Search results for "Rap1"

showing 8 items of 8 documents

Evaluation Of Massive Parallel Sequencing As A Diagnostic Tool For Familial Hypercholesterolemia

2015

Abstract Familial hypercholesterolemia (FH) is one of the most common single gene disorders, which is mostly inherited as an autosomal dominant trait. The physical signs of FH are elevated low density lipoprotein cholesterol (LDL-C), elevated total cholesterol (TC) levels and tendon xantomas. Identification and early treatment of affected individuals is desirable and in lack of physical symptoms DNA-based diagnosis provides confirmation of diagnosis and enables early patient management. The majority of FH cases are caused by mutations in four genes (APOB, LADLR, PCSK9, and LDLRAP1). There are commercial kits available for testing of the 20 most common FH causing mutations, but the spectrum …

Pediatricsmedicine.medical_specialtyldlrApolipoprotein Bldlrap1ScienceLow density lipoprotein cholesterolFamilial hypercholesterolemiachemistry.chemical_compoundngsmedicinepcsk9MultidisciplinaryMassive parallel sequencingfamilial hypercholesterolemiabiologyCholesterolPCSK9QAutosomal dominant traitmedicine.diseasechemistryapobLDL receptorbiology.proteinlipids (amino acids peptides and proteins)Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences.
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Regulatory T cell-derived adenosine induces dendritic cell migration through the Epac-Rap1 pathway.

2014

Abstract Dendritic cells (DC) are one target for immune suppression by regulatory T cells (Treg), because their interaction results in reduced T cell stimulatory capacity and secretion of inhibitory cytokines in DC. We show that DC in the presence of Treg are more mobile as compared with cocultures with conventional CD4+ T cells and form DC–Treg aggregates within 2 h of culture. The migration of DC was specifically directed toward Treg, as Treg, but not CD4+ T cells, attracted DC in Boyden chambers. Treg deficient for the ectonucleotidase CD39 were unable to attract DC. Likewise, addition of antagonists for A2A adenosine receptors abolished the formation of DC–Treg clusters, indicating a ro…

AdenosineRegulatory T cellT cellImmunologyMedizinchemical and pharmacologic phenomenaCell CommunicationBiologyT-Lymphocytes RegulatoryMiceAdenosine TriphosphateAntigens CDCell MovementmedicineImmunology and AllergyAnimalsGuanine Nucleotide Exchange FactorsDendritic cell migrationReceptors Adenosine A2Apyraserap1 GTP-Binding Proteinshemic and immune systemsDendritic CellsActin cytoskeletonAdenosineAdenosine receptorCell biologyActin Cytoskeletonmedicine.anatomical_structureRap1Signal transductionmedicine.drugSignal TransductionJournal of immunology (Baltimore, Md. : 1950)
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Efficacy of Lomitapide in the Treatment of Familial Homozygous Hypercholesterolemia: Results of a Real-World Clinical Experience in Italy

2017

Homozygous familial hypercholesterolaemia (HoFH) is a rare form of inherited dyslipidemia resistant to conventional cholesterol-lowering medications so that lipoprotein apheresis (LA) is usually required. Lomitapide has been approved for the treatment of HoFH. The aim of this study was to evaluate the benefits of lomitapide in HoFH patients followed with the usual clinical care. Homozygous familial hypercholesterolaemia (HoFH) is a rare form of inherited dyslipidemia resistant to conventional cholesterol-lowering medications so that lipoprotein apheresis (LA) is usually required. Lomitapide has been approved for the treatment of HoFH. The aim of this study was to evaluate the benefits of lo…

MaleSettore MED/09 - Medicina InternaHyperlipidemia Familial Combined030204 cardiovascular system & hematologyPharmacologyBenzimidazolecholesterol-lowering effect; clinical practice; genetics; lomitapide; severe hypercholesterolemia; medicine (all); pharmacology (medical)cholesterol-lowering effectchemistry.chemical_compound0302 clinical medicineRetrospective StudieAnticholesteremic Agentgenetics030212 general & internal medicineAged 80 and overAnticholesteremic AgentsHomozygoteGeneral MedicineMiddle Agedclinical practiceSafety profileItalylipids (amino acids peptides and proteins)FemaleHumanAdultmedicine.medical_specialtySocio-culturaleLiver ultrasoundLDLRAP1 geneHyperlipoproteinemia Type II03 medical and health sciencesGeneticInternal medicinemedicineHumansLiver damagemedicine (all)Familial homozygous hypercholesterolemiaAgedRetrospective Studieslomitapidebusiness.industrysevere hypercholesterolemiamedicine.diseaseRheumatologyLomitapidepharmacology (medical)chemistryBenzimidazolesbusinessDyslipidemia
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Disease-associated polymorphisms in ERAP1 do not alter endoplasmic reticulum stress in patients with ankylosing spondylitis

2014

The mechanism by which human leukocyte antigen B27 (HLA-B27) contributes to ankylosing spondylitis (AS) remains unclear. Genetic studies demonstrate that association with and interaction between polymorphisms of endoplasmic reticulum aminopeptidase 1 (ERAP1) and HLA-B27 influence the risk of AS. It has been hypothesised that ERAP1-mediated HLA-B27 misfolding increases endoplasmic reticulum (ER) stress, driving an interleukin (IL) 23-dependent, pro-inflammatory immune response. We tested the hypothesis that AS-risk ERAP1 variants increase ER-stress and concomitant pro-inflammatory cytokine production in HLA-B27(+) but not HLA-B27(-) AS patients or controls. Forty-nine AS cases and 22 healthy…

AdultMaleAnkylosing Spondylitismedicine.medical_treatmentImmunologyInflammationSingle-nucleotide polymorphismDiseaseBiologyERAP1AminopeptidasesPolymorphism Single NucleotideMinor Histocompatibility AntigensYoung AdultGene expressionGeneticsmedicineHumansSpondylitis AnkylosingERAP1 Ankylosing SpondylitisEndoplasmic Reticulum Chaperone BiPSpondylitisHLA-B27 AntigenGenetics (clinical)InflammationAnkylosing spondylitisEndoplasmic reticulumMiddle AgedEndoplasmic Reticulum Stressmedicine.diseaseCytokineImmunologyFemalemedicine.symptomGenes & Immunity
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Binding properties and stability of the Ras-association domain of Rap1-GTP interacting adapter molecule (RIAM).

2012

The Rap1-GTP interacting adapter protein (RIAM) is an important protein in Rap1-mediated integrin activation. By binding to both Rap1 GTPase and talin, RIAM recruits talin to the cell membrane, thus facilitating talin-dependent integrin activation. In this article, we studied the role of the RIAM Ras-association (RA) and pleckstrin-homology (PH) domains in the interaction with Rap1. We found that the RA domain was sufficient for GTP-dependent interaction with Rap1B, and the addition of the PH domain did not change the binding affinity. We also detected GTP-independent interaction of Rap1B with the N-terminus of RIAM. In addition, we found that the PH domain stabilized the RA domain both in …

TalinIntegrinsGTP'lcsh:MedicineGTPaseSignal transductionBiochemistryProtein structureMolecular cell biologyRIAMlcsh:Science0303 health sciencesMultidisciplinarybiologyProtein Stability030302 biochemistry & molecular biologySignal transducing adaptor proteinrap1 GTP-Binding ProteinssitoutuminenCell biologyPleckstrin homology domainRap1Research Articleendocrine systemvuorovaikutusProtein domainIntegrinSignaling in cellular processesPhosphoinositide Signal TransductionSignaling Pathways03 medical and health sciencesCell AdhesionHumansProtein InteractionsBiologyGTPase signaling030304 developmental biologyRas signalingAdaptor Proteins Signal Transducingintegriinitlcsh:RProteinsMembrane ProteinsRegulatory ProteinsProtein Structure TertiaryCytoskeletal Proteinsenzymes and coenzymes (carbohydrates)rap GTP-Binding ProteinsCell movement signalingbiology.proteinta1181lcsh:QPLoS ONE
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Next-generation-sequencing-based identification of familial hypercholesterolemia-related mutations in subjects with increased LDL–C levels in a latvi…

