Search results for " messenger"

showing 10 items of 1295 documents

RNA-mediated therapies in myotonic dystrophy

2018

Myotonic dystrophy 1 (DM1) is a multisystemic neuromuscular disease caused by a dominantly inherited 'CTG' repeat expansion in the gene encoding DM Protein Kinase (DMPK). The repeats are transcribed into mRNA, which forms hairpins and binds with high affinity to the Muscleblind-like (MBNL) family of proteins, sequestering them from their normal function. The loss of function of MBNL proteins causes numerous downstream effects, primarily the appearance of nuclear foci, mis-splicing, and ultimately myotonia and other clinical symptoms. Antisense and other RNA-mediated technologies have been applied to target toxic-repeat mRNA transcripts to restore MBNL protein function in DM1 models, such as…

musculoskeletal diseases0301 basic medicinePharmacologycongenital hereditary and neonatal diseases and abnormalitiesMessenger RNAMyotonin-protein kinaseRNABiologymedicine.diseaseMyotoniaMyotonic dystrophyMyotonin-Protein KinaseCell biology03 medical and health sciences030104 developmental biologyDrug DiscoverymedicineAnimalsHumansMyotonic DystrophyRNARNA MessengerTrinucleotide repeat expansionGeneLoss functionDrug Discovery Today
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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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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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Osteoprotegerin (OPG) and RANKL expression and distribution in developing human craniomandibular joint.

2005

Abstract During embryogenesis the bone tissue of craniomandibular joint (CMJ) is formed through two pathways: intramembranous ossification and endochondral ossification. The development process is under the control of regulatory factors.The osteoprotegerin (OPG) and the receptor activator of nuclear factor (NF)-κB ligand are key regulators of osteoclastogenesis. The aim of this study is the localization of OPG and RANKL mRNA and protein in the foetal CMJ by immunohistochemistry (IHC) and in situ hybridization (ISH). The main results were: OPG and RANKL mRNA and protein were co-localized in the same cell types; OPG and RANKL were specially immunolocated in osteogenic cells; immunolabeling wa…

musculoskeletal diseasesCartilage Articularmedicine.medical_specialtyReceptors Cytoplasmic and NuclearIn situ hybridizationBiologyBone tissueReceptors Tumor Necrosis FactorBone remodelingOsteoprotegerinOsteogenesisInternal medicineBone cellmedicineHumansRNA MessengerEndochondral ossificationIn Situ HybridizationGlycoproteinsMembrane GlycoproteinsReceptor Activator of Nuclear Factor-kappa BTemporomandibular JointRANK LigandOsteoprotegerinCell BiologyGeneral MedicineImmunohistochemistryCell biologyEndocrinologymedicine.anatomical_structureRANKLIntramembranous ossificationbiology.proteinCarrier ProteinsDevelopmental BiologyTissuecell
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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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mRNA expression profiles of primary high-grade central osteosarcoma are preserved in cell lines and xenografts

2011

Abstract Background Conventional high-grade osteosarcoma is a primary malignant bone tumor, which is most prevalent in adolescence. Survival rates of osteosarcoma patients have not improved significantly in the last 25 years. Aiming to increase this survival rate, a variety of model systems are used to study osteosarcomagenesis and to test new therapeutic agents. Such model systems are typically generated from an osteosarcoma primary tumor, but undergo many changes due to culturing or interactions with a different host species, which may result in differences in gene expression between primary tumor cells, and tumor cells from the model system. We aimed to investigate whether gene expressio…

musculoskeletal diseaseslcsh:Internal medicinelcsh:QH426-470Transplantation HeterologousHeterologousBone NeoplasmsBiologyMiceCell Line TumorGene expressionDatabases GeneticGeneticsmedicineAnimalsHumansGenetics(clinical)RNA Messengerlcsh:RC31-1245Survival rateneoplasmsGenetics (clinical)Oligonucleotide Array Sequence AnalysisOsteosarcomaGene Expression Profilingmedicine.diseasePrimary tumorMolecular biologyTransplantationGene expression profilinglcsh:GeneticsCell cultureCancer researchOsteosarcomaResearch ArticleBMC Medical Genomics
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Parathyroid hormone-related peptide and 8701-BC breast cancer cell growth and invasion in vitro: evidence for growth-inhibiting and invasion-promotin…

1995

It has been previously reported that 8701-BC cells, derived from a primary carcinoma of the breast, constitutively express parathyroid hormone-related peptide (PTHrP) gene and that N-terminal PTHrP immunoreactivity can be found in cell medium. Here we have firstly measured immunoreactive PTHrP in 8701-BC cell medium using antibodies raised against midregion and C-terminal fragments, and also demonstrated the expression of PTH/PTHrP receptor by 8701-BC cells. Secondly, we have examined the role, if any, elicited by diverse PTHrP domains on 8701-BC cell proliferation, and invasive behaviour in vitro related to production of extracellular proteolytic enzymes. Our data show that PTHrP [1-34], a…

musculoskeletal diseasesmedicine.medical_specialtyCell divisionMolecular Sequence DataParathyroid hormoneBreast NeoplasmsBiologyPolymerase Chain ReactionBiochemistryEndocrinologyInternal medicineEndopeptidasesTumor Cells CulturedmedicineExtracellularHumansNeoplasm InvasivenessProtease InhibitorsRNA MessengerReceptorMolecular BiologyReceptor Parathyroid Hormone Type 1Base SequenceParathyroid hormone-related proteinCell growthParathyroid Hormone-Related ProteinProteolytic enzymesProteinsRNA-Directed DNA PolymeraseIn vitroEndocrinologyParathyroid HormoneCancer researchReceptors Parathyroid HormoneCell Divisionhormones hormone substitutes and hormone antagonistsMolecular and Cellular Endocrinology
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The corticotrophin-releasing factor/urocortin system regulates white fat browning in mice through paracrine mechanisms.

2015

Objectives:\ud The corticotrophin-releasing factor (CRF)/urocortin system is expressed in the adipose tissue of mammals, but its functional role in this tissue remains unknown.\ud \ud Methods:\ud Pharmacological manipulation of the activity of CRF receptors, CRF1 and CRF2, was performed in 3T3L1 white pre-adipocytes and T37i brown pre-adipocytes during in vitro differentiation. The expression of genes of the CRF/urocortin system and of markers of white and brown adipocytes was evaluated along with mitochondrial biogenesis and cellular oxygen consumption. Metabolic evaluation of corticosterone-deficient or supplemented Crhr1-null (Crhr1−/−) mice and their wild-type controls was performed alo…

obesitycrf1Corticotropin-Releasing Hormonecrf2Endocrinology Diabetes and MetabolismIMPAIRED STRESS-RESPONSE[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionAdipocytes WhiteMedicine (miscellaneous)urocortinWhite adipose tissueMOUSEMicebrown adiposte tissue0302 clinical medicineBrowningUrocortinsUrocortin0303 health sciencesNutrition and Dietetics[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismParacrine mechanisms[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismImmunohistochemistryADIPOCYTESAdipocytes BrownADIPOSE-TISSUESKELETAL-MUSCLEhormones hormone substitutes and hormone antagonistsSignal TransductionEXPRESSIONmedicine.medical_specialtyendocrine systemTHERMOGENESISBiologycrfReceptors Corticotropin-Releasing Hormone03 medical and health scienceswhite adipose tissueInternal medicine3T3-L1 CellsmedicineAnimalsRNA MessengerGLUCOCORTICOIDS030304 developmental biologyENERGY HOMEOSTASISCorticotrophin releasing factoradipose plasticityPigments BiologicalUROCORTIN-II GENEQPEndocrinologyGene Expression Regulation[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgery
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Activation of the p38MAPK cascade is associated with upregulation of TNF alpha receptors in the spinal motor neurons of mouse models of familial ALS.

2005

Phosphorylated p38 mitogen-activated protein kinase (p38MAPK), but not activated c-jun-N-terminal kinase (JNK), increases in the motor neurons of transgenic mice overexpressing ALS-linked SOD1 mutants at different stages of the disease. This effect is associated with a selective increase of phosphorylated MKK3-6, MKK4 and ASK1 and a concomitant upregulation of the TNFalpha receptors (TNFR1 and TNFR2), but not IL1beta and Fas receptors. Activation of both p38 MAPK and JNK occurs in the activated microglial cells of SOD1 mutant mice at the advanced stage of the disease; however, this effect is not accompanied by the concomitant activation of the upstream kinases ASK1 and MKK3,4,6, while both …

p38 mitogen-activated protein kinasesMAP Kinase Kinase 3Mice TransgenicMAP Kinase Kinase 6BiologyMAP Kinase Kinase Kinase 5p38 Mitogen-Activated Protein KinasesReceptors Tumor Necrosis FactorCellular and Molecular NeuroscienceMiceSuperoxide Dismutase-1Downregulation and upregulationAnimalsHumansASK1RNA Messengerfas ReceptorPhosphorylationReceptorProtein kinase AMolecular BiologyP38MAPK cascadeMotor NeuronsKinaseSuperoxide DismutaseTumor Necrosis Factor-alphaAmyotrophic Lateral SclerosisJNK Mitogen-Activated Protein KinasesReceptors Interleukin-1Cell BiologyCell biologyEnzyme ActivationMice Inbred C57BLDisease Models AnimalTumor Necrosis Factor Decoy ReceptorsSpinal CordReceptors Tumor Necrosis Factor Type IDisease ProgressionTumor necrosis factor alphaSignal TransductionMolecular and cellular neurosciences
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Protein Phosphorylation by Peroxisome Proliferators: Species-specific Stimulation of Protein Kinases and Its Role in PP-induced Transcriptional Activ…

1996

p38 mitogen-activated protein kinasesMicrobodiesGene Expression Regulation EnzymologicGeneral Biochemistry Genetics and Molecular BiologyMAP2K7Retinoblastoma-like protein 1History and Philosophy of ScienceAnimalsHumansProtein phosphorylationClofibrateRNA MessengerAcetyl-CoA C-AcetyltransferaseProtein kinase ACells CulturedProtein Kinase CHypolipidemic AgentsbiologyChemistryKinaseGeneral NeuroscienceGRB10Autophagy-related protein 13PhosphoproteinsStaurosporineRats Inbred F344RatsCell biologybiology.proteinProtein KinasesAnnals of the New York Academy of Sciences
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