Search results for "BINDING PROTEIN"

showing 10 items of 1292 documents

Lamivudine/Adefovir Treatment Increases the Rate of Spontaneous Mutation of Hepatitis B Virus in Patients.

2016

The high levels of genetic diversity shown by hepatitis B virus (HBV) are commonly attributed to the low fidelity of its polymerase. However, the rate of spontaneous mutation of human HBV in vivo is currently unknown. Here, based on the evolutionary principle that the population frequency of lethal mutations equals the rate at which they are produced, we have estimated the mutation rate of HBV in vivo by scoring premature stop codons in 621 publicly available, full-length, molecular clone sequences derived from patients. This yielded an estimate of 8.7 × 10-5 spontaneous mutations per nucleotide per cell infection in untreated patients, which should be taken as an upper limit estimate becau…

0301 basic medicineMaleRNA virusesMutation ratelcsh:Medicinemedicine.disease_causeBiochemistryPolymerasesAdefovirFrameshift Mutationlcsh:SciencePathology and laboratory medicineeducation.field_of_studyMultidisciplinaryMicrobial MutationLamivudineMedical microbiologyResistance mutation3. Good healthLamivudineVirusesFemalePathogensSequence AnalysisImmunosuppressive Agentsmedicine.drugResearch ArticleHepatitis B virusSubstitution MutationPopulationOrganophosphonatesBiologyResearch and Analysis MethodsPolymorphism Single NucleotideMicrobiologyFrameshift mutation03 medical and health sciencesHepatitis B ChronicDrug Resistance ViralDNA-binding proteinsmedicineGeneticsHumanseducationMolecular Biology TechniquesSequencing TechniquesMolecular BiologyHepatitis B virusMedicine and health sciencesPoint mutationAdeninelcsh:RViral pathogensOrganismsBiology and Life SciencesProteinsVirologyMolecular biologyHepatitis virusesMicrobial pathogens030104 developmental biologyMutationlcsh:QCloningPLoS ONE
researchProduct

Mutations in SKI in Shprintzen-Goldberg syndrome lead to attenuated TGF-β responses through SKI stabilization.

2020

ABSTRACTShprintzen-Goldberg syndrome (SGS) is a multisystemic connective tissue disorder, with considerable clinical overlap with Marfan and Loeys-Dietz syndromes. These syndromes have commonly been associated with enhanced TGF-β signaling. In SGS patients, heterozygous point mutations have been mapped to the transcriptional corepressor SKI, which is a negative regulator of TGF-β signaling that is rapidly degraded upon ligand stimulation. The molecular consequences of these mutations, however, are not understood. Here we use a combination of structural biology, genome editing and biochemistry to show that SGS mutations in SKI abolish its binding to phosphorylated SMAD2 and SMAD3. This resul…

0301 basic medicineMaleSMADmedicine.disease_causeMarfan SyndromeActivin0302 clinical medicineGenome editingTransforming Growth Factor betaGene expressionBiology (General)MutationShprintzen-Goldberg syndromeGeneral NeuroscienceQRShprintzen–Goldberg syndromeGeneral MedicineLigand (biochemistry)Chromosomes and Gene ExpressionCell biologyDNA-Binding ProteinsMedicinePhosphorylationFemaleSignal TransductionResearch ArticleHumanTGF-βQH301-705.5ScienceBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCraniosynostosesstomatognathic systemBiochemistry and Chemical BiologyProto-Oncogene ProteinsmedicineHumansGeneral Immunology and MicrobiologyPoint mutationmedicine.diseaseSKIArachnodactyly030104 developmental biologyStructural biologyMutation030217 neurology & neurosurgerySMADTransforming growth factoreLife
researchProduct

Brief Report: Functional Interaction of Endoplasmic Reticulum Aminopeptidase 2 and HLA-B27 Activates the Unfolded Protein Response.

2017

Objective: The basic mechanisms underlying the pathogenesis of ankylosing spondylitis (AS) remain unresolved. We previously reported an association of the single-nucleotide polymorphism (SNP) rs2549782 in the endoplasmic reticulum aminopeptidase 2 gene (ERAP2) with AS. It is known that patients homozygous for the G allele (GG) of another ERAP2 SNP, rs2248374, lack expression of ERAP2 (ERAP2 null). The present study utilized this information to study the impact of ERAP2 deficiency on HLA–B27 expression in patients with AS, specifically focusing on the functional interaction of ERAP2 and HLA–B27 in peripheral blood mononuclear cells (PBMCs) from patients with AS and assessing the effects …

