Search results for "R2"

showing 10 items of 285 documents

WNT Signaling Perturbations Underlie the Genetic Heterogeneity of Robinow Syndrome

2018

International audience; Locus heterogeneity characterizes a variety of skeletal dysplasias often due to interacting or overlapping signaling pathways. Robinow syndrome is a skeletal disorder historically refractory to molecular diagnosis, potentially stemming from substantial genetic heterogeneity. All current known pathogenic variants reside in genes within the noncanonical Wnt signaling pathway including ROR2, WNT5A, and more recently, DVL1 and DVL3. However, ∼70% of autosomal-dominant Robinow syndrome cases remain molecularly unsolved. To investigate this missing heritability, we recruited 21 families with at least one family member clinically diagnosed with Robinow or Robinow-like pheno…

Male0301 basic medicineCandidate geneFrizzledGROWTH-PLATEDEP DOMAINlnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]PROTEINskeletal dysplasiaCraniofacial Abnormalities0302 clinical medicineLocus heterogeneityChromosome SegregationChild[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsWnt Signaling PathwayGenetics (clinical)Genes DominantGeneticsWnt signaling pathwayMiddle AgedRobinow syndromeMENDELIAN-INHERITANCEPhenotypeChild PreschoolFemaleNEURAL-TUBE DEFECTSVERTEBRATE GASTRULATIONhuman embryonic developmentRare cancers Radboud Institute for Health Sciences [Radboudumc 9]AdultAdolescentCELL POLARITYLimb Deformities CongenitalMutation MissenseDwarfismBiologyArticledual molecular diagnosisDiagnosis DifferentialGenetic Heterogeneity03 medical and health sciencesFrizzledAll institutes and research themes of the Radboud University Medical CenterSkeletal disorderGeneticsmedicineHumansGenetic Association StudiesNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Base SequenceGenetic heterogeneityMUTATIONSROR2medicine.diseaseDROSOPHILA TISSUE POLARITY030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsUrogenital AbnormalitiesAUTOSOMAL-DOMINANT030217 neurology & neurosurgery
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Systemic blockade of ACVR2B ligands attenuates muscle wasting in ischemic heart failure without compromising cardiac function

2020

Signaling through activin receptors regulates skeletal muscle mass and activin receptor 2B (ACVR2B) ligands are also suggested to participate in myocardial infarction (MI) pathology in the heart. In this study, we determined the effect of systemic blockade of ACVR2B ligands on cardiac function in experimental MI, and defined its efficacy to revert muscle wasting in ischemic heart failure (HF). Mice were treated with soluble ACVR2B decoy receptor (ACVR2B-Fc) to study its effect on post-MI cardiac remodeling and on later HF. Cardiac function was determined with echocardiography, and myocardium analyzed with histological and biochemical methods for hypertrophy and fibrosis. Pharmacological blo…

Male0301 basic medicineCardiac function curvemedicine.medical_specialtyActivin Receptors Type IIMyocardial IschemiaMyostatinBiochemistryMuscle hypertrophyMice03 medical and health sciences0302 clinical medicineInternal medicineGeneticsmedicineAnimalsMyocyteMyocardial infarctionMolecular BiologyVentricular Remodelingbiologybusiness.industrySkeletal muscleHeartmedicine.disease3. Good healthBlockadeMice Inbred C57BLDisease Models AnimalMuscular Atrophy030104 developmental biologymedicine.anatomical_structureCardiologybiology.proteinbusiness030217 neurology & neurosurgeryACVR2BSignal TransductionTranscription FactorsBiotechnologyThe FASEB Journal
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CD73 Overexpression in Podocytes: A Novel Marker of Podocyte Injury in Human Kidney Disease

2021

The CD73 pathway is an important anti-inflammatory mechanism in various disease settings. Observations in mouse models suggested that CD73 might have a protective role in kidney damage

