Search results for "Nuclear proteins"

showing 10 items of 295 documents

Multipotential nestin and Isl-1 positive mesenchymal stem cells isolated from human pancreatic islets.

2006

Mesenchymal cells in the developing pancreas express the neural stem cell marker nestin and the transcription factor islet-1 (Isl-1). Using defined culture conditions we isolated on a single cell basis nestin producing cells from human pancreatic islets. These cells were immortalized with lentiviral vectors coding for telomerase and mBmi. They are positive for Isl-1 and nestin and have the potential to adopt a pancreatic endocrine phenotype with expression of critical transcription factors including Ipf-1, Isl-1, Ngn-3, Pax4, Pax6, Nkx2.2, and Nkx6.1 as well as the islet hormones insulin, glucagon, and somatostatin. In addition, they can be differentiated into human albumin producing cells …

endocrine systemLIM-Homeodomain ProteinsBiophysicsCell Culture TechniquesNerve Tissue ProteinsBiologyBiochemistryNestinIslets of LangerhansIntermediate Filament ProteinsNeurosphereAlbuminsmedicineAdipocytesATP Binding Cassette Transporter Subfamily G Member 2HumansMolecular BiologyStem cell transplantation for articular cartilage repairHomeodomain ProteinsNeuronsOsteoblastsPancreatic isletsMesenchymal stem cellLentivirusNuclear ProteinsCell DifferentiationMesenchymal Stem CellsCell BiologyNestinNeural stem cellNeoplasm Proteinsmedicine.anatomical_structureHomeobox Protein Nkx-2.2Cancer researchPAX4ATP-Binding Cassette TransportersPancreasTranscription FactorsBiochemical and biophysical research communications
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Expression and regulation of mPer1 in immortalized GnRH neurons.

2003

Hypothalamic GnRH (gonadotropin-releasing hormone) neurons play a critical role in the initiation and maintenance of reproduction competence. Using the mouse GnRH neuronal cell line, GT1-7, we have characterized the expression of the gene mPer1, a recognized key element of the mammalian circadian clockwork. Both mPer1 transcripts and the 136 kDa mPER1 gene product could be detected in these cells. Immunocytochemical analysis also confirmed expression of mPER1 both in vitro and in vivo in GnRH neurons. Activation of cyclic AMP signalling pathways in vitro elevated GnRH secretion as well as mPer1 expression and nuclear mPER1 immunoreactivity. As mPER1 is known to feedback on transcriptional a…

endocrine systemmedicine.medical_specialtyCellImmunoblottingCell Cycle ProteinsBiologyGene productGonadotropin-Releasing HormoneMiceInternal medicineGene expressionmedicineAnimalsGeneCells CulturedRegulation of gene expressionNeuronsReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceColforsinNuclear ProteinsPeriod Circadian ProteinsImmunohistochemistryPreoptic AreaIn vitromedicine.anatomical_structureEndocrinologyNeuroprotective AgentsGene Expression RegulationCell cultureHypothalamushormones hormone substitutes and hormone antagonistsVasoactive Intestinal PeptideNeuroreport
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SAP30L interacts with members of the Sin3A corepressor complex and targets Sin3A to the nucleolus.

2006

Histone acetylation plays a key role in the regulation of gene expression. The chromatin structure and accessibility of genes to transcription factors is regulated by enzymes that acetylate and deacetylate histones. The Sin3A corepressor complex recruits histone deacetylases and in many cases represses transcription. Here, we report that SAP30L, a close homolog of Sin3-associated protein 30 (SAP30), interacts with several components of the Sin3A corepressor complex. We show that it binds to the PAH3/HID (Paired Amphipathic Helix 3/Histone deacetylase Interacting Domain) region of mouse Sin3A with residues 120–140 in the C-terminal part of the protein. We provide evidence that SAP30L induces…

entsyymitvuorovaikutustumajyvänenBiologySAP30Protein Sorting SignalsHistone DeacetylasesArticleCell Line03 medical and health sciencesMice0302 clinical medicineHistone H1Histone H2AGeneticsHistone codeAnimalsHumansGene Silencingnucleolus030304 developmental biologyNuclear receptor co-repressor 2Histone deacetylationGenetics0303 health sciencesgeenitbiokemiaNuclear ProteinsCell biologyRepressor ProteinsProtein TransportSin3 Histone Deacetylase and Corepressor Complextranskriptio (biologia)030220 oncology & carcinogenesisSin-associated proteinsHistone deacetylase complexhistonideasetylaatioHistone deacetylaseproteiinitCorepressorSin-assosioituvat proteiinitCell NucleolusNucleic acids research
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IFI16 expression is related to selected transcription factors during B-cell differentiation