0301 basic medicineMaleX-Box Binding Protein 1Aminopeptidases0302 clinical medicineImmunology and AllergyRNA Small InterferingEndoplasmic Reticulum Chaperone BiPHLA-B27 AntigenHeat-Shock ProteinsAlleleBlottingReverse Transcriptase Polymerase Chain ReactionHeat-Shock ProteinSingle NucleotideMiddle AgedFlow CytometryCCAAT-Enhancer-Binding Protein3. Good healthUp-RegulationFemaleWesternHumanAnkylosingAdultAminopeptidaseMononuclearImmunologyBlotting WesternSingle-nucleotide polymorphismBiologyMajor histocompatibility complexSmall InterferingPolymorphism Single NucleotideAdult; Alleles; Aminopeptidases; Blotting Western; CCAAT-Enhancer-Binding Proteins; Cell Line; Female; Flow Cytometry; HLA-B27 Antigen; Heat-Shock Proteins; Humans; Leukocytes Mononuclear; Male; Middle Aged; Polymorphism Single Nucleotide; RNA Small Interfering; Reverse Transcriptase Polymerase Chain Reaction; Spondylitis Ankylosing; Unfolded Protein Response; Up-Regulation; X-Box Binding Protein 1; Immunology and Allergy; Rheumatology; ImmunologyCell Line03 medical and health sciencesDownregulation and upregulationRheumatologyHumansSpondylitis AnkylosingAllelePolymorphismAlleles030203 arthritis & rheumatologySpondylitiHLA-B27LeukocyteEndoplasmic reticulum aminopeptidase 2X-Box Binding Protein 1Molecular biologySettore MED/16 - Reumatologia030104 developmental biologyUnfolded protein responsebiology.proteinCCAAT-Enhancer-Binding ProteinsLeukocytes MononuclearUnfolded Protein ResponseRNAArthritisrheumatology (Hoboken, N.J.)
researchProduct

Nonacidic Farnesoid X Receptor Modulators.

2017

As a cellular bile acid sensor, farnesoid X receptor (FXR) participates in regulation of bile acid, lipid and glucose homeostasis, and liver protection. Clinical results have validated FXR as therapeutic target in hepatic and metabolic diseases. To date, potent FXR agonists share a negatively ionizable function that might compromise their pharmacokinetic distribution and behavior. Here we report the development and characterization of a high-affinity FXR modulator not comprising an acidic residue.

0301 basic medicineMalemedicine.drug_classPyridinesPeroxisome proliferator-activated receptorReceptors Cytoplasmic and NuclearATP-binding cassette transporterCholesterol 7 alpha-hydroxylase01 natural sciencesRats Sprague-Dawley03 medical and health sciencesStructure-Activity RelationshipDrug StabilityDrug DiscoverymedicineGlucose homeostasisAnimalsHumansPPAR alphaReceptorCholesterol 7-alpha-HydroxylaseATP Binding Cassette Transporter Subfamily B Member 11chemistry.chemical_classificationBile acid010405 organic chemistryChemistryHEK 293 cellsImidazolesMembrane Transport ProteinsHep G2 Cells0104 chemical sciencesMolecular Docking SimulationZolpidem030104 developmental biologyHEK293 CellsBiochemistryMolecular MedicineFarnesoid X receptorATP-Binding Cassette TransportersSterol Regulatory Element Binding Protein 1HeLa CellsJournal of medicinal chemistry
researchProduct

Dietary protein restriction reduces circulating VLDL triglyceride levels via CREBH-APOA5-dependent and -independent mechanisms

2018

Hypertriglyceridemia is an independent risk factor for cardiovascular disease. Dietary interventions based on protein restriction (PR) reduce circulating triglycerides (TGs), but underlying mechanisms and clinical relevance remain unclear. Here, we show that 1 week of a protein-free diet without enforced calorie restriction significantly lowered circulating TGs in both lean and diet-induced obese mice. Mechanistically, the TG-lowering effect of PR was due, in part, to changes in very low-density lipoprotein (VLDL) metabolism both in liver and peripheral tissues. In the periphery, PR stimulated VLDL-TG consumption by increasing VLDL-bound APOA5 expression and promoting VLDL-TG hydrolysis and…

0301 basic medicineMalemedicine.medical_specialtyVery low-density lipoproteinDietary proteinFGF21Calorie restrictionmTORC1Lipoproteins VLDLMechanistic Target of Rapamycin Complex 1Protein Serine-Threonine Kinases03 medical and health sciencesMice0302 clinical medicineRisk FactorsInternal medicinemedicineDiet Protein-RestrictedIntegrated stress responseAnimalsHumansCyclic AMP Response Element-Binding ProteinTriglyceridesRandomized Controlled Trials as TopicHypertriglyceridemiaChemistryHydrolysisHypertriglyceridemianutritional and metabolic diseasesGeneral Medicinemedicine.diseaseLipid Metabolism030104 developmental biologyEndocrinologyApolipoproteinsHypotriglyceridemiaLiverApolipoprotein A-Vlipids (amino acids peptides and proteins)Female030217 neurology & neurosurgeryLipoproteinResearch Article
researchProduct

