Search results for "Transcription"

showing 10 items of 2278 documents

IL-27 controls the development of inducible regulatory T cells and Th17 cells via differential effects on STAT1

2007

IL-27 is an IL-12-related cytokine frequently present at sites of inflammation that can promote both anti- and pro-inflammatory immune responses. Here, we have analyzed the mechanisms how IL-27 may drive such divergent immune responses. While IL-27 suppressed the development of proinflammatory Th17 cells, a novel role for this cytokine in inhibiting the development of anti-inflammatory, inducible regulatory T cells (iTreg) was identified. In fact, IL-27 suppressed the development of adaptive, TGF-beta-induced Forkhead box transcription factor p3-positive (Foxp3(+)) Treg. Whereas the blockade of Th17 development was dependent on the transcription factor STAT1, the suppression of iTreg develo…

medicine.medical_treatmentImmunologyMice Transgenicchemical and pharmacologic phenomenaInflammationBiologyT-Lymphocytes RegulatoryProinflammatory cytokineMiceImmune systemT-Lymphocyte SubsetsmedicineAnimalsImmunology and AllergySTAT1IL-2 receptorTranscription factorInterleukinsFOXP3Forkhead Transcription FactorsFlow CytometryCoculture TechniquesCell biologySTAT1 Transcription FactorCytokineImmunologybiology.proteinmedicine.symptomEuropean Journal of Immunology
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A MiR-142-3p/EGR2 Feedback Circuitry In Human CSF-1 Driven Differentiation of Monocytes Into Macrophages

2011

Abstract Abstract 2366 Colony-stimulating factor-1 (CSF-1 or M-CSF) triggers the differentiation of human peripheral blood monocytes into macrophages through and integrated cytokine/transcription factors circuitry. Using microarray profiling to explore the role of microRNAs (miRNAs) in this molecular circuitry, we identified the down-regulation of miR-142-3p in human macrophages obtained from CSF-1-treated monocytes. We show that miR-142-3p is a repressor of the transcription factor EGR2 (Early Growth Response 2) through direct 3'UTR interactions. Interestingly, EGR2 binds the promoter of the pre-miR-142-3p gene to negatively regulate its expression, identifying a self-regulatory feedback l…

medicine.medical_treatmentImmunologyRepressorChronic myelomonocytic leukemiaCell BiologyHematologyBiologyColony-stimulating factormedicine.diseaseBiochemistryCell biologyCytokinemicroRNAmedicineGeneTranscription factorProto-oncogene tyrosine-protein kinase SrcBlood
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Translation of HTT mRNA with expanded CAG repeats is regulated by the MID1-PP2A protein complex.

2012

Expansion of CAG repeats is a common feature of various neurodegenerative disorders, including Huntington's disease. Here we show that expanded CAG repeats bind to a translation regulatory protein complex containing MID1, protein phosphatase 2A and 40S ribosomal S6 kinase. Binding of the MID1-protein phosphatase 2A protein complex increases with CAG repeat size and stimulates translation of the CAG repeat expansion containing messenger RNA in a MID1-, protein phosphatase 2A- and mammalian target of rapamycin-dependent manner. Our data indicate that pathological CAG repeat expansions upregulate protein translation leading to an overproduction of aberrant protein and suggest that the MID1-com…

metabolism [Microtubule Proteins]General Physics and AstronomyHTT protein humanRibosomal s6 kinaseMice0302 clinical medicinemetabolism [Transcription Factors]Protein Phosphatase 2Luciferasesgenetics [Nerve Tissue Proteins]genetics [Protein Biosynthesis]0303 health sciencesHuntingtin ProteinMultidisciplinarybiologyTOR Serine-Threonine KinasesNuclear ProteinsTranslation (biology)3. Good healthmetabolism [Luciferases]Microtubule Proteinsddc:500metabolism [Nuclear Proteins]genetics [Trinucleotide Repeat Expansion]Protein Bindingcongenital hereditary and neonatal diseases and abnormalitiesMTOR protein humanUbiquitin-Protein LigasesBlotting WesternNerve Tissue Proteinsmetabolism [TOR Serine-Threonine Kinases]metabolism [RNA Messenger]General Biochemistry Genetics and Molecular Biology03 medical and health sciencesgenetics [RNA Messenger]mental disordersHuntingtin ProteinAnimalsHumansEukaryotic Small Ribosomal SubunitRNA MessengerNucleotide Motifs030304 developmental biologyMessenger RNAmetabolism [Nerve Tissue Proteins]RNAmetabolism [Protein Phosphatase 2]General ChemistryProtein phosphatase 2Molecular biologynervous system diseasesProtein Biosynthesisbiology.proteinTrinucleotide repeat expansionTrinucleotide Repeat Expansion030217 neurology & neurosurgeryMid1 protein humanHeLa CellsTranscription FactorsNature communications
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The E3 Ubiquitin Ligase MID1 Catalyzes Ubiquitination and Cleavage of Fu

