Search results for " Signal Transducing"

showing 10 items of 133 documents

New insights into the clinical and molecular spectrum of the novel CYFIP2-related neurodevelopmental disorder and impairment of the WRC-mediated acti…

2021

International audience; Purpose: A few de novo missense variants in the cytoplasmic FMRP-interacting protein 2 (CYFIP2) gene have recently been described as a novel cause of severe intellectual disability, seizures, and hypotonia in 18 individuals, with p.Arg87 substitutions in the majority.Methods: We assembled data from 19 newly identified and all 18 previously published individuals with CYFIP2 variants. By structural modeling and investigation of WAVE-regulatory complex (WRC)-mediated actin polymerization in six patient fibroblast lines we assessed the impact of CYFIP2 variants on the WRC.Results: Sixteen of 19 individuals harbor two previously described and 11 novel (likely) disease-ass…

0301 basic medicine[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyWAVEregulatory complex (WRC)030105 genetics & heredityBiologyArticleIntellectual disability; Epilepsy; CYFIP2; WAVE-regulatory complex (WRC); WASF03 medical and health sciencesNeurodevelopmental disorderSeizuresWAVE-regulatory complex (WRC)medicineCYFIP2Missense mutationHumansGenetics(clinical)WASFGeneGenetics (clinical)ActinAdaptor Proteins Signal TransducingGenetics/dk/atira/pure/subjectarea/asjc/2700/2716medicine.diseaseActin cytoskeletonPhenotypeHypotoniaActins3. Good healthddc:030104 developmental biology[SDV.BDD.EO]Life Sciences [q-bio]/Development Biology/Embryology and OrganogenesisNeurodevelopmental Disordersintellectual disabilityCYFIP2epilepsymedicine.symptom
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Structural Basis of the High Affinity Interaction between the Alphavirus Nonstructural Protein-3 (nsP3) and the SH3 Domain of Amphiphysin-2

2016

We show that a peptide from Chikungunya virus nsP3 protein spanning residues 1728–1744 binds the amphiphysin-2 (BIN1) Src homology-3 (SH3) domain with an unusually high affinity (Kd 24 nM). Our NMR solution complex structure together with isothermal titration calorimetry data on several related viral and cellular peptide ligands reveal that this exceptional affinity originates from interactions between multiple basic residues in the target peptide and the extensive negatively charged binding surface of amphiphysin-2 SH3. Remarkably, these arginines show no fixed conformation in the complex structure, indicating that a transient or fluctuating polyelectrostatic interaction accounts for this …

0301 basic medicinenuclear magnetic resonance (NMR)Amino Acid MotifsStatic ElectricityPeptideTarget peptidePlasma protein bindingViral Nonstructural ProteinsBiologyhost-pathogen interactionBiochemistrySH3 domainsrc Homology Domainsamphiphysin SH3Structure-Activity Relationship03 medical and health sciencesProtein structuredynaminHumansShort linear motifprotein structureNuclear Magnetic Resonance BiomolecularMolecular BiologySrc homology 3 domain (SH3 domain)Adaptor Proteins Signal Transducingchemistry.chemical_classificationTumor Suppressor Proteinsta1182Nuclear ProteinsIsothermal titration calorimetryCell Biologyintrinsically disordered protein030104 developmental biologychemistryBiochemistrynsP3Protein Structure and FoldingAmphiphysinBiophysicsPeptidesChikungunya virusProtein BindingJournal of Biological Chemistry
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STRIPAK Members Orchestrate Hippo and Insulin Receptor Signaling to Promote Neural Stem Cell Reactivation

2019

Summary Adult stem cells reactivate from quiescence to maintain tissue homeostasis and in response to injury. How the underlying regulatory signals are integrated is largely unknown. Drosophila neural stem cells (NSCs) also leave quiescence to generate adult neurons and glia, a process that is dependent on Hippo signaling inhibition and activation of the insulin-like receptor (InR)/PI3K/Akt cascade. We performed a transcriptome analysis of individual quiescent and reactivating NSCs harvested directly from Drosophila brains and identified the conserved STRIPAK complex members mob4, cka, and PP2A (microtubule star, mts). We show that PP2A/Mts phosphatase, with its regulatory subunit Widerbors…

