Search results for "Phosphoprotein"

showing 10 items of 160 documents

pRb2/p130-E2F4/5-HDAC1-SUV39H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 multimolecular complexes mediate the transcription of estrogen receptor-…

2003

The estrogen receptor-alpha (ER) plays a crucial role in normal breast development and is also linked to development and progression of mammary carcinoma. The transcriptional repression of ER-alpha gene in breast cancer is an area of active investigation with potential clinical significance. However, the molecular mechanisms that regulate the ER-alpha gene expression are not fully understood. Here we show a new molecular mechanism of ER-alpha gene inactivation mediated by pRb2/p130 in ER-negative breast cancer cells. We investigated in vivo occupancy of ER-alpha promoter by pRb2/p130-E2F4/5-HDAC1-SUV39 H1-p300 and pRb2/p130-E2F4/5-HDAC1-SUV39H1-DNMT1 complexes, and provided a link between p…

Cancer ResearchTranscription GeneticEstrogen receptorHistone Deacetylase 1HistonesTumor Cells CulturedDNA (Cytosine-5-)-MethyltransferasesReceptorPromoter Regions GeneticE2F4Nuclear ProteinsAcetylationChromatinDNA-Binding ProteinsGene Expression Regulation NeoplasticReceptors Estrogenembryonic structuresDNA methylationFemalepRb2/p130; chromatin-modifying enzymes; estrogen receptor-alpha; breast carcinomabiological phenomena cell phenomena and immunityDNA (Cytosine-5-)-Methyltransferase 1medicine.medical_specialtyanimal structuresmedicine.drug_classMacromolecular SubstancesBreast NeoplasmsE2F4 Transcription FactorBiologyHistone DeacetylasesBreast cancerInternal medicineGeneticsmedicineEstrogen Receptor betaHumansMolecular BiologyEstrogen receptor betaE2F5 Transcription FactorRetinoblastoma-Like Protein p130Estrogen Receptor alphaProteinsMethyltransferasesDNA Methylationmedicine.diseasePhosphoproteinsRepressor Proteinsenzymes and coenzymes (carbohydrates)EndocrinologyEstrogenCancer researchTrans-ActivatorsEstrogen receptor alphaTranscription FactorsOncogene
researchProduct

Nuclear insulin receptor substrate 1 interacts with estrogen receptor alpha at ERE promoters.

2004

Insulin receptor substrate 1 (IRS-1) is a major signaling molecule activated by the insulin and insulin-like growth factor I receptors. Recent data obtained in different cell models suggested that in addition to its conventional role as a cytoplasmic signal transducer, IRS-1 has a function in the nuclear compartment. However, the role of nuclear IRS-1 in breast cancer has never been addressed. Here we report that in estrogen receptor alpha (ERalpha)-positive MCF-7 cells, (1) a fraction of IRS-1 was translocated to the nucleus upon 17-beta-estradiol (E2) treatment; (2) E2-dependent nuclear translocation of IRS-1 was blocked with the antiestrogen ICI 182,780; (3) nuclear IRS-1 colocalized and…

Cancer Researchmedicine.medical_specialtyTranscription Geneticmedicine.medical_treatmentBlotting WesternEstrogen receptorBiologyInsulin-like growth factorInternal medicineCell Line TumorGeneticsmedicineAnimalsHumansReceptorPromoter Regions GeneticMolecular BiologyNuclear receptor co-repressor 1DNA PrimersBase SequenceReverse Transcriptase Polymerase Chain ReactionEstrogen Receptor alphaPromoterAntiestrogenPhosphoproteinsPrecipitin TestsIRS1Cell biologyProtein TransportEndocrinologyNuclear receptorReceptors EstrogenInsulin Receptor Substrate ProteinsProtein BindingOncogene
researchProduct

Autocrine production of interleukin-4 and interleukin-10 is required for survival and growth of thyroid cancer cells.

