Search results for "Transducin"

showing 9 items of 169 documents

MiR-33a Controls hMSCS Osteoblast Commitment Modulating the Yap/Taz Expression Through EGFR Signaling Regulation

2019

Mesenchymal stromal cells (hMSCs) display a pleiotropic function in bone regeneration. The signaling involved in osteoblast commitment is still not completely understood, and that determines the failure of current therapies being used. In our recent studies, we identified two miRNAs as regulators of hMSCs osteoblast differentiation driving hypoxia signaling and cytoskeletal reorganization. Other signalings involved in this process are epithelial to mesenchymal transition (EMT) and epidermal growth factor receptor (EGFR) signalings through the regulation of Yes-associated protein (YAP)/PDZ-binding motif (TAZ) expression. In the current study, we investigated the role of miR-33a family as a (…

epithelial mesenchymal transitionregenerative medicinePDZ DomainsCell CommunicationArticlemicroRNAmedicineHumansEpidermal growth factor receptorEpithelial–mesenchymal transitionBone regenerationCells CulturedEGFR inhibitorsAdaptor Proteins Signal TransducingOsteoblastsmicroRNAbiologyMesenchymal stem cellComputational BiologyOsteoblastMesenchymal Stem CellsYAP-Signaling ProteinsGeneral MedicinePhenotypeCell biologymicroRNAsErbB Receptorsmedicine.anatomical_structureTranscriptional Coactivator with PDZ-Binding Motif Proteinsmesenchymal stromal cellbiology.proteinTrans-Activatorsmesenchymal stromal cellsEGFR signalingSignal TransductionTranscription FactorsCells
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Light-dependent CK2-mediated phosphorylation of centrins regulates complex formation with visual G-protein.

2008

AbstractCentrins are Ca2+-binding EF-hand proteins. All four known centrin isoforms are expressed in the ciliary apparatus of photoreceptor cells. Cen1p and Cen2p bind to the visual G-protein transducin in a strictly Ca2+-dependent way, which is thought to regulate light driven movements of transducin between photoreceptor cell compartments. These relatively slow motile processes represent a novel paradigm in light adaptation of photoreceptor cells.Here we validated specific phosphorylation as a novel regulator of centrins in photoreceptors. Centrins were differentially phosphorylated during photoreceptor dark adaptation. Inhibitor treatments revealed protein kinase CK2 as the major protein…

genetic structuresLightG proteinVisionChromosomal Proteins Non-HistoneBlotting WesternDark AdaptationBiologySignal transductionMicrotubulesPhotoreceptor cellMass SpectrometryCa2+-binding proteinsSubstrate SpecificityRats Sprague-DawleyMiceHeterotrimeric G proteinmedicineAnimalsCiliaTransducinPhosphorylationProtein kinase ACasein Kinase IIFluorescent Antibody Technique IndirectMicroscopy ImmunoelectronMolecular BiologyCytoskeletonCiliumCalcium-Binding ProteinsCell BiologyCell biologyRatsMice Inbred C57BLmedicine.anatomical_structureCentrinPhosphorylationHeterotrimeric G-proteinCalciumCattleTransducinsense organsMolecular translocationPhotoreceptor Cells VertebrateProtein BindingBiochimica et biophysica acta
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Interaction of glutamic-acid-rich proteins with the cGMP signalling pathway in rod photoreceptors.

1999

The assembly of signalling molecules into macromolecular complexes (transducisomes) provides specificity, sensitivity and speed in intracellular signalling pathways. Rod photoreceptors in the eye contain an unusual set of glutamic-acid-rich proteins (GARPs) of unknown function. GARPs exist as two soluble forms, GARP1 and GARP2, and as a large cytoplasmic domain (GARP' part) of the beta-subunit of the cyclic GMP-gated channel. Here we identify GARPs as multivalent proteins that interact with the key players of cGMP signalling, phosphodiesterase and guanylate cyclase, and with a retina-specific ATP-binding cassette transporter (ABCR), through four, short, repetitive sequences. In electron mic…

genetic structuresPhosphodiesterase InhibitorsMolecular Sequence DataCyclic Nucleotide-Gated Cation ChannelsGlutamic AcidNerve Tissue ProteinsPlasma protein bindingBiologyIn Vitro TechniquesRetinal Rod Photoreceptor CellsAnimalsAmino Acid SequenceTransducinEye ProteinsPeptide sequenceCyclic GMPMultidisciplinaryPhosphoric Diester HydrolasesPhosphodiesteraseProteinsTransporterGlutamic acidRod Cell Outer SegmentRecombinant ProteinsCell biologyBiochemistryCytoplasmGuanylate CyclaseATP-Binding Cassette TransportersCattleTransducinSignal transductionProtein BindingSignal TransductionNature
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Progenitor death drives retinal dysplasia and neuronal degeneration in a mouse model of Atrip-Seckel syndrome

