Search results for "Receptor Cross-Talk"

showing 10 items of 15 documents

Direct estrogen receptor (ER) / HER family crosstalk mediating sensitivity to lumretuzumab and pertuzumab in ER+ breast cancer.

2017

Bidirectional cross talk between members of the human epidermal growth factor family of receptors (HER) and the estrogen receptor (ER) is believed to underlie resistance mechanisms that develop in response to treatment with anti-HER agents and endocrine therapy. We investigated the interaction between HER2, HER3 and the ER in vitro using human embryonic kidney cells transfected with human HER2, HER3, and ERα. We also investigated the additive efficacy of combination regimens consisting of anti-HER3 (lumretuzumab), anti-HER2 (pertuzumab), and endocrine (fulvestrant) therapy in vivo. Our data show that both HER2 and HER3 can directly complex with the ER and can mediate phosphorylation of the …

0301 basic medicineCell signalingReceptor ErbB-3Receptor ErbB-2Cancer TreatmentEstrogen receptorlcsh:MedicineSignal transductionBiochemistryMice0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsBreast TumorsMedicine and Health SciencesReceptorlcsh:Scienceskin and connective tissue diseasesMultidisciplinaryRemission InductionEndocrine TherapySignaling cascadesPrecipitation TechniquesTreatment OutcomeReceptors EstrogenOncology030220 oncology & carcinogenesisMonoclonalCell linesFemalePertuzumabBiological culturesmedicine.drugResearch ArticleAdultCell biologyMAPK signaling cascadesPaclitaxelBreast NeoplasmsAntibodies Monoclonal Humanized03 medical and health sciencesBreast cancerCell Line TumorBreast CancermedicineEndocrine systemAnimalsHumansImmunoprecipitationFulvestrantbusiness.industrylcsh:RHEK 293 cellsCancers and NeoplasmsBiology and Life SciencesEstrogensReceptor Cross-TalkLumretuzumabmedicine.diseaseXenograft Model Antitumor AssaysHormonesResearch and analysis methods030104 developmental biologyCancer researchlcsh:QbusinessPloS one
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Crosstalk between receptor tyrosine kinases (RTKs) and G protein-coupled receptors (GPCR) in the brain: Focus on heteroreceptor complexes and related…

2019

Neuronal events are regulated by the integration of several complex signaling networks in which G protein-coupled receptors (GPCRs) and receptor tyrosine kinases (RTKs) are considered key players of an intense bidirectional cross-communication in the cell, generating signaling mechanisms that, at the same time, connect and diversify the traditional signal transduction pathways activated by the single receptor. For this receptor-receptor crosstalk, the two classes of receptors form heteroreceptor complexes resulting in RTKs transactivation and in growth-promoting signals. In this review, we describe heteroreceptor complexes between GPCR and RTKs in the central nervous system (CNS) and their …

0301 basic medicineG proteinRTKHeteroreceptorSettore BIO/09 - FisiologiaReceptor tyrosine kinaseReceptors G-Protein-Coupled03 medical and health sciencesCellular and Molecular NeuroscienceTransactivation0302 clinical medicineGPCRReceptor Fibroblast Growth Factor Type 1Receptor Fibroblast Growth Factor Type 2ReceptorG protein-coupled receptorPharmacologyTransactivationbiologyChemistryReceptor Protein-Tyrosine KinasesBrainReceptor Cross-TalkCrosstalk (biology)030104 developmental biologyHeteroreceptor complexebiology.proteinSignal transductionNeuroscience030217 neurology & neurosurgerySignal Transduction
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Serotonin Heteroreceptor Complexes and Their Integration of Signals in Neurons and Astroglia—Relevance for Mental Diseases

2021

The heteroreceptor complexes present a novel biological principle for signal integration. These complexes and their allosteric receptor–receptor interactions are bidirectional and novel targets for treatment of CNS diseases including mental diseases. The existence of D2R-5-HT2AR heterocomplexes can help explain the anti-schizophrenic effects of atypical antipsychotic drugs not only based on blockade of 5-HT2AR and of D2R in higher doses but also based on blocking the allosteric enhancement of D2R protomer signaling by 5-HT2AR protomer activation. This research opens a new understanding of the integration of DA and 5-HT signals released from DA and 5-HT nerve terminal networks. The biologica…