2015

Background Familial hypercholesterolemia (FH) is one of the commonest monogenic disorders, predominantly inherited as an autosomal dominant trait. When untreated, it results in early coronary heart disease. The vast majority of FH remains undiagnosed in Latvia. The identification and early treatment of affected individuals remain a challenge worldwide. Most cases of FH are caused by mutations in one of four genes, APOB, LDLR, PCSK9, or LDLRAP1. The spectrum of disease-causing variants is very diverse and the variation detection panels usually used in its diagnosis cover only a minority of the disease-causing gene variants. However, DNA-based tests may provide an FH diagnosis for FH patients…

MaleNonsynonymous substitutionApolipoprotein BCoronary Artery DiseaseFamilial hypercholesterolemiaDiseaseCohort StudiesPCSK9Genetics(clinical)Family historyGenetics (clinical)Aged 80 and overGeneticseducation.field_of_studybiologySerine EndopeptidasesHigh-Throughput Nucleotide SequencingAutosomal dominant traitMiddle AgedLDLRAP1Apolipoprotein B-100Femalelipids (amino acids peptides and proteins)Proprotein ConvertasesProprotein Convertase 9APOBResearch ArticleAdultPopulationPolymorphism Single NucleotideLDLHyperlipoproteinemia Type IIYoung AdultGeneticsmedicineHumanseducationAdaptor Proteins Signal TransducingAgedDiagnostic toolsPCSK9Cholesterol LDLmedicine.diseaseLatviaGenetics PopulationLDLRReceptors LDLMutationNext-generation sequencingbiology.proteinBMC Medical Genetics
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Reciprocal regulation of human platelet function by endogenous prostanoids and through multiple prostanoid receptors

2014

Platelets are permanently exposed to a variety of prostanoids formed by blood cells or the vessel wall. The two major prostanoids, prostacyclin and thromboxane act through well established pathways mediated by their respective G-protein coupled receptors inhibiting or promoting platelet aggregation accordingly. Yet the role of other prostanoids and prostanoid receptors for platelet function regulation has not been thoroughly investigated. We aimed at a comprehensive analysis of prostanoid effects on platelets, the receptors and pathways involved and functional consequences. We analyzed cAMP formation and phosphorylation of proteins pivotal to platelet function as well as functional platelet…

Blood PlateletsSerotoninmedicine.medical_specialtyPlatelet AggregationProstaglandin E2 receptorReceptors ProstaglandinProstaglandinProstacyclinchemistry.chemical_compoundAdenosine TriphosphateP2Y12Internal medicineCyclic AMPmedicineHumansPlateletPlatelet activationReceptorMitogen-Activated Protein Kinase KinasesPharmacologyChemistryMicrofilament Proteinsrap1 GTP-Binding ProteinsProstanoidrespiratory systemPhosphoproteinsCell biologyAdenosine DiphosphateP-SelectinEndocrinologyProstaglandinscardiovascular systemCalciumlipids (amino acids peptides and proteins)Cell Adhesion Moleculesmedicine.drugEuropean Journal of Pharmacology
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Can you blame cold feet on Epac (and Rap1A)? Focus on “Cyclic AMP-Rap1A signaling activates RhoA to induce α2C-adrenoceptor translocation to the cell…

2012

Intracellular signaling by the second messenger cyclic AMP (cAMP) activates the Ras-related small GTPase Rap1 through the guanine exchange factor Epac. This activation leads to effector protein interactions, activation, and biological responses in the vasculature, including vasorelaxation. In vascular smooth muscle cells derived from human dermal arterioles (microVSM), Rap1 selectively regulates expression of G protein-coupled α2C-adrenoceptors (α2C-ARs) through JNK-c-jun nuclear signaling. The α2C-ARs are generally retained in the trans-Golgi compartment and mobilize to the cell surface and elicit vasoconstriction in response to cellular stress. The present study used human microVSM to exa…

medicine.medical_specialtyRHOAPhysiologyMyocytes Smooth MuscleCellChromosomal translocationSmooth muscleReceptors Adrenergic alpha-2Internal medicineCyclic AMPmedicineAnimalsHumansReceptorbiologyrap1 GTP-Binding ProteinsArticlesCell Biologyα2c adrenoceptorCell biologyProtein Transportmedicine.anatomical_structureEndocrinologybiology.proteinmedicine.symptomrhoA GTP-Binding ProteinVasoconstrictionAmerican Journal of Physiology-Cell Physiology
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