Search results for "Insulin receptor substrate"

showing 5 items of 15 documents

Genetic and environmental aspect of polycystic ovary syndrome.

2004

Polycystic ovary syndrome (PCOS) is a heterogeneous syndrome determined in most patients by the association of two main factors: hyperandrogenism and insulin resistance. These characters are probably independent of each other and seem to be inherited by several different mechanisms. In some patients homozygous gene alteration has been found but in most patients PCOS seems to be determined by the association of gene polymorphisms that are common in the general population but alone are unable to determine phenotypic consequences. Alteration of genes that regulate the initial steps of ovarian steroidogenesis is probably the main causal factor of hyperandrogenism. Insulin resistance may be the …

medicine.medical_specialtyEndocrinology Diabetes and MetabolismPopulationBiologyEatingEndocrinologyInsulin resistanceInternal medicineInsulin receptor substratemedicineHumansGenetic Predisposition to DiseaseObesityeducationGeneeducation.field_of_studyHyperandrogenismmedicine.diseaseObesityPhenotypePolycystic ovaryEndocrinologyFemaleInsulin ResistanceEnergy MetabolismHyperandrogenismPolycystic Ovary SyndromeJournal of endocrinological investigation
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The estrogen receptor α:insulin receptor substrate 1 complex in breast cancer: structure–function relationships

2007

Background: Insulin receptor substrate 1 (IRS-1) is a signaling molecule that exerts a key role in mediating cross talk between estrogen receptor a (ERa) and insulin-like growth factor 1 (IGF-1) in breast cancer cells. Previously, we demonstrated that a fraction of IRS-1 binds ERa, translocates to the nucleus, and modulates ERa-dependent transcription at estrogen response elements (ERE). Here, we studied structure-function relationships of the ER-a:IRS-1 complex under IGF-1 and/or estradiol (E 2 ) stimulation. Materials and methods: ERa and IRS-1 deletion mutants were used to analyze structural and functional ERα/IRS-1 interactions. IRS-1 binding to ERE and IRS-1 role in ERa-dependent ERE t…

medicine.medical_specialtyInsulin Receptor Substrate ProteinsActive Transport Cell NucleusEstrogen receptorRepressorBreast NeoplasmsBiologyStructure-Activity Relationshipestrogen receptor alpha (ERa) Insulin receptor substrate 1 (IRS-1) breast cancerCell Line TumorInternal medicineCoactivatormedicineHumansInsulin-Like Growth Factor IReceptors InterferonEstradiolEstrogen Receptor alphaHematologyDNA-binding domainPhosphoproteinsPeptide FragmentsReceptor InsulinProtein Structure TertiaryCell biologyIRS1Repressor ProteinsPleckstrin homology domainEndocrinologyOncologyInsulin Receptor Substrate ProteinsFemaleChromatin immunoprecipitationProtein BindingAnnals of Oncology
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IRS-2 deficiency impairs NMDA receptor-dependent long-term potentiation

2011

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License.-- et al.

medicine.medical_specialtyPatch-Clamp TechniquesCognitive Neurosciencemedicine.medical_treatmentBlotting WesterneducationHippocampusComputingMilieux_LEGALASPECTSOFCOMPUTINGNeurotransmissionBiologyHippocampusReceptors N-Methyl-D-AspartateSynaptic TransmissionMiceCellular and Molecular NeuroscienceInternal medicinemedicineAnimalsImmunoprecipitationlong-term potentiationMice Knockoutsynaptic plasticitydiabetesInsulinDiabetesLong-term potentiationArticlesNMDA receptorIRS2insulin receptor signalingSynaptic fatigueEndocrinologynervous systemSynaptic plasticityInsulin Receptor Substrate ProteinsNMDA receptorFemaleNeuroscienceCerebral Cortex
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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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Increased dosage of Ink4/Arf protects against glucose intolerance and insulin resistance associated with aging

2013

Recent genome-wide association studies have linked type-2 diabetes mellitus to a genomic region in chromosome 9p21 near the Ink4/Arf locus, which encodes tumor suppressors that are up-regulated in a variety of mammalian organs during aging. However, it is unclear whether the susceptibility to type-2 diabetes is associated with altered expression of the Ink4/Arf locus. In the present study, we investigated the role of Ink4/Arf in age-dependent alterations of insulin and glucose homeostasis using Super-Ink4/Arf mice which bear an extra copy of the entire Ink4/Arf locus. We find that, in contrast to age-matched wild-type controls, Super-Ink4/Arf mice do not develop glucose intolerance with agi…

p16ink4amedicine.medical_specialtyAgingGlucose uptakemedicine.medical_treatmentMice TransgenicCarbohydrate metabolismCDKN2BMiceCDKN2AInsulin resistanceInsulin receptor substrateInternal medicineDiabetes mellitusinsulin resistanceGlucose IntolerancemedicineGlucose homeostasisAnimalsInsulininsulin signalingCyclin-Dependent Kinase Inhibitor p16biologydiabetesADP-Ribosylation FactorsInsulin18F-fluorodeoxyglucose-PETARFCell Biologypancreatic isletmedicine.diseaseMice Inbred C57BLInsulin receptorEndocrinologyGlucosebiology.proteinInsulin Resistancep15ink4bGenome-Wide Association Study
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