0301 basic medicineReviewheteroreceptor complexesTropomyosin receptor kinase BReceptor tyrosine kinasechemistry.chemical_compound0302 clinical medicineG protein-coupled receptorsserotonin receptorsReceptor Serotonin 5-HT2ABiology (General)astrogliabiologyChemistryMental DisordersBrainGeneral MedicineAntidepressive AgentsdepressionG protein-coupled receptors; astroglia; depression; heteroreceptor complexes; rapid antidepressant drugs; receptor tyrosine kinase; serotonin receptors.medicine.symptomAntipsychotic AgentsSerotonergic NeuronsSignal TransductionProto-oncogene tyrosine-protein kinase Srcserotonin receptorheteroreceptor complexeQH301-705.5Astroglia; Depression; G protein-coupled receptors; Heteroreceptor complexes; Rapid antidepressant drugs; Receptor tyrosine kinase; Serotonin receptors;Allosteric regulationserotonin receptors heteroreceptor complexes depression astroglia receptor tyrosine kinase rapid antidepressant drugs G protein-coupled receptors.depression astroglia receptor tyrosine kinase rapid antidepressant drugs G protein-coupled receptorsHeteroreceptorNO03 medical and health sciencesmedicineAnimalsHumansReceptor Fibroblast Growth Factor Type 1rapid antidepressant drugsG protein-coupled receptorReceptors Dopamine D2Dopaminergic NeuronsTyrosine phosphorylationReceptor Cross-TalkReceptor Galanin Type 1Receptor Galanin Type 2030104 developmental biologyMechanism of actionAstrocytesreceptor tyrosine kinasebiology.proteinReceptors Serotonin 5-HT1Neuroscience030217 neurology & neurosurgeryCells
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TSH/IGF-1 Receptor Cross-Talk Rapidly Activates Extracellular Signal-Regulated Kinases in Multiple Cell Types

2017

We previously showed that thyrotropin (TSH)/insulinlike growth factor (IGF)-1 receptor cross-talk appears to be involved in Graves’ orbitopathy (GO) pathogenesis and upregulation of thyroid-specific genes in human thyrocytes. In orbital fibroblasts from GO patients, coadministration of TSH and IGF-1 induces synergistic increases in hyaluronan secretion. In human thyrocytes, TSH plus IGF-1 synergistically increased expression of the sodium-iodide symporter that appeared to involve ERK1/2 activation. However, the details of ERK1/2 activation were not known, nor was whether ERK1/2 was involved in this synergism in other cell types. Using primary cultures of GO fibroblasts (GOFs) and human thyr…

0301 basic medicinemedicine.medical_specialtyCell typeendocrine systemendocrine system diseasesMAP Kinase Signaling SystemThyrotropinPertussis toxinReceptor IGF Type 103 medical and health sciencesEndocrinologyDownregulation and upregulationInternal medicinemedicineHumansSecretionHyaluronic AcidInsulin-Like Growth Factor IPhosphorylationReceptorResearch ArticlesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3SymportersChemistryHEK 293 cellsReceptors ThyrotropinReceptor Cross-TalkFibroblastsSignalingGraves Ophthalmopathy030104 developmental biologyEndocrinologyHEK293 CellsThyroid Epithelial CellsSymporterPhosphorylationhormones hormone substitutes and hormone antagonistsEndocrinology
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TSH/IGF-1 Receptor Cross Talk in Graves' Ophthalmopathy Pathogenesis.

2016

AbstractContext:The TSH receptor (TSHR) is considered the main target of stimulatory autoantibodies in the pathogenesis of Graves' ophthalmopathy (GO); however, it has been suggested that stimulatory IGF-1 receptor (IGF-1R) autoantibodies also play a role.Objective:We previously demonstrated that a monoclonal stimulatory TSHR antibody, M22, activates TSHR/IGF-1R cross talk in orbital fibroblasts/preadipocytes obtained from patients with GO (GO fibroblasts [GOFs]). We show that cross talk between TSHR and IGF-1R, not direct IGF-1R activation, is involved in the mediation of GO pathogenesis stimulated by Graves' autoantibodies.Design/Setting/Participants:Immunoglobulins were purified from the…