EGFL7 enhances surface expression of integrin α5β1 to promote angiogenesis in malignant brain tumors

2018

Abstract Glioblastoma (GBM) is a typically lethal type of brain tumor with a median survival of 15 months postdiagnosis. This negative prognosis prompted the exploration of alternative treatment options. In particular, the reliance of GBM on angiogenesis triggered the development of anti‐VEGF (vascular endothelial growth factor) blocking antibodies such as bevacizumab. Although its application in human GBM only increased progression‐free periods but did not improve overall survival, physicians and researchers still utilize this treatment option due to the lack of adequate alternatives. In an attempt to improve the efficacy of anti‐VEGF treatment, we explored the role of the egfl7 gene in ma…

0301 basic medicineMedicine (General)Vascular Biology & AngiogenesisAngiogenesisEndothelial Growth FactorsQH426-470chemistry.chemical_compoundangiogenesisMice0302 clinical medicineAntineoplastic Agents ImmunologicalResearch ArticlesCancerNeovascularization PathologicBrain NeoplasmsEndothelial stem cellVascular endothelial growth factormedicine.anatomical_structureTreatment Outcome030220 oncology & carcinogenesisendothelial cellMolecular MedicineHeterograftsEGFL7PericyteEGFL7medicine.drugResearch ArticleIntegrin alpha5beta1EGF Family of ProteinsintegrinBrain tumor03 medical and health sciencesR5-920GliomamedicineGeneticsHuman Umbilical Vein Endothelial CellsAnimalsHumansddc:610Cell ProliferationTemozolomidebusiness.industryCalcium-Binding ProteinsglioblastomaEndothelial Cellsmedicine.diseaseSurvival AnalysisDisease Models Animal030104 developmental biologychemistryCancer researchbusinessNeoplasm TransplantationNeuroscienceEMBO Molecular Medicine
researchProduct

Apoptotic Activity of MeCP2 Is Enhanced by C-Terminal Truncating Mutations.

2016

Methyl-CpG binding protein 2 (MeCP2) is a widely abundant, multifunctional protein most highly expressed in post-mitotic neurons. Mutations causing Rett syndrome and related neurodevelopmental disorders have been identified along the entire MECP2 locus, but symptoms vary depending on mutation type and location. C-terminal mutations are prevalent, but little is known about the function of the MeCP2 C-terminus. We employ the genetic efficiency of Drosophila to provide evidence that expression of p.Arg294* (more commonly identified as R294X), a human MECP2 E2 mutant allele causing truncation of the C-terminal domains, promotes apoptosis of identified neurons in vivo. We confirm this novel find…

0301 basic medicineMethyl-CpG-Binding Protein 2lcsh:MedicineApoptosisBiochemistryPhosphoserine0302 clinical medicineAnimal CellsDrosophila ProteinsPost-Translational ModificationPhosphorylationlcsh:ScienceNeuronsMotor NeuronsGeneticsMultidisciplinaryCell DeathbiologyDrosophila MelanogasterAnimal ModelsInsectsFOXG1Cell ProcessesCaspasesPhosphorylationDrosophilaBiological CulturesCellular TypesDrosophila melanogasterResearch ArticleGene isoformcongenital hereditary and neonatal diseases and abnormalitiesArthropodaProtein domainMouse ModelsMotor ActivityResearch and Analysis MethodsTransfectionModels BiologicalMECP203 medical and health sciencesModel OrganismsProtein Domainsmental disordersAnimalsHumansMolecular Biology TechniquesImmunohistochemistry TechniquesMolecular BiologyTranscription factorBinding proteinlcsh:ROrganismsBiology and Life SciencesProteinsCell BiologyCell Culturesbiology.organism_classificationInvertebratesHistochemistry and Cytochemistry TechniquesHEK293 Cells030104 developmental biologyCellular NeuroscienceMutationImmunologic TechniquesMutant Proteinslcsh:Q030217 neurology & neurosurgeryNeuroscienceTranscription FactorsPLoS ONE
researchProduct

Staphylococcal cassette chromosome mec typing and mecA sequencing in methicillin-resistant staphylococci from Algeria: a highly diversified element w…

2016

Genetic mechanisms of methicillin resistance are still relevant in staphylococci. The aims of this study are to assess the possible exchanges of staphylococcal cassette chromosome mec (SCCmec) among isolates of methicillin-resistant staphylococci (MRS) and to check for known or new mutations in mecA DNA. A total of 35 MRS non-repetitive isolates were recovered, including 20 Staphylococcus haemolyticus, 7 Staphylococcus aureus, 4 Staphylococcus sciuri, 2 Staphylococcus saprophyticus and 1 isolate each of Staphylococcus xylosus and Staphylococcus lentus. Only 16 of the 35 strains were assigned to known SCCmec types: 7 SCCmec VII, 6 SCCmec IV and 3 SCCmec III, with possible horizontal transfer…