2015

The interferon-inducible DNA sensor IFI16 is involved in the modulation of cellular survival, proliferation, and differentiation. In the hematopoietic system, IFI16 is consistently expressed in the CD34+ stem cells and in peripheral blood lymphocytes; however, little is known regarding its regulation during maturation of B- and T-cells. We explored the role of IFI16 in normal B-cell subsets by analysing its expression and relationship with the major transcription factors involved in germinal center (GC) development and plasma-cell (PC) maturation.IFI16mRNA was differentially expressed in B-cell subsets with significant decrease inIFI16mRNA in GC and PCs with respect to naïve and memory subs…

lcsh:Immunologic diseases. AllergyAdultMaleXBP1Article SubjectLymphoid TissueTranscription FactorCellular differentiationPlasma CellsImmunologyB-Lymphocyte SubsetsBiologySettore MED/08 - Anatomia PatologicaAdult; B-Lymphocyte Subsets; B-Lymphocytes; Enzyme Activation; Female; Gene Expression Profiling; Germinal Center; Humans; Lymphoid Tissue; Male; NF-kappa B; Nuclear Proteins; Phosphoproteins; Plasma Cells; RNA Messenger; Transcription Factors; Cell Differentiation; Gene Expression Regulation; Immunology; Immunology and AllergyGene expressionImmunology; Immunology and AllergyHumansImmunology and AllergyRNA MessengerTranscription factorB-Lymphocyte SubsetsNuclear ProteinRegulation of gene expressionB-Lymphocyte SubsetB-LymphocytesRELBGene Expression ProfilingB-LymphocyteNF-kappa BNuclear ProteinsCell DifferentiationGeneral MedicineB-Cell DifferentiationPhosphoproteinsGerminal CenterMolecular biologyGene expression profilingEnzyme ActivationGene Expression RegulationPhosphoproteinImmunology interferon-inducible DNA sensor IFI16 B-Cell DifferentiationPlasma Cellinterferon-inducible DNA sensor IFI16Femalelcsh:RC581-607Transcription FactorsResearch ArticleHuman
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Increased autophagy and apoptosis contribute to muscle atrophy in a myotonic dystrophy type 1 Drosophila model

2015

ABSTRACT Muscle mass wasting is one of the most debilitating symptoms of myotonic dystrophy type 1 (DM1) disease, ultimately leading to immobility, respiratory defects, dysarthria, dysphagia and death in advanced stages of the disease. In order to study the molecular mechanisms leading to the degenerative loss of adult muscle tissue in DM1, we generated an inducible Drosophila model of expanded CTG trinucleotide repeat toxicity that resembles an adult-onset form of the disease. Heat-shock induced expression of 480 CUG repeats in adult flies resulted in a reduction in the area of the indirect flight muscles. In these model flies, reduction of muscle area was concomitant with increased apopto…

lcsh:MedicineMedicine (miscellaneous)Genes InsectApoptosisDystrophyInhibitor of Apoptosis ProteinsAnimals Genetically ModifiedCTG repeat expansion0302 clinical medicineImmunology and Microbiology (miscellaneous)Drosophila ProteinsMyotonic DystrophyMyocyte0303 health sciencesTOR Serine-Threonine KinasesMyotonin-protein kinaseNuclear ProteinsMuscle atrophyUp-RegulationCell biologyMuscular AtrophyDrosophila melanogastermedicine.anatomical_structureFemalemedicine.symptomSignal TransductionResearch Articlelcsh:RB1-214congenital hereditary and neonatal diseases and abnormalitiesProgrammed cell deathNeuroscience (miscellaneous)BiologyMyotonic dystrophyMyotonin-Protein KinaseMuscleblindGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesAutophagylcsh:PathologymedicineAnimalsHumans030304 developmental biologylcsh:RAutophagyDystrophySkeletal musclemedicine.diseaseMolecular biologyDisease Models AnimalMuscle atrophyTrinucleotide Repeat Expansion030217 neurology & neurosurgeryDisease Models & Mechanisms
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Aberrant copy numbers of ALK gene is a frequent genetic alteration in neuroblastomas.

