Search results for "Growth factor receptor"

showing 7 items of 307 documents

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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The nicotinic acetylcholine receptor agonist (±)-epibatidine increases FGF-2 mRNA and protein levels in the rat brain

2000

Abstract In a previous work, we showed that acute intermittent nicotine treatment up-regulates the level of fibroblast growth factor-2 (FGF-2) mRNA in brain regions of tel- and mesencephalon of rats suggesting that neuroprotective effect of (−)nicotine may, at least in part, involve an activation of the neuronal FGF-2 signalling. The present experiments were designed to extend the study on the nicotinic receptor mediated up-regulation of FGF-2 mRNA levels to the use of the potent nicotinic acetylcholine receptor (nAChR) agonist (±)-epibatidine. The (±)-epibatidine treatment led to a strong and long lasting up-regulation of FGF-2 mRNA expression in the cerebral cortex, in the hippocampal for…

medicine.medical_specialtyTime FactorsNicotinic acetylcoline receptor agonistPyridinesBlotting WesternNerve Tissue ProteinsNicotinic AntagonistsFibroblast growth factor-2MecamylamineBiologyHippocampusRats Sprague-DawleyNicotineCellular and Molecular NeuroscienceInternal medicineMecamylaminemedicineGlial cell line-derived neurotrophic factorAnimalsGlial Cell Line-Derived Neurotrophic FactorNerve Growth FactorsNicotinic AgonistsRNA MessengerMolecular BiologyIn Situ HybridizationEpibatidineCerebral CortexBrain-derived neurotrophic factorDose-Response Relationship DrugBrain-Derived Neurotrophic FactorBrainBridged Bicyclo Compounds HeterocyclicCorpus StriatumRatsSpecific Pathogen-Free OrganismsNicotinic acetylcholine receptorEndocrinologyNicotinic agonistGene Expression RegulationEpibatidinebiology.proteinFibroblast Growth Factor 2Alpha-4 beta-2 nicotinic receptorFibroblast growth factor receptor-1medicine.drugMolecular Brain Research
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Abnormal development of pacinian corpuscles in double trkB;trkC knockout mice.

2006

Pacinian corpuscles depend on either Aalpha or Abeta nerve fibers of the large- and intermediate-sized sensory neurons for the development and maintenance of the structural integrity. These neurons express TrkB and TrkC, two members of the family of signal transducing neurotrophin receptors, and mice lacking TrkB and TrkC lost specific neurons and the sensory corpuscles connected to them. The impact of single or double targeted mutations in trkB and trkC genes in the development of Pacinian corpuscles was investigated in 25-day-old mice using immunohistochemistry and ultrastructural techniques. Single mutations on trkB or trkC genes were without effect on the structure and S100 protein expr…

medicine.medical_specialtyanimal structuresTropomyosin receptor kinase BBiologyTropomyosin receptor kinase CS100 proteinMiceMicroscopy Electron TransmissionInternal medicinemedicineLow-affinity nerve growth factor receptorAnimalsReceptor trkBReceptor trkCReceptorMice Knockoutmusculoskeletal neural and ocular physiologyGeneral NeuroscienceImmunohistochemistryCell biologyMice Inbred C57BLEndocrinologynervous systemAnimals NewbornTrk receptorembryonic structuresKnockout mousebiology.proteinPacinian CorpusclesNeurotrophinNeuroscience letters
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Role of insulin-like growth factors in autocrine growth of human retinoblastoma Y79 cells.