2006

AbstractAlthough CD95 and its ligand are expressed in thyroid cancer, the tumor cell mass does not seem to be affected by such expression. We have recently shown that thyroid carcinomas produce interleukin (IL)-4 and IL-10, which promote resistance to chemotherapy through the up-regulation of Bcl-xL. Here, we show that freshly purified thyroid cancer cells were completely refractory to CD95-induced apoptosis despite the consistent expression of Fas-associated death domain and caspase-8. The analysis of potential molecules able to prevent caspase-8 activation in thyroid cancer cells revealed a remarkable up-regulation of cellular FLIPL (cFLIPL) and PED/PEA-15, two antiapoptotic proteins whos…

Cancer Researchmedicine.medical_treatmentNF-KAPPA-BOligonucleotidesC-FLIPCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisSuppressor of Cytokine Signaling ProteinsSIGNALING COMPLEXThyroid cancerTumorCARCINOMA CELLSANDROGEN RECEPTORIntracellular Signaling Peptides and ProteinsInterleukinHASHIMOTOS-THYROIDITISMiddle AgedProtein-Tyrosine KinasesInterleukin-10Up-RegulationMALIGNANT GLIOMA-CELLSInterleukin 10CytokineOncologyAged; Antibodies; Apoptosis; CASP8 and FADD-Like Apoptosis Regulating Protein; Cell Growth Processes; Cell Line Tumor; Humans; Interleukin-10; Interleukin-4; Intracellular Signaling Peptides and Proteins; Janus Kinase 1; Middle Aged; Oligonucleotides Antisense; Phosphoproteins; Protein-Tyrosine Kinases; Repressor Proteins; STAT6 Transcription Factor; Suppressor of Cytokine Signaling 1 Protein; Suppressor of Cytokine Signaling Proteins; Thyroid Neoplasms; Up-Regulation; fas Receptor; Oncology; Cancer Researchmedicine.medical_specialtyANTIAPOPTOTIC PROTEINSCell Growth ProcessesAntibodiesCell LineThyroid carcinomaSuppressor of Cytokine Signaling 1 ProteinSettore MED/04 - PATOLOGIA GENERALEInternal medicineCell Line TumormedicineHumansThyroid Neoplasmsfas ReceptorAntisenseAutocrine signallingInterleukin 4AgedAPOPTOSIS-INDUCING LIGANDbusiness.industryJanus Kinase 1Oligonucleotides Antisensemedicine.diseasePhosphoproteinsRepressor ProteinsEndocrinologyCancer cellCancer researchInterleukin-4businessApoptosis Regulatory ProteinsSTAT6 Transcription FactorCancer research
researchProduct

Mechanisms of Increased Vascular Superoxide Production in an Experimental Model of Idiopathic Dilated Cardiomyopathy

2005

Objective— In the present study, we sought to identify mechanisms underlying increased oxidative stress in vascular tissue in an experimental animal model of chronic congestive heart failure (CHF). Methods and Results— Superoxide and nitric oxide (NO) was measured in vessels from cardiomyopathic hamsters (CHF hamsters) and golden Syrian hamsters. We also determined expression of endothelial nitric oxide synthase (NOSIII), the soluble guanylyl cyclase, the cGMP-dependent kinase, and the NADPH oxidase. To analyze the contribution of the renin-angiotensin system to oxidative stress, CHF hamsters were treated with the angiotensin-converting enzyme inhibitor captopril for 200 days (120 mg · kg …

Cardiomyopathy DilatedMalemedicine.medical_specialtyCaptoprilNitric Oxide Synthase Type IIIReceptors Cytoplasmic and NuclearAngiotensin-Converting Enzyme InhibitorsNitric Oxidemedicine.disease_causeNitric oxideRenin-Angiotensin Systemchemistry.chemical_compoundSoluble Guanylyl CyclaseSuperoxidesCricetinaeInternal medicineIdiopathic dilated cardiomyopathymedicineAnimalsHeart FailureNADPH oxidaseMesocricetusbiologybusiness.industrySuperoxideMyocardiumBody WeightMicrofilament ProteinsNADPH OxidasesCaptoprilOrgan SizePhosphoproteinsDisease Models AnimalOxidative StressEndocrinologychemistryGuanylate CyclaseACE inhibitorbiology.proteinFemaleCardiology and Cardiovascular MedicinebusinessSoluble guanylyl cyclaseCell Adhesion MoleculesOxidative stressmedicine.drugArteriosclerosis, Thrombosis, and Vascular Biology
researchProduct

NF-κB inducing kinase (NIK) is an essential post-transcriptional regulator of T-cell activation affecting F-actin dynamics and TCR signaling