Male0301 basic medicinePathologyCCR2podocyte030232 urology & nephrologyGene ExpressionKidneyPodocyte0302 clinical medicineFocal segmental glomerulosclerosisMedicineMinimal change diseaseBiology (General)5'-NucleotidaseSpectroscopyAged 80 and overKidneymedicine.diagnostic_testPodocytesGlomerulonephritisGeneral MedicineMiddle AgedComputer Science ApplicationsChemistryProteinuriaminimal change diseasemedicine.anatomical_structureImmunohistochemistryFemaleKidney DiseasesAdultmedicine.medical_specialtyQH301-705.5Receptors CCR2GPI-Linked ProteinsImmunofluorescenceArticleCatalysisInorganic Chemistry03 medical and health sciencesHumansPhysical and Theoretical ChemistryQD1-999Molecular BiologyAgedbusiness.industryOrganic Chemistrymedicine.disease030104 developmental biologyGene Expression RegulationCD73CCR2businessBiomarkersInternational Journal of Molecular Sciences
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Skraban‐Deardorff syndrome: Six new cases of WDR 26 ‐related disease and expansion of the clinical phenotype

2021

International audience; Skraban-Deardorff syndrome (a disease related to variations in the WDR26 gene; OMIM #617616) was first described in a cohort of 15 individuals in 2017. The syndrome comprises intellectual deficiency, severe speech impairment, ataxic gait, seizures, mild hypotonia with feeding difficulties during infancy, and dysmorphic features. Here, we report on six novel heterozygous de novo pathogenic variants in WDR26 in six probands. The patients’ phenotypes were consistent with original publication. One patient displayed marked hypotonia with an abnormal muscle biopsy; this finding warrants further investigation. Gait must be closely monitored, in order to highlight any muscul…

Male0301 basic medicineProbandPediatricsmedicine.medical_specialtyAdolescent[SDV]Life Sciences [q-bio]Developmental DisabilitiesSkraban-Deardorff syndromeDisease030105 genetics & heredityYoung Adult03 medical and health sciencesIntellectual disabilityGeneticsmedicineWDR26HumansAbnormalities MultiplehypotoniaAtaxic GaitChildGenetics (clinical)Adaptor Proteins Signal Transducing[SDV.GEN]Life Sciences [q-bio]/GeneticsMuscle biopsymedicine.diagnostic_testbusiness.industryInfantSyndromemedicine.diseaseGaitHypotonia3. Good health[SDV] Life Sciences [q-bio]Phenotype030104 developmental biologyspeech therapyintellectual disabilityChild PreschoolMutationCohortlanguage development disordersFemalemedicine.symptombusinessClinical Genetics
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Systemic blockade of ACVR2B ligands protects myocardium from acute ischemia-reperfusion injury

2019

Activin A and myostatin, members of the transforming growth factor (TGF)-β superfamily of secreted factors, are potent negative regulators of muscle growth, but their contribution to myocardial ischemia-reperfusion (IR) injury is not known. The aim of this study was to investigate if activin 2B (ACVR2B) receptor ligands contribute to myocardial IR injury. Mice were treated with soluble ACVR2B decoy receptor (ACVR2B-Fc) and subjected to myocardial ischemia followed by reperfusion for 6 or 24 h. Systemic blockade of ACVR2B ligands by ACVR2B-Fc was protective against cardiac IR injury, as evidenced by reduced infarcted area, apoptosis, and autophagy and better preserved LV systolic function fo…

MaleActivin Receptors Type IIiskemialihaksetSmad2 ProteinMyostatinPharmacologyMice0302 clinical medicineDrug DiscoverykasvutekijätMyocytes CardiacCardioprotection0303 health sciences318 Medical biotechnologybiologysydänactivins1184 Genetics developmental biology physiologyII RECEPTORS3. Good health030220 oncology & carcinogenesisMolecular MedicineOriginal ArticleSignal TransductionCardiac function curvegrowth differentiation factorsProgrammed cell deathBLOCKINGischemia-reperfusion injuryIschemiaMyocardial Reperfusion InjuryMASSta311103 medical and health sciencesMYOSTATIN-KNOCKOUTCARDIOPROTECTIONGeneticsmedicineAnimalsMolecular Biologylihassolut030304 developmental biologyPharmacologySKELETAL-MUSCLE GROWTHbusiness.industryMyocardiumFOLLISTATINMyostatinmedicine.diseaseACVR2BMice Inbred C57BLACTIVIN-AGDF11GDF11biology.protein3111 BiomedicineproteiinitbusinessReperfusion injuryDIFFERENTIATION FACTOR 11ACVR2BTranscription Factors
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Combination of KIR 2DL2 and HLA-C1 (Asn 80) confers susceptibility to type 1 diabetes in Latvians.

2008

Summary Killer immunoglobulin-like receptors (KIRs) are known to modulate natural killer (NK) and NK T-cell function by interacting with human leucocyte antigen (HLA) class I ligands on target cells. The aim of our study was to investigate the influence of KIR2D genes with their HLA-C ligands in susceptibility to type 1 diabetes. A total of 98 type 1 diabetes patients and 70 healthy subjects from Latvia were typed for KIR genes and HLA-C ligands using polymerase chain reaction-based genotyping. The HLA C1+/C2+ combination was positively, and C1–/C2+ combination was negatively, associated with type 1 diabetes. Stratification analysis of KIR/HLA-C ligand combinations showed 2DL2+/C1+, 2DL3+/C…

MaleAdolescentGenotypeImmunologyHuman leukocyte antigenHLA-C AntigensBiologyWhite Peoplelaw.inventionImmune systemGene FrequencylawGeneticsmedicineHumansGenetic Predisposition to DiseaseReceptorChildMolecular BiologyGenotypingGeneGenetics (clinical)Polymerase chain reactionType 1 diabetesInfant NewbornInfantGeneral Medicinemedicine.diseaseLatviaDiabetes Mellitus Type 1Child PreschoolReceptors KIR2DL2ImmunologyFemaleFunction (biology)International journal of immunogenetics
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HLA association is different in children and adults with severe acquired aplastic anemia

2007

Background Severe aplastic anemia (SAA) is defined as pancytopenia caused by bone marrow failure. The pathogenesis of SAA is thought to involve autoimmune processes. Increased susceptibility to autoimmunity has been shown to be associated with several different HLA alleles. In SAA, few large studies based on data mainly from adults describe a positive HLA correlation with HLA-DR2 (DRB1*15) and HLA-B14. Procedure This study explored the HLA constitution of 181 children with SAA who were enrolled in the prospective multi-center study SAA94 between January 1994 and January 2002. The control group consisted of 303 healthy individuals of comparable demographic background. Allelic frequencies bet…

MaleAdolescentHuman leukocyte antigenmedicine.disease_causeAutoimmunityPathogenesisHLA-B14 AntigenHLA Antigenshemic and lymphatic diseasesmedicineHumansHLA-DR2 AntigenProspective StudiesChildAllelesbusiness.industryBone marrow failureAnemia AplasticInfantHematologymedicine.diseasePancytopeniaPathophysiologyExact testOncologyHLA-B AntigensChild PreschoolPediatrics Perinatology and Child HealthImmunologyCohortFemalebusinessPediatric Blood & Cancer
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Trastuzumab therapy vs tetracycline controlled ERBB2 downregulation: influence on tumour development in an ERBB2-dependent mouse tumour model

2008

Trastuzumab (Herceptin) has improved therapy of breast cancer. Only patients overexpressing ERBB2 are treated with trastuzumab, whereas its use in tumours without ERBB2 expression is useless. This led to the concept that the subgroup of trastuzumab-sensitive tumours is ‘ERBB2-dependent', meaning that ERBB2 signalling is indispensable for growth of these tumours. We used a mouse model that allows anhydrotetracycline (ATc)-controlled downregulation of ERBB2 in tumour tissue. ERBB2 mRNA and protein expression were downregulated below detection limit leading to a macroscopically complete tumour remission within 14 days. Tumour remission was accompanied by a strong decrease in proliferation, a m…