2014

Sonic Hedgehog (SHH)-GLI signalling plays an important role during embryogenesis and in tumorigenesis. The survival and growth of several types of cancer depend on autonomously activated SHH-GLI signalling. A protein complex containing the ubiquitin-ligase MID1 and protein phosphatase 2A (PP2A) regulates the nuclear localization and transcriptional activity of GLI3, a transcriptional effector molecule of SHH, in cancer cell lines with autonomously activated SHH signalling. However, the exact molecular mechanisms that mediate the interaction between MID1 and GLI3 remained unknown. Here, we show that MID1 catalyses the ubiquitination and proteasomal cleavage of the GLI3-regulator Fu. Our data…

metabolism [Microtubule Proteins]Ubiquitin-conjugating enzymeBiochemistrymetabolism [Protein Serine-Threonine Kinases]Ubiquitinmetabolism [Transcription Factors]Nuclear proteinSonic hedgehogbiologymetabolism [Protein-Serine-Threonine Kinases]Nuclear Proteinsrespiratory systemProtein-Serine-Threonine KinasesUbiquitin ligaseGene Expression Regulation NeoplasticGLI3 protein humanBiochemistryddc:540embryonic structuresMicrotubule Proteinsmetabolism [Hedgehog Proteins]Function and Dysfunction of the Nervous Systemmetabolism [Nuclear Proteins]Signal Transductionmetabolism [Kruppel-Like Transcription Factors]Proteasome Endopeptidase Complexanimal structuresSTK36 protein humanUbiquitin-Protein LigasesKruppel-Like Transcription FactorsNerve Tissue ProteinsProtein Serine-Threonine Kinaseschemistry [Ubiquitin-Protein Ligases]CatalysisZinc Finger Protein Gli3Cell Line TumorGLI3HumansHedgehog Proteinsmetabolism [Proteasome Endopeptidase Complex]metabolism [Cell Nucleus]Molecular Biologychemistry [Lysine]DNA PrimersCell Nucleusmetabolism [Nerve Tissue Proteins]UbiquitinLysineUbiquitinationCell BiologyProtein phosphatase 2chemistry [Ubiquitin]Proteasomebiology.proteinSHH protein humanhuman activitiesMid1 protein humanHeLa CellsTranscription FactorsJournal of Biological Chemistry
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Functions of the translation factor eIF5A in cellular metabolism and transcriptional control

2023

El factor de inicio de traducción de eucariotas 5A (eIF5A) es una proteína esencial y conservada con funciones en las tres fases de la traducción. eIF5A está codificado por dos genes parálogos, TIF51A/TIF51B y EIF5A1/EIF5A2 en levadura y humanos respectivamente. eIF5A es la única proteína que contiene hipusina, una modificación esencial para su actividad, y se une a los ribosomas para facilitar la traducción de motivos con prolinas consecutivas o combinaciones de prolina con glicina y aminoácidos cargados. eIF5A participa en otras funciones y procesos como exporte de mRNAs nucleares, proliferación y apoptosis. Su asociación con enfermades como el cáncer es de interés. En esta tesis se han u…

mitochondriacollagenUNESCO::CIENCIAS DE LA VIDAtranslationgene expression regulationtranscriptionmetabolism
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A SUMOylation-defective MITF germline mutation predisposes to melanoma and renal carcinoma

