Search results for "EXPRESSION"

showing 10 items of 5168 documents

Myotonic dystrophy: candidate small molecule therapeutics

2017

Myotonic dystrophy type 1 (DM1) is a rare multisystemic neuromuscular disorder caused by expansion of CTG trinucleotide repeats in the noncoding region of the DMPK gene. Mutant DMPK transcripts are toxic and alter gene expression at several levels. Chiefly, the secondary structure formed by CUGs has a strong propensity to capture and retain proteins, like those of the muscleblind-like (MBNL) family. Sequestered MBNL proteins cannot then fulfill their normal functions. Many therapeutic approaches have been explored to reverse these pathological consequences. Here, we review the myriad of small molecules that have been proposed for DM1, including examples obtained from computational rational …

musculoskeletal diseases0301 basic medicineTherapeutic gene modulationcongenital hereditary and neonatal diseases and abnormalitiesMutantComputational biologyBiologyMyotonic dystrophyMyotonin-Protein Kinase03 medical and health sciences0302 clinical medicineTrinucleotide RepeatsDrug DiscoveryGene expressionmedicineAnimalsHumansMyotonic DystrophyGenePharmacologyRegulation of gene expressionGeneticsDrug RepositioningRational designmedicine.diseaseSmall moleculeHigh-Throughput Screening Assays030104 developmental biologyGene Expression RegulationDrug Design030217 neurology & neurosurgeryDrug Discovery Today
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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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Expanded CCUG repeat RNA expression in Drosophila heart and muscle trigger Myotonic Dystrophy type 1-like phenotypes and activate autophagocytosis ge…

2016

AbstractMyotonic dystrophies (DM1–2) are neuromuscular genetic disorders caused by the pathological expansion of untranslated microsatellites. DM1 and DM2, are caused by expanded CTG repeats in the 3′UTR of the DMPK gene and CCTG repeats in the first intron of the CNBP gene, respectively. Mutant RNAs containing expanded repeats are retained in the cell nucleus, where they sequester nuclear factors and cause alterations in RNA metabolism. However, for unknown reasons, DM1 is more severe than DM2. To study the differences and similarities in the pathogenesis of DM1 and DM2, we generated model flies by expressing pure expanded CUG ([250]×) or CCUG ([1100]×) repeats, respectively, and compared …

musculoskeletal diseases0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesRNA SplicingScienceGene ExpressionBiologyMyotonic dystrophyMyotonin-Protein KinaseArticle03 medical and health sciencesGene expressionAutophagymedicineAnimalsMyotonic DystrophyMuscle SkeletalGeneDNA Repeat ExpansionMultidisciplinaryMyocardiumQRIntronRNAArrhythmias CardiacDNA Repeat Expansionmedicine.diseaseMolecular biologyDisease Models AnimalCell nucleus030104 developmental biologymedicine.anatomical_structureRNA splicingMedicineDrosophilaLocomotionScientific Reports
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Influence of the anti-inflammatory cytokine interleukin-4 on human joint capsule myofibroblasts

2016

Post-traumatic joint contracture was reported to be associated with elevated numbers of contractile myofibroblasts (MFs) in the healing capsule. During the physiological healing process, the number of MFs declines; however, in fibroconnective disorders, MFs persist. The manifold interaction of the cytokines regulating the appearance and persistence of MFs in the pathogenesis of joint contracture remains to be elucidated. The objective of our current study was to analyze the impact of the anti-inflammatory cytokine interleukin (IL)-4 on functional behavior of MFs. Cells were isolated from human joint capsule specimens and challenged with three different concentrations of IL-4 with or without…

musculoskeletal diseases0301 basic medicinemedicine.medical_treatmentInterleukinBiology03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structureCytokineJoint capsuleGene expressionImmunologyCancer researchmedicineOrthopedics and Sports MedicineJoint ContractureReceptorMyofibroblastInterleukin 4030215 immunologyJournal of Orthopaedic Research
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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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Mouse CSB protein is important for gene expression in the presence of a single-strand break in the non-transcribed DNA strand.

2010

CSB protein is required for strand-specific repair of bulky DNA lesions in transcribed genes and mediates transcription recovery after exposure to DNA-damaging agents. We enzymatically generated DNA single-strand breaks (SSBs) with 3'-OH and 5'-phosphate termini in defined positions of a plasmid-borne gene and measured their effect on transcription in cell lines with different statuses of the Csb gene. A single SSB in the transcribed region of the gene caused significant decrease of gene expression. In all tested cell lines of mouse and human origin, a SSB in the transcribed DNA strand was less harmful for gene expression than a SSB situated in the opposing DNA strand. CSB deficiency exhibi…

musculoskeletal diseasesBase SequenceDNA damageDNA Single-StrandedGene ExpressionCell BiologyBiologyBiochemistryMolecular biologychemistry.chemical_compoundMiceDNA Repair EnzymeschemistryTranscription (biology)Cell cultureCoding strandGene expressionAnimalsPoly-ADP-Ribose Binding ProteinsMolecular BiologyGeneDNATranscription bubbleDNA DamageDNA PrimersDNA repair
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Sense and Antisense DMPK RNA Foci Accumulate in DM1 Tissues during Development.