0301 basic medicinereactivationendocrine systemMitosisNerve Tissue ProteinsProtein Serine-Threonine KinasesBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyAnimals Genetically ModifiedPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineNeural Stem CellsAnimalsDrosophila ProteinsquiescenceProtein Phosphatase 2lcsh:QH301-705.5Protein kinase BCells CulturedPI3K/AKT/mTOR pathwayTissue homeostasisAdaptor Proteins Signal TransducingCell ProliferationHippo signaling pathwayGene Expression ProfilingHippo signalingInR/PI3K/Akt signalingfungiIntracellular Signaling Peptides and ProteinsBrainSTRIPAK membersProtein phosphatase 2Receptor InsulinNeural stem cellCell biologyDrosophila melanogaster030104 developmental biologylcsh:Biology (General)nervous systemHippo signalingSingle-Cell AnalysisTranscriptomeProto-Oncogene Proteins c-akt030217 neurology & neurosurgeryAdult stem cellCell Reports
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Advanced mechanotherapy: Biotensegrity  for governing metastatic tumor cell fate via modulating the extracellular matrix.

2021

Mechano-transduction is the procedure of mechanical stimulus translation via cells, among substrate shear flow, topography, and stiffness into a biochemical answer. TAZ and YAP are transcriptional coactivators which are recognized as relay proteins that promote mechano-transduction within the Hippo pathway. With regard to healthy cells in homeostasis, mechano-transduction regularly restricts proliferation, and TAZ and YAP are totally inactive. During cancer development a YAP/TAZ - stimulating positive response loop is formed between the growing tumor and the stiffening ECM. As tumor developments, local stromal and cancerous cells take advantage of mechanotransduction to enhance proliferatio…

0303 health sciencesHippo signaling pathwayStromal cellChemistryPharmaceutical ScienceCell Differentiation02 engineering and technologyCell fate determination021001 nanoscience & nanotechnologyPhosphoproteinsMechanotransduction CellularCell biologyExtracellular MatrixExtracellular matrix03 medical and health sciencesMechanobiologyTumor progressionNeoplasmsHumansMechanotransduction0210 nano-technologyMechanotherapy030304 developmental biologyAdaptor Proteins Signal TransducingJournal of controlled release : official journal of the Controlled Release Society
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TCTN3 Mutations Cause Mohr-Majewski Syndrome

2012

Orofaciodigital syndromes (OFDSs) consist of a group of heterogeneous disorders characterized by abnormalities in the oral cavity, face, and digits and associated phenotypic abnormalities that lead to the delineation of 13 OFDS subtypes. Here, by a combined approach of homozygozity mapping and exome ciliary sequencing, we identified truncating TCTN3 mutations as the cause of an extreme form of OFD associated with bone dysplasia, tibial defect, cystic kidneys, and brain anomalies (OFD IV, Mohr-Majewski syndrome). Analysis of 184 individuals with various ciliopathies (OFD, Meckel, Joubert, and short rib polydactyly syndromes) led us to identify four additional truncating TCTN3 mutations in un…

AdolescentFoot Deformities CongenitalMolecular Sequence DataCiliopathiesJoubert syndromeYoung AdultFetusReportCerebellumGLI3medicineGeneticsHumansExomeHedgehog ProteinsGenetics(clinical)Sonic hedgehogChildExomeGenetics (clinical)Adaptor Proteins Signal TransducingCystic kidneyGeneticsBase SequencebiologyHomozygoteIntracellular Signaling Peptides and ProteinsMembrane ProteinsCiliary transition zoneSequence Analysis DNAOrofaciodigital Syndromesmedicine.diseaseCleft PalateCiliopathyPhenotypeMutationbiology.proteinApoptosis Regulatory ProteinsHand Deformities CongenitalSignal TransductionThe American Journal of Human Genetics
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A Roma founder BIN1 mutation causes a novel phenotype of centronuclear myopathy with rigid spine

