Search results for "Retinitis pigmentosa"

showing 10 items of 78 documents

PCARE and WASF3 regulate ciliary F-actin assembly that is required for the initiation of photoreceptor outer segment disk formation

2020

Significance The photoreceptor outer segments are primary cilia, modified for phototransduction by incorporation of stacked opsin-loaded membrane disks that are continuously regenerated. This process is disrupted in several types of inherited retinal dystrophy, but the driving force remained unclear. We show that C2orf71/PCARE (photoreceptor cilium actin regulator), associated with inherited retinal dystrophy subtype RP54, efficiently recruits the Arp2/3 complex activator WASF3 to the cilium. This activates an actin dynamics-driven expansion of the ciliary tip, resembling membrane evagination in lamellipodia formation. Colocalization of this actin dynamics module to the base of the outer se…

ciliummacromolecular substancesSensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]Actin-Related Protein 2-3 Complexchemistry.chemical_compoundMiceAll institutes and research themes of the Radboud University Medical Centerretinitis pigmentosaRetinitis pigmentosamedicineGeneticsAnimalsHumansCiliaRNA Small InterferingCiliary tipEye ProteinsCiliary membraneActinMice KnockoutMultidisciplinaryCiliumouter segmentsRetinalBiological Sciencesmedicine.diseaseRod Cell Outer SegmentPhotoreceptor outer segmentphotoreceptorActinsCell biologyWiskott-Aldrich Syndrome Protein FamilyDisease Models AnimalRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]chemistryPNAS PlusGene Expression RegulationRetinal Cone Photoreceptor Cellssense organsactinCone-Rod DystrophiesVisual phototransductionProceedings of the National Academy of Sciences USA
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Genetic analysis of 2299delG and C759F mutations (USH2A) in patients with visual and/or auditory impairments

2004

The most common mutation in the USH2A gene (Usherin), 2299delG, causes both typical Usher (USH) syndrome type II and atypical USH syndrome, two autosomal recessive disorders, characterised by moderate to severe sensorineural hearing loss and retinitis pigmentosa (RP). Furthermore, the C759F mutation in the USH2A gene has been described in 4.5% of patients with nonsyndromic recessive RP. We have investigated the presence of the 2299delG and/or the C759F mutations in 191 unrelated Spanish patients with different syndromic and nonsyndromic retinal diseases, or with nonsyndromic hearing impairment. The 2299delG mutation was observed in patients with clinical signs of USHII or of atypical USH sy…

GenotypeHearing Loss SensorineuralEye diseaseDNA Mutational AnalysisMutation MissenseGenetic analysisGene FrequencyGenotypeRetinitis pigmentosaotorhinolaryngologic diseasesGeneticsmedicineHumansAlleleAllelesPolymorphism Single-Stranded ConformationalGenetics (clinical)Sequence DeletionGeneticsExtracellular Matrix Proteinsbusiness.industryDNAmedicine.diseasePhenotypePhenotypeSpainMutation (genetic algorithm)Sensorineural hearing lossbusinessRetinitis PigmentosaEuropean Journal of Human Genetics
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Suppression and Replacement Gene Therapy for Autosomal Dominant Disease in a Murine Model of Dominant Retinitis Pigmentosa

2011

For dominantly inherited disorders development of gene therapies, targeting the primary genetic lesion has been impeded by mutational heterogeneity. An example is rhodopsin-linked autosomal dominant retinitis pigmentosa with over 150 mutations in the rhodopsin gene. Validation of a mutation-independent suppression and replacement gene therapy for this disorder has been undertaken. The therapy provides a means of correcting the genetic defect in a mutation-independent manner thereby circumventing the mutational diversity. Separate adeno-associated virus (AAV) vectors were used to deliver an RNA interference (RNAi)-based rhodopsin suppressor and a codon-modified rhodopsin replacement gene res…

genetic structuresGenetic enhancementMice TransgenicPolymerase Chain ReactionPhotoreceptor cellMiceRNA interferenceRetinitis pigmentosaDrug DiscoverymedicineGeneticsElectroretinographyAnimalsGeneMolecular BiologyPharmacologyGene therapy of the human retinabiologyAutosomal dominant traitGenetic Therapymedicine.diseaseMolecular biologyDisease Models Animalmedicine.anatomical_structureRhodopsinbiology.proteinMolecular MedicineOriginal Articlesense organsRetinitis PigmentosaMolecular Therapy
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Differential Distribution of Harmonin Isoforms and Their Possible Role in Usher-1 Protein Complexes in Mammalian Photoreceptor Cells

