Search results for "Signaling"

showing 10 items of 1125 documents

NG2/CSPG4 and progranulin in the posttraumatic glial scar.

2018

Traumatic injury of the central nervous system is one of the leading causes of death and disability in young adults. Failure of regeneration is caused by autonomous neuronal obstacles and by formation of the glial scar, which is essential to seal the injury but also constitutes a barrier for regrowing axons. The scar center is highly inflammatory and populated by NG2+ glia, whereas astrocytes form the sealing border and trap regrowing axons, suggesting that the non-permissive environment of activated astrocytes and extracellular matrix components is one of the reasons for the regenerative failure. Particularly, secreted chondroitin-sulfate proteoglycans, CSPGs, of the lectican family hinder…

0301 basic medicineCentral nervous systemPerlecanCell CommunicationBiologyGlial scarExtracellular matrix03 medical and health scienceschemistry.chemical_compoundCicatrix0302 clinical medicineProgranulinsmedicineLecticanAnimalsHumansMolecular BiologyMicrogliaReceptors NotchMembrane ProteinsCell biology030104 developmental biologymedicine.anatomical_structurenervous systemchemistryChondroitin Sulfate ProteoglycansChondroitin sulfate proteoglycanBrain InjuriesImmunologybiology.proteinSynaptic signalingNeuroglia030217 neurology & neurosurgeryHeparan Sulfate ProteoglycansSignal TransductionMatrix biology : journal of the International Society for Matrix Biology
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The NG2 Protein Is Not Required for Glutamatergic Neuron-NG2 Cell Synaptic Signaling.

2014

NG2 glial cells (as from now NG2 cells) are unique in receiving synaptic input from neurons. However, the components regulating formation and maintenance of these neuron–glia synapses remain elusive. The transmembrane protein NG2 has been considered a potential mediator of synapse formation and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) clustering, because it contains 2 extracellular Laminin G/Neurexin/Sex Hormone-Binding Globulin domains, which in neurons are crucial for formation of transsynaptic neuroligin– neurexin complexes. NG2 is connected via Glutamate Receptor-Interacting Protein with GluA2/3-containing AMPARs, thereby possibly mediating receptor clus…

0301 basic medicineCognitive NeuroscienceNeurexinSynaptogenesisGlutamic AcidNeuroliginMice TransgenicBiologyNeurotransmissionHippocampusSynaptic Transmission03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinePostsynaptic potentialAnimalsReceptors AMPAAntigensNeuronsMembrane Proteins030104 developmental biologynervous systemSynaptic plasticitySynapsesProteoglycansSynaptic signalingNeurosciencePostsynaptic densityNeuroglia030217 neurology & neurosurgeryCerebral cortex (New York, N.Y. : 1991)
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Synaptic Phospholipid Signaling Modulates Axon Outgrowth via Glutamate-dependent Ca2+-mediated Molecular Pathways.

2015

Abstract Altered synaptic bioactive lipid signaling has been recently shown to augment neuronal excitation in the hippocampus of adult animals by activation of presynaptic LPA2-receptors leading to increased presynaptic glutamate release. Here, we show that this results in higher postsynaptic Ca2+ levels and in premature onset of spontaneous neuronal activity in the developing entorhinal cortex. Interestingly, increased synchronized neuronal activity led to reduced axon growth velocity of entorhinal neurons which project via the perforant path to the hippocampus. This was due to Ca2+-dependent molecular signaling to the axon affecting stabilization of the actin cytoskeleton. The spontaneous…

0301 basic medicineCognitive NeuroscienceNeuronal OutgrowthHippocampusGlutamic AcidAxon hillockSynaptic Transmission03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicinePostsynaptic potentialmedicinePremovement neuronal activityAnimalsbioactive phospholipidsCalcium SignalingAxonearly synchronized activityCells CulturedPhospholipidsChemistryOriginal ArticlesEntorhinal cortexPerforant pathActin cytoskeletonAxonsCell biologyCa2+-signalingentorhinal–hippocampal formation030104 developmental biologymedicine.anatomical_structureaxon outgrowthnervous systemCalcium030217 neurology & neurosurgeryMetabolic Networks and PathwaysCerebral cortex (New York, N.Y. : 1991)
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Succinate Activates EMT in Intestinal Epithelial Cells through SUCNR1: A Novel Protagonist in Fistula Development

2020

The pathogenesis of Crohn&rsquo

0301 basic medicineCrohn’s diseaseFistulaSuccinic Acid610 Medicine & healthVimentinArticleReceptors G-Protein-CoupledPathogenesis03 medical and health sciencesHT29 Cells0302 clinical medicineCrohn DiseaseFibrosismedicineGene silencingAnimalsHumansfistulaReceptorlcsh:QH301-705.5InflammationbiologyChemistryMesenchymal stem cellWnt signaling pathwayEpithelial CellsGeneral Medicinemedicine.diseaseCadherinssuccinateFibrosisdigestive system diseasesIntestinesCrohn's disease10219 Clinic for Gastroenterology and Hepatology030104 developmental biologylcsh:Biology (General)030220 oncology & carcinogenesisbiology.proteinCancer research
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NF-κB Is a Potential Molecular Drug Target in Triple-Negative Breast Cancers.

