Search results for "G proteins"

showing 10 items of 992 documents

Genome-wide Trans-ethnic Meta-analysis Identifies Seven Genetic Loci Influencing Erythrocyte Traits and a Role for RBPMS in Erythropoiesis

2017

Genome-wide association studies (GWASs) have identified loci for erythrocyte traits in primarily European ancestry populations. We conducted GWAS meta-analyses of six erythrocyte traits in 71,638 individuals from European, East Asian, and African ancestries using a Bayesian approach to account for heterogeneity in allelic effects and variation in the structure of linkage disequilibrium between ethnicities. We identified seven loci for erythrocyte traits including a locus (RBPMS/GTF2E2) associated with mean corpuscular hemoglobin and mean corpuscular volume. Statistical fine-mapping at this locus pointed to RBPMS at this locus and excluded nearby GTF2E2. Using zebrafish morpholino to evaluat…

0301 basic medicineMaleLinkage disequilibriumAsiaErythrocytesGenome-wide association studyLocus (genetics)RBPMS030105 genetics & heredityBiologyEasternGenomeMedical and Health SciencesArticleLinkage Disequilibrium03 medical and health sciencesGeneticsEthnicityAnimalsHumansErythropoiesisAlleleGenetics (clinical)Loss functionAllelesZebrafishGenetic associationGeneticsGenetics & HeredityAsia EasternHuman GenomeRacial GroupsRNA-Binding ProteinsBioBank Japan ProjectBayes TheoremHematologyBiological SciencesR13. Good healthEurope030104 developmental biologyAfricaFemaleGenome-Wide Association Study
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Levosimendan prevents doxorubicin-induced cardiotoxicity in time- and dose-dependent manner: implications for inotropy.

2019

Abstract Aims Levosimendan (LEVO) a clinically-used inodilator, exerts multifaceted cardioprotective effects. Case-studies indicate protection against doxorubicin (DXR)-induced cardiotoxicity, but this effect remains obscure. We investigated the effect and mechanism of different regimens of levosimendan on sub-chronic and chronic doxorubicin cardiotoxicity. Methods and results Based on preliminary in vivo experiments, rats serving as a sub-chronic model of doxorubicin-cardiotoxicity and were divided into: Control (N/S-0.9%), DXR (18 mg/kg-cumulative), DXR+LEVO (LEVO, 24 μg/kg-cumulative), and DXR+LEVO (acute) (LEVO, 24 μg/kg-bolus) for 14 days. Protein kinase-B (Akt), endothelial nitric oxi…

0301 basic medicineMaleMice 129 StrainTime FactorsHeart DiseasesNitric Oxide Synthase Type IIIPhysiology030204 cardiovascular system & hematologyPharmacology03 medical and health sciences0302 clinical medicineEnosPhysiology (medical)medicineCyclic AMPCyclic GMP-Dependent Protein KinasesAnimalsDoxorubicinMyocytes CardiacCalcium SignalingRats WistarProtein kinase BCyclic GMPCells CulturedSimendanCardioprotectionMice KnockoutCardiotoxicityAntibiotics AntineoplasticbiologyDose-Response Relationship DrugChemistryCalcium-Binding ProteinsMammary Neoplasms ExperimentalCardiovascular AgentsLevosimendanbiology.organism_classificationCyclic AMP-Dependent Protein KinasesMyocardial ContractionCardiotoxicityPhospholambanMice Inbred C57BL030104 developmental biologyDoxorubicinMilrinoneFemaleCardiology and Cardiovascular MedicineProto-Oncogene Proteins c-aktmedicine.drugCardiovascular research
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Mutation-specific pathophysiological mechanisms define different neurodevelopmental disorders associated with SATB1 dysfunction

2021

AbstractWhereas large-scale statistical analyses can robustly identify disease-gene relationships, they do not accurately capture genotype-phenotype correlations or disease mechanisms. We use multiple lines of independent evidence to show that different variant types in a single gene,SATB1, cause clinically overlapping but distinct neurodevelopmental disorders. Clinical evaluation of 42 individuals carryingSATB1variants identified overt genotype-phenotype relationships, associated with different pathophysiological mechanisms, established by functional assays. Missense variants in the CUT1 and CUT2 DNA-binding domains result in stronger chromatin binding, increased transcriptional repression…

0301 basic medicineMaleModels MolecularMISSENSE MUTATIONSCHROMATINTranscription GeneticCellMedizinDiseaseHaploinsufficiencymedicine.disease_cause0302 clinical medicineMissense mutationde novo variantsGenetics (clinical)INTERLEUKIN-2seizuresGenetics0303 health sciencesMutationChromatin bindingneurodevelopmental disordersMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]SATB1Phenotypemedicine.anatomical_structureintellectual disabilityFemaleHaploinsufficiencyteeth abnormalitiesProtein BindingNeuroinformaticsEXPRESSIONGENESMutation MissenseBiologyBINDING PROTEINREGION03 medical and health sciencesSATB1Protein DomainsReportGeneticsmedicineHPO-based analysisHumansGenetic Association StudiesHpo-based Analysis ; Satb1 ; Cell-based Functional Assays ; De Novo Variants ; Intellectual Disability ; Neurodevelopmental Disorders ; Seizures ; Teeth Abnormalities030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Matrix Attachment Region Binding Proteins030104 developmental biologyNeurodevelopmental DisordersMutationNanomedicine Radboud Institute for Molecular Life Sciences [Radboudumc 19]030217 neurology & neurosurgerycell-based functional assays
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Maternal Inheritance of a Recessive RBP4 Defect in Canine Congenital Eye Disease