2020

ABSTRACT Seckel syndrome is a type of microcephalic primordial dwarfism (MPD) that is characterized by growth retardation and neurodevelopmental defects, including reports of retinopathy. Mutations in key mediators of the replication stress response, the mutually dependent partners ATR and ATRIP, are among the known causes of Seckel syndrome. However, it remains unclear how their deficiency disrupts the development and function of the central nervous system (CNS). Here, we investigated the cellular and molecular consequences of ATRIP deficiency in different cell populations of the developing murine neural retina. We discovered that conditional inactivation of Atrip in photoreceptor neurons …

lcsh:MedicineMedicine (miscellaneous)315BlindnessMicechemistry.chemical_compoundImmunology and Microbiology (miscellaneous)Cell DeathneurodevelopmentStem CellsNeurodegenerationapoptosisneurodegenerationSyndromeCell biologyDNA-Binding Proteinsdna damage responsemedicine.anatomical_structurePhotoreceptor Cells VertebrateResearch Articlelcsh:RB1-214NeurogenesisNeuroscience (miscellaneous)Embryonic DevelopmentBiologyRetinaGeneral Biochemistry Genetics and Molecular Biologylcsh:PathologymedicineAnimalsAbnormalities MultipleProgenitor cellVision OcularAdaptor Proteins Signal TransducingCell ProliferationProgenitorRetinalcsh:RRetinalEmbryo Mammalianmedicine.diseasephotoreceptorDisease Models AnimalSeckel syndromechemistryvisual system developmentNerve DegenerationRetinal dysplasiaRetinal DysplasiaTumor Suppressor Protein p53Primordial dwarfismDNA DamageDisease Models & Mechanisms
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Inhibition of Delta-like 4 mediated signaling induces abortion in mice due to deregulation of decidual angiogenesis.

2013

Objective: To explore whether the Dll4/Notch1 pathway plays a key role in regulating the vascular endothelial growth factor (VEGF)/VEGF receptor 2 (VEGFR2) driven decidual angiogenesis and related pregnancy through induction of a tip/stalk phenotype. Methods: Progesterone-replaced ovariectomized pregnant mice received a single injection of YW152F (Dll4 blocking antibody, BAb) or placebo at embryonic day (E) 4.5. Animals were sacrificed at different time points; blood and uterus were collected for further analysis. Number of embryos and implantation site, uteri weight, and serum progesterone levels were assessed. Alterations in the tip/stalk phenotype were determined by quantitative immunofl…

medicine.medical_specialtyAngiogenesisNotch pathwayNotch signaling pathwayUterusEmbryonic DevelopmentNeovascularization PhysiologicApoptosisGestational AgeDll4BiologyPregnancy disruptionAndrologychemistry.chemical_compoundMicePregnancyInternal medicinemedicineDeciduaAnimalsAntibodies BlockingAdaptor Proteins Signal TransducingCell ProliferationCell growthDeciduaCalcium-Binding ProteinsIntracellular Signaling Peptides and ProteinsObstetrics and GynecologyMembrane ProteinsEmbryoVEGFVascular Endothelial Growth Factor Receptor-2Vascular endothelial growth factorDisease Models Animalmedicine.anatomical_structureEndocrinologyReproductive MedicinechemistryApoptosiscardiovascular systemEmbryo LossFemaleAngiogenesisDevelopmental BiologySignal TransductionPlacenta
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Microarray-based mutation analysis of 183 Spanish families with Usher syndrome.

2010

PURPOSE. The purpose of this study was to test the ability of the genotyping microarray for Usher syndrome (USH) to identify the mutations responsible for the disease in a cohort of 183 patients with USH. METHODS. DNA from 183 patients with Usher syndrome from the Spanish population was analyzed using a genotyping microarray containing 429 previously identified disease-associated variants in eight USH genes. Mutations detected by the array were confirmed by direct sequencing. Haplotype analysis was also performed in families carrying common Spanish mutations. RESULTS. The genotyping microarray identified 43 different variants, divided into 32 disease causative and 11 probably non-pathologic…

medicine.medical_specialtyGenotypeMicroarrayUsher syndromeDNA Mutational AnalysisCadherin Related ProteinsCell Cycle ProteinsNerve Tissue ProteinsMyosinsBiologymedicine.disease_causePolymerase Chain ReactionReceptors G-Protein-CoupledMolecular geneticsGenotypemedicineotorhinolaryngologic diseasesHumansGenotypingAllelesAdaptor Proteins Signal TransducingOligonucleotide Array Sequence AnalysisGeneticsExtracellular Matrix ProteinsMutationGene Expression ProfilingHaplotypeMembrane ProteinsCadherinsmedicine.diseaseGene expression profilingCytoskeletal ProteinsSpainMyosin VIIaMutationUsher Syndromes
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The antiapoptotic protein BAG3 is expressed in thyroid carcinomas and modulates apoptosis mediated by tumor necrosis factor-related apoptosis-inducin…