2017

Breast cancer continues to cause significant burden in global health morbidity and mortality. Triple-negative breast cancers (TNBCs) are highly aggressive with poor prognosis and are characterized by lack of expression of estrogen receptor, progesterone receptor, and human epidermal growth factor receptor (Her-2). TNBCs are often resistant to cytotoxic chemotherapy and pose major difficulty in achieving personalized medicine due to their molecular heterogeneity. There is increasing evidence that the aberrant activation of nuclear factor (NF)-κB signaling is a frequent characteristic of TNBCs. We evaluated the effects of different potential NF-κB inhibitors, such as bisindolylmaleimide I (BI…

0301 basic medicineCurcuminEstrogen receptorTriple Negative Breast NeoplasmsPharmacologydiagnostics drug targets NF-kB signaling personalized medicine triple-negative breast cancerBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBreast cancerCell Line TumorMG132Progesterone receptorGeneticsmedicineGene silencingHumansPrecision MedicineMolecular BiologyTriple-negative breast cancerbusiness.industryCyclohexanonesNF-kappa BCancermedicine.disease030104 developmental biologychemistry030220 oncology & carcinogenesisBenzamidesProteasome inhibitorCancer researchMolecular MedicineFemalebusinessBiotechnologymedicine.drugSignal TransductionOmics : a journal of integrative biology
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Transmembrane signaling and cytoplasmic signal conversion by dimeric transmembrane helix 2 and a linker domain of the DcuS sensor kinase

2020

Transmembrane (TM) signaling is a key process of membrane-bound sensor kinases. The C4-dicarboxylate (fumarate) responsive sensor kinase DcuS of Escherichia coli is anchored by TM helices TM1 and TM2 in the membrane. Signal transmission across the membrane relies on the piston-type movement of the periplasmic part of TM2. To define the role of TM2 in TM signaling, we use oxidative Cys cross-linking to demonstrate that TM2 extends over the full distance of the membrane and forms a stable TM homodimer in both the inactive and fumarate-activated state of DcuS. An S186xxxGxxxG194 motif is required for the stability and function of the TM2 homodimer. The TM2 helix further extends on the periplas…

0301 basic medicineCytoplasmGpA glycophorin AC4DC C4-dicarboxylateCL cross-linkingpiston-typeMBP maltose-binding proteinBiochemistry03 medical and health sciencesProtein DomainsDcuSEscherichia coli(Gly)xxx(Gly) motifMolecular Biologysensor kinasefumarate030102 biochemistry & molecular biologyChemistryEscherichia coli ProteinsCell MembraneHistidine kinaseGene Expression Regulation BacterialCell BiologyPeriplasmic spacelinkerTransmembrane proteinoxidative Cys cross-linkingTransmembrane domain030104 developmental biologyMembrane proteinProtein kinase domainHelixBiophysicsProtein MultimerizationProtein Kinasestransmembrane signalingLinkerResearch ArticleTM transmembraneJournal of Biological Chemistry
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Tumor- and cytokine-primed human natural killer cells exhibit distinct phenotypic and transcriptional signatures.

2019

An emerging cellular immunotherapy for cancer is based on the cytolytic activity of natural killer (NK) cells against a wide range of tumors. Although in vitro activation, or "priming," of NK cells by exposure to pro-inflammatory cytokines, such as interleukin (IL)-2, has been extensively studied, the biological consequences of NK cell activation in response to target cell interactions have not been thoroughly characterized. We investigated the consequences of co-incubation with K562, CTV-1, Daudi RPMI-8226, and MCF-7 tumor cell lines on the phenotype, cytokine expression profile, and transcriptome of human NK cells. We observe the downregulation of several activation receptors including CD…