2011

International audience; So far, no common environmental and/or phenotypic factor has been associated with melanoma and renal cell carcinoma (RCC). The known risk factors for melanoma include sun exposure, pigmentation and nevus phenotypes; risk factors associated with RCC include smoking, obesity and hypertension. A recent study of coexisting melanoma and RCC in the same patients supports a genetic predisposition underlying the association between these two cancers. The microphthalmia-associated transcription factor (MITF) has been proposed to act as a melanoma oncogene; it also stimulates the transcription of hypoxia inducible factor (HIF1A), the pathway of which is targeted by kidney canc…

multidisciplinary sciencesMESH : Germ-Line MutationSUMO proteinurologic and male genital diseasesmedicine.disease_causeMESH : Neoplasm Invasiveness[ SDV.CAN ] Life Sciences [q-bio]/CancerMESH : Carcinoma Renal Cell0302 clinical medicineGene FrequencyCell MovementMESH: Germ-Line MutationMESH : Cell MovementMESH : Gene FrequencyMESH: Cell MovementComputingMilieux_MISCELLANEOUSGenetics0303 health sciencesMultidisciplinaryMESH: SumoylationMelanomaMESH : SumoylationMESH: Genetic Predisposition to Diseaserenal carcinomaMESH: Carcinoma Renal CellMicrophthalmia-associated transcription factorMESH : Microphthalmia-Associated Transcription Factor3. Good healthgermline mutation030220 oncology & carcinogenesisMESH: Microphthalmia-Associated Transcription Factorscience and technologyMESH: MelanomasumoMESH : Melanoma[SDV.CAN]Life Sciences [q-bio]/CancerBiology03 medical and health sciencesGermline mutationmelanomaMESH: Gene FrequencyGenetic predispositionmedicineHumansGenetic Predisposition to DiseaseNeoplasm InvasivenessCarcinoma Renal CellneoplasmsTranscription factorGerm-Line Mutation030304 developmental biologyMicrophthalmia-Associated Transcription FactorMESH: HumansMESH : HumansSumoylationMESH: Neoplasm Invasivenessmedicine.diseaseHIF1Acancer cellsCancer researchMESH : Genetic Predisposition to DiseaseCarcinogenesis
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Myostatin/activin blocking combined with exercise reconditions skeletal muscle expression profile of mdx mice

2015

Duchenne Muscular Dystrophy is characterized by muscle wasting and decreased aerobic metabolism. Exercise and blocking of myostatin/activin signaling may independently or combined counteract muscle wasting and dystrophies. The effects of myostatin/activin blocking using soluble activin receptor-Fc (sActRIIB-Fc) administration and wheel running were tested alone or in combination for seven weeks in dystrophic mdx mice. Expression microarray analysis revealed decreased aerobic metabolism in the gastrocnemius muscle of mdx mice compared to healthy mice. This was not due to reduced home-cage physical activity, and was further downregulated upon sActRIIB-Fc treatment in enlarged muscles. However…

muscular dystrophymedicine.medical_specialtyDuchenne muscular dystrophyActivin Receptors Type IIRecombinant Fusion Proteinsphysical activityMyostatinBiologyta3111BiochemistryMuscle hypertrophy03 medical and health sciencesGastrocnemius muscleMice0302 clinical medicineEndocrinologyoxidative metabolismInternal medicinePhysical Conditioning AnimalGene expressionmedicineSTAT5 Transcription FactorAnimalsmuscle hypertrophyMuscular dystrophyPhosphorylationta315Muscle SkeletalMolecular BiologyWasting030304 developmental biologyInhibin-beta Subunits0303 health sciencesPhysical activitySkeletal muscleMyostatinmusculoskeletal systemmedicine.diseaseMuscular dystrophymRNA profilingEndocrinologymedicine.anatomical_structurebiology.proteinMice Inbred mdxOxidative metabolismMuscle hypertrophymedicine.symptom030217 neurology & neurosurgery
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The utility of SATB2 immunohistochemical expression in distinguishing between osteosarcomas and their malignant bone tumor mimickers, such as Ewing s…