2018

ObjectiveTo describe a large series of BIN1 patients, in which a novel founder mutation in the Roma population of southern Spain has been identified.MethodsPatients diagnosed with centronuclear myopathy (CNM) at 5 major reference centers for neuromuscular disease in Spain (n = 53) were screened for BIN1 mutations. Clinical, histologic, radiologic, and genetic features were analyzed.ResultsEighteen patients from 13 families carried the p.Arg234Cys variant; 16 of them were homozygous for it and 2 had compound heterozygous p.Arg234Cys/p.Arg145Cys mutations. Both BIN1 variants have only been identified in Roma, causing 100% of CNM in this ethnic group in our cohort. The haplotype analysis confi…

Adult0301 basic medicinemedicine.medical_specialtyRomaNeuromuscular diseaseAdolescentPopulationMallory BodiesCompound heterozygosityArticleMuscular DystrophiesCohort StudiesYoung Adult03 medical and health sciences0302 clinical medicineInternal medicinemedicineHumansProspective StudiesCentronuclear myopathyChildeducationProspective cohort studyAdaptor Proteins Signal TransducingRetrospective Studieseducation.field_of_studybusiness.industryTumor Suppressor ProteinsHaplotypeNuclear ProteinsRetrospective cohort studyMiddle Agedmedicine.diseaseFounder EffectPhenotype030104 developmental biologyScoliosisSpainMutation[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Neurology (clinical)business030217 neurology & neurosurgeryMyopathies Structural CongenitalFounder effect
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Common missense variant in the glucokinase regulatory protein gene is associated with increased plasma triglyceride and C-reactive protein but lower …

2008

OBJECTIVE—Using the genome-wide association approach, we recently identified the glucokinase regulatory protein gene (GCKR, rs780094) region as a novel quantitative trait locus for plasma triglyceride concentration in Europeans. Here, we sought to study the association of GCKR variants with metabolic phenotypes, including measures of glucose homeostasis, to evaluate the GCKR locus in samples of non-European ancestry and to fine- map across the associated genomic interval. RESEARCH DESIGN AND METHODS—We performed association studies in 12 independent cohorts comprising >45,000 individuals representing several ancestral groups (whites from Northern and Southern Europe, whites from the …

AdultBlood GlucoseMaleLinkage disequilibriummedicine.medical_specialtyGenotypeEndocrinology Diabetes and MetabolismMutation Missense030209 endocrinology & metabolismLocus (genetics)Single-nucleotide polymorphismBiologyQuantitative trait locusPolymorphism Single Nucleotide03 medical and health sciences0302 clinical medicineGene FrequencyInternal medicineInternal MedicinemedicineGeneticsGlucose homeostasisHumansTriglycerides030304 developmental biologyGenetic associationAdaptor Proteins Signal TransducingAgedGenetics0303 health sciencesAnalysis of VarianceGlucokinase regulatory proteinGlucokinaseFastingMiddle AgedEndocrinologyC-Reactive Proteinbiology.proteinFemaleDiabetes
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A genome-wide association study identifies two loci associated with heart failure due to dilated cardiomyopathy

2011

Dilated cardiomyopathy (DCM) is a major cause of heart failure with a high familial recurrence risk. So far, the genetics of DCM remains largely unresolved. We conducted the first genome-wide association study (GWAS) to identify loci contributing to sporadic DCM.One thousand one hundred and seventy-nine DCM patients and 1108 controls contributed to the discovery phase. Pools of DNA stratified on disease status, population, age, and gender were constituted and used for testing association of DCM with 517 382 single nucleotide polymorphisms (SNPs). Three DCM-associated SNPs were confirmed by individual genotyping (P5.0 10(-7)), and two of them, rs10927875 and rs2234962, were replicated in ind…