0301 basic medicineCytotoxicity ImmunologicPhysiologymedicine.medical_treatmentCytotoxicityGene ExpressionNK cellsLymphocyte ActivationToxicologyPathology and Laboratory MedicineMolecular biology assays and analysis techniquesChemokine receptor0302 clinical medicineNeoplasmsImmune PhysiologyCellular typesGene Regulatory NetworksIL-2 receptorReceptorInnate Immune SystemMultidisciplinaryNucleic acid analysisQImmune cellsRRNA analysisKiller Cells NaturalCytokinePhenotype030220 oncology & carcinogenesisMCF-7 CellsMedicineCytokinesWhite blood cellsTumor necrosis factor alphaImmunotherapyInflammation MediatorsResearch ArticleCell signalingCell biologyBlood cellsScienceImmunologyCD16BiologyResearch and Analysis Methods03 medical and health sciencesExtraction techniquesCell Line TumormedicineGeneticsHumansMolecular Biology TechniquesMolecular BiologySecretionMedicine and health sciencesBiology and life sciencesMolecular DevelopmentNKG2DRNA extraction030104 developmental biologyAnimal cellsImmune SystemCancer researchK562 CellsTranscriptomePhysiological ProcessesDevelopmental BiologyCloningPloS one
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NOTCH signalling in ovarian cancer angiogenesis

2020

The Notch signalling pathway is involved in the new vessel formation process by regulating tip and stalk cells, which are key cells in the sprout formation. This process is essential in both normal ovary and cancer angiogenesis and is regulated by Notch-VEGF crosstalk. Furthermore, Notch has been linked in ovary with stem cell maintenance and epithelial mesenchymal transition processes. Dysregulation of the Notch pathway is frequent in ovarian cancer (OC) and it has been associated with impaired survival and advanced stages or lymph node involvement. Notch also plays a role in chemoresistance to platinum. In this context, this pathway has emerged as an attractive target for precision medici…

0301 basic medicineDemcizumabAngiogenesisNotch signaling pathway610 Medicine & healthContext (language use)General MedicineBiologymedicine.disease10174 Clinic for Gynecology03 medical and health sciencesReview Article on Ovarian Cancer: State of the Art and Perspectives of Clinical Research030104 developmental biology0302 clinical medicine030220 oncology & carcinogenesismedicineCancer researchEpithelial–mesenchymal transitionStem cellOvarian cancerGamma secretaseAnnals of Translational Medicine
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Intra-neuronal Competition for Synaptic Partners Conserves the Amount of Dendritic Building Material

2017

Brain development requires correct targeting of multiple thousand synaptic terminals onto staggeringly complex dendritic arbors. The mechanisms by which input synapse numbers are matched to dendrite size, and by which synaptic inputs from different transmitter systems are correctly partitioned onto a postsynaptic arbor, are incompletely understood. By combining quantitative neuroanatomy with targeted genetic manipulation of synaptic input to an identified Drosophila neuron, we show that synaptic inputs of two different transmitter classes locally direct dendrite growth in a competitive manner. During development, the relative amounts of GABAergic and cholinergic synaptic drive shift dendrit…

0301 basic medicineDendritic spinePresynaptic TerminalsBiologyReceptors NicotinicArticleSynapse03 medical and health sciencesDendrite (crystal)Calcium Channels T-Type0302 clinical medicinePostsynaptic potentialSynaptic augmentationmedicineAnimalsDrosophila ProteinsCalcium Signalinggamma-Aminobutyric AcidNeuronsNeuronal PlasticityGeneral NeuroscienceDendritesReceptors GABA-AAcetylcholine030104 developmental biologySynaptic fatiguemedicine.anatomical_structurenervous systemSynaptic plasticitySynapsesDrosophilaNeuronNeuroscience030217 neurology & neurosurgery
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Loss-of-Function Mutations in UNC45A Cause a Syndrome Associating Cholestasis, Diarrhea, Impaired Hearing, and Bone Fragility

2018

International audience; Despite the rapid discovery of genes for rare genetic disorders, we continue to encounter individuals presenting with syndromic manifestations. Here, we have studied four affected people in three families presenting with cholestasis, congenital diarrhea, impaired hearing, and bone fragility. Whole-exome sequencing of all affected individuals and their parents identified biallelic mutations in Unc-45 Myosin Chaperone A (UNC45A) as a likely driver for this disorder. Subsequent in vitro and in vivo functional studies of the candidate gene indicated a loss-of-function paradigm, wherein mutations attenuated or abolished protein activity with concomitant defects in gut dev…

0301 basic medicineDiarrheaMaleCandidate geneAdolescentBone fragilityArticleBone and Bones03 medical and health sciencesYoung AdultCholestasisLoss of Function MutationGCUNC-45MyosinGeneticsMedicineAnimalsHumansFamilyLymphocytes[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsHearing LossGeneGenetics (clinical)Loss functionZebrafishCholestasisbusiness.industryInfant NewbornIntracellular Signaling Peptides and ProteinsSyndromeFibroblastsmedicine.disease3. Good healthPedigreeDiarrhea030104 developmental biologyPhenotype[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsConcomitantChild PreschoolImmunologyFemalemedicine.symptombusinessGastrointestinal Motility
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