Search results for " Transcription factor"

showing 10 items of 656 documents

Antibodies to New Beta Cell Antigen ICA12 in Latvian Diabetes Patients

2006

In Latvia diabetes mellitus is diagnosed using the WHO's clinical criteria, and assays for the detection of autoantibodies are not available. In consequence, slowly progressive autoimmune diabetes or LADA is likely to be missed. Antibodies to GAD65 and IA-2 are the major immunological markers in autoimmune diabetes. Recently, a new beta cell antigen, called ICA12, has been identified, which has a homology to the SOX family of transcription factors. The aim of the study was to analyze the prevalence of ICA12 antibodies in diabetes mellitus patients and controls from Latvia and to see whether this antigen is important in revealing autoimmunity when antibodies against major antigens are not pr…

Maleendocrine systemAdolescentendocrine system diseasesmedicine.disease_causeAutoantigensGeneral Biochemistry Genetics and Molecular BiologyAutoimmunityIslets of LangerhansHistory and Philosophy of ScienceAntigenHLA-DQ AntigensDiabetes mellitusmedicineHumansChildAutoantibodiesgeographygeography.geographical_feature_categorybiologyGlutamate Decarboxylasebusiness.industryGeneral NeuroscienceHigh Mobility Group ProteinsAutoantibodyInfantnutritional and metabolic diseasesmedicine.diseaseIsletLatviaIsoenzymesDiabetes Mellitus Type 2Child PreschoolAutoimmune diabetesImmunologybiology.proteinFemaleDisease SusceptibilityBeta cellAntibodybusinessSOXD Transcription FactorsBiomarkersAnnals of the New York Academy of Sciences
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Acetylcholine leads to signal transducer and activator of transcription 1 (STAT-1) mediated oxidative/nitrosative stress in human bronchial epithelia…

2013

AbstractThe induction of nitric oxide synthase (iNOS) expression via the signal transducer and activator of transcription 1 (STAT-1) is involved in the mechanism of oxidative/nitrosative stress. We investigated whether acetylcholine (ACh) generates oxidative/nitrosative stress in bronchial epithelial cells during airway inflammation of COPD and evaluated the effects of Tiotropium, a once-daily antimuscarinic drug, and Olodaterol, a long-acting β2-agonist on these mechanisms. Human bronchial epithelial cells (16-HBE) were stimulated (4h, 37°C) with induced sputum supernatants (ISSs) from healthy controls (HC) (n=10), healthy smokers (HS) (n=10) or COPD patients (n=10), as well as with ACh (f…

Malemedicine.medical_specialtyBlotting WesternNitric Oxide Synthase Type IIBronchiOxidative phosphorylationCholinergic AgonistsFlow cytometrychemistry.chemical_compoundPulmonary Disease Chronic ObstructiveWestern blotInternal medicinemedicineHumansRNA Small InterferingMolecular BiologyCells Culturedchemistry.chemical_classificationReactive oxygen speciesbiologymedicine.diagnostic_testNitrotyrosineEpithelial CellsMiddle AgedAcetylcholinerespiratory tract diseasesEpithelial cellNitric oxide synthaseOxidative StressEndocrinologySTAT1 Transcription FactorchemistrySTAT proteinbiology.proteinOxidative/nitrosative stressTyrosineMolecular MedicineSTAT-1FemaleReactive Oxygen SpeciesAcetylcholinemedicine.drugBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Altered REDD1, myostatin, and Akt/mTOR/FoxO/MAPK signaling in streptozotocin-induced diabetic muscle atrophy

2011

Type 1 diabetes, if poorly controlled, leads to skeletal muscle atrophy, decreasing the quality of life. We aimed to search highly responsive genes in diabetic muscle atrophy in a common diabetes model and to further characterize associated signaling pathways. Mice were killed 1, 3, or 5 wk after streptozotocin or control. Gene expression of calf muscles was analyzed using microarray and protein signaling with Western blotting. We identified translational repressor protein REDD1 (regulated in development and DNA damage responses) that increased seven- to eightfold and was associated with muscle atrophy in diabetes. The diabetes-induced increase in REDD1 was confirmed at the protein level. …

