Search results for "GTP-Binding Proteins"

showing 10 items of 117 documents

TBC1D24-TLDc-related epilepsy exercise-induced dystonia: rescue by antioxidants in a disease model

2019

Genetic mutations in TBC1D24 have been associated with multiple phenotypes, with epilepsy being the main clinical manifestation. The TBC1D24 protein consists of the unique association of a Tre2/Bub2/Cdc16 (TBC) domain and a TBC/lysin motif domain/catalytic (TLDc) domain. More than 50 missense and loss-of-function mutations have been described and are spread over the entire protein. Through whole genome/exome sequencing we identified compound heterozygous mutations, R360H and G501R, within the TLDc domain, in an index family with a Rolandic epilepsy exercise-induced dystonia phenotype (http://omim.org/entry/608105). A 20-year long clinical follow-up revealed that epilepsy was self-limited in…

MaleModels Molecular0301 basic medicineProtein ConformationAmino Acid Motifsalpha-TocopherolMutantCrystallography X-RayPHENOTYPECompound heterozygosityAntioxidantsAnimals Genetically ModifiedEpilepsy0302 clinical medicineCatalytic DomainDrosophila ProteinsMissense mutationoxidative stressChildTLDC DOMAINVITAMIN-EExome sequencingSequence DeletionNeuronsDystoniaGeneticsexercise-induced dystoniaTBC1D24GTPase-Activating ProteinsANNOTATIONSEpilepsy RolandicPhenotypeRecombinant ProteinsPedigree3. Good healthRolandic epilepsyDystoniaDrosophila melanogasterChild PreschoolFemaleSettore MED/26 - NeurologiaSynaptic VesiclesDrosophila melanogasterPROTEIN STABILITYLife Sciences & BiomedicineLocomotionAdolescentPhysical ExertionMutation MissenseClinical NeurologyPREDICTIONSBiology03 medical and health sciencesmedicineAnimalsHumansAmino Acid SequenceCOMPARTMENToxidative streScience & TechnologySequence Homology Amino AcidMUTATIONSNeurosciencesInfantBiological TransportDEGRADATIONmedicine.diseasebiology.organism_classificationAcetylcysteineDisease Models AnimalOxidative Stress030104 developmental biologyrab GTP-Binding ProteinsSEIZURESNeurosciences & NeurologyNeurology (clinical)Reactive Oxygen SpeciesSequence Alignment030217 neurology & neurosurgery
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Sulfhydryl G Proteins and Phospholipase A2-Associated G Proteins Are Involved in Adrenergic Signal Transduction in the Rat Pineal Gland

2001

The rat pineal gland with its circadian noradrenaline-regulated melatonin rhythm is an excellent model for studying adrenergic signal transduction with respect to cAMP and cGMP formation. The stimulatory G(s) proteins play a well-established role in this process. In contrast, the potential roles of the inhibitory G(i) proteins, the functionally unclear other G(o) proteins, and a number of G protein subtypes are not known. The present study examines the effects on beta(1)- and beta(1)-plus-alpha(1)-stimulated cAMP and cGMP formation of a number of G protein modulators in rat pinealocyte suspension cultures. The effects of the nitric oxide donor sodium nitroprusside on cGMP were also examined…

MaleNitroprussideArylamine N-AcetyltransferaseG proteinAdrenergicWasp VenomsPhospholipaseBiologyNitric OxidePertussis toxinBenzylisoquinolinesPineal GlandPhospholipases APinealocyteRats Sprague-DawleyPhenylephrineAlkaloidsEndocrinologyPhospholipase A2GTP-Binding ProteinsCyclic AMPAnimalsp-Methoxy-N-methylphenethylamineVirulence Factors BordetellaCyclic GMPSulfhydryl ReagentsIsoproterenolAdrenergic beta-AgonistsRatsReceptors AdrenergicPhospholipases A2Pertussis ToxinBiochemistryEthylmaleimideMastoparanbiology.proteinIntercellular Signaling Peptides and ProteinsAnimal Science and ZoologySignal transductionPeptidesAdrenergic alpha-AgonistsSignal TransductionGeneral and Comparative Endocrinology
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Translational read-through of the RP2 Arg120stop mutation in patient iPSC-derived retinal pigment epithelium cells.

