Search results for "Myosins"

showing 10 items of 36 documents

Flexible Structure of Peptide-Bound Filamin A Mechanosensor Domain Pair 20-21.

2015

Filamins (FLNs) are large, multidomain actin cross-linking proteins with diverse functions. Besides regulating the actin cytoskeleton, they serve as important links between the extracellular matrix and the cytoskeleton by binding cell surface receptors, functioning as scaffolds for signaling proteins, and binding several other cytoskeletal proteins that regulate cell adhesion dynamics. Structurally, FLNs are formed of an amino terminal actin-binding domain followed by 24 immunoglobulin-like domains (IgFLNs). Recent studies have demonstrated that myosin-mediated contractile forces can reveal hidden protein binding sites in the domain pairs IgFLNa18-19 and 20-21, enabling FLNs to transduce me…

Models MolecularDIMERIZATIONMagnetic Resonance SpectroscopyFilaminsProtein domainlcsh:MedicinePlasma protein bindingmacromolecular substancesBiologyMyosinsFilaminCrystallography X-RayLigandsfilaminsFORCEProtein structureAUTO-INHIBITIONBINDINGEscherichia coliCytoskeletonPHOSPHORYLATIONlcsh:ScienceCytoskeletonFRAGMENTMultidisciplinaryBinding Siteslcsh:Rta1182Signal transducing adaptor proteinfilamiinitSMALL-ANGLE SCATTERINGActin cytoskeletonActinsRecombinant ProteinsCell biologyProtein Structure TertiaryMODELBIOLOGICAL MACROMOLECULESCytoskeletal Proteinspeptiditpeptides1182 Biochemistry cell and molecular biologylcsh:QPeptidesINTEGRINBinding domainProtein BindingResearch ArticlePloS one
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MyRIP, a novel Rab effector, enables myosin VIIa recruitment to retinal melanosomes

2002

Defects of the myosin VIIa motor protein cause deafness and retinal anomalies in humans and mice. We report on the identification of a novel myosin-VIIa-interacting protein that we have named MyRIP (myosin-VIIa- and Rab-interacting protein), since it also binds to Rab27A in a GTP-dependent manner. In the retinal pigment epithelium cells, MyRIP, myosin VIIa and Rab27A are associated with melanosomes. In transfected PC12 cells, overexpression of MyRIP was shown to interfere with the myosin VIIa tail localization. We propose that a molecular complex composed of Rab27A, MyRIP and myosin VIIa bridges retinal melanosomes to the actin cytoskeleton and thereby mediates the local trafficking of thes…

Molecular Sequence Datamacromolecular substancesMyosinsBiologyBiochemistryRetinarab27 GTP-Binding ProteinsMotor proteinMicechemistry.chemical_compoundTwo-Hybrid System Techniquesotorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansAmino Acid SequenceRAB27Molecular BiologyGene LibraryMelanosomesRetinal pigment epitheliumScientific ReportsDyneinsRetinalActin cytoskeletonCell biologymedicine.anatomical_structurechemistryOrgan Specificityrab GTP-Binding ProteinsMelanosome transportMyosin VIIaMelanophilinsense organsRabSequence Alignmentcirculatory and respiratory physiologyEMBO reports
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Changes of energy metabolism, myosin light chain composition, lactate dehydrogenase isozyme pattern and fibre type distribution of denervated fast-tw…

1985

The influence of low frequency (8-10 Hz) electrical stimulation on denervated fast-twitch muscle from rabbit was investigated. Prolonged direct stimulation of denervated muscle resulted in higher oxidative enzyme activities. Furthermore, single fibre analyses for succinate dehydrogenase showed a more uniform distribution of activity in stimulated-denervated muscle when compared to normal muscle. As was also the case following stimulation of innervated muscle, glycolytic enzymes were decreased in activity and the LDH-isozyme pattern was also shifted towards heart type. No change of the myosin light chain pattern could be observed after 56 days of stimulation.

Myosin light-chain kinaseChemical PhenomenaPhysiologyClinical BiochemistryStimulationMyosinschemistry.chemical_compoundPhysiology (medical)Lactate dehydrogenaseMyosinAnimalsDenervationMuscle DenervationLagomorphaL-Lactate DehydrogenasebiologyHistocytochemistryChemistryMusclesSuccinate dehydrogenasebiology.organism_classificationElectric StimulationMuscle DenervationIsoenzymesChemistrybiology.proteinBiophysicsRabbitsEnergy MetabolismPfl�gers Archiv European Journal of Physiology
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The giant spectrin βV couples the molecular motors to phototransduction and Usher syndrome type I proteins along their trafficking route.

