Search results for "Transcription factor"

showing 10 items of 1493 documents

Survivin is regulated by interleukin-4 in colon cancer stem cells

2010

Colorectal cancer has provided an important model to test the stem cell hypothesis of cancer origin, which implies that cancer arises as a result of genetic aberrations in stem cells leading to deregulation of the proliferation/differentiation balance. We and others have demonstrated that, similarly to other solid tumors, colon carcinogenesis and progression are dictated by highly apoptosis-resistant stem-like cells. Our data have suggested that protection from apoptosis is achieved by autocrine production of interleukin-4 (IL-4) through up-regulation of anti-apoptotic mediators. In this study, we extend our analysis to another apoptosis inhibitor widely expressed in tumors, namely survivin…

Organoplatinum CompoundsPhysiologyColorectal cancerSurvivinmedicine.medical_treatmentClinical BiochemistryFluorescent Antibody TechniqueAntineoplastic AgentsApoptosisBiologyInhibitor of Apoptosis ProteinsSurvivin inetrleukin-4Cancer stem cellSurvivinIn Situ Nick-End LabelingmedicineHumansPhosphorylationAutocrine signallingInterleukin 4Staining and LabelingCancerIsoxazolesCell Biologymedicine.diseaseGene Expression Regulation NeoplasticOxaliplatinProtein TransportCytokineImmunologyNeoplastic Stem CellsCancer researchInterleukin-4Stem cellColorectal NeoplasmsSTAT6 Transcription FactorMicrotubule-Associated ProteinsLeflunomideJournal of Cellular Physiology
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The transcription factor IRF1 dictates the IL-21-dependent anticancer functions of TH9 cells

2014

The TH9 subset of helper T cells was initially shown to contribute to the induction of autoimmune and allergic diseases, but subsequent evidence has suggested that these cells also exert antitumor activities. However, the molecular events that account for their effector properties are elusive. Here we found that the transcription factor IRF1 enhanced the effector function of TH9 cells and dictated their anticancer properties. Under TH9-skewing conditions, interleukin 1β (IL-1β) induced phosphorylation of the transcription factor STAT1 and subsequent expression of IRF1, which bound to the promoters of Il9 and Il21 and enhanced secretion of the cytokines IL-9 and IL-21 from TH9 cells. Further…

OvalbuminGreen Fluorescent ProteinsImmunologyMelanoma ExperimentalProto-Oncogene Proteins c-fyn3T3 cellsCell LineInterferon-gammaMicemedicineAnimalsImmunology and AllergySTAT1PhosphorylationRNA Small InterferingSTAT4Transcription factorInterleukin 3Mice KnockoutBase SequencebiologySequence Analysis RNAChemistryEffectorInterleukinsInterleukin-9Promoter3T3 CellsT-Lymphocytes Helper-InducerInterleukin-10Cell biologyMice Inbred C57BLSTAT1 Transcription Factormedicine.anatomical_structureCell culturebiology.proteinFemaleRNA InterferenceInterferon Regulatory Factor-1Nature Immunology
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Phospho-p38 MAPK expression in COPD patients and asthmatics and in challenged bronchial epithelium

2015

<b><i>Background:</i></b> The role of mitogen-activated protein kinases (MAPK) in regulating the inflammatory response in the airways of patients with chronic obstructive pulmonary disease (COPD) and asthmatic patients is unclear. <b><i>Objectives:</i></b> To investigate the expression of activated MAPK in lungs of COPD patients and in bronchial biopsies of asthmatic patients and to study MAPK expression in bronchial epithelial cells in response to oxidative and inflammatory stimuli. <b><i>Methods:</i></b> Immunohistochemical expression of phospho (p)-p38 MAPK, p-JNK1 and p-ERK1/2 was measured in bronchial mucosa in pat…

