. The data were compared with status of MYCN, 11q, 17q, and 1p36. We observed ALK aberrations (amplification, 1 of 45; gain, 15 of 45 and loss/imbalance, 11 of 45) in a total of 27 (60%) of 45 neuroblastomas. Synchronic MYCN and ALK aberrations accounted for 23 of 45 (51%) tumors; however, MYCN alterations were also detected in 11 (60%) of 18 tumors without ALK aberrations. Our data suggest that copy number aberrations of the ALK gene is a frequent genetic event in the development of neurobla…

medicine.medical_specialtyPathologyGene DosageBiologyPathology and Forensic MedicineNeuroblastomahemic and lymphatic diseasesNeuroblastomamedicineAnaplastic lymphoma kinaseHumansAnaplastic Lymphoma KinaseCopy number aberrationneoplasmsIn Situ Hybridization FluorescenceOncogene ProteinsN-Myc Proto-Oncogene Proteinmedicine.diagnostic_testGenetic AlterationCancerNuclear ProteinsReceptor Protein-Tyrosine KinasesAnatomical pathologyProtein-Tyrosine Kinasesmedicine.diseaseTissue Array AnalysisCancer researchAutonomic neuropathyFluorescence in situ hybridizationHuman pathology
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Ethanol inhibits astroglial cell proliferation by disruption of phospholipase D-mediated signaling.

2002

The activation of phospholipase D (PLD) is a common response to mitogenic stimuli in various cell types. As PLD-mediated signaling is known to be disrupted in the presence of ethanol, we tested whether PLD is involved in the ethanol-induced inhibition of cell proliferation in rat cortical primary astrocytes. Readdition of fetal calf serum (FCS) to serum-deprived astroglial cultures caused a rapid, threefold increase of PLD activity and a strong mitogenic response; both effects were dependent on tyrosine kinases but not on protein kinase C. Ethanol (0.1-2%) suppressed the FCS-induced, PLD-mediated formation of phosphatidic acid (PA) as well as astroglial cell proliferation in a concentration…

medicine.medical_specialtyPlatelet-derived growth factorIndolestert-Butyl Alcoholmedicine.medical_treatmentButanolsBecaplerminPhosphatidic AcidsNerve Tissue ProteinsBiologyBiochemistryCulture Media Serum-FreeCellular and Molecular Neurosciencechemistry.chemical_compound1-ButanolInternal medicineLysophosphatidic acidmedicinePhospholipase DAnimalsPhosphorylationProtein kinase APlatelet-Derived Growth FactorEndothelin-1EthanolPhospholipase DCell growthGrowth factorPhosphatidic acidDNAProto-Oncogene Proteins c-sisProtein-Tyrosine KinasesGenisteinGrowth InhibitorsCell biologyRatsEndocrinologychemistryFetal Alcohol Spectrum DisordersAstrocyteslipids (amino acids peptides and proteins)Signal transductionVanadatesProtein Processing Post-TranslationalCell DivisionSignal TransductionJournal of neurochemistry
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Acute estradiol protects CA1 neurons from ischemia-induced apoptotic cell death via the PI3K/Akt pathway

2010

Global ischemia arising during cardiac arrest or cardiac surgery causes highly selective, delayed death of hippocampal CA1 neurons. Exogenous estradiol ameliorates global ischemia-induced neuronal death and cognitive impairment in male and female rodents. However, the molecular mechanisms by which a single acute injection of estradiol administered after the ischemic event intervenes in global ischemia-induced apoptotic cell death are unclear. Here we show that acute estradiol acts via the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling cascade to protect CA1 neurons in ovariectomized female rats. We demonstrate that global ischemia promotes early activation of glycogen syn…

medicine.medical_specialtyProgrammed cell deathmedicine.drug_classOvariectomyBlotting WesternIschemiaApoptosisHippocampusArticleBrain IschemiaBrain ischemiaPhosphatidylinositol 3-KinasesInternal medicinemedicineAnimalsMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCaspaseNeuronsbiologyEstradiolGeneral NeuroscienceEstrogensmedicine.diseaseRatsEndocrinologyEstrogenApoptosisNerve DegenerationCancer researchbiology.proteinFemaleNeurology (clinical)Proto-Oncogene Proteins c-aktDevelopmental BiologySignal Transduction
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Expression of differentiation antigens and growth-related genes in normal kidney, autosomal dominant polycystic kidney disease, and renal cell carcin…

