Search results for "JUNB"

showing 9 items of 9 documents

miR-155 regulative network in FLT3 mutated acute myeloid leukemia

2015

Abstract Background Acute myeloid leukemia (AML) represents a heterogeneous disorder with recurrent chromosomal alterations and molecular abnormalities. Among AML with normal karyotype (NK-AML) FLT3 activating mutation, internal tandem duplication (FLT3-ITD), is present in about 30% of patients, conferring unfavorable outcome. Our previous data demonstrated specific up-regulation of miR-155 in FLT3-ITD+ AML. miR-155 is known to be directly implicated in normal hematopoiesis and in some pathologies such as myeloid hyperplasia and acute lymphoblastic leukemia. Methods and results To investigate about the potential influence of miR-155 de-regulation in FLT3-mutated AML we generated a transcrip…

AdultMaleCancer ResearchMyeloidJUNBNetworkBiologyYoung Adultchemistry.chemical_compoundAMLhemic and lymphatic diseasesmicroRNACEBPBmedicineHumansGene silencingGene Regulatory NetworksAML; MicroRNA; NetworkAgedAged 80 and overGene Expression Regulation LeukemicGene Expression ProfilingMyeloid leukemiaMicroRNAHematologyMiddle AgedLeukemia Myeloid AcuteMicroRNAsmedicine.anatomical_structurefms-Like Tyrosine Kinase 3OncologyRUNX1chemistryMutationCancer researchFemaleMyelopoiesisK562 Cells
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Resveratrol decreases the levels of miR-155 by upregulating miR-663, a microRNA targeting JunB and JunD.

2010

An inflammatory component is present in the microenvironment of most neoplastic tissues, including those not causally related to an obvious inflammatory process. Several microRNAs, and especially miR-155, play an essential role in both the innate and adaptative immune response. Resveratrol (trans-3,4#,5-trihydroxystilbene) is a natural antioxidant with anti-inflammatory properties that is currently at the stage of preclinical studies for human cancer prevention. Here, we establish that, in human THP-1 monocytic cells as well as in human blood monocytes, resveratrol upregulates miR- 663, a microRNA potentially targeting multiple genes implicated in the immune response. In THP-1 cells, miR-66…

LipopolysaccharidesCancer ResearchJUNBProto-Oncogene Proteins c-junBlotting WesternResveratrolBiologyMonocytesmiR-15503 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmune systemDownregulation and upregulationRNA interferencemicroRNAStilbenesBiomarkers TumorHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRNA MessengerLuciferases[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCells Cultured030304 developmental biologyOligonucleotide Array Sequence AnalysisCancer Biology0303 health sciencesInnate immune systemmicroRNAReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingmicroRNA; ResveratrolGeneral MedicineAntineoplastic Agents Phytogenic3. Good healthUp-RegulationTranscription Factor AP-1MicroRNAschemistryGene Expression RegulationResveratrol030220 oncology & carcinogenesisCancer research
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Suppression of ischemia-induced fos expression and AP-1 activity by an antisense oligodeoxynucleotide to c-fos mRNA.

1994

The molecular events of brain adaptation to injury that may underlie functional recovery after stroke remain largely undefined. Recent observations of altered gene expression in ischemic brain using animal stroke models have opened new avenues for exploration of the biochemical cascades after stroke [1–11]. These postischemic events include an increase in extracellular excitatory amino acid neurotransmitters such as glutamate. Glutamate receptor–mediated activation of phospholipases and protein kinases results in the alteration of nuclear regulatory processes, including the expression of immediate early genes such as c-fos, junB, and c-jun [5, 12]. The Fos, Jun, and JunB proteins have been …

Messenger RNAbiologyBase SequenceJUNBEffectorOligonucleotideMolecular Sequence DataGene ExpressionOligonucleotides Antisensec-FosMolecular biologyReceptor tyrosine kinaseArticleRatsTranscription Factor AP-1NeurologyTranscription (biology)Ischemic Attack TransientGene expressionbiology.proteinAnimalsNeurology (clinical)RNA MessengerProto-Oncogene Proteins c-fosAnnals of neurology
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Soluble interleukin 6 (IL-6) receptor influences the expression of the protooncogene junB and the production of fibrinogen in the HepG2 human hepatom…

