Search results for "Cytoskeletal Proteins"

showing 9 items of 119 documents

Impairing Otp homeodomain function in oral ectoderm cells affects skeletogenesis in sea urchin embryos

2003

AbstractIn the sea urchin embryo skeletogenesis is the result of a complex series of molecular and cellular events that coordinate the morphogenetic process. Past and recent evidence strongly indicate that skeletal initiation and growth are strictly dependent on signals emanating from the oral ectodermal wall. As previously suggested, Orthopedia (Otp), a homeodomain-containing transcription factor specifically expressed in a small subset of oral ectoderm cells, might be implicated in this signalling pathway. In this study, we utilize three different strategies to address the issue of whether Otp is an upstream regulator of sketelogenesis. We describe the effects of microinjection of Otp mor…

Transcriptional Activationanimal structuresMorpholinoOrthopedia homeoboxMolecular Sequence DataEctodermNerve Tissue ProteinsBiologyFusion geneEctodermmedicineSkeletogenesisAnimalsAmino Acid SequenceSea urchin embryoTranscription factorMolecular BiologyMessenger RNAExtracellular Matrix ProteinsBone DevelopmentEmbryoCell BiologyMolecular biologyHedgehog signaling pathwayMorpholino oligonucleotidesCytoskeletal Proteinsmedicine.anatomical_structureProtein BiosynthesisSea Urchinsembryonic structuresHomeoboxDevelopmental BiologyDevelopmental Biology
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Fertility and Polarized Cell Growth Depends on eIF5A for Translation of Polyproline-Rich Formins in Saccharomyces cerevisiae

2014

eIF5A is an essential and evolutionary conserved translation elongation factor, which has recently been proposed to be required for the translation of proteins with consecutive prolines. The binding of eIF5A to ribosomes occurs upon its activation by hypusination, a modification that requires spermidine, an essential factor for mammalian fertility that also promotes yeast mating. We show that in response to pheromone, hypusinated eIF5A is required for shmoo formation, localization of polarisome components, induction of cell fusion proteins, and actin assembly in yeast. We also show that eIF5A is required for the translation of Bni1, a proline-rich formin involved in polarized growth during …

TranslationSaccharomyces cerevisiae ProteinsSaccharomyces cerevisiaePeptide Chain Elongation TranslationalForminsRNA-binding proteinSaccharomyces cerevisiaeInvestigationsPeptide Initiation FactorsMorphogenesisGeneticsQc-SNARE ProteinsPolyproline helixPolarisomeGeneticsMatingbiologyMicrofilament ProteinsMembrane ProteinsRNA-Binding ProteinsTranslation (biology)Polarized growthbiology.organism_classificationActinsProtein Structure TertiaryCell biologyCytoskeletal ProteinsMating of yeastForminsMutationbiology.proteinEIF5APeptidesRibosomesEIF5A
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Interactions in the network of Usher syndrome type 1 proteins

2004

International audience; Defects in myosin VIIa, harmonin (a PDZ domain protein), cadherin 23, protocadherin 15 and sans (a putative scaffolding protein), underlie five forms of Usher syndrome type I (USH1). Mouse mutants for all these proteins exhibit disorganization of their hair bundle, which is the mechanotransduction receptive structure of the inner ear sensory cells, the cochlear and vestibular hair cells. We have previously demonstrated that harmonin interacts with cadherin 23 and myosin VIIa. Here we address the extent of interactions between the five known USH1 proteins. We establish the previously suggested sans-harmonin interaction and find that sans also binds to myosin VIIa. We …

[SDV]Life Sciences [q-bio]Hearing Loss SensorineuralStereocilia (inner ear)PDZ domainCadherin Related ProteinsProtocadherinCell Cycle ProteinsNerve Tissue ProteinsCuticular plateMyosinsBiologyMiceTwo-Hybrid System TechniquesHair Cells AuditoryBone plateMyosinotorhinolaryngologic diseasesGeneticsAnimalsHumansProtein PrecursorsMolecular BiologyGenetics (clinical)GeneticsStereociliumDyneinsSyndromeGeneral MedicineCadherinsCell biologyCytoskeletal ProteinsMyosin VIIaMutationsense organsCarrier ProteinsRetinitis PigmentosaPCDH15HeLa CellsProtein BindingHuman Molecular Genetics
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Intraflagellar transport protein 172 is essential for primary cilia formation and plays a vital role in patterning the mammalian brain