P38 MAPKMaleMAPK/ERK pathwayAsthma phenotypeSMOKERespiratory SystemMitogen-activated protein kinases; p65; Pathology of chronic obstructive pulmonary disease; Chronic obstructive pulmonary disease phenotypes; Asthma phenotypesPathology of chronic obstructive pulmonary diseasep38 Mitogen-Activated Protein KinasesChronic obstructive pulmonary disease phenotypePulmonary Disease Chronic ObstructiveOXIDATIVE STRESSMACROPHAGESRespiratory systemMitogen-activated protein kinasesChronic obstructive pulmonary disease phenotypesMitogen-activated protein kinases; p65; pathology of chronic obstructive pulmonary disease phenotypes; asthma phenotypesCOPDp65KinaseAsthma phenotypes; Chronic obstructive pulmonary disease phenotypes; Mitogen-activated protein kinases; p65; Pathology of chronic obstructive pulmonary disease; Pulmonary and Respiratory MedicineACTIVATED PROTEIN-KINASEInterleukinMiddle AgedImmunohistochemistrypathology of chronic obstructive pulmonary disease phenotypesAsthma phenotypesFemaleLife Sciences & BiomedicinePulmonary and Respiratory Medicinep38 mitogen-activated protein kinasesBlotting WesternINHIBITIONSocio-culturaleBronchiRespiratory MucosaOBSTRUCTIVE PULMONARY-DISEASE1102 Cardiovascular Medicine And HaematologyCell LinemedicineHumansLymphocyte CountInterleukin 8AgedAsthmaScience & Technologybusiness.industryInterleukin-8Transcription Factor RelAPATHWAYSMitogen-activated protein kinasemedicine.diseaseAsthmarespiratory tract diseasesSEVERITYCase-Control StudiesCELLSImmunologybusiness
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miR-205-5p-mediated downregulation of ErbB/HER receptors in breast cancer stem cells results in targeted therapy resistance

2015

AbstractThe ErbB tyrosine kinase receptor family has been shown to have an important role in tumorigenesis, and the expression of its receptor members is frequently deregulated in many types of solid tumors. Various drugs targeting these receptors have been approved for cancer treatment. Particularly, in breast cancer, anti-Her2/EGFR molecules represent the standard therapy for Her2-positive malignancies. However, in a number of cases, the tumor relapses or progresses thus suggesting that not all cancer cells have been targeted. One possibility is that a subset of cells capable of regenerating the tumor, such as cancer stem cells (CSCs), may not respond to these therapeutic agents. Accumula…

P63cancer stem cellsCancer ResearchReceptor ErbB-2oncogenesmedicine.medical_treatmentmedicine.disease_causeTargeted therapyERBB3Molecular Targeted TherapyDEATHErbB ReceptorsGene Expression Regulation NeoplasticNeoplastic Stem CellsFemaleOriginal Articlemedicine.drugCARCINOMAMIGRATIONCancer Stem Cells; Breast CancerImmunologyBreast NeoplasmsCancer Stem CellMIR-205miR-205-5pBiologyLapatinibcancer treatmentNOCellular and Molecular Neurosciencebreast cancerBreast cancerErbBCancer stem cellCell Line TumormedicineHumansSUPPRESSIONCell ProliferationMESENCHYMAL TRANSITIONtumorigenesis cancer treatment cancer stem cells miR-205-5p oncogenes breast cancerMICRORNA EXPRESSIONTumor Suppressor ProteinsLapatinibCell BiologyTrastuzumabmedicine.diseaseGENEMicroRNAstumorigenesisDrug Resistance NeoplasmCancer cellQuinazolinesCancer researchNeoplasm Recurrence LocalCarcinogenesisTranscription FactorsCell Death & Disease
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Common variants conferring risk of schizophrenia

2009

Schizophrenia is a complex disorder, caused by both genetic and environmental factors and their interactions. Research on pathogenesis has traditionally focused on neurotransmitter systems in the brain, particularly those involving dopamine. Schizophrenia has been considered a separate disease for over a century, but in the absence of clear biological markers, diagnosis has historically been based on signs and symptoms. A fundamental message emerging from genome-wide association studies of copy number variations (CNVs) associated with the disease is that its genetic basis does not necessarily conform to classical nosological disease boundaries. Certain CNVs confer not only high relative ris…