2015

International audience; Myotonic dystrophy type 1 (DM1) is caused by an unstable expanded CTG repeat located within the DMPK gene 3'UTR. The nature, severity and age at onset of DM1 symptoms are very variable in patients. Different forms of the disease are described, among which the congenital form (CDM) is the most severe. Molecular mechanisms of DM1 are well characterized for the adult form and involve accumulation of mutant DMPK RNA forming foci in the nucleus. These RNA foci sequester proteins from the MBNL family and deregulate CELF proteins. These proteins are involved in many cellular mechanisms such as alternative splicing, transcriptional, translational and post-translational regul…

musculoskeletal diseasesCCAAT-Enhancer-Binding Protein-deltacongenital hereditary and neonatal diseases and abnormalities[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiologylcsh:MedicineMice Transgenic[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human genetics[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMyotonin-Protein KinaseMice[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]AnimalsHumansMyotonic DystrophyRNA AntisenseRNA Messengerlcsh:ScienceMuscle SkeletalCell NucleusMyocardiumlcsh:R[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyBrainGene Expression Regulation DevelopmentalRNA-Binding Proteins[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyEmbryo MammalianAlternative SplicingDisease Models Animal[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAnimals Newborn[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]lcsh:QTrinucleotide Repeat ExpansionSignal TransductionResearch ArticlePloS one
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Clonal heterogeneity of the growth and invasive response of a human breast carcinoma cell line to parathyroid hormone-related peptide fragments

1997

It has been previously reported that 8701-BC cells, derived from a primary carcinoma of the breast, constitutively express parathyroid hormone (PTH)-related peptide (PTHrP) and PTH/PTHrP receptor (PTH/PTHrP-R) genes, that N-terminal, mid-regional and C-terminal immunoreactive PTHrP can be found in cell conditioned medium and, furthermore, that exogenously added PTHrP (1-34), (67-86) and, to a minor extent, (107-139) are anti-mitogenic but promote Matrigel invasion by this cell line. It has also been reported that PTHrP gene expression is selectively switched on in those 8701-BC clonal lines endowed with a higher proliferation rate and invasive ability in vitro. Here we have first examined t…

musculoskeletal diseasesCancer Researchmedicine.medical_specialtyPopulationParathyroid hormoneBreast NeoplasmsBiologyInternal medicineGene expressionTumor Cells CulturedmedicineHumansNeoplasm Invasivenesseducationeducation.field_of_studyParathyroid hormone-related proteinCell growthParathyroid hormone receptorParathyroid Hormone-Related ProteinProteinsGeneral Medicinemusculoskeletal systemMolecular biologyPeptide FragmentsNeoplasm ProteinsEndocrinologyParathyroid HormoneCell cultureFemaleClone (B-cell biology)Cell Divisionhormones hormone substitutes and hormone antagonistsCarcinogenesis
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Osteogenic differentiation of periodontal fibroblasts is dependent on the strength of mechanical strain

2012

Abstract Objective During orthodontic therapy the correct strength of mechanical strain plays a key role for bone remodelling during tooth movement. Aim of this study was to investigate the osteogenic differentiation of human periodontal ligament fibroblasts (HPdLF) depending on the applied strength of mechanical strain compared to osteoblasts (HOB). Design HPdLF and HOB were loaded with different strengths (1%, 5% and 10%) of static mechanical strain (SMS) for 12 h in vitro. Viability was verified by MTT and apoptosis by TUNEL assay. Gene expression of cyclin D1, collagen type-1 (COL-I), alkaline phosphatase (ALP), osteocalcin, osteoprotegerin (OPG) and receptor activator of the NF-κB liga…

musculoskeletal diseasesCell SurvivalPeriodontal LigamentGene ExpressionDentistryApoptosisEnzyme-Linked Immunosorbent AssayReal-Time Polymerase Chain ReactionCollagen Type IBone remodelingAndrologyCyclin D1OsteoprotegerinOsteogenesisIn Situ Nick-End LabelingHumansPeriodontal fiberCyclin D1RNA MessengerGeneral DentistryCells CulturedAnalysis of VarianceOsteoblastsTUNEL assaybiologybusiness.industryChemistryRANK LigandOsteoprotegerinCell DifferentiationCell BiologyGeneral MedicineFibroblastsAlkaline PhosphataseOtorhinolaryngologyRANKLOsteocalcinbiology.proteinAlkaline phosphataseStress MechanicalbusinessArchives of Oral Biology
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Functional characterization of osteosarcoma cell lines provides representative models to study the human disease

2011

Cancer cell lines represent in vitro models for studying malignancies, general cell biology, drug discovery and more. Whether they can be considered as exact representative models of the parental tumors remains uncertain given the acquisition of additional ex vivo changes of the cells and the lack of tissue architecture and stroma. Previously, within the EuroBoNeT consortium, we characterized a collection of bone sarcoma cell lines on genomic and proteomic level. Here, we address the phenotypical and functional characterization of the unique set of osteosarcoma cell lines (n=19) in vitro and in vivo. For functional analysis of differentiation capacity, cells were stimulated towards osteobla…

musculoskeletal diseasesPathologymedicine.medical_specialtyMice NudeBone NeoplasmsBiologymedicine.disease_causePathology and Forensic MedicineMiceHuman diseasecontaminationU2OSCell Line TumorMNNGmedicineoriginAnimalsHumansNeoplasm MetastasisneoplasmsMolecular BiologyOsteosarcomaGene Expression ProfilingHOSCell DifferentiationCell Biologymedicine.diseaseImmunohistochemistrytumorigenesisCell cultureCancer geneticsCancer researchOsteosarcomamisidentificationSarcoma ExperimentalSarcomaCarcinogenesisNeoplasm Transplantation
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