Malemedicine.medical_specialtyMAP Kinase Signaling SystemPhysiologyEndocrinology Diabetes and MetabolismFOXO1P70-S6 Kinase 1MyostatinBiologyMiceRandom Allocation03 medical and health sciences0302 clinical medicinePhysiology (medical)Internal medicinemedicineAnimalsRNA MessengerPhosphorylationMuscle SkeletalProtein kinase BPI3K/AKT/mTOR pathwayOligonucleotide Array Sequence Analysis030304 developmental biology0303 health sciencesForkhead Box Protein O1Gene Expression ProfilingTOR Serine-Threonine KinasesUbiquitinationForkhead Transcription FactorsOrgan SizeMyostatinProtein ubiquitinationMuscle atrophyMuscular AtrophyDNA Repair EnzymesDiabetes Mellitus Type 1EndocrinologyGene Expression Regulationbiology.proteinPhosphorylationmedicine.symptomProto-Oncogene Proteins c-akt030217 neurology & neurosurgeryTranscription FactorsAmerican Journal of Physiology-Endocrinology and Metabolism
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The Adult Pituitary Shows Stem/Progenitor Cell Activation in Response to Injury and Is Capable of Regeneration

2012

The pituitary gland constitutes, together with the hypothalamus, the regulatory core of the endocrine system. Whether the gland is capable of cell regeneration after injury, in particular when suffered at adult age, is unknown. To investigate the adult pituitary's regenerative capacity and the response of its stem/progenitor cell compartment to damage, we constructed a transgenic mouse model to conditionally destroy pituitary cells. GHCre/iDTR mice express diphtheria toxin (DT) receptor after transcriptional activation by Cre recombinase, which is driven by the GH promoter. Treatment with DT for 3 d leads to gradual GH+ (somatotrope) cell obliteration with a final ablation grade of 80–90% 1…

Malemedicine.medical_specialtyPituitary glandTime FactorsSomatotropic cellMice TransgenicBiologyMiceEndocrinologySOX2Internal medicinemedicineAnimalsRegenerationCell LineageProgenitor cellPromoter Regions GeneticSOXB1 Transcription FactorsStem CellsDeoxyuridineEndothelial stem cellEndocrinologymedicine.anatomical_structureGrowth HormonePituitary GlandIntercellular Signaling Peptides and ProteinsFemaleStem cellHeparin-binding EGF-like Growth FactorAdult stem cellEndocrine glandEndocrinology
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Fludarabine prevents smooth muscle proliferation in vitro and neointimal hyperplasia in vivo through specific inhibition of STAT-1 activation.

2007

Drug-eluting stents are increasingly used to reduce in-stent restenosis and adverse cardiac events after percutaneous coronary interventions. However, the race for the ideal drug-eluting stent is still on, with special regard to the best stent-coating system and the most effective and less toxic drug. Fludarabine, a nucleoside analog, has both anti-inflammatory and antiproliferative cellular effects. The aim of the present study was to assess the cellular and molecular effects of fludarabine on vascular smooth muscle cell (VSMC) growth in vitro and in vivo and the feasibility and efficacy of a fludarabine-eluting stent. To study the biomolecular effects of fludarabine on VSMC proliferation…

Malemedicine.medical_specialtyVascular smooth muscleTime FactorsPhysiologyMyocytes Smooth MusclePharmacologyProsthesis DesignTransfectionMuscle Smooth VascularRestenosisIn vivoPhysiology (medical)medicineAnimalsCarotid StenosisRNA AntisensePhosphorylationRats WistarAortaCells CulturedCell ProliferationNeointimal hyperplasiaHyperplasiaDose-Response Relationship Drugbusiness.industryCardiovascular AgentsHyperplasiaJanus Kinase 2medicine.diseaseFludarabineSurgeryRatsDisease Models AnimalSTAT1 Transcription FactorCardiovascular agentSTAT proteinFeasibility StudiesStentsRabbitsCardiology and Cardiovascular MedicinebusinessCarotid Artery InjuriesTunica IntimaAngioplasty BalloonVidarabinemedicine.drug
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A non-redundant role for OX40 in the competitive fitness of Treg in response to IL-2.

