Search results for "PATHWAY"

showing 10 items of 1685 documents

Arrestin-β-1 Physically Scaffolds TSH and IGF1 Receptors to Enable Crosstalk

2019

Endogenously expressed TSH receptors (TSHRs) on orbital fibroblasts of patients with Graves ophthalmopathy (GO) use crosstalk with IGF1 receptors (IGF1R) to synergistically stimulate secretion of hyaluronan (HA), a major component of GO pathology. We previously showed crosstalk occurred upstream of mitogen-activated protein kinase (ERK) phosphorylation. Because other G protein-coupled receptors engage arrestin-β-1 (ARRB1) and ERK, we tested whether ARRB1 was a necessary component of TSHR/IGF1R crosstalk. HA secretion was stimulated by the TSHR-stimulating monoclonal antibodies M22 and KSAb1, or immunoglobulins from patients with GO (GO-Igs). Treatment with M22, as previously shown, resulted…

0301 basic medicineMAPK/ERK pathwaymedicine.medical_specialty030209 endocrinology & metabolismStimulationReceptor tyrosine kinaseCell LineReceptor IGF Type 103 medical and health sciencesMice0302 clinical medicineEndocrinologyInternal medicinemedicineArrestinAnimalsHumansPhosphorylationProtein kinase AReceptorResearch ArticlesbiologyChemistryReceptors Thyrotropinbody regionsGraves OphthalmopathyCrosstalk (biology)030104 developmental biologyEndocrinologybeta-Arrestin 1Thyroid Epithelial CellsGene Knockdown Techniquesbiology.proteinPhosphorylationSignal Transduction
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The Role of ERK Signaling in Experimental Autoimmune Encephalomyelitis

2017

Extracellular signal-regulated kinase (ERK) signaling plays a crucial role in regulating immune cell function and has been implicated in autoimmune disorders. To date, all commercially available inhibitors of ERK target upstream components, such as mitogen-activated protein (MAP) kinase/ERK kinase (MEKs), but not ERK itself. Here, we directly inhibit nuclear ERK translocation by a novel pharmacological approach (Glu-Pro-Glu (EPE) peptide), leading to an increase in cytosolic ERK phosphorylation during T helper (Th)17 cell differentiation. This was accompanied by diminished secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine influencing the encephalitogenicity …

0301 basic medicineMAPK/ERK pathwaymedicine.medical_treatmentCellular differentiationexperimental autoimmune encephalomyelitisLymphocyte Activationmedicine.disease_causemultiple sclerosisAutoimmunitylcsh:ChemistryMice0302 clinical medicineT-Lymphocyte SubsetsPhosphorylationExtracellular Signal-Regulated MAP Kinaseslcsh:QH301-705.5SpectroscopyKinaseExperimental autoimmune encephalomyelitisInterleukinGeneral MedicineComputer Science ApplicationsCell biologyProtein TransportCytokine030220 oncology & carcinogenesisFemaleERK pathwayCell signalingEncephalomyelitis Autoimmune ExperimentalMAP Kinase Signaling SystemT cellsBiologyModels BiologicalArticleCatalysisInorganic Chemistry03 medical and health sciencesmedicineAnimalscell signalingPhysical and Theoretical ChemistryEPE peptideMolecular BiologyT cells; ERK pathway; EPE peptide; experimental autoimmune encephalomyelitis; multiple sclerosis; cell signalingOrganic ChemistryGranulocyte-Macrophage Colony-Stimulating Factormedicine.diseaseDisease Models Animal030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Th17 CellsInternational Journal of Molecular Sciences
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ESCRT Requirements for Murine Leukemia Virus Release

2016

The Murine Leukemia Virus (MLV) is a gammaretrovirus that hijack host components of the endosomal sorting complex required for transport (ESCRT) for budding. To determine the minimal requirements for ESCRT factors in MLV viral and viral-like particles (VLP) release, an siRNA knockdown screen of ESCRT(-associated) proteins was performed in MLV-producing human cells. We found that MLV VLPs and virions primarily engage the ESCRT-I factor Tsg101 and marginally the ESCRT-associated adaptors Nedd4-1 and Alix to enter the ESCRT pathway. