Search results for "muta"

showing 10 items of 6895 documents

A TRAPPC6B splicing variant associates to restless legs syndrome

2016

Abstract INTRODUCTION: RLS is a common movement disorders with a strong genetic component in its pathophysiology, but, up to now, no causative mutation has been reported. METHODS: We re-evaluated the previously described RLS2 family by exome sequencing. RESULTS: We identified fifteen variations in the 14q critical region. The c.485G > A transition of the TRAPPC6B gene segregates with the RLS2 haplotype, is absent in 200 local controls and is extremely rare in 12988 exomes from the Exome Variant Server (EVS). This variant alters a splicing site and hampers the normal transcript processing by promoting exon 3-skipping as demonstrated by minigene transfection and by patient transcripts. CON…

0301 basic medicineExome sequencingMaleVesicular Transport ProteinsLocus (genetics)VariationGene mutationBiologySplicingTransfection03 medical and health sciencesExonGene FrequencyRLSRestless Legs SyndromeAnimalsHumansGenetic Predisposition to DiseaseRNA MessengerRestless legs syndromeExomeExome sequencingMovement disorderCells CulturedGeneticsChromosomes Human Pair 14Family HealthSleep disorderHaplotypeExonsRats030104 developmental biologyAuthors report no disclosureNeurologyHaplotypesRNA splicingMutationFemaleNeurology (clinical)Geriatrics and GerontologyNeurological diseaseMinigene
researchProduct

FGFR a promising druggable target in cancer: Molecular biology and new drugs.

2017

Abstract: Introduction: The Fibroblast Growth Factor Receptor (FGFR) family consists of Tyrosine Kinase Receptors (TKR) involved in several biological functions. Recently, alterations of FGFR have been reported to be important for progression and development of several cancers. In this setting, different studies are trying to evaluate the efficacy of different therapies targeting FGFR. Areas Covered: This review summarizes the current status of treatments targeting FGFR, focusing on the trials that are evaluating the FGFR profile as inclusion criteria: Multi-Target, Pan-FGFR Inhibitors and anti-FGF (Fibroblast Growth Factor)/FGFR Monoclonal Antibodies. Expert opinion: Most of the TKR share …

0301 basic medicineFibroblast Growth FactorDruggabilityFibroblast growth factorTyrosine-kinase inhibitorReceptor tyrosine kinase0302 clinical medicineNeoplasmsFGFR inhibitorsFGFMolecular Targeted TherapyCancerCancer; FGF; FGFR; FGFR inhibitors; Drug Resistance Neoplasm; Fibroblast Growth Factors; Gene Fusion; Humans; Molecular Targeted Therapy; Mutation; Neoplasms; Protein Kinase Inhibitors; Receptors Fibroblast Growth Factor; Signal Transduction; Hematology; Oncology; Geriatrics and GerontologybiologyFGFRHematologyFGFR inhibitorOncologyFibroblast growth factor receptor030220 oncology & carcinogenesisembryonic structuresSignal transductionbiological phenomena cell phenomena and immunityGene FusionHumanSignal Transductionmusculoskeletal diseasesanimal structuresmedicine.drug_classProtein Kinase Inhibitor03 medical and health sciencesmedicineHumansProtein Kinase InhibitorsCancer; FGF; FGFR; FGFR inhibitorsbusiness.industryCancermedicine.diseaseMolecular biologyReceptors Fibroblast Growth FactorFibroblast Growth Factors030104 developmental biologyDrug Resistance NeoplasmCancer cellMutationbiology.proteinNeoplasmHuman medicineGeriatrics and GerontologybusinessCritical reviews in oncology/hematology
researchProduct

Skeletal Dysplasia Mutations Effect on Human Filamins’ Structure and Mechanosensing

2016

AbstractCells’ ability to sense mechanical cues in their environment is crucial for fundamental cellular processes, leading defects in mechanosensing to be linked to many diseases. The actin cross-linking protein Filamin has an important role in the conversion of mechanical forces into biochemical signals. Here, we reveal how mutations in Filamin genes known to cause Larsen syndrome and Frontometaphyseal dysplasia can affect the structure and therefore function of Filamin domains 16 and 17. Employing X-ray crystallography, the structure of these domains was first solved for the human Filamin B. The interaction seen between domains 16 and 17 is broken by shear force as revealed by steered mo…

0301 basic medicineFilaminsScienceProtein domainPeptide bindingPlasma protein bindingmacromolecular substancesBiologyMolecular Dynamics SimulationFilaminmedicine.disease_causeBioinformaticsCrystallography X-RayOsteochondrodysplasiasMechanotransduction CellularArticlecomputational biophysics03 medical and health sciences0302 clinical medicineProtein DomainsmedicineHumansLarsen syndromeForeheadMechanotransductionNMR-spektroskopiaActinMutationMultidisciplinaryBinding SitesQRSAXSmedicine.diseasecytoskeletal proteinsActinsCell biologybody regions030104 developmental biologyMutationMedicine030217 neurology & neurosurgeryröntgenkristallografiaProtein Binding
researchProduct

Evolutionary conserved role of eukaryotic translation factor eIF5A in the regulation of actin-nucleating formins

2017

AbstractElongation factor eIF5A is required for the translation of consecutive prolines, and was shown in yeast to translate polyproline-containing Bni1, an actin-nucleating formin required for polarized growth during mating. Here we show that Drosophila eIF5A can functionally replace yeast eIF5A and is required for actin-rich cable assembly during embryonic dorsal closure (DC). Furthermore, Diaphanous, the formin involved in actin dynamics during DC, is regulated by and mediates eIF5A effects. Finally, eIF5A controls cell migration and regulates Diaphanous levels also in mammalian cells. Our results uncover an evolutionary conserved role of eIF5A regulating cytoskeleton-dependent processes…

0301 basic medicineFluorescent Antibody Techniquelcsh:Medicinemacromolecular substancesBiologyArticleMiceEukaryotic cells03 medical and health sciencesEukaryotic translationCell MovementPeptide Initiation FactorsCitosqueletProtein biosynthesisAnimalsProtein Interaction Domains and Motifslcsh:ScienceCytoskeletonActinMultidisciplinaryCèl·lules eucariotesMicrofilament Proteinsfungilcsh:RGene Expression Regulation DevelopmentalRNA-Binding ProteinsTranslation (biology)Biological EvolutionActinsDorsal closureCell biologyElongation factor030104 developmental biologyProtein BiosynthesisForminsMutationbiology.proteinDrosophilalcsh:QEIF5AScientific Reports
researchProduct

Hog1p activation by marasmic acid through inhibition of the histidine kinase Sln1p

2016

BACKGROUND The histidine kinase (HK) MoHik1p within the high-osmolarity glycerol (HOG) pathway is known to be the target of the fungicide fludioxonil. Treatment of the fungus with fludioxonil causes an uncontrolled hyperactivation of the pathway and cell death. In this study, we used a target-based in vivo test system with mutant strains of the rice blast fungus Magnaporthe oryzae to search for new fungicidal compounds having various target locations within the HOG pathway. Mutants with inactivated HOG signalling are resistant to fungicides having the target located in the HOG pathway. RESULTS The HK MoSln1p was identified as being involved in the new antifungal mode of action of marasmic a…

0301 basic medicineFungal proteinMagnaporthebiologyMutantHistidine kinaseGeneral MedicineFludioxonilbiology.organism_classificationMicrobiology03 medical and health sciencesMetabolic pathway030104 developmental biologyBiochemistryInsect SciencePhosphorylationMode of actionAgronomy and Crop SciencePest Management Science
researchProduct

The Amino-Terminal Domain of GRK5 Inhibits Cardiac Hypertrophy through the Regulation of Calcium-Calmodulin Dependent Transcription Factors.