2014

Mutations in the RP2 gene lead to a severe form of X-linked retinitis pigmentosa. RP2 patients frequently present with nonsense mutations and no treatments are currently available to restore RP2 function. In this study, we reprogrammed fibroblasts from an RP2 patient carrying the nonsense mutation c.519C>T (p.R120X) into induced pluripotent stem cells (iPSC), and differentiated these cells into retinal pigment epithelial cells (RPE) to study the mechanisms of disease and test potential therapies. RP2 protein was undetectable in the RP2 R120X patient cells, suggesting a disease mechanism caused by complete lack of RP2 protein. The RP2 patient fibroblasts and iPSC-derived RPE cells showed phe…

MaleNonsense mutationInduced Pluripotent Stem CellsGene ExpressionRetinal Pigment EpitheliumBiologymedicine.disease_causeBioinformaticschemistry.chemical_compoundYoung AdultGTP-Binding ProteinsRetinitis pigmentosaGeneticsmedicineHumansCiliaFibroblastInduced pluripotent stem cellEye ProteinsMolecular BiologyGenetics (clinical)MutationOxadiazolesRetinal pigment epitheliumIntracellular Signaling Peptides and ProteinsMembrane ProteinsRetinalCell DifferentiationEpithelial CellsGeneral MedicineArticlesFibroblastsmedicine.diseaseCellular Reprogramming3. Good healthAtalurenCell biologyProtein Transportmedicine.anatomical_structurePhenotypechemistryProtein BiosynthesisMutationHuman molecular genetics
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Low Prevalence of Celiac Disease among Patients with Functional Gastrointestinal Disorders in Latvia.

2020

Background and Aims: Studies suggest that the prevalence of celiac disease (CD) is increased in individuals with functional gastrointestinal disorders (FGIDs), in particular, irritable bowel syndrome (IBS); however, the evidence is conflicting. We aimed to analyze the prevalence of CD in patients with FGIDs in Latvia.
 Methods: This retrospective study included patients with FGIDs, referred for a gastroenterologist consultation in a secondary gastroenterology practice unit. Patients were divided into three groups – patients only with IBS (IBS group), patients only with functional dyspepsia (FD) (FD group), patients with mixed symptoms IBS and FD (Mixed group). Patient levels of tissue …

Malemedicine.medical_specialtyGastrointestinal DiseasesDiseaseGastroenterologySerologyIrritable Bowel SyndromeGTP-Binding ProteinsInternal medicineBiopsymedicinePrevalenceHumansMixed groupIn patientProtein Glutamine gamma Glutamyltransferase 2Serologic TestsDuodenoscopyIrritable bowel syndromeAutoantibodiesRetrospective StudiesRoutine screeningTransglutaminasesmedicine.diagnostic_testbusiness.industryGastroenterologyRetrospective cohort studyMiddle Agedmedicine.diseaseLatviaImmunoglobulin ACeliac DiseaseFemaleSymptom AssessmentbusinessJournal of gastrointestinal and liver diseases : JGLD
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Rac1 GTPase, a multifunctional player in the regulation of genotoxic stress response

2013

The Ras-related C3 botulinum toxin substrate 1 (Rac1) belongs to the Ras-homologous (Rho) family of small GTPases, which transduce signals from the outside to the inside of a cell. Rac1 becomes activated upon ligand binding of a variety of receptors, including receptor tyrosine kinases and heterotrimeric G-protein-coupled receptors. After GTP loading by guanine exchange factors (GEFs), GTP-bound Rac1 engages numerous effector proteins, thereby eventually regulating cell motility and adhesion, cell cycle progression through G1, mitosis and meiosis, as well as cell death and metastasis.1 Besides, Rac1 adjusts cellular responses to genotoxic agents, such as UV light and alkylating agents, by r…

Malerac1 GTP-Binding Proteintopoisomerase IIAgingRHOADNA repairDNA damagep38 mitogen-activated protein kinasesApoptosisRAC1Editorials: Cell Cycle FeaturesDNA damage responseReceptor tyrosine kinasechemical carcinogenesisHistonesMiceTransforming Growth Factor betaRho GTPasesAnimalsMolecular BiologyTranscription factoranthracyclinesMice KnockoutbiologyKinaseNeuropeptidesConnective Tissue Growth FactorHMG-CoA reductase inhibitors (statins)Cell BiologyFibrosisgenotoxic stressActinsrac GTP-Binding ProteinsCell biologyOxidative Stressnormal tissue damageGene Expression RegulationLiverBiochemistryDoxorubicinGamma Raysbiology.proteinFemaleDNA DamageMutagensSignal TransductionDevelopmental BiologyCell Cycle
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Deficient p27 Phosphorylation at Serine 10 Increases Macrophage Foam Cell Formation and Aggravates Atherosclerosis Through a Proliferation-Independen…

2011

OBJECTIVE: Genetic ablation of the growth suppressor p27(Kip1) (p27) in the mouse aggravates atherosclerosis coinciding with enhanced arterial cell proliferation. However, it is unknown whether molecular mechanisms that limit p27's protective function contribute to atherosclerosis development and whether p27 exerts proliferation-independent activities in the arterial wall. This study aims to provide insight into both questions by investigating the role in atherosclerosis of p27 phosphorylation at serine 10 (p27-phospho-Ser10), a major posttranslational modification of this protein. METHODS AND RESULTS: Immunoblotting studies revealed a marked reduction in p27-phospho-Ser10 in atheroscleroti…

Malerho GTP-Binding ProteinsRHOAMoesinMiceApolipoproteins ERadixinSerinemedicineAnimalsHumansProtein phosphorylationPhosphorylationProtein kinase ACell ProliferationFoam cellMice Knockoutrho-Associated KinasesbiologyArteriesAtherosclerosismedicine.diseaseCell biologyMice Inbred C57BLDisease Models AnimalAtheromaCase-Control StudiesImmunologyDisease Progressionbiology.proteinPhosphorylationFemalerhoA GTP-Binding ProteinCardiology and Cardiovascular MedicineCyclin-Dependent Kinase Inhibitor p27Foam CellsSignal TransductionArteriosclerosis, Thrombosis, and Vascular Biology
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Itraconazole inhibits nuclear delivery of extracellular vesicle cargo by disrupting the entry of late endosomes into the nucleoplasmic reticulum

2021

ABSTRACT Extracellular vesicles (EVs) are mediators of intercellular communication under both healthy and pathological conditions, including the induction of pro‐metastatic traits, but it is not yet known how and where functional cargoes of EVs are delivered to their targets in host cell compartments. We have described that after endocytosis, EVs reach Rab7+ late endosomes and a fraction of these enter the nucleoplasmic reticulum and transport EV biomaterials to the host cell nucleoplasm. Their entry therein and docking to outer nuclear membrane occur through a tripartite complex formed by the proteins VAP‐A, ORP3 and Rab7 (VOR complex). Here, we report that the antifungal compound itracona…

Models MolecularHistologyAntifungal AgentsEndosomeNuclear EnvelopeNucleoplasmic reticulumActive Transport Cell NucleusVesicular Transport ProteinsHost cell nucleoplasmEndosomesEndocytosisFatty Acid-Binding ProteinsExosomeCell LineExtracellular VesiclesCell MovementSettore BIO/13 - Biologia ApplicataHumanscancerexosomemetastasisendosomeResearch ArticlesCholestenonesmicro‐vesicleQH573-671Chemistryrab7 GTP-Binding ProteinsCell BiologyExtracellular vesicleSaponinsEndocytosisCell biologyKetoconazoleCancer cellintercellular communicationnucleoplasmic reticulumcancer endosome exosome intercellular communication metastasis micro-vesicle nucleoplasmicreticulumItraconazoleCytologyIntracellularResearch ArticleJournal of Extracellular Vesicles
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MyRIP, a novel Rab effector, enables myosin VIIa recruitment to retinal melanosomes