2010

OX40 stimulation is known to enhance activation of effector T cells and to inhibit induction and suppressive function of Treg. Here we uncovered a novel role of OX40 in sustaining Treg competitive fitness in vivo, during repopulation of lymphopenic hosts and reconstitution of BM chimeras. Defective expansion of OX40-null Treg diminished their ability to suppress inflammation in a model of lymphopenia-driven colitis. OX40-mediated promotion of Treg fitness spanned beyond lymphopenic environments, as endogenous Treg in OX40-null mice showed decreased accumulation during thymic development, enhanced susceptibility to antibody-mediated depletion and defective turnover following thymectomy. In v…

Malemedicine.medical_treatmentImmunologyBlotting Westernchemical and pharmacologic phenomenaEndogenyInflammationSuppressor of Cytokine Signaling ProteinsT-Lymphocytes RegulatoryMiceSuppressor of Cytokine Signaling 1 ProteinLymphopeniaOX40; Treg; IL-2.medicineSTAT5 Transcription FactorImmunology and AllergyAnimalsOX40PhosphorylationReceptorSTAT5Cell ProliferationMice KnockoutbiologyEffectorCell growthSuppressor of cytokine signaling 1hemic and immune systemsReceptors OX40IL-2.ColitisFlow Cytometrycytokinescompetitive fitnessSpecific Pathogen-Free OrganismsThymectomyMice Inbred C57BLTregRadiation ChimeraImmunologybiology.proteinInterleukin-2costimulatory moleculesmedicine.symptomcompetitive fitness; costimulatory molecules; cytokines; treg
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Targeting transcription factor Stat4 uncovers a role for interleukin-18 in the pathogenesis of severe lupus nephritis in mice

2011

Polymorphisms in the transcription factor Stat4 gene have been implicated as risk factors for systemic lupus erythematosus. Although some polymorphisms have a strong association with autoantibodies and nephritis, their impact on pathophysiology is still unknown. To explore this further we used signal transducers and activators of transcription 4 (Stat4) knockout MRL/MpJ-Fas(lpr)/Fas(lpr) (MRL-Fas(lpr)) mice and found that they did not differ in survival or renal function from Stat4-intact MRL-Fas(lpr) mice. Circulating interleukin (IL)-18 levels, however, were elevated in Stat4-deficient compared to Stat4-intact mice, suggesting that this interleukin might contribute to the progression of l…

Malemusculoskeletal diseasesMice Inbred MRL lprchronic inflammationLupus nephritisKidneyInterleukin-23ArticleProinflammatory cytokineOligodeoxyribonucleotides AntisenseGene Knockout TechniquesInterferon-gammaMiceimmune system diseasesmedicineAnimalsskin and connective tissue diseasesSTAT4DNA PrimersAutoimmune diseaseMice Knockoutlupus nephritisMice Inbred BALB CBase Sequencebusiness.industryGene Transfer TechniquesInterleukin-18InterleukinGlomerulonephritishemic and immune systemsSTAT4 Transcription Factormedicine.diseaseInterleukin-12chronic glomerulonephritisNephrologyImmunologyInterleukin 18FemalebusinessNephritisKidney International
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In-vitro regulation of odontogenic gene expression in human embryonic tooth cells and SHED cells