1998

Abstract Interleukin 6 (IL-6) belongs to a family of cytokines using receptors sharing a common signal-transducing chain, gp130 and containing a specific ligand-binding chain (IL-6Rα). It was shown that both the membrane-bound and the soluble form (sIL-6R) of this ligand specific receptor chain occurs naturally. The soluble form of IL-6 receptor was found to be able to associate with the membrane-bound gp130 and to generate active IL-6 receptor complex capable of inducing signal transduction. This study on a human hepatoma cell line and primary rat hepatocytes examined how the effectiveness of IL-6 is modified by the presence of soluble IL-6 receptor and whether the sIL-6R in the absence of…

Receptor complexCarcinoma HepatocellularJUNBProto-Oncogene Proteins c-junImmunologyBiologyBiochemistryPolymerase Chain Reactionhemic and lymphatic diseasesGene expressionTumor Cells CulturedImmunology and AllergyAnimalsHumansRNA MessengerReceptorMolecular BiologyTranscription factorCells CulturedFibrinogenHematologyGlycoprotein 130Molecular biologyReceptors Interleukin-6RatsGene Expression RegulationLiverSolubilityInterleukin-6 receptorSignal transductionCytokine
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A differential role of CREB phosphorylation in cAMP-inducible gene expression in the rat pineal

2000

In the rat pineal gland cAMP mediates nocturnal induction of the enzyme arylalkylamine N-acetyltransferase (AA-NAT) as well as of transcription factors such as inducible cAMP early repressor (ICER), Fos-related antigen-2 (Fra-2) and JunB. Cyclic AMP stimulates the phosphorylation of the DNA binding protein cAMP response element binding protein (CREB). While cAMP-induced CREB phosphorylation appears to be a prerequisite for AA-NAT and ICER gene expression, it is not known whether CREB phosphorylation accounts for the full cAMP response of the two genes. Furthermore, the significance of CREB phosphorylation in cAMP-activated Fra-2 and JunB transcription is unknown. In the present in vitro stu…

Transcriptional Activationendocrine systemCAMP-Responsive Element ModulatorArylamine N-AcetyltransferaseProto-Oncogene Proteins c-junJUNBBlotting WesternNerve Tissue ProteinsFos-Related Antigen-2CREBPineal GlandGene Expression Regulation EnzymologicCyclic AMP Response Element ModulatorRats Sprague-DawleyOkadaic AcidGene expressionAnimalsRNA MessengerEnzyme InhibitorsPhosphorylationCyclic AMP Response Element-Binding ProteineducationMolecular BiologyTranscription factorRegulation of gene expressioneducation.field_of_studybiologyReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceMolecular biologyRatsDNA-Binding ProteinsRepressor ProteinsBucladesinebiology.proteinPhosphorylationNeurology (clinical)CREB1Proto-Oncogene Proteins c-fosSignal TransductionTranscription FactorsDevelopmental BiologyBrain Research
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Measles virus enhances the expression of cellular immediate-early genes and DNA-binding of transcription factor AP-1 in lung epithelial A549 cells.

2002

In this work we investigated the effect of measles virus (MV) infection on the expression of immediate-early genes junB, c-jun and c-fos mRNA as well as AP-1 DNA-binding activity in the lung epithelial-like adenocarcinoma cell line A549. The transcription factor AP-1, which is a group of dimeric complexes of the Fos and Jun family proteins, is an important regulator in many cellular responses to different extracellular stimuli. Membrane cofactor protein CD46, which acts as a receptor for laboratory-adapted and vaccine strains of MV, has been reported to associate with beta1 integrin molecules, which are known to trigger signaling events and activate immediate-early genes. The expression of …

