Search results for "MUTATION"

showing 10 items of 2830 documents

Zasp/Cypher internal ZM-motif containing fragments are sufficient to co-localize with α-actinin—Analysis of patient mutations

2005

Z-band alternatively spliced PDZ-containing protein (ZASP/Cypher) has an important role in maintaining Z-disc stability in striated and cardiac muscle. ZASP/Cypher interacts through its PDZ domain with the major Z-disc actin cross-linker, alpha-actinin. ZASP/Cypher also has a conserved sequence called the ZM-motif, and it is found in two alternatively spliced exons 4 and 6. We have shown earlier that the ZM-motif containing internal regions of two related proteins ALP and CLP36 interact with alpha-actinin rod region, and that the ZM-motif is important in targeting ALP to the alpha-actinin containing structures in cell. Here, we show that the ZASP/Cypher internal fragments containing either …

SarcomeresAmino Acid MotifsPDZ domainCHO Cellsmacromolecular substancesBiologyConserved sequenceStress fiber assemblyMyoblastsMiceExonCricetinaeStress FibersmedicineAnimalsHumansMyocyteActininMuscle SkeletalActinAdaptor Proteins Signal TransducingOrganellesGeneticsMyocardiumPoint mutationCardiac muscleExonsIntracellular MembranesCell BiologyLIM Domain Proteinsmusculoskeletal systemPeptide FragmentsCell biologymedicine.anatomical_structureMutationCardiomyopathiesProtein BindingExperimental Cell Research
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Biallelic gephyrin variants lead to impaired GABAergic inhibition in a patient with developmental and epileptic encephalopathy

2021

Abstract Synaptic inhibition is essential for shaping the dynamics of neuronal networks, and aberrant inhibition is linked to epilepsy. Gephyrin (Geph) is the principal scaffolding protein at inhibitory synapses and is essential for postsynaptic clustering of glycine (GlyRs) and GABA type A receptors. Consequently, gephyrin is crucial for maintaining the relationship between excitation and inhibition in normal brain function and mutations in the gephyrin gene (GPHN) are associated with neurodevelopmental disorders and epilepsy. We identified bi-allelic variants in the GPHN gene, namely the missense mutation c.1264G > A and splice acceptor variant c.1315-2A > G, in a patient wi…

Scaffold proteinBiologyInhibitory postsynaptic potentialEpilepsyPostsynaptic potentialGeneticsmedicineHumansMissense mutationReceptorBiologyMolecular BiologyGenetics (clinical)Brain DiseasesEpilepsyGephyrinMembrane ProteinsGeneral MedicineReceptors GABA-Amedicine.diseaseCell biologyChemistrySynapsesbiology.proteinHuman medicineReceptor clusteringCarrier ProteinsHuman Molecular Genetics
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Gene-based treatment options for Usher type 1C by translational read-through of a nonsense mutation

2012

The Usher syndrome (USH) is the most frequent cause of inherited combined deaf-blindness. The ciliopathy is clinically and genetically heterogeneous, assigned to three clinical USH types of which the most severe type is USH1. The USH1C gene encodes the PDZ containing scaffold protein harmonin which is expressed in form of numerous alternatively spliced variants. Hamonin binds directly to all USH1/2 proteins and is a key organizer of USH protein networks in photoreceptor cells. So far no effective treatment for the ophthalmic component of USH exists. Translational read-through was introduced as an innovative therapy option for several non-ocular diseases caused by nonsense mutations leading …

Scaffold proteinGeneticslcsh:CytologyUsher syndromePDZ domainNonsense mutationCell BiologyBiologymedicine.diseaseCiliopathiesPhotoreceptor cellCell biologyCiliopathymedicine.anatomical_structureotorhinolaryngologic diseasesmedicineOral Presentationlcsh:QH573-671GeneCilia
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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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The GRIP1/14-3-3 Pathway Coordinates Cargo Trafficking and Dendrite Development

2014

SummaryRegulation of cargo transport via adaptor molecules is essential for neuronal development. However, the role of PDZ scaffolding proteins as adaptors in neuronal cargo trafficking is still poorly understood. Here, we show by genetic deletion in mice that the multi-PDZ domain scaffolding protein glutamate receptor interacting protein 1 (GRIP1) is required for dendrite development. We identify an interaction between GRIP1 and 14-3-3 proteins that is essential for the function of GRIP1 as an adaptor protein in dendritic cargo transport. Mechanistically, 14-3-3 binds to the kinesin-1 binding region in GRIP1 in a phospho-dependent manner and detaches GRIP1 from the kinesin-1 motor protein …

Scaffold proteinPDZ domainKinesinsNerve Tissue ProteinsDendriteBiologyGeneral Biochemistry Genetics and Molecular BiologyMotor proteinGene Knockout TechniquesMiceMicrotubulemedicineAnimalsMolecular BiologyAdaptor Proteins Signal TransducingPoint mutationSignal transducing adaptor proteinDendritesCell BiologyCell biologyProtein Transportmedicine.anatomical_structure14-3-3 ProteinsMutationCarrier ProteinsFunction (biology)Protein BindingSignal TransductionTranscription FactorsDevelopmental BiologyDevelopmental Cell
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Cystic Fibrosis Transmembrane Conductance Regulator Interacts with Multiple Immunoglobulin Domains of Filamin A

2010

Mutations of the chloride channel cystic fibrosis transmembrane conductance regulator (CFTR) that impair its apical localization and function cause cystic fibrosis. A previous report has shown that filamin A (FLNa), an actin-cross-linking and -scaffolding protein, interacts directly with the cytoplasmic N terminus of CFTR and that this interaction is necessary for stability and confinement of the channel to apical membranes. Here, we report that the CFTR N terminus has sequence similarity to known FLNa-binding partner-binding sites. FLNa has 24 Ig (IgFLNa) repeats, and a CFTR peptide pulled down repeats 9, 12, 17, 19, 21, and 23, which share sequence similarity yet differ from the other FLN…

Scaffold proteincongenital hereditary and neonatal diseases and abnormalitiesFilaminsMolecular Sequence DataCystic Fibrosis Transmembrane Conductance RegulatorImmunoglobulinsBiologymedicine.disease_causeFilaminBiochemistryContractile ProteinsProtein structureCricetinaemedicineAnimalsHumansFLNAAmino Acid SequenceMolecular BiologyPeptide sequenceMutationSequence Homology Amino AcidCell MembraneMicrofilament ProteinsCell Biologyrespiratory systemMolecular biologyActinsCystic fibrosis transmembrane conductance regulatorProtein Structure Tertiaryrespiratory tract diseasesCell biologySolubilityMutationProtein Structure and FoldingChloride channelbiology.proteinPeptidesDimerizationProtein BindingJournal of Biological Chemistry
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Michel Bernard : un passeur culturel à l’ENSEP, ou les germes d’une petite révolution philosophique (1949-1968)

2021

En centrant l’analyse sur une étape du parcours de Michel Bernard, durant laquelle il intervient à l’École normale supérieure d’Éducation physique, notre propos vise à reconsidérer l’apport de cet acteur comme étant révélateur d’une mutation théorique fondamentale dans ce secteur professionnel, à travers l’introduction des sciences humaines. La perspective adoptée sous l’angle d’une biographie herméneutique permet de rendre compte, à travers la singularité du personnage, des évolutions et des tensions collectives qui se dessinent autour des représentations du corps et des velléités d’émancipation qui caractérisent les années précédant mai 1968.

Sciences humainesMai 1968ActeurMutation sociale[SHS.EDU] Humanities and Social Sciences/EducationEnseignement de l'éducation physique et sportiveÉducation physique et sportiveBiographie
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Compromised nuclear envelope integrity drives tumor cell invasion

2020

AbstractWhile mutations leading to a fragile envelope of the cell nucleus are well known to cause diseases such as muscular dystrophies or accelerated aging, the pathophysiological consequences of the recently discovered mechanically induced nuclear envelope ruptures in cells harboring no mutation are less known. Here we show that repeated loss of nuclear envelope integrity in nuclei experiencing mechanical constraints promotes senescence in nontransformed cells, and induces an invasive phenotype including increased collagen degradation in human breast cancer cells, both in vitro and in a mouse xenograft model of breast cancer progression. We show that these phenotypic changes are due to th…

SenescenceCell nucleusMutationmedicine.anatomical_structureCytoplasmChemistryDNA damageCancer cellmedicinemedicine.disease_causePhenotypeExtracellular Matrix DegradationCell biology
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Long-term effects of delayed parenthood.

1998

The present study aims to define, characterize and compare the long-term effects on offspring of delayed parenthood. Data published so far on this topic show that maternal and paternal ageing may affect offspring by different mechanisms. Delayed motherhood is characterized by increased probability of obstetric complications and/or fetal and perinatal problems which, in turn, may increase the risks of mortality and morbidity in newborns and later life. Furthermore, maternal ageing is distinguished by a decreased ratio of male to female infants and higher odds of conceiving a trisomic child and/or an individual suffering from mitochondrial DNA disorders. In contrast, delayed fatherhood is ass…

SenescenceMaleMitochondrial DNAmedicine.medical_specialtyDNA RepairOffspringDiseaseBiologymedicine.disease_causePaternal AgeAndrologyPregnancyInternal medicinemedicineHumansFetusPregnancyRehabilitationPregnancy OutcomeObstetrics and Gynecologymedicine.diseasePregnancy ComplicationsEndocrinologyReproductive MedicineAgeingMutationFemaleOxidative stressMaternal AgeHuman reproduction (Oxford, England)
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Phylogenetic relationship of ubiquitin repeats in the polyubiquitin gene from the marine sponge Geodia cydonium

1994

Ubiquitin is a 76-residue protein which is highly conserved among eukaryotes. Sponge (Porifera) ubiquitin, isolated from Geodia cydonium, is encoded by a gene (termed GCUBI) with six repeats, GCUBI-1 to GCUBI-6. All repeat units encode the same protein (with one exception: GCUBI-4 encodes ubiquitin with a change of Leu to Val at position 71). On the nt level the sequences of the six repeats differ considerably. All changes (except in GCUBI-4) are silent substitutions, which do not affect the protein structure. However, there is one major difference between the repeats: Codons from both codon families (TCN and AGPy) are simultaneously used for the serine at position 65. Using this characteri…

Sequence analysisMolecular Sequence Datamedicine.disease_causeUbiquitinPhylogeneticsGene duplicationGeneticsmedicineAnimalsGeodiaAmino Acid SequenceUbiquitinsMolecular BiologyGenePhylogenyEcology Evolution Behavior and SystematicsRepetitive Sequences Nucleic AcidGeneticsMutationBase SequencebiologyPhylogenetic treeDNASequence Analysis DNAbiology.organism_classificationBiological EvolutionPoriferaMutationbiology.proteinJournal of Molecular Evolution
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