2018

We have recently demonstrated that the amino-terminal domain of G protein coupled receptor kinase (GRK) type 5, (GRK5-NT) inhibits NFκB activity in cardiac cells leading to a significant amelioration of LVH. Since GRK5-NT is known to bind calmodulin, this study aimed to evaluate the functional role of GRK5-NT in the regulation of calcium-calmodulin-dependent transcription factors. We found that the overexpression of GRK5-NT in cardiomyoblasts significantly reduced the activation and the nuclear translocation of NFAT and its cofactor GATA-4 in response to phenylephrine (PE). These results were confirmed in vivo in spontaneously hypertensive rats (SHR), in which intramyocardial adenovirus-med…

0301 basic medicineG-Protein-Coupled Receptor Kinase 5MalecalmodulinMutantWistarPlasma protein binding030204 cardiovascular system & hematologyCatalysilcsh:ChemistryPhenylephrine0302 clinical medicineRats Inbred SHRMyocytes Cardiaclcsh:QH301-705.5SpectroscopybiologyChemistrycardiac hypertrophyNFATComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineLeft VentricularComputer Science ApplicationsCell biologycardiac hypertrophy; transcription factors; calmodulin; GRKGRKHypertrophy Left VentricularCardiacProtein BindingInbred SHRCalmodulinCalmodulin; Cardiac hypertrophy; GRK; Transcription factors; Animals; Binding Sites; Calmodulin; Cell Line; G-Protein-Coupled Receptor Kinase 5; GATA4 Transcription Factor; Hypertrophy Left Ventricular; Male; Myocytes Cardiac; NFATC Transcription Factors; Phenylephrine; Protein Binding; Rats; Rats Inbred SHR; Rats Wistar; Catalysis; Molecular Biology; Spectroscopy; Computer Science Applications1707 Computer Vision and Pattern Recognition; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic ChemistryCatalysisArticleCell LineInorganic Chemistry03 medical and health sciencesG-Protein-Coupled Receptor Kinase 5transcription factorsAnimalsPhysical and Theoretical ChemistryRats WistarTranscription factorMolecular BiologyG protein-coupled receptor kinaseMyocytesBinding SitesNFATC Transcription FactorsOrganic ChemistryHypertrophyNFATC Transcription FactorsGATA4 Transcription FactorRats030104 developmental biologylcsh:Biology (General)lcsh:QD1-999biology.proteinTranscription factorInternational journal of molecular sciences
researchProduct

Increased Motor-Impairing Effects of the Neuroactive Steroid Pregnanolone in Mice with Targeted Inactivation of the GABAA Receptor γ2 Subunit in the …

2016

Endogenous neurosteroids and neuroactive steroids have potent and widespread actions on the brain via inhibitory GABAA receptors. In recombinant receptors and genetic mouse models their actions depend on the α, β, and δ subunits of the receptor, especially on those that form extrasynaptic GABAA receptors responsible for non-synaptic (tonic) inhibition, but they also act on synaptically enriched γ2 subunit-containing receptors and even on αβ binary receptors. Here we tested whether behavioral sensitivity to the neuroactive steroid agonist 5β-pregnan-3α-ol-20-one is altered in genetically engineered mouse models that have deficient GABAA receptor-mediated synaptic inhibition in selected neuro…

0301 basic medicineGAMMA-2-SUBUNITCerebellumNeuroactive steroidcerebellumDISORDERSPurkinje cellINHIBITIONBiologyPharmacologyGABAA-rho receptor03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCRE RECOMBINASE EXPRESSIONmedicinePharmacology (medical)Pharmacology & PharmacyReceptorPARVALBUMIN-POSITIVE INTERNEURONSIN-VIVOOriginal ResearchPregnanolonePharmacologyScience & TechnologyGABAA receptorAllopregnanolonelcsh:RM1-950POINT MUTATIONA RECEPTORS3. Good health030104 developmental biologymedicine.anatomical_structurelcsh:Therapeutics. Pharmacologychemistrynervous systemPurkinje cellsALLOPREGNANOLONEextrasynaptic GABAA receptorsmotor performance1115 Pharmacology And Pharmaceutical Sciences3111 BiomedicineneurosteroidsLife Sciences & Biomedicine030217 neurology & neurosurgeryextrasynaptic GABA(A) receptors
researchProduct

Redox signaling in the gastrointestinal tract.