Pair 6/geneticsGenetics and epigenetic pathways of disease [NCMLS 6]Genome-wide association studyAetiology screening and detection [ONCOL 5]1Q21.1Major Histocompatibility Complex/geneticsMajor Histocompatibility ComplexTranscription Factor 40302 clinical medicineChemicals And Cas Registry NumbersPerception and Action [DCN 1]Copy-number variationPOPULATIONGeneticsPair 18/genetics0303 health scienceseducation.field_of_studyGenomeHuman/geneticsMultidisciplinaryBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsSchizophrenia/*genetics/immunologyGenetic Predisposition to Disease/*genetics3. Good healthDNA-Binding ProteinsNeurogranin/geneticsDISEASESChromosomes Human Pair 6Single Nucleotide/*geneticsFunctional Neurogenomics [DCN 2]Zinc finger protein 804AHumanGenetic MarkersPsychosisGenotypePopulationTranscription Factors/geneticsSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideChromosomesPair 11/geneticsArticleChromosomes; Human; Pair 11/genetics; Pair 18/genetics; Pair 6/genetics; DNA-Binding Proteins/genetics; Genetic Markers/genetics; Genetic Predisposition to Disease/*genetics; Genome; Human/genetics; Genome-Wide Association Study; Genotype; Humans; Major Histocompatibility Complex/genetics; Neurogranin/genetics; Polymorphism; Single Nucleotide/*genetics; Schizophrenia/*genetics/immunology; Transcription Factors/geneticsGenomic disorders and inherited multi-system disorders [IGMD 3]Molecular epidemiology [NCEBP 1]03 medical and health sciencesTranslational research [ONCOL 3]medicineHumansSNPGenetic Predisposition to DiseasePolymorphismGENOME-WIDE ASSOCIATIONeducation030304 developmental biologyGenetic associationGenetic Markers/geneticsHereditary cancer and cancer-related syndromes [ONCOL 1]Genome HumanChromosomes Human Pair 11MEMORYmedicine.diseaseGENENEUROGRANINDELETIONSSchizophreniabiology.proteinNeurograninChromosomes Human Pair 18DNA-Binding Proteins/geneticsMENTAL-RETARDATIONSCAN030217 neurology & neurosurgeryGenome-Wide Association StudyTranscription Factors
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Melanocortins in Brain Inflammation: The Role of Melanocortin Receptor Subtypes

2010

The melanocortins (MC) are released from neurons and paracrine cells in the CNS where they are involved in important physiological functions, including regulation of body temperature and immune responses. MC bind to melanocortin receptors, a class of cell surface G-protein-coupled receptors. Of the five subtypes of MC receptors that have been cloned in mammals, the MC1, MC3, MC4 and MC5 receptors are expressed in brain tissues. Expression of MC receptors in both brain cells and cells of the immune system suggests direct involvement of MC in regulation of inflammatory processes in the brain. The binding of MC to MC receptors induces activation of adenylate cyclase, increase in intracellular …

Paracrine signallingImmune systemMelanocortin receptormedicineInflammationBiologymedicine.symptomPharmacologyMelanocortinReceptorTranscription factorMelanocortinsCell biology
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Distribution and Dynamics of Transcription-Associated Proteins during Parvovirus Infection

2012

ABSTRACT Canine parvovirus (CPV) infection leads to reorganization of nuclear proteinaceous subcompartments. Our studies showed that virus infection causes a time-dependent increase in the amount of viral nonstructural protein NS1 mRNA. Fluorescence recovery after photobleaching showed that the recovery kinetics of nuclear transcription-associated proteins, TATA binding protein (TBP), transcription factor IIB (TFIIB), and poly(A) binding protein nuclear 1 (PABPN1) were different in infected and noninfected cells, pointing to virus-induced alterations in binding dynamics of these proteins.

Parvovirus CanineViral nonstructural proteinvirusesImmunologyMicrobiologyParvoviridae Infections03 medical and health sciencesVirologyAnimalsTranscription factor030304 developmental biology0303 health sciencesbiologyParvovirusBinding protein030302 biochemistry & molecular biologyCanine parvovirusFluorescence recovery after photobleachingbiology.organism_classificationMolecular biology3. Good healthVirus-Cell InteractionsCell CompartmentationInsect Sciencebiology.proteinTATA-binding proteinTranscription factor II BSubcellular FractionsTranscription Factors
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Modulation of Hedgehog target gene expression by the Fused serine-threonine kinase in wing imaginal discs

1998

0925-4773 doi: DOI: 10.1016/S0925-4773(98)00130-0; The Fused (Fu) serine–threonine kinase and the Suppressor of fused (Su(fu)) product are part of the Hedgehog (Hh) signalling pathway both in embryos and in imaginal discs. In wing imaginal discs, the Hh signal induces Cubitus interruptus (Ci) accumulation and activates patched (ptc) and decapentaplegic (dpp) expression along the anterior/posterior (A/P) boundary. In this paper, we have examined the role of the Fu and Su(fu) proteins in the regulation of Hh target gene expression in wing imaginal discs, by using different classes of fu alleles and an amorphic Su(fu) mutation. We show that, at the A/P boundary, Fu kinase activity is involved …