Lung NeoplasmsJUNBBiologyMeasles virusMembrane Cofactor Protein03 medical and health sciencesAntigens CDVirologyGene expressionTumor Cells CulturedHumansMononegaviralesTranscription factorGenes Immediate-Early030304 developmental biologyA549 cell0303 health sciencesMembrane GlycoproteinsCD46Interleukin-6030302 biochemistry & molecular biologyGeneral MedicineDNAbiology.organism_classificationVirology3. Good healthTranscription Factor AP-1Gene Expression RegulationMeasles virusImmediate early geneArchives of virology
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Epidermal IL-17A leads to bone loss through inhibition of osteoblast differentiation

2012

The AP-1 transcription factor family is a central regulator of skin and bone homeostasis. We have previously shown that specific deletion of JunB/AP-1 in epidermis (JunBmice) results in skin inflammation,myeloproliferative disease, lupus-like disease and osteopenia. While upregulation of serum IL-6 and G-CSF are observed in this model, genetic deletion of these cytokines does not rescue osteopenia in JunB mice. Thus, we carried out a screen for other cytokines that are regulated by the loss of JunB in the epidermis. We have identified IL-17A as a cytokine expressed in JunB epidermis in vivo, and hypothesize that IL-17A leads to osteopenia in JunBmice. To test this,we carried out osteoblast …

HistologyEpidermis (botany)PhysiologyJUNBEndocrinology Diabetes and Metabolismmedicine.medical_treatmentInflammationOsteoblastBiologyCytokinemedicine.anatomical_structureDownregulation and upregulationOsteoclastmedicineCancer researchCytotoxic T cellmedicine.symptomBone
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Hypertrophic agonists induce the binding of c-Fos to an AP-1 site in cardiac myocytes: implications for the expression of GLUT1

2003

Objectives: Serum is among the agents known to induce hypertrophy of cardiac myocytes, which occurs concomitant with an increase in AP-1-mediated transcription. We have examined if this effect correlates with changes in the relative abundance of particular AP-1 heterodimers, as their exact composition under these conditions is unknown. Furthermore, we obtained insight on the specific role of c-Fos from studying the induction of the glucose transporter GLUT1 by serum in fibroblasts. Methods: We characterised the AP-1 heterodimers expressed in neonatal cardiac myocytes by supershift electrophoretic mobility shift assay (EMSA) analysis. Quantitative changes in transcription were measured using…

Monosaccharide Transport ProteinsTranscription GeneticMAP Kinase Signaling SystemPyridinesPhysiologyJUNBBlotting WesternElectrophoretic Mobility Shift Assayc-FosCell LineMicePhysiology (medical)Gene expressionAnimalsMyocyteMyocytes CardiacElectrophoretic mobility shift assayCells CulturedFlavonoidsGlucose Transporter Type 1biologyImidazolesGlucose transporterFibroblastsMolecular biologyRatsEnzyme ActivationTranscription Factor AP-1Animals Newbornbiology.proteinGLUT1Mitogen-Activated Protein KinasesCardiology and Cardiovascular MedicineProto-Oncogene Proteins c-fosGene DeletionProtein BindingFOSBCardiovascular Research
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Inducible Responses and Protective Functions of Mammalian Cells Upon Exposure to UV Light and Ionizing Radiation

1999

In mammalian cells, ultraviolet (UV) light as well as ionizing radiation (IR) transcriptionally activate the early-responsive genes c-fos, c jun,junB and junD. The induction of fos and jun by UV-C is currently understood to occur via activation of the EGF receptor and the Ras, Raf, ERK and JNK cascade leading ultimately to phosphorylation of transcription factors such as Fos and Jun (AP-1). This, finally, gives rise to transcriptional activation of AP-1 dependent target genes. Another gene we have recently demonstrated to be immediate-early inducible upon UV-irradiation encodes the Ras-related small GTPase RhoB. The pathway of rhoB induction appears to be different from fos/jun because (i) …

MAPK/ERK pathwayMutationChemistryDNA repairJUNBDNA damageRHOBc-junmedicinemedicine.disease_causeTranscription factorCell biology
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