2018

NF-κB inducing kinase (NIK) is the key protein of the non-canonical NF-κB pathway and is important for the development of lymph nodes and other secondary immune organs. We elucidated the specific role of NIK in T cells using T-cell specific NIK-deficient (NIKΔT) mice. Despite showing normal development of lymphoid organs, NIKΔT mice were resistant to induction of CNS autoimmunity. T cells from NIKΔT mice were deficient in late priming, failed to up-regulate T-bet and to transmigrate into the CNS. Proteomic analysis of activated NIK-/- T cells showed de-regulated expression of proteins involved in the formation of the immunological synapse: in particular, proteins involved in cytoskeleton dy…

Central Nervous System0301 basic medicineEncephalomyelitis Autoimmune ExperimentalT-LymphocytesT cellPrimary Cell CultureImmunologyReceptors Antigen T-CellPriming (immunology)Protein Serine-Threonine KinasesBiologyLymphocyte ActivationImmunological synapseMice03 medical and health sciences0302 clinical medicineImmune systemmedicineAnimalsImmunology and AllergyProtein kinase BAdaptor Proteins Signal TransducingMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3ZAP-70 Protein-Tyrosine KinasePhospholipase C gammaGene Expression ProfilingZAP70T-cell receptorMembrane ProteinsPhosphoproteinsActinsPeptide FragmentsCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureGene Expression Regulation030220 oncology & carcinogenesisMyelin-Oligodendrocyte GlycoproteinLymph NodesSignal transductionT-Box Domain ProteinsProto-Oncogene Proteins c-aktSpleenSignal TransductionJournal of Autoimmunity
researchProduct

Inhibitory effects of N-acetylcysteine on the functional responses of human eosinophils in vitro

2007

Background Oxidative stress appears to be relevant in the pathogenesis of inflammation in allergic diseases like bronchial asthma. Eosinophils are oxidant-sensitive cells considered as key effectors in allergic inflammation. Objective The aim of this work was to study the effects of the clinically used antioxidant N-acetyl-L-cysteine (NAC) on the functional responses of human-isolated eosinophils. Methods Human eosinophils were purified from the blood of healthy donors by a magnetic bead separation system. The effects of NAC were investigated on the generation of reactive oxygen species (chemiluminescence and flow cytometry), Ca2+ signal (fluorimetry), intracellular glutathione (GSH; flow c…

Chemokine CCL11EotaxinLuminescenceImmunologyhuman eosinophilsBiologyPharmacologymedicine.disease_causeTranslocation GeneticAllergic inflammationAcetylcysteinechemistry.chemical_compoundmedicineHumansImmunology and Allergychemistry.chemical_classificationreactive oxygen speciesEosinophil cationic proteinReactive oxygen speciesCell DeathEosinophil Cationic ProteinNADPH OxidasesFree Radical ScavengersGlutathioneEosinophilPhosphoproteinsGlutathioneN-acetylcysteineAcetylcysteineEosinophilsN-Formylmethionine Leucyl-Phenylalaninemedicine.anatomical_structurechemistryBiochemistryChemokines CCeosinophil cationic proteinCalciumReactive Oxygen SpeciesOxidative stressp47(phox)medicine.drugp67(phox)
researchProduct

Gliadin, zonulin and gut permeabilità: effects on celiac and non-celiac intestinal mucosa and intestinal cell lines.

2006

Objective. Little is known about the interaction of gliadin with intestinal epithelial cells and the mechanism(s) through which gliadin crosses the intestinal epithelial barrier. We investigated whether gliadin has any immediate effect on zonulin release and signaling. Material and methods. Both ex vivo human small intestines and intestinal cell monolayers were exposed to gliadin, and zonulin release and changes in paracellular permeability were monitored in the presence and absence of zonulin antagonism. Zonulin binding, cytoskeletal rearrangement, and zonula occludens-1 (ZO-1) redistribution were evaluated by immunofluorescence microscopy. Tight junction occludin and ZO-1 gene expression …

Cholera ToxinGene ExpressionEnzyme-Linked Immunosorbent AssayOccludindigestive systemCoeliac diseaseGliadinPermeabilityTight JunctionsIntestinal mucosaOccludinIntestine SmallmedicineAnimalsHumansIntestinal MucosaProtein PrecursorsCells CulturedIntestinal permeabilitybiologyTight junctionHaptoglobinsGastroenterologynutritional and metabolic diseasesZonulinMembrane ProteinsEpithelial Cellsmedicine.diseasePhosphoproteinsMolecular biologydigestive system diseasesRatsCeliac DiseaseMicroscopy FluorescenceParacellular transportImmunologybiology.proteinZonula Occludens-1 ProteinGliadin
researchProduct

Exploiting Cryo-EM Structural Information and All-Atom Simulations To Decrypt the Molecular Mechanism of Splicing Modulators.