0301 basic medicinemedicine.medical_specialtyLinsitinibEndocrinology Diabetes and MetabolismClinical Biochemistry030209 endocrinology & metabolismContext (language use)BiochemistryThyrotropin receptorReceptor IGF Type 1Graves' ophthalmopathyPathogenesis03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEndocrinologyInternal medicineCyclic AMPMedicineHumansHyaluronic AcidReceptorCells Culturedbusiness.industryBiochemistry (medical)AutoantibodyReceptors ThyrotropinReceptor Cross-TalkOriginal Articlesmedicine.diseaseGraves Ophthalmopathy030104 developmental biologyEndocrinologychemistryMonoclonalbusinessOrbitThe Journal of clinical endocrinology and metabolism
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Interruption of CD28-mediated costimulation during allergen challenge protects mice from allergic airway disease

2012

Background Allergic asthma is a T H 2-promoted hyperreactivity with an immediate, IgE, and mast cell–dependent response followed by eosinophil-dominated inflammation and airway obstruction. Objective Because costimulation by CD28 is essential for T H 2 but not T H 1 responses, we investigated the effect of selective interference with this pathway in mice using the models of ovalbumin and house dust mite–induced airway inflammation. Methods To study the role of CD28 in the effector phase of allergic airway inflammation, we developed an inducibly CD28-deleting mouse strain or alternatively used a CD28 ligand-binding site–specific mouse anti-mouse mAb blocking CD28 engagement. Results We show …

Allergic asthmaLymphocyte ActivationImmunoglobulin Emedicine.disease_causeT-Lymphocytes RegulatoryMice0302 clinical medicineAirway resistanceAllergenImmunology and AllergySensitizationMice Inbred BALB C0303 health sciencesbiologyAntibodies Monoclonalovalbuminrespiratory system3. Good healthmedicine.anatomical_structurecostimulationconditional CD28 knockout miceFemalemedicine.symptomImmunologyInflammation03 medical and health sciencesTh2 CellsCD28 AntigensRespiratory HypersensitivitymedicineAnimalsHumansAntigens DermatophagoidesLymphocyte CountAntibodies Blocking030304 developmental biologyHouse dust miteCD28-specific mAbbusiness.industryReceptor Cross-TalkAirway obstructionmedicine.diseasebiology.organism_classificationMice Mutant Strainsrespiratory tract diseasesDisease Models AnimalCTLA-4Immunologybiology.proteinbusiness030215 immunology
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Central role of IL-6 and MMP-1 for cross talk between human intestinal mast cells and human intestinal fibroblasts.

2012

Mast cells (MC) are key effector cells in allergic reactions but also involved in host defence, tissue remodeling, angiogenesis, and fibrogenesis. Here, we show that human intestinal fibroblasts (FB) suppress apoptosis in human intestinal MC dependent on IL-6. Intestinal FB produced IL-6 upon direct stimulation by intestinal MC in co-culture or by MC mediators such as TNF-α, IL-1β, tryptase or histamine. MC incubated with IL-6 survived for up to 3 weeks similar to MC co-cultured with FB and MC survival could be blocked by neutralizing anti-IL-6 Abs. Moreover, FB stimulated by MC mediators upregulated their expression of matrix metalloproteinase-1 (MMP-1), a key fibrolytic enzyme. Noteworthy…

AngiogenesisCell SurvivalImmunologyInflammationTryptaseApoptosisCell CommunicationMatrix metalloproteinaseBiologychemistry.chemical_compoundDownregulation and upregulationmedicineImmunology and AllergyHumansMast CellsIntestinal MucosaInterleukin 6Protein Kinase InhibitorsFlavonoidsInterleukin-6HematologyReceptor Cross-TalkFibroblastsMolecular biologyCoculture TechniqueschemistryApoptosisImmunologybiology.proteinmedicine.symptomMatrix Metalloproteinase 1HistamineImmunobiology
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Receptor phosphorylation does not mediate cross talk between muscarinic M(3) and bradykinin B(2) receptors.