PatchedEmbryologyanimal structuresReceptors Cell SurfaceBiologyProtein Serine-Threonine KinasesSignal transductionCubitus interruptusImaginal disc developmentMorphogenesisAnimalsDrosophila ProteinsWings AnimalHedgehog ProteinsKinase activitySuppressor of fusedGeneticsSerine/threonine-specific protein kinaseHomeodomain ProteinsDecapentaplegicFusedGene Expression Regulation DevelopmentalMembrane ProteinsCi proteinHedgehog signaling pathwayCell biologyDNA-Binding ProteinsRepressor ProteinsImaginal discDrosophila melanogasterInsect ProteinsDrosophilaHedgehogMorphogenTranscription FactorsDevelopmental Biology
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Endothelial Wnt/β-catenin signaling inhibits glioma angiogenesis and normalizes tumor blood vessels by inducing PDGF-B expression

2012

Wnt modulates glioma vascularization by regulating PDGF-B expression.

PathologyAngiogenesisCentral Nervous System NeoplasmsMice0302 clinical medicineImmunology and AllergyWnt Signaling Pathwaybeta Catenin0303 health sciencesbiologyNeovascularization PathologicBrain NeoplasmsWnt signaling pathwayIntracellular Signaling Peptides and ProteinsForkhead Transcription FactorsGliomaProto-Oncogene Proteins c-sis3. Good healthmedicine.anatomical_structureBlood-Brain Barrier030220 oncology & carcinogenesiscardiovascular systemIntercellular Signaling Peptides and ProteinsFemalemedicine.medical_specialtyBeta-cateninEndotheliumImmunologyNotch signaling pathwayMice NudeWnt1 ProteinMural cellArticle03 medical and health sciencesGliomamedicineAnimalsHumansddc:610neoplasms030304 developmental biologyAdaptor Proteins Signal TransducingCalcium-Binding ProteinsMembrane Proteinsmedicine.diseaseXenograft Model Antitumor Assaysnervous system diseasesDKK1Cancer researchbiology.proteinEndothelium VascularNeoplasm Grading
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IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease

2011

Interleukin (IL)-22 is an effector cytokine, which acts primarily on epithelial cells in the skin, gut, liver and lung. Both pro- and anti-inflammatory properties have been reported for IL-22 depending on the tissue and disease model. In a murine model of allergic airway inflammation, we found that IL-22 is predominantly produced by innate lymphoid cells in the inflamed lungs, rather than TH cells. To determine the impact of IL-22 on airway inflammation, we used allergen-sensitized IL-22-deficient mice and found that they suffer from significantly higher airway hyperreactivity upon airway challenge. IL-22-deficiency led to increased eosinophil infiltration lymphocyte invasion and production…

PathologyPulmonologymedicine.medical_treatmentT-LymphocytesIntracellular Spacelcsh:Medicine10263 Institute of Experimental ImmunologyInterleukin 22Mice0302 clinical medicineLymphocytesPhosphorylationlcsh:ScienceLung0303 health sciencesMultidisciplinaryInterleukin-13T CellsAllergy and HypersensitivityInnate lymphoid cellInterleukinrespiratory systemInnate ImmunityRecombinant Proteins3. Good healthCytokinemedicine.anatomical_structureInterleukin 13CytokinesMedicineTumor necrosis factor alphaBiological Markersmedicine.symptomResearch ArticleSTAT3 Transcription Factormedicine.medical_specialtyImmune CellsImmunologyAntigen-Presenting CellsImmunoglobulinsInflammation610 Medicine & health1100 General Agricultural and Biological SciencesBiology03 medical and health sciences1300 General Biochemistry Genetics and Molecular BiologymedicineRespiratory HypersensitivityAnimalsBiology030304 developmental biologyInflammation1000 MultidisciplinaryTumor Necrosis Factor-alphaInterleukinslcsh:RImmunityEpithelial CellsEosinophilAllergensAsthmaImmunity Innaterespiratory tract diseasesImmune SystemImmunology570 Life sciences; biologylcsh:QImmunizationBiomarkers030215 immunology
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