2019

Splicing modulators (SMs) pladienolides, herboxidienes, and spliceostatins exert their antitumor activity by altering the ability of SF3B1 and PHF5A proteins, components of SF3b splicing factor, to recognize distinct intron branching point sequences, thus finely calibrating constitutive/alternative/aberrant splicing of pre-mRNA. Here, by exploiting structural information obtained from cryo-EM data, and by performing multiple μs-long all-atom simulations of SF3b in apo form and in complex with selected SMs, we disclose how these latter seep into the narrow slit at the SF3B1/PHF5A protein interface. This locks the intrinsic open/closed conformational transitions of SFB1's solenoidal structure…

Cryo-electron microscopyGeneral Chemical EngineeringRNA SplicingComputational biologyLibrary and Information SciencesEncryption01 natural sciencesSplicing factorAtom (programming language)0103 physical sciencesRNA PrecursorsAberrant splicingPhysics010304 chemical physicsbusiness.industryCryoelectron MicroscopyIntronGeneral ChemistryPhosphoproteins0104 chemical sciencesComputer Science Applications010404 medicinal & biomolecular chemistrySettore CHIM/03 - Chimica Generale E InorganicaRNA splicingMolecular mechanismRNA Splicing FactorsbusinessJournal of chemical information and modeling
researchProduct

Dense Bodies of Human Cytomegalovirus Induce both Humoral and Cellular Immune Responses in the Absence of Viral Gene Expression

2000

ABSTRACTInfection of fibroblast cell cultures with human cytomegalovirus (HCMV) leads to the production of significant amounts of defective enveloped particles, termed dense bodies (DB). These noninfectious structures contain major antigenic determinants which are responsible for induction of both the humoral and the cellular immune response against HCMV. We tested the hypothesis that, by virtue of their unique antigenic and structural properties, DB could induce a significant immune response in the absence of infectious virus. Mice were immunized with gradient-purified DB, which were either left untreated or subjected to sequential rounds of sonication and freeze-thawing to prevent cellula…

Cytotoxicity ImmunologicHuman cytomegalovirusImmunologyAntigen presentationCytomegalovirusGene ExpressionMice TransgenicBiologyAntibodies ViralMicrobiologyImmunoglobulin GDefective virusViral Matrix ProteinsMiceImmune systemViral Envelope ProteinsAntigenVirologyHLA-A2 AntigenVaccines and Antiviral AgentsTumor Cells CulturedmedicineAnimalsHumansAntigens ViralAntigen PresentationMice Inbred BALB CVaccinationH-2 AntigensDefective Viruses3T3 CellsTh1 Cellsbiochemical phenomena metabolism and nutritionPhosphoproteinsmedicine.diseaseVirologyCTL*Insect ScienceImmunologybiology.proteinAntibodyT-Lymphocytes CytotoxicJournal of Virology
researchProduct

Inhibition of the NKp30 activating receptor by pp65 of human cytomegalovirus.

2005

Human cytomegalovirus, a chief pathogen in immunocompromised people, can persist in a healthy immunocompetent host throughout life without being eliminated by the immune system. Here we show that pp65, the main tegument protein of human cytomegalovirus, inhibited natural killer cell cytotoxicity by an interaction with the activating receptor NKp30. This interaction was direct and specific, leading to dissociation of the linked CD3zeta from NKp30 and, consequently, to reduced killing. Thus, pp65 is a ligand for the NKp30 receptor and demonstrates a unique mechanism by which an intracellular viral protein causes general suppression of natural killer cell cytotoxicity by specific interaction w…

Cytotoxicity ImmunologicHuman cytomegalovirusViral proteinvirusesImmunologyCytomegalovirusReceptors Cell SurfaceBiologymedicine.disease_causeNatural killer cellViral Matrix ProteinsMiceImmune systemmedicineAnimalsHumansImmunology and AllergyReceptors ImmunologicCytotoxicityReceptorCells CulturedMembrane GlycoproteinsNatural Cytotoxicity Triggering Receptor 3virus diseasesPhosphoproteinsmedicine.diseaseVirologyImmunoglobulin Fc FragmentsCell biologyKiller Cells NaturalNatural Cytotoxicity Triggering Receptor 3Kineticsmedicine.anatomical_structureGene Expression RegulationIntracellularProtein BindingNature immunology
researchProduct