2003

PURPOSE. Human Usher syndrome is the most common form of combined deafness and blindness. Usher type I (USH1), the most severe form, is characterized by profound congenital deafness, constant vestibular dysfunction, and prepubertal onset retinitis pigmentosa. Previous studies have shown that the USH1-proteins myosin VIIa, harmonin, and cadherin 23 interact and form a functional network during hair cell differentiation in the inner ear. The purpose of the present study was to analyze the molecular and cellular functions of these USH1 proteins in the mammalian retina. METHODS. Antibodies to USH1 proteins were generated and used in Western blot analysis of subcellular photoreceptor fractions a…

Gene isoformUsher syndromeBlotting WesternSynaptophysinCell Cycle ProteinsMyosinsBiologyPhotoreceptor cellMiceRetinitis pigmentosaotorhinolaryngologic diseasesmedicineAnimalsProtein IsoformsRats WistarFluorescent Antibody Technique IndirectMicroscopy ImmunoelectronCytoskeletonGeneticsRetinaHair cell differentiationReverse Transcriptase Polymerase Chain ReactionCadherinDyneinsCadherinsmedicine.diseaseeye diseasesRatsCell biologyMice Inbred C57BLCytoskeletal Proteinsmedicine.anatomical_structureMicroscopy FluorescenceMyosin VIIasense organsCarrier ProteinsPhotoreceptor Cells VertebrateSubcellular FractionsInvestigative Opthalmology & Visual Science
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A comparative evaluation of NB30, NB54 and PTC124 in translational read-through efficacy for treatment of an USH1C nonsense mutation

2012

Translational read-through-inducing drugs (TRIDs) promote read-through of nonsense mutations, placing them in the spotlight of current gene-based therapeutic research. Here, we compare for the first time the relative efficacies of new-generation aminoglycosides NB30, NB54 and the chemical compound PTC124 on retinal toxicity and read-through efficacy of a nonsense mutation in the USH1C gene, which encodes the scaffold protein harmonin. This mutation causes the human Usher syndrome, the most common form of inherited deaf-blindness. We quantify read-through efficacy of the TRIDs in cell culture and show the restoration of harmonin function. We do not observe significant differences in the read…

MaleRetinal DisorderUsher syndromemedia_common.quotation_subjectNonsenseNonsense mutationPeptide Chain Elongation TranslationalCell Cycle ProteinsIn Vitro TechniquesBiologyPharmacologymedicine.disease_causeRetinaCell LineMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRetinal DiseasesIn vivoretinitis pigmentosaRetinitis pigmentosaotorhinolaryngologic diseasesmedicineAnimalsHumansResearch ArticlesAdaptor Proteins Signal Transducingpharmacogenetics030304 developmental biologymedia_commonOxadiazoles0303 health sciencesMutationsensoneuronal degenerationRetinalmedicine.diseasedrug therapy3. Good healthMice Inbred C57BLCytoskeletal ProteinsAminoglycosideschemistryCodon NonsenseMolecular MedicineFemaleUsher syndrome030217 neurology & neurosurgeryEMBO Molecular Medicine
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The retinitis pigmentosa protein RP2 links pericentriolar vesicle transport between the Golgi and the primary cilium.

2010

Photoreceptors are complex ciliated sensory neurons. The basal body and periciliary ridge of photoreceptors function in association with the Golgi complex to regulate the export of proteins from the inner segment to the outer segment sensory axoneme. Here, we show that the retinitis pigmentosa protein RP2, which is a GTPase activating protein (GAP) for Arl3, localizes to the ciliary apparatus, namely the basal body and the associated centriole at the base of the photoreceptor cilium. Targeting to the ciliary base was dependent on N-terminal myristoylation. RP2 also localized to the Golgi and periciliary ridge of photoreceptors, which suggested a role for RP2 in regulating vesicle traffic an…

CentriolePhotoreceptor Connecting CiliumGolgi ApparatusBiologysymbols.namesakeMiceIntraflagellar transportGTP-Binding ProteinsGeneticsBasal bodyAnimalsHumansKIF3APhotoreceptor CellsCiliaEye ProteinsTransport VesiclesMolecular BiologyGenetics (clinical)Cells CulturedCentriolesADP-Ribosylation FactorsCiliumCiliary BodyIntracellular Signaling Peptides and ProteinsMembrane ProteinsBiological TransportGeneral MedicineGolgi apparatusCell biologysymbolssense organsCiliary baseRetinitis PigmentosaHuman molecular genetics
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Mutation ofPOC1Bin a Severe Syndromic Retinal Ciliopathy

2014

We describe a consanguineous Iraqi family with Leber congenital amaurosis (LCA), Joubert syndrome (JBTS), and polycystic kidney disease (PKD). Targeted next-generation sequencing for excluding mutations in known LCA and JBTS genes, homozygosity mapping, and whole-exome sequencing identified a homozygous missense variant, c.317G>C (p.Arg106Pro), in POC1B, a gene essential for ciliogenesis, basal body, and centrosome integrity. In silico modeling suggested a requirement of p.Arg106 for the formation of the third WD40 repeat and a protein interaction interface. In human and mouse retina, POC1B localized to the basal body and centriole adjacent to the connecting cilium of photoreceptors and in …