1996

In this study, we have demonstrated that human retinoblastoma Y79 cells produce insulin-like growth factors (IGFs) type I and type II and release them into the medium. We have also ascertained, by means of competitive studies and cross-linking procedure, that Y79 cells contain the type-I IGF receptor (IGF-IR). Furthermore, surface-bound IGF-I is internalised by the receptor, then degraded to amino acids. Insulin, IGF-I and IGF-II caused down-regulation of IGF-IR; the effect is concentration and time dependant. Scatchard analysis demonstrated that incubation with insulin markedly decreased the binding capacity measured for IGF-I while the apparent Kd value calculated for IGF-I binding was no…

medicine.medical_specialtymedicine.medical_treatmentBiologyBiochemistryBinding CompetitiveReceptor IGF Type 1chemistry.chemical_compoundInsulin-Like Growth Factor IIInternal medicineInsulin receptor substratemedicineHumansInsulinInsulin-Like Growth Factor IAutocrine signallingPhosphotyrosineInsulin-like growth factor 1 receptorInsulinRetinoblastomaTyrosine phosphorylationPhosphoproteinsIRS2Insulin receptorautocrine growthEndocrinologychemistrybiology.proteinInsulin Receptor Substrate ProteinsPlatelet-derived growth factor receptorCell DivisionSignal TransductionEuropean journal of biochemistry
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Posttraumatic Propofol Neurotoxicity Is Mediated via the Pro–Brain-Derived Neurotrophic Factor-p75 Neurotrophin Receptor Pathway in Adult Mice*

2016

Objectives:The gamma-aminobutyric acid modulator propofol induces neuronal cell death in healthy immature brains by unbalancing neurotrophin homeostasis via p75 neurotrophin receptor signaling. In adulthood, p75 neurotrophin receptor becomes down-regulated and propofol loses its neurotoxic effect. H

musculoskeletal diseases0301 basic medicineBrain-derived neurotrophic factorProgrammed cell deathbiologybusiness.industryNeurotoxicityCaspase 3PharmacologyCritical Care and Intensive Care Medicinemedicine.disease03 medical and health sciences030104 developmental biology0302 clinical medicinenervous systemAnesthesiamedicinebiology.proteinLow-affinity nerve growth factor receptorReceptorbusiness030217 neurology & neurosurgeryHomeostasisNeurotrophinCritical Care Medicine
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2016

Background Contractile myofibroblasts (MFs) accumulate in the joint capsules of patients suffering from posttraumatic joint stiffness. MF activation is controlled by a complex local network of growth factors and cytokines, ending in the increased production of extracellular matrix components followed by soft tissue contracture. Despite the tremendous growth of knowledge in this field, inconsistencies remain in practice and prevention.

musculoskeletal diseases0301 basic medicinePathologymedicine.medical_specialtyPlatelet-derived growth factormacromolecular substancesBiologyExtracellular matrix03 medical and health scienceschemistry.chemical_compound0302 clinical medicineJoint capsulemedicine030222 orthopedicsMultidisciplinaryCell biology030104 developmental biologymedicine.anatomical_structurechemistrybiology.proteinContracturemedicine.symptomSignal transductionMyofibroblastPlatelet-derived growth factor receptorTransforming growth factorPLOS ONE
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Pfeiffer syndrome: clinical and genetic findings in five Brazilian families

2014

Pfeiffer syndrome (PS) is mainly characterized by craniosysnostosis, midface hypoplasia, great toes with partial syndactyly of the digits and broad and medially deviated thumbs. It is caused by allelic mutations in the fibroblast growth factor receptor 1 and 2 (FGFR1 and 2) genes. This study describes the clinical and genetic features of five Brazilian families affected by PS. All patients exhibited the classical phenotypes related to PS. The genetic analysis was able to detect the mutations Cys278Phe, Cys342Arg, and Val359Leu in three of these families. Two mutations were de novo, with one familial. We identified pathogenic mutations in four PS cases in five Brazilian families by PCR seque…

musculoskeletal diseasesAdultMaleAdolescentAcrocephalosyndactyliaOdontologíaBiologymedicine.disease_causeGenetic analysisExonmedicineHumansAlleleChildGeneral DentistryGeneticsMutationOral Medicine and PathologyResearchFibroblast growth factor receptor 1Crouzon syndromeAcrocephalosyndactyliaMiddle Agedmedicine.disease:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludPedigreePhenotypeOtorhinolaryngologyChild PreschoolMutationUNESCO::CIENCIAS MÉDICASPfeiffer syndromeFemaleSurgeryBrazil
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