1992

Cellular differentiation and mRNA levels of genes involved in kidney growth were investigated in normal kidney cells, cyst-lining epithelial cells of polycystic kidney disease, and renal carcinoma cells (RCC). All cells comparatively studied exhibited an antigenic phenotype of proximal tubular cells as shown by the expression of a panel of brush border membrane enzymes and kidney-associated cell surface antigens. The epithelial developmental antigen Exo-1 was expressed in 50% to 80% of cyst-lining epithelia in polycystic kidney tissue and in 20% to 30% of polycystic kidney cells cultured in vitro. Normal kidney cells and RCC were negative under identical culture conditions. The expression o…

medicine.medical_specialtyTGF alphaCellular differentiationAutosomal dominant polycystic kidney diseaseGene ExpressionBiologyKidneyEpitheliumProto-Oncogene Proteins c-mycGrowth factor receptorEpidermal growth factorInternal medicinemedicinePolycystic kidney diseaseHumansRNA MessengerGrowth SubstancesCarcinoma Renal CellCells CulturedKidneyurogenital systemAntibodies MonoclonalTransforming Growth Factor alphamedicine.diseasePolycystic Kidney Autosomal DominantAntigens DifferentiationImmunohistochemistryKidney NeoplasmsErbB ReceptorsEndocrinologymedicine.anatomical_structureGenesNephrologyAntigens SurfaceCancer researchTransforming growth factorAmerican journal of kidney diseases : the official journal of the National Kidney Foundation
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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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Specific mutations of the RET proto-oncogene are related to disease phenotype in MEN 2A and FMTC.

1994

We have analysed 118 families with inherited medullary thyroid carcinoma (MTC) for mutations of the RET proto-oncogene. These included cases of multiple endocrine neoplasia types 2A (MEN 2A) and 2B (MEN 2B) and familial MTC (FMTC). Mutations at one of 5 cysteines in the extracellular domain were found in 97% of patients with MEN 2A and 86% with FMTC but not in MEN 2B patients or normal controls. 84% of the MEN2A mutations affected codon 634. MEN 2A patients with a Cys634 to Arg substitution had a greater risk of developing parathyroid disease than those with other codon 634 mutations. Our data show a strong correlation between disease phenotype and the nature and position of the RET mutatio…

medicine.medical_specialtyendocrine system diseasesOncogene RETDNA Mutational AnalysisMolecular Sequence DataMultiple endocrine neoplasia type 2RET proto-oncogeneBiologymedicine.disease_causeProto-Oncogene MasInternal medicineProto-Oncogene ProteinsProto-OncogenesGeneticsmedicineDrosophila ProteinsHumansPoint MutationThyroid NeoplasmsMultiple endocrine neoplasiaDNA PrimersMutationBase SequencePoint mutationMultiple Endocrine NeoplasiaProto-Oncogene Proteins c-retReceptor Protein-Tyrosine KinasesExonsmedicine.diseasePhenotypeEndocrinologyPhenotypeProto-Oncogene Proteins c-retCarcinoma MedullaryCancer researchNature genetics
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A MiR-142-3p/EGR2 Feedback Circuitry In Human CSF-1 Driven Differentiation of Monocytes Into Macrophages

2011

Abstract Abstract 2366 Colony-stimulating factor-1 (CSF-1 or M-CSF) triggers the differentiation of human peripheral blood monocytes into macrophages through and integrated cytokine/transcription factors circuitry. Using microarray profiling to explore the role of microRNAs (miRNAs) in this molecular circuitry, we identified the down-regulation of miR-142-3p in human macrophages obtained from CSF-1-treated monocytes. We show that miR-142-3p is a repressor of the transcription factor EGR2 (Early Growth Response 2) through direct 3'UTR interactions. Interestingly, EGR2 binds the promoter of the pre-miR-142-3p gene to negatively regulate its expression, identifying a self-regulatory feedback l…

medicine.medical_treatmentImmunologyRepressorChronic myelomonocytic leukemiaCell BiologyHematologyBiologyColony-stimulating factormedicine.diseaseBiochemistryCell biologyCytokinemicroRNAmedicineGeneTranscription factorProto-oncogene tyrosine-protein kinase SrcBlood
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