2009

A total of 50 neuroblastomas were assessed for frequency of ALK gene copy number aberrations by interphase fluorescence in situ hybridization using a break-apart fluorescence in situ hybridization probe. The data were compared with status of MYCN, 11q, 17q, and 1p36. We observed ALK aberrations (amplification, 1 of 45; gain, 15 of 45 and loss/imbalance, 11 of 45) in a total of 27 (60%) of 45 neuroblastomas. Synchronic MYCN and ALK aberrations accounted for 23 of 45 (51%) tumors; however, MYCN alterations were also detected in 11 (60%) of 18 tumors without ALK aberrations. Our data suggest that copy number aberrations of the ALK gene is a frequent genetic event in the development of neurobla…

medicine.medical_specialtyPathologyGene DosageBiologyPathology and Forensic MedicineNeuroblastomahemic and lymphatic diseasesNeuroblastomamedicineAnaplastic lymphoma kinaseHumansAnaplastic Lymphoma KinaseCopy number aberrationneoplasmsIn Situ Hybridization FluorescenceOncogene ProteinsN-Myc Proto-Oncogene Proteinmedicine.diagnostic_testGenetic AlterationCancerNuclear ProteinsReceptor Protein-Tyrosine KinasesAnatomical pathologyProtein-Tyrosine Kinasesmedicine.diseaseTissue Array AnalysisCancer researchAutonomic neuropathyFluorescence in situ hybridizationHuman pathology
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Retarded thymic involution and massive germinal center formation in NF-ATp-deficient mice.

1998

NF-ATp and NF-ATc are the most prominent nuclear NF-AT transcription factors in peripheral T lymphocytes. After T cell activation both factors bind to and control the promoters and enhancers of numerous lymphokine and receptor ligand genes. In order to define a specific role for NF-ATp in vivo we have inactivated the NF-ATp gene by gene targeting in mice. We show that NF-ATp deficiency leads to the accumulation of peripheral T cells with a “preactivated” phenotype, enhanced immune responses of T cells after secondary stimulation in vitro and severe defects in the proper termination of antigen responses, as shown by a reduced deletion of superantigen-reactive CD4+ T cells. These alterations …

medicine.medical_specialtyT cellT-LymphocytesImmunologyApoptosisThymus GlandBiologyPolymerase Chain ReactionMiceImmune systemAntigenInternal medicinemedicineImmunology and AllergyCytotoxic T cellAnimalsfas ReceptorDNA PrimersMice KnockoutThymic involutionSuperantigensBase SequenceNFATC Transcription FactorsLymphokineGerminal centerNuclear ProteinsGerminal CenterMolecular biologyDNA-Binding ProteinsEndocrinologymedicine.anatomical_structureLymphatic systemPhenotypeTranscription FactorsEuropean journal of immunology
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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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Derepressing muscleblind expression by miRNA sponges ameliorates myotonic dystrophy-like phenotypes in Drosophila

2016

AbstractMyotonic Dystrophy type 1 (DM1) originates from alleles of the DMPK gene with hundreds of extra CTG repeats in the 3′ untranslated region (3′ UTR). CUG repeat RNAs accumulate in foci that sequester Muscleblind-like (MBNL) proteins away from their functional target transcripts. Endogenous upregulation of MBNL proteins is, thus, a potential therapeutic approach to DM1. Here we identify two miRNAs, dme-miR-277 and dme-miR-304, that differentially regulate muscleblind RNA isoforms in miRNA sensor constructs. We also show that their sequestration by sponge constructs derepresses endogenous muscleblind not only in a wild type background but also in a DM1 Drosophila model expressing non-co…

musculoskeletal diseases0301 basic medicineUntranslated regioncongenital hereditary and neonatal diseases and abnormalitiesMotor ActivityBiologyMyotonic dystrophyArticle03 medical and health sciences0302 clinical medicineRNA IsoformsmicroRNAmedicineAnimalsDrosophila ProteinsMyotonic DystrophyRegulation of gene expressionGeneticsMultidisciplinaryWild typeNuclear Proteinsmedicine.diseaseMicroRNAsDrosophila melanogasterPhenotype030104 developmental biologyGene Expression RegulationFlight AnimalTrinucleotide Repeat ExpansionTrinucleotide repeat expansion030217 neurology & neurosurgeryDrosophila ProteinScientific Reports
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