2013

International audience; Mutations in the myosin VIIa gene cause Usher syndrome type IB (USH1B), characterized by deaf-blindness. A delay of opsin trafficking has been observed in the retinal photoreceptor cells of myosin VIIa-deficient mice. We identified spectrin bV, the mammalian b-heavy spectrin, as a myosin VIIa-and rhodopsin-interacting partner in photoreceptor cells. Spectrin bV displays a polarized distribution from the Golgi apparatus to the base of the outer segment, which, unlike that of other b spectrins, matches the trafficking route of opsin and other phototransduction proteins. Formation of spectrin bV-rhodopsin complex could be detected in the differentiating photoreceptors a…

OpsinRhodopsinLight Signal Transductiongenetic structures[SDV]Life Sciences [q-bio]Cell Cycle Proteinsmacromolecular substancesBiologyMyosinsOpsin transportRetinaMotor protein03 medical and health sciencesMice0302 clinical medicineMyosinotorhinolaryngologic diseasesGeneticsAnimalsHumansSpectrinMolecular BiologyGenetics (clinical)030304 developmental biologyAdaptor Proteins Signal Transducing0303 health sciencesEPB41SpectrinGeneral Medicineeye diseasesCell biologyCytoskeletal ProteinsRhodopsinMyosin VIIabiology.proteinMicrotubule Proteinssense organsUsher Syndromes030217 neurology & neurosurgeryVisual phototransductionHeLa CellsPhotoreceptor Cells VertebrateHuman molecular genetics
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CD59 (homologous restriction factor 20), a plasma membrane protein that protects against complement C5b-9 attack, in human atherosclerotic lesions

1992

Blood cells express a cell membrane protein, termed homologous restriction factor 20 (HRF20) and identical to CD59, that can inhibit complement C5b-9 insertion into their membranes. In this report, we investigated by immunohistochemistry whether CD59 was present on cells in human atherosclerotic lesions since membranous C5b-9(m) has been found in lesions. Using a monoclonal anti-CD59 antibody, a cellular CD59 staining pattern was apparent in nearly all lesion specimens. CD59 stain co-localised with macrophage (CD14), T lymphocyte (CD7), endothelial cell (anti-factor VIII related antigen) and smooth muscle cell cytoskeletal-specific antigens (anti-alpha actin and muscle myosin). Endothelial …

Pathologymedicine.medical_specialtyCell typeArteriosclerosisCD59 Antigenschemical and pharmacologic phenomenaComplement Membrane Attack ComplexMyosinsBiologyAntigenAntigens CDMyosinmedicineHumansMacrophageSaphenous VeinActinComplement Inactivator ProteinsMembrane GlycoproteinsImmunohistochemistryActinsEndothelial stem cellCarotid ArteriesCD59 antigenEndothelium VascularCardiology and Cardiovascular MedicineComplement membrane attack complexAtherosclerosis
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Actinopathies and Myosinopathies

2009

The currently recognized two forms of "anabolic" protein aggregate myopathies, that is, defects in development, maturation and final formation of respective actin and myosin filaments encompass actinopathies and myosinopathies. The former are marked by mutations in the ACTA1 gene, largely of the de novo type. Aggregates of actin filaments are deposited within muscle fibers. Early clinical onset is often congenital; most patients run a rapidly progressive course and die during their first 2 years of life. Myosinopathies or myosin storage myopathies also commence in childhood, but show a much more protracted course owing to mutations in the myosin heavy chain gene MYH7. Protein aggregation co…

Rapidly progressive courseGeneral Neurosciencemacromolecular substancesMyosinsProtein aggregationBiologyClinical onsetActinsPathology and Forensic MedicineCell biologyProtracted courseMuscular DiseasesBiochemistryMyosinHumansMYH7Neurology (clinical)MINI‐SYMPOSIUM: Protein Aggregate MyopathiesGeneActinBrain Pathology
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Rhodopsin transport in the membrane of the connecting cilium of mammalian photoreceptor cells

2000

The transport of the photopigment rhodopsin from the inner segment to the photosensitive outer segment of vertebrate photoreceptor cells has been one of the main remaining mysteries in photoreceptor cell biology. Because of the lack of any direct evidence for the pathway through the photoreceptor cilium, alternative extracellular pathways have been proposed. Our primary aim in the present study was to resolve rhodopsin trafficking from the inner to the outer segment. We demonstrate, predominantly by high-sensitive immunoelectron microscopy, that rhodopsin is also densely packed in the membrane of the photoreceptor connecting cilium. Present prominent labeling of rhodopsin in the ciliary mem…

RhodopsinOpsingenetic structuresPhotoreceptor Connecting CiliumImmunoblottingMolecular Sequence Datamacromolecular substancesMyosinsBiologyPhotoreceptor cellRats Sprague-DawleyMiceRetinal Rod Photoreceptor CellsStructural BiologymedicineAnimalsHumansPhotopigmentAmino Acid SequenceCiliaMicroscopy ImmunoelectronCiliary membraneCiliumRod OpsinsAntibodies MonoclonalDyneinsBiological TransportCell BiologyMiddle AgedRod Cell Outer SegmentActin cytoskeletonImmunohistochemistryActinseye diseasesRatsCell biologyMice Inbred C57BLmedicine.anatomical_structureRhodopsinMyosin VIIabiology.proteinCattleFemalesense organsRetinitis PigmentosaCell Motility and the Cytoskeleton
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Molecular basis of human Usher syndrome: deciphering the meshes of the Usher protein network provides insights into the pathomechanisms of the Usher …