2008

AbstractIFT172, also known as Selective Lim-domain Binding protein (SLB), is a component of the intraflagellar transport (IFT) complex. In order to evaluate the biological role of the Ift172 gene, we generated a loss-of-function mutation in the mouse. The resulting Slb mutant embryos die between E12.5 and 13.0, and exhibit severe cranio-facial malformations, failure to close the cranial neural tube, holoprosencephaly, heart edema and extensive hemorrhages. Cilia outgrowth in cells of the neuroepithelium is initiated but the axonemes are severely truncated and do not contain visible microtubules. Morphological and molecular analyses revealed a global brain-patterning defect along the dorsal–…

animal structuresBody PatterningNodal ProteinSlbNodalBiologyArticleMiceFGF8Intraflagellar transportHoloprosencephalymedicineMHB boundaryAnimalsHedgehog ProteinsRNA MessengerCiliaNodeMolecular BiologyAdaptor Proteins Signal TransducingBody PatterningGeneticsMammalsCell DeathCiliumEndodermNeural tubeIntracellular Signaling Peptides and ProteinsBrainGene Expression Regulation DevelopmentalCell BiologyEmbryo MammalianCell biologyNeuroepithelial cellGastrulationCytoskeletal Proteinsmedicine.anatomical_structurePhenotypeIFT172Gene Targetingembryonic structuresNODALBiomarkersGene DeletionDevelopmental BiologySignal TransductionDevelopmental Biology
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Role of genetic polymorphisms in myocardial infarction at young age

2010

Acute myocardial infarction (AMI) in young adult presents a typical pattern of risk factors, clinical, angiographic and prognostic characteristics. In the last years we demonstrated that hemorheological profile is altered in these patients in a persistent way and independently of the number of risk factors and of the extent of coronary lesions. Thus, the hyperviscosity syndrome following AMI could be considered an intrinsic characteristic of these patients. Consequently it is possible to hypothesise the presence of a genetic background at the origin of this predisposition. If this background is able to influence the risk of ischemic heart disease, this should be particularly evident in youn…

cardiovascular risk factorsAdultMalePathologymedicine.medical_specialtyPhysiologyPopulationMyocardial InfarctionCoronary DiseaseSingle-nucleotide polymorphismDiseaseBiologyPolymorphism Single NucleotideConnexinsPhysiology (medical)Genetic predispositionmedicineHumansSNPGenetic Predisposition to DiseaseMyocardial infarctionAlleleeducationAged 80 and overInflammationeducation.field_of_studyHaplotypeHematologyMiddle AgedPyrinmedicine.diseaseInterleukin-10Platelet Endothelial Cell Adhesion Molecule-1Toll-Like Receptor 4Juvenile myocardial infarctiongenetic patternCytoskeletal ProteinsC-Reactive ProteinImmunologyFemaleCardiology and Cardiovascular MedicineClinical Hemorheology and Microcirculation
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miR-31-5p Is a LIPUS-Mechanosensitive MicroRNA that Targets HIF-1α Signaling and Cytoskeletal Proteins

2019

The roles of low-intensity pulsed ultrasound (LIPUS) and microRNAs (miRNAs) on hMSCs commitments have already been investigated

endocrine systemAngiogenesisregenerative medicineArticleCatalysisCell LineInorganic ChemistryRho family proteinlcsh:Chemistry03 medical and health sciences0302 clinical medicinemicroRNAmedicineHumansPhysical and Theoretical ChemistryBone regenerationCytoskeletonMolecular Biologylcsh:QH301-705.5Spectroscopy030304 developmental biologyMesenchymal stem cell0303 health sciencesmesenchymal stem cellsOsteoblastsChemistryhypoxiaOrganic ChemistryMesenchymal stem cellCell DifferentiationOsteoblastMicroRNAGeneral MedicineHypoxia-Inducible Factor 1 alpha Subunitequipment and suppliesUp-RegulationComputer Science ApplicationsCell biologymicroRNAsmir-31Cytoskeletal Proteinsmedicine.anatomical_structureUltrasonic Waveslcsh:Biology (General)lcsh:QD1-999030220 oncology & carcinogenesisMechanosensitive channelsInternational Journal of Molecular Sciences
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Microarray-based mutation analysis of 183 Spanish families with Usher syndrome.