1999

This study examined cross talk between phospholipase C-coupled muscarinic M3and bradykinin B2receptors coexpressed in Chinese hamster ovary (CHO) cells. Agonists of either receptor enhanced phosphoinositide signaling (which rapidly desensitized) and caused protein kinase C (PKC)-independent, homologous receptor phosphorylation. Muscarinic M3but not bradykinin B2receptors were also phosphorylated after phorbol ester activation of PKC. Consistent with this, muscarinic M3receptors were phosphorylated in a PKC-dependent fashion after bradykinin B2receptor activation, but muscarinic M3receptor activation did not influence bradykinin B2receptor phosphorylation. Despite heterologous phosphorylatio…

Atropinemedicine.medical_specialtyReceptor Bradykinin B2PhysiologyGene ExpressionCHO CellsInositol 145-TrisphosphateMuscarinic AntagonistsBiologyMuscarinic AgonistsBradykininTransfectionTritiumInternal medicineCricetinaeMuscarinic acetylcholine receptor M5Muscarinic acetylcholine receptormedicineMuscarinic acetylcholine receptor M4AnimalsHumansBradykinin receptorPhosphorylationReceptorMethacholine ChlorideReceptor Muscarinic M3Receptors BradykininMuscarinic acetylcholine receptor M3Muscarinic acetylcholine receptor M2Cell BiologyMuscarinic acetylcholine receptor M1Receptor Cross-TalkReceptors MuscarinicRecombinant ProteinsEndocrinologyType C PhospholipasesCalciumInositolSignal TransductionThe American journal of physiology
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Crosstalk between leukemia-associated proteins MOZ and MLL regulates HOX gene expression in human cord blood CD34+ cells

2010

MOZ and MLL, encoding a histone acetyltransferase (HAT) and a histone methyltransferase, respectively, are targets for recurrent chromosomal translocations found in acute myeloblastic or lymphoblastic leukemia. In MOZ (MOnocytic leukemia Zinc-finger protein)/CBP- or mixed lineage leukemia (MLL)-rearranged leukemias, abnormal levels of HOX transcription factors have been found to be critical for leukemogenesis. We show that MOZ and MLL cooperate to regulate these key genes in human cord blood CD34+ cells. These chromatin-modifying enzymes interact, colocalize and functionally cooperate, and both are recruited to multiple HOX promoters. We also found that WDR5, an adaptor protein essential fo…

Cancer ResearchAntigens CD34HistonesHistone H3hemic and lymphatic diseasesHistone methylationGeneticsHumansWDR5Tissue DistributionPromoter Regions GeneticHox geneneoplasmsMolecular BiologyCells CulturedHistone AcetyltransferasesHomeodomain ProteinsGeneticsBlood CellsbiologyIntracellular Signaling Peptides and ProteinsHistone-Lysine N-MethyltransferaseReceptor Cross-TalkU937 CellsHistone acetyltransferaseFetal BloodHematopoiesisCell biologyGene Expression RegulationHistone methyltransferasebiology.proteinMyeloid-Lymphoid Leukemia ProteinH3K4me3K562 CellsMyeloid-Lymphoid Leukemia ProteinProtein BindingOncogene
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The Functional Role of the Second NPXY Motif of the LRP1 β-Chain in Tissue-type Plasminogen Activator-mediated Activation of N-Methyl-D-aspartate Rec…

2008

The low density lipoprotein receptor-related protein 1 (LRP1) emerges to play fundamental roles in cellular signaling pathways in the brain. One of its prominent ligands is the serine proteinase tissue-type plasminogen activator (tPA), which has been shown to act as a key activator of neuronal mitogen-activated protein kinase pathways via the N-methyl-D-aspartate (NMDA) receptor. However, here we set out to examine whether LRP1 and the NMDA receptor might eventually act in a combined fashion to mediate tPA downstream signaling. By blocking tPA from binding to LRP1 using the receptor-associated protein, we were able to completely inhibit NMDA receptor activation. Additionally, inhibition of …

Cell signalingAmino Acid MotifsPDZ domainIntracellular SpaceBiologyReceptors N-Methyl-D-AspartateBiochemistryProtein Structure SecondaryCell LineRats Sprague-DawleyMiceStructure-Activity RelationshipAnimalsHumansAmino Acid SequencePhosphorylationRNA Small InterferingReceptorProtein kinase AMolecular BiologyMitogen-Activated Protein Kinase 1NeuronsMitogen-Activated Protein Kinase 3Activator (genetics)Intracellular Signaling Peptides and ProteinsMembrane ProteinsReceptor Cross-TalkCell BiologyLRP1RatsCell biologyEnzyme ActivationBiochemistryTissue Plasminogen ActivatorDisks Large Homolog 4 ProteinCalciumDisks Large Homolog 4 ProteinGuanylate KinasesPlasminogen activatorLow Density Lipoprotein Receptor-Related Protein-1PlasmidsSignal TransductionJournal of Biological Chemistry
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