2018

SUMMARY Maternally skewed transmission of traits has been associated with genomic imprinting and oocyte-derived mRNA. We report canine congenital eye malformations, caused by an amino acid deletion (K12del) near the N terminus of retinol-binding protein (RBP4). The disease is only expressed when both dam and offspring are deletion homozygotes. RBP carries vitamin A (retinol) from hepatic stores to peripheral tissues, including the placenta and developing eye, where it is required to synthesize retinoic acid. Gestational vitamin A deficiency is a known risk factor for ocular birth defects. The K12del mutation disrupts RBP folding in vivo, decreasing its secretion from hepatocytes to serum. T…

0301 basic medicineMaleNon-Mendelian inheritanceProtein Foldingcongenital eye defectEye Diseasesgenetic structuresNATIVE DISULFIDE BONDSMedical PhysiologyRetinoic acidReproductive health and childbirth413 Veterinary scienceMicrophthalmiavitamin Achemistry.chemical_compoundPlasmaA-vitamiini2.1 Biological and endogenous factorsMicrophthalmosPrealbuminCRYSTAL-STRUCTUREAetiologyBase Pairinglcsh:QH301-705.5Sequence DeletionPediatricwhole genome sequencingVITAMIN-A-DEFICIENCYANOPHTHALMIAPenetrancePedigreemedicine.anatomical_structurePhenotypeFemalemedicine.medical_specialtyGenotypeENDOPLASMIC-RETICULUMGenes RecessiveMETABOLISMBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesDogscanine geneticsInternal medicinePlacentaRETINOL-BINDING-PROTEINGeneticsmedicineAnimalsHumansRecessiveMALFORMATIONSBIOCHEMICAL BASISAmino Acid SequenceAlleleEye Disease and Disorders of VisionNutritiongenome-wide association study030102 biochemistry & molecular biologywestern blottingMUTATIONSta1184RBP4maternal inheritancemedicine.diseaseRetinol-Binding ProteinsRetinol binding proteinnuclear magnetic resonance030104 developmental biologyEndocrinologychemistryGeneslcsh:Biology (General)microphthalmiaGenetic LociHela Cells1182 Biochemistry cell and molecular biologyCongenital Structural Anomalies3111 BiomedicineBiochemistry and Cell BiologyDigestive DiseasesGenomic imprintingRetinol-Binding Proteins PlasmaHeLa Cells
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Short-Term Effects of Microglia-Specific Mitochondrial Dysfunction on Amyloidosis in Transgenic Models of Alzheimer's Disease.

2018

Reduction of mitochondrial activity is a subtle and early event in the pathogenesis of Alzheimer’s disease. Mitochondrial damage and consequentially enhanced production of reactive oxygen species is particularly occurring in the vicinity of amyloid plaques. Since all cells are affected by mitochondrial damage, analyses of cell type-specific effects are challenging. To study the impact of mitochondrial alterations on microglial activity in a homogeneous genetic background, we generated bone marrow chimeras of irradiated 46-days-old APP-transgenic mice. For reconstitution, bone marrow from CX3CR1-eGFP mice with mitochondria of either non-obese diabetic or C57BL/6J animals was utilized. Succes…

0301 basic medicineMalePathologymedicine.medical_specialtyMitochondrial DiseasesAmyloidCellGreen Fluorescent ProteinsCX3C Chemokine Receptor 1Mice TransgenicPlaque AmyloidBiologyMitochondrionPathogenesis03 medical and health sciencesAmyloid beta-Protein Precursor0302 clinical medicineAlzheimer DiseaseMice Inbred NODCX3CR1medicinePresenilin-1AnimalsHumansMicrogliaGeneral NeuroscienceAmyloidosisCalcium-Binding ProteinsMicrofilament ProteinsGeneral MedicineAmyloidosismedicine.diseaseMitochondriaMice Inbred C57BLPsychiatry and Mental healthClinical PsychologyDisease Models Animal030104 developmental biologymedicine.anatomical_structureFemaleBone marrowMicrogliaGeriatrics and Gerontology030217 neurology & neurosurgeryJournal of Alzheimer's disease : JAD
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Detection of Missing Proteins Using the PRIDE Database as a Source of Mass Spectrometry Evidence

2016

The current catalogue of the human proteome is not yet complete, as experimental proteomics evidence is still elusive for a group of proteins known as the missing proteins. The Human Proteome Project (HPP) has been successfully using technology and bioinformatic resources to improve the characterization of such challenging proteins. In this manuscript, we propose a pipeline starting with the mining of the PRIDE database to select a group of data sets potentially enriched in missing proteins that are subsequently analyzed for protein identification with a method based on the statistical analysis of proteotypic peptides. Spermatozoa and the HEK293 cell line were found to be a promising source…

0301 basic medicineMaleProteomicsFrontal cortexFuture studiesProteomePlacentaBiologyMass spectrometrycomputer.software_genreTandem mass spectrometryProteomicsBiochemistryArticleRetina03 medical and health sciencesPregnancyTandem Mass SpectrometryMS/MS proteomicsHuman proteome projectHumansDatabases ProteinAortaPRIDE databaseDatabaseC-HPPComputational BiologyGeneral ChemistrySpermatozoaFrontal Lobe030104 developmental biologyHEK293 CellsProteomeProtein identificationFemalemissing proteinscomputerJournal of Proteome Research
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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
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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
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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.)
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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
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