MaleRetinal degenerationgenetic structuresAmino Acid MotifsLeber Congenital AmaurosisMolecular Sequence DataCell Cycle ProteinsBiologyKidneyArticleRetinaJoubert syndromeMiceCerebellar DiseasesCerebellumCiliogenesisRetinitis pigmentosaGeneticsmedicineAnimalsHumansAbnormalities MultipleAmino Acid SequenceCiliaEye AbnormalitiesChildZebrafishGenetics (clinical)Cystic kidneyGeneticsCiliumKidney Diseases Cysticmedicine.diseaseDisease gene identificationeye diseasesPedigreeCiliopathyGene Knockdown TechniquesIraqMutationsense organsHuman Mutation
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Identification of a novel mutation of MTP gene in a patient with abetalipoproteinemia.

2011

Abetalipoproteinemia (ABL), or Bassen-Kornzweig syndrome, is a rare autosomal recessive disorder of lipoprotein metabolism, characterized by fat malabsorption, hypocholesterolemia retinitis pigmentosa, progressive neuropathy and acanthocytosis from early infancy. We describe the clinical and molecular characterization of a 6-month-old infant born of consanguineous, apparently healthy parents from Iran. The patient was hospitalized because of failure to thrive, greasy stool and vomiting. The patient's serum lipid profile, the clinical phenotype and the duodenal histology suggested the clinical diagnosis of ABL. The MTP gene analysis by direct sequencing revealed a novel homozygous mutation (…

medicine.medical_specialtyHeterozygoteSettore MED/09 - Medicina InternaDuodenumSpecialties of internal medicineInternal medicineRetinitis pigmentosamedicineHumansgeneticsFamily HealthMTP gene mutations.ABLHepatologymedicine.diagnostic_testApoB-containing lipoproteins.business.industryAbetalipoproteinemiaInfantAbetalipoproteinemia.Heterozygote advantageGeneral Medicinemedicine.diseaseLipidsAbetalipoproteinemiaFat malabsorptionHypocholesterolemiaEndocrinologyPhenotypeRC581-951Failure to thriveFemaleHypocholesterolemia.medicine.symptomLipid profilebusinessCarrier Proteins
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Altered antioxidant-oxidant status in the aqueous humor and peripheral blood of patients with retinitis pigmentosa.

2013

Retinitis Pigmentosa is a common form of hereditary retinal degeneration constituting the largest Mendelian genetic cause of blindness in the developed world. It has been widely suggested that oxidative stress possibly contributes to its pathogenesis. We measured the levels of total antioxidant capacity, free nitrotyrosine, thiobarbituric acid reactive substances (TBARS) formation, extracellular superoxide dismutase (SOD3) activity, protein, metabolites of the nitric oxide/cyclic GMP pathway, heme oxygenase-I and inducible nitric oxide synthase expression in aqueous humor or/and peripheral blood from fifty-six patients with retinitis pigmentosa and sixty subjects without systemic or ocular …

Retinal degenerationAdultMalePathologymedicine.medical_specialtygenetic structuresSOD3lcsh:MedicineGene ExpressionPharmacologymedicine.disease_causeNitric OxideAntioxidantsNitric oxideAqueous Humorchemistry.chemical_compoundRetinitis pigmentosaTBARSmedicineCluster AnalysisHumanslcsh:ScienceCyclic GMPMultidisciplinarybiologySuperoxide DismutaseNitrotyrosinelcsh:RMiddle Agedmedicine.diseaseOxidantseye diseasesNitric oxide synthasechemistryCase-Control Studiesbiology.proteinLeukocytes MononuclearMetabolomelcsh:QFemalesense organsOxidative stressBiomarkersHeme Oxygenase-1Retinitis PigmentosaResearch ArticlePloS one
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Identification of three novel mutations in the MYO7A gene

1999

Three new mutations in the myosin VIIA gene involved in the pathogenesis of Usher syndrome type Ib are reported. These mutations are K1080X in exon 25, E1170K in exon 28, and Y1719C in exon 37. It is presumed that these mutations are involved in the Usher syndrome Ib phenotype. Hum Mutat 14:181, 1999. Copyright 1999 Wiley-Liss, Inc.

MaleMYO7AHearing Loss SensorineuralUsher syndromeMyosinsBiologymedicine.disease_causeExonRetinitis pigmentosaMyosinotorhinolaryngologic diseasesGeneticsmedicineHumansGenePolymorphism Single-Stranded ConformationalGenetics (clinical)GeneticsMutationBase SequenceChromosomes Human Pair 11fungiDyneinsSyndromemedicine.diseasePhenotypeeye diseasesPedigreePhenotypeMyosin VIIaMutationFemaleRetinitis PigmentosaHuman Mutation
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