MaleCancer ResearchReceptor ErbB-2AKT1AKT2ApoptosisMiceTrastuzumabPKBskin and connective tissue diseasesERBB2Mitogen-Activated Protein Kinase 3biologyERK1/2herceptinAntibodies MonoclonalCytochromes cImmunohistochemistrynude miceGene Expression Regulation NeoplasticOncologyTetracyclinesKi-67Ki-67Femalemedicine.drugmedicine.medical_specialtyBlotting WesternDown-RegulationMice NudeAntineoplastic AgentsProtein Serine-Threonine KinasesAntibodies Monoclonal Humanizedresistance3-Phosphoinositide-Dependent Protein Kinasesbreast cancerDownregulation and upregulationresponse to therapyInternal medicineHER2medicineAnimalsRNA Messengercytochrome c releaseProtein kinase Bneoplasmstumour developmentCell Proliferationhumanised monoclonal antibodyAktCancerMammary Neoplasms ExperimentalTrastuzumabmedicine.diseaseEndocrinologyKi-67 AntigenApoptosisDrug Resistance Neoplasmbiology.proteinCancer researchreceptor tyrosine kinaseTranslational TherapeuticsProto-Oncogene Proteins c-aktBritish Journal of Cancer
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A Pilot Study on Prostate Cancer Risk and Pro-Inflammatory Genotypes: Pathophysiology and Therapeutic Implications

2010

Host genetic factors are crucial risk determinants for many human cancers. In this framework, an interesting model is represented by prostate cancer (PC), which is featured by a complex pathophysiology with a strong genetic component. Multiple genes seem to influence PC risk and several single nucleotide polymorphisms (SNPs) of candidate genes modifying PC susceptibility have been identified. It is noteworthy the potential association of common SNPs in pro-inflammatory genes with PC risk, since chronic inflammation is assumed to play a key role in prostate carcinogenesis. With the aim to identify candidate genes as an experimental basis to develop new strategies for both prevention and trea…

MaleCandidate geneGenotypePilot ProjectsSingle-nucleotide polymorphismBioinformaticsPolymorphism Single NucleotideProstate cancerRisk FactorsDrug DiscoveryGenotypemedicineHumansSNPSettore MED/05 - Patologia ClinicaGeneAgedAged 80 and overInflammationPharmacologySettore MED/04 - Patologia Generalebusiness.industryProstatic NeoplasmsCancerMiddle AgedProstate cancer (PC) inflammation genetics TLR4 TLR2 PTGS2 5-LO SNP.medicine.diseaseImmunologyTLR4Inflammation Mediatorsbusiness
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X-linked primary ciliary dyskinesia due to mutations in the cytoplasmic axonemal dynein assembly factor PIH1D3

2017

By moving essential body fluids and molecules, motile cilia and flagella govern respiratory mucociliary clearance, laterality determination and the transport of gametes and cerebrospinal fluid. Primary ciliary dyskinesia (PCD) is an autosomal recessive disorder frequently caused by non-assembly of dynein arm motors into cilia and flagella axonemes. Before their import into cilia and flagella, multi-subunit axonemal dynein arms are thought to be stabilized and pre-assembled in the cytoplasm through a DNAAF2–DNAAF4–HSP90 complex akin to the HSP90 co-chaperone R2TP complex. Here, we demonstrate that large genomic deletions as well as point mutations involving PIH1D3 are responsible for an X-li…

MaleCytoplasmProtein FoldingAxoneme[SDV]Life Sciences [q-bio][SDV.GEN] Life Sciences [q-bio]/Genetics[SDV.MHEP.PSR]Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractouterGenes X-LinkedChilddefectsPhylogenyZebrafisharmsSequence DeletionvariantsIntracellular Signaling Peptides and ProteinsGenetic Diseases X-LinkedPedigreeMultidisciplinary Sciences[SDV] Life Sciences [q-bio]motilityChild PreschoolMicrotubule ProteinsSperm MotilityScience & Technology - Other TopicsFemaleAdultAdolescentinnerUK10K Rare Groupr2tp complexof-function mutationsArticleMicroscopy Electron TransmissionMD MultidisciplinaryExome SequencingAnimalsHumansPoint MutationCiliaHSP90 Heat-Shock Proteins[SDV.GEN]Life Sciences [q-bio]/GeneticsScience & TechnologyKartagener SyndromeInfant NewbornAxonemal DyneinsDisease Models AnimalHEK293 Cells[SDV.MHEP.PSR] Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractidentifies mutationsproteinApoptosis Regulatory ProteinsSequence AlignmentMolecular ChaperonesNature Communications
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