2006

Usher syndrome (USH) is the most frequent cause of combined deaf-blindness in man. It is clinically and genetically heterogeneous and at least 12 chromosomal loci are assigned to three clinical USH types, namely USH1A-G, USH2A-C, USH3A (Davenport, S.L.H., Omenn, G.S., 1977. The heterogeneity of Usher syndrome. Vth Int. Conf. Birth Defects, Montreal; Petit, C., 2001. Usher syndrome: from genetics to pathogenesis. Annu. Rev. Genomics Hum. Genet. 2, 271-297). Mutations in USH type 1 genes cause the most severe form of USH. In USH1 patients, congenital deafness is combined with a pre-pubertal onset of retinitis pigmentosa (RP) and severe vestibular dysfunctions. Those with USH2 have moderate to…

Scaffold proteinModels MolecularUsher syndromePDZ domainProtocadherinCadherin Related ProteinsCell Cycle ProteinsNerve Tissue ProteinsBiologyDeafnessMyosinsCellular and Molecular NeuroscienceRetinitis pigmentosaotorhinolaryngologic diseasesmedicineAnimalsHumansAdaptor Proteins Signal TransducingGeneticsExtracellular Matrix ProteinsModels GeneticCadherinRetinal DegenerationSignal transducing adaptor proteinDyneinsMembrane Proteinsmedicine.diseaseCadherinsSensory SystemsOphthalmologyCytoskeletal ProteinsDisease Models AnimalMembrane proteinMyosin VIIaMutationMicrotubule ProteinsVestibule LabyrinthUsher SyndromesExperimental eye research
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An Extended Filament Based Lamellipodium Model Produces Various Moving Cell Shapes in the Presence of Chemotactic Signals

2015

The Filament Based Lamellipodium Model (FBLM) is a two-phase two-dimensional continuum model, describing the dynamcis of two interacting families of locally parallel actin filaments (C.Schmeiser and D.Oelz, How do cells move? Mathematical modeling of cytoskeleton dynamics and cell migration. Cell mechanics: from single scale-based models to multiscale modeling. Chapman and Hall, 2010). It contains accounts of the filaments' bending stiffness, of adhesion to the substrate, and of cross-links connecting the two families. An extension of the model is presented with contributions from nucleation of filaments by branching, from capping, from contraction by actin-myosin interaction, and from a pr…

Statistics and ProbabilityNucleationNanotechnologymacromolecular substancesMyosinsBranching (polymer chemistry)Models BiologicalGeneral Biochemistry Genetics and Molecular BiologyPolymerizationQuantitative Biology::Cell BehaviorProtein filamentQuantitative Biology::Subcellular ProcessesCell Behavior (q-bio.CB)CoulombAnimalsComputer SimulationPseudopodiaCytoskeletonCell ShapeActinPhysicsGeneral Immunology and MicrobiologyApplied MathematicsChemotaxisChemotaxisNumerical Analysis Computer-AssistedGeneral Medicine92C17Actin CytoskeletonClassical mechanicsModeling and SimulationFOS: Biological sciencesQuantitative Biology - Cell BehaviorLamellipodiumGeneral Agricultural and Biological SciencesSignal Transduction
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A core cochlear phenotype in USH1 mouse mutants implicates fibrous links of the hair bundle in its cohesion, orientation and differential growth

2008

The planar polarity and staircase-like pattern of the hair bundle are essential to the mechanoelectrical transduction function of inner ear sensory cells. Mutations in genes encoding myosin VIIa, harmonin, cadherin 23,protocadherin 15 or sans cause Usher syndrome type I (USH1, characterized by congenital deafness, vestibular dysfunction and retinitis pigmentosa leading to blindness) in humans and hair bundle disorganization in mice. Whether the USH1 proteins are involved in common hair bundle morphogenetic processes is unknown. Here, we show that mouse models for the five USH1 genetic forms share hair bundle morphological defects. Hair bundle fragmentation and misorientation (25-52° mean ki…

Stereocilia (inner ear)Cadherin Related ProteinsProtocadherinCell Cycle ProteinsNerve Tissue ProteinsMyosinsBiologyMechanotransduction CellularMiceCDH23Pregnancyotorhinolaryngologic diseasesmedicineAnimalsHumansInner earProtein PrecursorsMolecular BiologyActinMice KnockoutCadherinDyneinsAnatomyCadherinsMice Mutant StrainsCochleaCell biologyCytoskeletal ProteinsDisease Models AnimalPhenotypemedicine.anatomical_structureMyosin VIIaMicroscopy Electron ScanningFemalesense organsCarrier ProteinsUsher SyndromesTip linkPCDH15Developmental BiologyDevelopment
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