0301 basic medicineMicrobiology (medical)Methicillin-Resistant Staphylococcus aureusSettore MED/07 - Microbiologia E Microbiologia ClinicaStaphylococcus030106 microbiologyMicrobial Sensitivity TestsBiologymedicine.disease_causebeta-LactamsMicrobiologyBacterial geneticsMicrobiology03 medical and health sciencesBacterial ProteinsmedicineMissense mutationHumansPenicillin-Binding ProteinsTypingmecAGeneticsMutationSCCmecChromosomeGeneral Medicinerespiratory systembiochemical phenomena metabolism and nutritionChromosomes BacterialStaphylococcal Infectionsbacterial infections and mycosesStaphylococcus aureusStaphylococcus aureus; Methicillin Resistance; mecAAlgeriaHorizontal gene transferMutationStaphylococcus aureuMethicillin ResistanceJournal of medical microbiology
researchProduct

Mitochondria during sea urchin oogenesis.

2017

SummarySea urchin represents an ideal model for studies on fertilization and early development, but the achievement of egg competence and mitochondrial behaviour during oogenesis remain to be enlightened. Oocytes of echinoid, such as sea urchin, unlike other echinoderms and other systems, complete meiotic maturation before fertilization. Mitochondria, the powerhouse of eukaryotic cells, contain a multi-copy of the maternally inherited genome, and are involved directly at several levels in the reproductive processes, as their functional status influences the quality of oocytes and contributes to fertilization and embryogenesis. In the present paper, we report our latest data on mitochondrial…

0301 basic medicineMitochondrial DNAEmbryo NonmammalianMitoTrackerHsp56MitochondrionOogenesisDNA MitochondrialParacentrotus lividusOxidative PhosphorylationTacrolimus Binding Proteins03 medical and health sciencesOogenesisMeiosisbiology.animalPicoGreenAnimalsConfocal laser scanning microscopySettore BIO/06 - Anatomia Comparata E CitologiaSea urchinGerminal vesiclebiologymtDNAAnatomyCell Biologybiology.organism_classificationCell biologyMitochondria030104 developmental biologySea UrchinsOocytesFemaleDevelopmental biologyDevelopmental BiologyZygote (Cambridge, England)
researchProduct

rbFOX1/MBNL1 competition for CCUG RNA repeats binding contributes to myotonic dystrophy type 1/type 2 differences

2018

Myotonic dystrophy type 1 and type 2 (DM1, DM2) are caused by expansions of CTG and CCTG repeats, respectively. RNAs containing expanded CUG or CCUG repeats interfere with the metabolism of other RNAs through titration of the Muscleblind-like (MBNL) RNA binding proteins. DM2 follows a more favorable clinical course than DM1, suggesting that specific modifiers may modulate DM severity. Here, we report that the rbFOX1 RNA binding protein binds to expanded CCUG RNA repeats, but not to expanded CUG RNA repeats. Interestingly, rbFOX1 competes with MBNL1 for binding to CCUG expanded repeats and overexpression of rbFOX1 partly releases MBNL1 from sequestration within CCUG RNA foci in DM2 muscle ce…

0301 basic medicineModels MolecularProtein Conformation alpha-Helical[SDV]Life Sciences [q-bio]General Physics and AstronomyGene ExpressionRNA-binding proteinCrystallography X-Raychemistry.chemical_compoundMOLECULAR-BASISGene expressionMBNL1Myotonic DystrophyComputingMilieux_MISCELLANEOUSMultidisciplinaryCHLORIDE CHANNELQRNA-Binding ProteinsRecombinant Proteins3. Good healthCell biologyCONGENITAL HEART-DISEASEDrosophila melanogasterThermodynamicsSKELETAL-MUSCLERNA Splicing FactorsCUG REPEATSProtein BindingRNA Splicing Factorsmusculoskeletal diseasesSTEADY-STATEcongenital hereditary and neonatal diseases and abnormalitiesScienceRBFOX1BiologyMyotonic dystrophyBinding CompetitiveGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesmedicineEscherichia coliAnimalsHumansProtein Interaction Domains and MotifsBinding siteNucleotide MotifsMuscle SkeletalSPLICING REGULATOR RBFOX2MUSCLEBLIND PROTEINSBinding SitesPRE-MESSENGER-RNARNAGeneral Chemistrymedicine.diseaseDisease Models AnimalKinetics030104 developmental biologychemistryTRIPLET REPEATRNAProtein Conformation beta-Strand3111 Biomedicine
researchProduct