2007

Abstract Context: We previously showed that BAG3 protein, a member of the BAG (Bcl-2-associated athanogene) co-chaperone family, modulates apoptosis in human leukemias. The expression of BAG3 in other tumor types has not been extensively investigated so far. Objective: The objective of this study was to analyze BAG3 expression in thyroid neoplastic cells and investigate its influence in cell apoptotic response to TNF-related apoptosis-inducing ligand (TRAIL). Design, Setting, and Patients: We investigated BAG3 expression in human thyroid carcinoma cell lines, including NPA, and the effect of BAG3-specific small interfering RNA on TRAIL-induced apoptosis in NPA cells. Subsequently, we analyz…

medicine.medical_specialtySmall interfering RNAProgrammed cell deathEndocrinology Diabetes and MetabolismClinical BiochemistryApoptosisBiologyBiochemistryThyroid carcinomaTNF-Related Apoptosis-Inducing LigandEndocrinologyWestern blotInternal medicineCell Line TumormedicineHumansThyroid NeoplasmsRNA Small InterferingThyroid cancerAdaptor Proteins Signal Transducingmedicine.diagnostic_testDose-Response Relationship DrugBiochemistry (medical)ThyroidCarcinomamedicine.diseaseImmunohistochemistryEndocrinologymedicine.anatomical_structureApoptosisCancer researchTumor necrosis factor alphaApoptosis Regulatory Proteins
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Nuclear localization but not PML protein is required for incorporation of the papillomavirus minor capsid protein L2 into virus-like particles.

2004

ABSTRACT Recent reports suggest that nuclear domain(s) 10 (ND10) is the site of papillomavirus morphogenesis. The viral genome replicates in or close to ND10. In addition, the minor capsid protein, L2, accumulates in these subnuclear structures and recruits the major capsid protein, L1. We have now used cell lines deficient for promyelocytic leukemia (PML) protein, the main structural component of ND10, to study the role of this nuclear protein for L2 incorporation into virus-like particles (VLPs). L2 expressed in PML protein knockout (PML −/− ) cells accumulated in nuclear dots, which resemble L2 aggregates forming at ND10 in PML protein-containing cells. These L2 assemblies also attracted…

virusesImmunologyActive Transport Cell NucleusNuclear dotsBiologyPromyelocytic Leukemia ProteinMicrobiologyCell LinePromyelocytic leukemia proteinMiceDeath-associated protein 6Virus-like particleVirologymedicineAnimalsHumansNuclear proteinPapillomaviridaeAdaptor Proteins Signal TransducingCell NucleusTumor Suppressor ProteinsStructure and AssemblyIntracellular Signaling Peptides and ProteinsVirionvirus diseasesNuclear ProteinsOncogene Proteins Viralbiochemical phenomena metabolism and nutritionMolecular biologyCell biologyNeoplasm ProteinsCell nucleusMicroscopy Electronmedicine.anatomical_structureInsect ScienceMutationbiology.proteinCapsid ProteinsNuclear transportCarrier ProteinsCo-Repressor ProteinsNuclear localization sequenceMolecular ChaperonesTranscription FactorsJournal of virology
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PTC124-mediated translational readthrough of a nonsense mutation causing Usher syndrome type 1C.

2011

We investigated the therapeutic potential of the premature termination codon (PTC) readthrough-inducing drug PTC124 in treating the retinal phenotype of Usher syndrome, caused by a nonsense mutation in the USH1C gene. Applications in cell culture, organotypic retina cultures, and mice in vivo revealed significant readthrough and the recovery of protein function. In comparison with other readthrough drugs, namely the clinically approved readthrough-inducing aminoglycoside gentamicin, PTC124 exhibits significant better retinal biocompatibility. Its high readthrough efficiency in combination with excellent biocompatibility makes PTC124 a promising therapeutic agent for PTCs in USH1C, as well a…

virusesUsher syndromeGenetic enhancementNonsense mutationGenetic VectorsCell Cycle ProteinsRetina03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineIn vivootorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansMolecular BiologyCells Cultured030304 developmental biologyAdaptor Proteins Signal TransducingGenetics0303 health sciencesOxadiazolesbusiness.industryfungiAminoglycosideTranslational readthroughmedicine.diseasePhenotype3. Good healthAtalurenMice Inbred C57BLCytoskeletal ProteinsLuminescent ProteinsElectroporationchemistryMicroscopy FluorescenceCodon NonsenseCancer researchMolecular MedicineGentamicinsbusinessUsher Syndromes030217 neurology & neurosurgeryHuman gene therapy
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