2002

Defects of the myosin VIIa motor protein cause deafness and retinal anomalies in humans and mice. We report on the identification of a novel myosin-VIIa-interacting protein that we have named MyRIP (myosin-VIIa- and Rab-interacting protein), since it also binds to Rab27A in a GTP-dependent manner. In the retinal pigment epithelium cells, MyRIP, myosin VIIa and Rab27A are associated with melanosomes. In transfected PC12 cells, overexpression of MyRIP was shown to interfere with the myosin VIIa tail localization. We propose that a molecular complex composed of Rab27A, MyRIP and myosin VIIa bridges retinal melanosomes to the actin cytoskeleton and thereby mediates the local trafficking of thes…

Molecular Sequence Datamacromolecular substancesMyosinsBiologyBiochemistryRetinarab27 GTP-Binding ProteinsMotor proteinMicechemistry.chemical_compoundTwo-Hybrid System Techniquesotorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansAmino Acid SequenceRAB27Molecular BiologyGene LibraryMelanosomesRetinal pigment epitheliumScientific ReportsDyneinsRetinalActin cytoskeletonCell biologymedicine.anatomical_structurechemistryOrgan Specificityrab GTP-Binding ProteinsMelanosome transportMyosin VIIaMelanophilinsense organsRabSequence Alignmentcirculatory and respiratory physiologyEMBO reports
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CXCR3-ligand-mediated skin inflammation in cutaneous lichenoid graft-versus-host disease.

2007

Background Lichenoid graft-versus-host disease (liGVHD) histologically shares several common features with other lichenoid dermatoses, such as cutaneous lupus erythematosus and lichen planus (LP), which collectively show a junctional infiltrate of cytotoxic lymphocytes with liquefaction of the basal layer ("interface dermatitis"). Because recent studies have shown a role for type I interferon (IFN)–associated inflammation, including lymphocyte recruitment via CXCR3 ligand interaction in cutaneous lupus erythematosus and LP, we hypothesized that similar mechanisms might also be involved in liGVHD. Methods Ten representative lesional skin biopsies taken from patients with different subsets of…

Myxovirus Resistance ProteinsChemokinePathologymedicine.medical_specialtyLichenoid EruptionsReceptors CXCR3CD3T-LymphocytesGraft vs Host DiseaseInflammationDermatitisDermatologyIn situ hybridizationCXCR3LigandsChemokine CXCL9Skin DiseasesGTP-Binding ProteinsMedicineCXCL10HumansLymphocytesRNA MessengerIn Situ Hybridizationbiologybusiness.industryLichen PlanusInterferon-alphaChemokine CXCL10stomatognathic diseasesImmunologyChronic DiseaseInterferon Type Ibiology.proteinCXCL9Immunohistochemistrymedicine.symptomEpidermisbusinessJournal of the American Academy of Dermatology
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Interferon-alpha inhibits hepatitis C virus subgenomic RNA replication by an MxA-independent pathway.

2001

Hepatitis C virus (HCV) persists in the majority of infected individuals and is a major cause of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma. Chronic hepatitis C is currently treated with interferon (IFN)-α or with a combination of IFN-α and ribavirin. The availability of an HCV replicon system (Lohmann et al., Science 285, 110–113, 1999) allowed the investigation of the effects of IFN on genuine HCV replication in cultured cells. It is shown here that IFN-α inhibits subgenomic HCV RNA replication in HuH-7 human hepatoma cells. Immunofluorescence, Western blot and Northern blot analysis revealed that levels of both HCV protein and replicon RNA were reduced after treatme…

Myxovirus Resistance ProteinsHepatitis C virusHepacivirusBiologyViral Nonstructural Proteinsmedicine.disease_causeAntiviral Agentschemistry.chemical_compoundInterferonGTP-Binding ProteinsVirologymedicineTumor Cells CulturedHumansRepliconNorthern blotSubgenomic mRNADose-Response Relationship DrugRibavirinvirus diseasesRNAInterferon-alphaProteinsVirologyMolecular biologydigestive system diseasesNS2-3 proteasechemistryRNA ViralRepliconmedicine.drugThe Journal of general virology
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