2017

Redox signaling regulates physiological self-renewal, proliferation, migration and differentiation in gastrointestinal epithelium by modulating Wnt/β-catenin and Notch signaling pathways mainly through NADPH oxidases (NOXs). In the intestine, intracellular and extracellular thiol redox status modulates the proliferative potential of epithelial cells. Furthermore, commensal bacteria contribute to intestine epithelial homeostasis through NOX1- and dual oxidase 2-derived reactive oxygen species (ROS). The loss of redox homeostasis is involved in the pathogenesis and development of a wide diversity of gastrointestinal disorders, such as Barrett's esophagus, esophageal adenocarcinoma, peptic ulc…

0301 basic medicineGastrointestinal DiseasesNotch signaling pathwaymedicine.disease_causeBiochemistryGastrointestinal epitheliumSuperoxide dismutase03 medical and health scienceschemistry.chemical_compoundPhysiology (medical)medicineHumansSulfhydryl CompoundsIntestinal MucosaWnt Signaling PathwayCell Proliferationchemistry.chemical_classificationReactive oxygen speciesbiologySuperoxideWnt signaling pathwayNADPH OxidasesDual oxidase 2digestive system diseasesGastrointestinal TractIntestinesOxidative Stress030104 developmental biologychemistryImmunologybiology.proteinCancer researchReactive Oxygen SpeciesOxidation-ReductionOxidative stressFree radical biologymedicine
researchProduct

NOX2ko Mice Show Largely Increased Expression of a Mutated NOX2 mRNA Encoding an Inactive NOX2 Protein

2020

Background: The superoxide-generating enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2 or gp91phox, the phagocytic isoform) was reported as a major source of oxidative stress in various human diseases. Genetic deletion is widely used to study the impact of NOX2-derived reactive oxygen species (ROS) on disease development and progression in various animal models. Here, we investigate why NOX2 knockout mice show no NOX2 activity but express NOX2 mRNA and protein. Methods and Results: Oxidative burst (NOX2-dependent formation of ROS) was measured by L-012-based chemiluminescence and was largely absent in whole blood of NOX2 knockout mice. Protein expression was still de…

0301 basic medicineGene isoformPhysiologyClinical Biochemistrynext generation sequencing (NGS)030204 cardiovascular system & hematologymedicine.disease_causeBiochemistryArticlenicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2) knockout mice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineWestern blotmedicineMolecular BiologyGeneMessenger RNAmedicine.diagnostic_testurogenital systemCell BiologyMolecular biologyRespiratory burst030104 developmental biologychemistryKnockout mousecardiovascular systemoxidative stress related diseasetruncated and inactive mutanthormones hormone substitutes and hormone antagonistsOxidative stressNicotinamide adenine dinucleotide phosphatecirculatory and respiratory physiologyAntioxidants
researchProduct

Zymography Methods to Simultaneously Analyze Superoxide Dismutase and Catalase Activities: Novel Application for Yeast Species Identification

2017

We provide an optimized protocol for a double staining technique to analyze superoxide dismutase enzymatic isoforms Cu-Zn SOD (Sod1) and Mn-SOD (Sod2) and catalase in the same polyacrylamide gel. The use of NaCN, which specifically inhibits yeast Sod1 isoform, allows the analysis of Sod2 isoform while the use of H2O2 allows the analysis of catalase. The identification of a different zymography profiling of SOD and catalase isoforms in different yeast species allowed us to propose this technique as a novel yeast identification and classification strategy.

0301 basic medicineGene isoformchemistry.chemical_classificationbiologySOD2Molecular biologyYeastSuperoxide dismutase03 medical and health sciences030104 developmental biology0302 clinical medicineEnzymechemistryCatalasebiology.proteinZymographyPolyacrylamide gel electrophoresis030217 neurology & neurosurgery
researchProduct