2012

The bud-to-cap stage transition during early tooth development is a time when the tooth-inducing potential becomes restricted to the mesenchyme. Several key genes, expressed in the mesenchyme at this stage, are an absolute requirement for the progression of tooth development. These include the transcription factors Msx1 and Pax9. The inductive potential of tooth mesenchyme cells is a key requisite for whole-tooth bioengineering and thus identification of cells that can retain this property following expansion in culture is an important as yet unresolved, goal. We show here that in-vitro culture of embryonic human tooth mesenchyme cells and SHED cells express low levels of PAX9 and MSX1 and …

MesodermCell signalingHistologyMesenchymeSHEDPAX9MSX1tissue engineering cell signallingBone Morphogenetic Protein 4BiologyCell LinePathology and Forensic MedicineMesodermstomatognathic systemmedicineHumansChildMSX1 Transcription FactorRegulation of gene expressionMesenchymal stem cellGene Expression Regulation DevelopmentalCell BiologyEmbryonic stem cellCell biologystomatognathic diseasesmedicine.anatomical_structureBone morphogenetic protein 4Cell cultureImmunologyOdontogenesisPAX9 Transcription FactorToothSignal TransductionCell and Tissue Research
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Serpent and a hibris reporter are co-expressed in migrating cells during Drosophila hematopoiesis and Malpighian tubule formation

2006

Motile mesodermal cells contribute several cell types to developing embryos. In Drosophila, blood cell precursors or prohemocytes, are first detected in the procephalic mesoderm by the expression of the GATA transcription factor Serpent. Once specified, a subset of prohemocytes migrate posteriorly to populate most of the embryo and further differentiate as plasmatocytes. Similarly, Drosophila nephrogenesis involves integration of posterior mesodermal cells into the Malpighian tubule primordia where these cells differentiate as stellate cells. Here we investigated the possibility that the immunoglobulin-domain protein Hibris and the GATA factor Serpent were co-expressed in motile mesodermal …

MesodermMalpighian tubule systemCell typeanimal structuresOrganogenesisEmbryoGeneral MedicineAnatomyEmbryonic TissueBiologyCell biologymedicine.anatomical_structureembryonic structuresGeneticsmedicineGATA transcription factorDrosophila ProteinHereditas
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Pancreatic T cell protein-tyrosine phosphatase deficiency ameliorates cerulein-induced acute pancreatitis.

2014

Background Acute pancreatitis (AP) is a common clinical problem whose incidence has been progressively increasing in recent years. Onset of the disease is trigged by intra-acinar cell activation of digestive enzyme zymogens that induce autodigestion, release of pro-inflammatory cytokines and acinar cell injury. T-cell protein tyrosine phosphatase (TCPTP) is implicated in inflammatory signaling but its significance in AP remains unclear. Results In this study we assessed the role of pancreatic TCPTP in cerulein-induced AP. TCPTP expression was increased at the protein and messenger RNA levels in the early phase of AP in mice and rats. To directly determine whether TCPTP may have a causal rol…

MessengerWistarProtein tyrosine phosphataseInbred C57BLBiochemistryOral and gastrointestinalSTAT3Mice2.1 Biological and endogenous factorsPhosphorylationAetiologySTAT3Non-Receptor Type 2CeruletideCancerMice KnockoutProtein Tyrosine Phosphatase Non-Receptor Type 2Pancreatitis Acute NecrotizingNF-kappa B3. Good healthAcute NecrotizingAmylasesTumor necrosis factor alphaTCPTPCell activationCeruletideSTAT3 Transcription Factormedicine.medical_specialtyBiochemistry & Molecular BiologyKnockoutBiologyProinflammatory cytokinePancreatic CancerRare DiseasesInternal medicineAcinar cellmedicineGeneticsAnimalsRNA MessengerRats WistarMolecular BiologyInflammationTumor Necrosis Factor-alphaInterleukin-6ResearchCell BiologyLipaseNFKB1RatsAcute pancreatitisMice Inbred C57BLEndocrinologyPancreatitisbiology.proteinRNAProtein Tyrosine PhosphataseBiochemistry and Cell BiologyDigestive DiseasesKnockout mice
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