AdultCardiomyopathy DilatedMaleCandidate genemedicine.medical_specialtyHeterozygoteHeart diseaseCardiomyopathyHSP27 Heat-Shock ProteinsMutation MissenseGenome-wide association studySingle-nucleotide polymorphism030204 cardiovascular system & hematologycomplex mixturesPolymorphism Single Nucleotide03 medical and health sciences0302 clinical medicineChloride ChannelsInternal medicinemedicineHumanscardiovascular diseasesComputingMilieux_MISCELLANEOUS030304 developmental biologyAdaptor Proteins Signal TransducingHeart Failure0303 health sciences[SDV.GEN]Life Sciences [q-bio]/GeneticsCLCNKAbiologybusiness.industryChromosomes Human Pair 10Dilated cardiomyopathyMiddle Agedmusculoskeletal systemmedicine.diseaseFasttrack Clinical3. Good healthChromosomes Human Pair 1Genetic LociHeart failurecardiovascular systemCardiologybiology.proteinFemaleCardiology and Cardiovascular MedicinebusinessApoptosis Regulatory ProteinsGenome-Wide Association Study
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Causal relationship of hepatic fat with liver damage and insulin resistance in nonalcoholic fatty liver

2017

Abstract Background and Aims Nonalcoholic fatty liver disease is epidemiologically associated with hepatic and metabolic disorders. The aim of this study was to examine whether hepatic fat accumulation has a causal role in determining liver damage and insulin resistance. Methods We performed a Mendelian randomization analysis using risk alleles in PNPLA3, TM6SF2, GCKR and MBOAT7, and a polygenic risk score for hepatic fat, as instruments. We evaluated complementary cohorts of at‐risk individuals and individuals from the general population: 1515 from the liver biopsy cohort (LBC), 3329 from the Swedish Obese Subjects Study (SOS) and 4570 from the population‐based Dallas Heart Study (DHS). Re…

AdultGenetic MarkersLiver CirrhosisMalenonalcoholic fatty liver diseaseNon-alcoholic Fatty Liver Diseaseinsulin resistanceHumansgeneticsProspective StudiesAdaptor Proteins Signal TransducingSettore MED/12 - GastroenterologiafibrosisMembrane ProteinsOriginal ArticlesLipaseMendelian Randomization AnalysisAdipose TissueDiabetes Mellitus Type 2Chronic Diseasemendelian randomizationOriginal ArticleFemaletype 2 diabetesgeneticfibrosiAcyltransferases
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Phenotype and natural history of inherited neuropathies caused byHSJ1c.352+1G>A mutation

2015

Mutations in the HSJ1 ( Heat-Shock Protein J1 ) gene, also called DNAJB2 (DnaJ (Hsp40) homologue, subfamily B, member 2), have been recently described as a cause of hereditary neuropathies. The HSJ1 c.352+1G>A mutation in homozygote state has been reported as the causative mutation in a single family with autosomal recessive distal hereditary motor neuropathy (dHMN).1 Since then, two other families with different HSJ1 mutations have been described: one with a dHMN phenotype and the other with a Charcot-Marie-Tooth disease type 2 (CMT2) phenotype.2 We identified the HSJ1 c.352+1G>A mutation in 10 patients who underwent long-lasting follow-up. We describe their phenotype and clinical evolutio…

AdultMale0301 basic medicineNeural ConductionCell Cycle ProteinsNeurological examinationDisease03 medical and health sciencessymbols.namesake0302 clinical medicineCharcot-Marie-Tooth DiseasemedicineHumansGeneHeat-Shock ProteinsExome sequencingAdaptor Proteins Signal TransducingGenetic testingGeneticsSanger sequencingmedicine.diagnostic_testbusiness.industryNuclear ProteinsMiddle AgedPhenotypePsychiatry and Mental healthPhenotype030104 developmental biologySpainMutationMutation (genetic algorithm)symbolsFemaleSurgeryNeurology (clinical)Hereditary Sensory and Motor Neuropathybusiness030217 neurology & neurosurgeryJournal of Neurology, Neurosurgery & Psychiatry
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