2016

SATB2 is commonly expressed in osteosarcomas. Although apparently being a valuable diagnostic marker for differentiating between small cell osteosarcoma (SCO) and other small round cell tumors of bone, for instance Ewing sarcoma family of tumors (ESFT), it has not been tested in a large series of ESFT and chondrosarcomas so far. We studied the immunohistochemical expression of SATB2 in 42 osteosarcomas, 31 chondrosarcomas, and 371 genetically confirmed ESFT. SATB2 positivity was detected in 90.4% of osteosarcomas, 87.5% of SCO, 91.3% of osteoblastic osteosarcomas, and in all chondroblastic and parosteal osteosarcomas. The osteoblastic and SCO subtypes expressed SATB2 more intensely than oth…

musculoskeletal diseases0301 basic medicinePathologymedicine.medical_specialtyCD99ChondrosarcomaBone NeoplasmsSarcoma EwingSensitivity and SpecificitySmall Cell OsteosarcomaPathology and Forensic MedicineDiagnosis Differential03 medical and health sciences0302 clinical medicineChondroblastic OsteosarcomaBiomarkers TumormedicineHumansRetrospective StudiesOsteosarcomabusiness.industryOsteoidMatrix Attachment Region Binding ProteinsCell Biologymusculoskeletal systemmedicine.diseaseImmunohistochemistry030104 developmental biology030220 oncology & carcinogenesisImmunohistochemistryOsteosarcomaSarcomaChondrosarcomabusinessTranscription FactorsPathology - Research and Practice
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Transcriptional profiles from patients with dystrophinopathies and limb girdle muscular dystrophies as determined by qRT-PCR.

2003

Mutations in genes coding for the dystrophin-glycoprotein complex (DGC) cause inherited muscular dystrophies (MD), including Morbus Duchenne (DMD) and M. Becker (BMB) as well as limb-girdle muscular dystrophies (LGMD). New insights into the pathophysiology of the dystrophic muscle, the identification of compensatory mechanisms and additional proteins interacting with dystrophin are essential for developing new treatments. In order to define molecular mechanisms induced by lack of dystrophin and the subsequent counter-regulatory transcriptional response of degenerating muscle fibres, we have investigated the mRNA expression of 19 functionally linked genes in biopsies of patients with MD by m…

musculoskeletal diseasesAdultMaleAdolescentTranscription GeneticGene Expressionmedicine.disease_causeMuscular DystrophiesStatistics NonparametricDystrophinGenetic linkageGene expressionmedicineHumansRNA MessengerMuscular dystrophyChildGeneGlycoproteinsMutationbiologyReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingMusclesMiddle Agedmedicine.diseaseCell biologyGene expression profilingMuscular Dystrophy DuchenneNeurologyChild PreschoolMutationbiology.proteinFemaleNeurology (clinical)DystrophinNeuroscienceLimb-girdle muscular dystrophyJournal of neurology
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Phenotypic spectrum and genomics of undiagnosed arthrogryposis multiplex congenital

2022

BackgroundArthrogryposis multiplex congenita (AMC) is characterised by congenital joint contractures in two or more body areas. AMC exhibits wide phenotypic and genetic heterogeneity. Our goals were to improve the genetic diagnosis rates of AMC, to evaluate the added value of whole exome sequencing (WES) compared with targeted exome sequencing (TES) and to identify new genes in 315 unrelated undiagnosed AMC families.MethodsSeveral genomic approaches were used including genetic mapping of disease loci in multiplex or consanguineous families, TES then WES. Sanger sequencing was performed to identify or validate variants.ResultsWe achieved disease gene identification in 52.7% of AMC index pati…

musculoskeletal diseasesArtrogriposi múltiple congènitaSettore BIO/18 - GENETICAhuman geneticsneuromuscular diseasesGenomicsBiologyCONTRACTURESCLASSIFICATIONdiseasessymbols.namesakeDiagnòsticGene mappingarthrogryposis multiplex congenitaExome SequencingOF-FUNCTION MUTATIONSGeneticsMedicine and Health SciencesgenomicsHumansGenetics (clinical)Exome sequencingArthrogryposisSanger sequencingGeneticsArthrogryposis multiplex congenitaGenetic heterogeneitySPINAL MUSCULAR-ATROPHYProteinsnervous system malformationsDYSTROPHYDisease gene identificationGENEHuman geneticsPedigreeETIOLOGYPhenotypesymbolsneuromuscularGenèticaTranscription Factors
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