2010

PURPOSE. The purpose of this study was to test the ability of the genotyping microarray for Usher syndrome (USH) to identify the mutations responsible for the disease in a cohort of 183 patients with USH. METHODS. DNA from 183 patients with Usher syndrome from the Spanish population was analyzed using a genotyping microarray containing 429 previously identified disease-associated variants in eight USH genes. Mutations detected by the array were confirmed by direct sequencing. Haplotype analysis was also performed in families carrying common Spanish mutations. RESULTS. The genotyping microarray identified 43 different variants, divided into 32 disease causative and 11 probably non-pathologic…

medicine.medical_specialtyGenotypeMicroarrayUsher syndromeDNA Mutational AnalysisCadherin Related ProteinsCell Cycle ProteinsNerve Tissue ProteinsMyosinsBiologymedicine.disease_causePolymerase Chain ReactionReceptors G-Protein-CoupledMolecular geneticsGenotypemedicineotorhinolaryngologic diseasesHumansGenotypingAllelesAdaptor Proteins Signal TransducingOligonucleotide Array Sequence AnalysisGeneticsExtracellular Matrix ProteinsMutationGene Expression ProfilingHaplotypeMembrane ProteinsCadherinsmedicine.diseaseGene expression profilingCytoskeletal ProteinsSpainMyosin VIIaMutationUsher Syndromes
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Abnormalities in alpha-dystroglycan expression in MDC1C and LGMD2I muscular dystrophies

2004

We recently identified mutations in the fukutin related protein (FKRP) gene in patients with congenital muscular dystrophy type 1C (MDC1C) and limb girdle muscular dystrophy type 2I (LGMD2I). The sarcolemma of these patients typically displays an immunocytochemical reduction of alpha-dystroglycan. In this report we extend these observations and report a clear correlation between the residual expression of alpha-dystroglycan and the phenotype. Three broad categories were identified. Patients at the severe end of the clinical spectrum (MDC1C) were compound heterozygote between a null allele and a missense mutation or carried two missense mutations and displayed a profound depletion of alpha-d…

musculoskeletal diseasesAdultPathologymedicine.medical_specialtyNonsense mutationBlotting WesternDNA Mutational AnalysisMedizinCompound heterozygosityPolymerase Chain ReactionMuscular DystrophiesPathology and Forensic MedicineFetusDystroglycanmedicineMissense mutationHumansPentosyltransferasesMuscular dystrophyChildDystroglycansMuscle SkeletalGeneticsFukutin-related proteinMembrane GlycoproteinsbiologyProteinsmedicine.diseasemusculoskeletal systemImmunohistochemistryCytoskeletal ProteinsPhenotypeMutationbiology.proteinCongenital muscular dystrophyLimb-girdle muscular dystrophyRegular Articles
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PTC124-mediated translational readthrough of a nonsense mutation causing Usher syndrome type 1C.

2011

We investigated the therapeutic potential of the premature termination codon (PTC) readthrough-inducing drug PTC124 in treating the retinal phenotype of Usher syndrome, caused by a nonsense mutation in the USH1C gene. Applications in cell culture, organotypic retina cultures, and mice in vivo revealed significant readthrough and the recovery of protein function. In comparison with other readthrough drugs, namely the clinically approved readthrough-inducing aminoglycoside gentamicin, PTC124 exhibits significant better retinal biocompatibility. Its high readthrough efficiency in combination with excellent biocompatibility makes PTC124 a promising therapeutic agent for PTCs in USH1C, as well a…

virusesUsher syndromeGenetic enhancementNonsense mutationGenetic VectorsCell Cycle ProteinsRetina03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineIn vivootorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansMolecular BiologyCells Cultured030304 developmental biologyAdaptor Proteins Signal TransducingGenetics0303 health sciencesOxadiazolesbusiness.industryfungiAminoglycosideTranslational readthroughmedicine.diseasePhenotype3. Good healthAtalurenMice Inbred C57BLCytoskeletal ProteinsLuminescent ProteinsElectroporationchemistryMicroscopy FluorescenceCodon NonsenseCancer researchMolecular MedicineGentamicinsbusinessUsher Syndromes030217 neurology & neurosurgeryHuman gene therapy
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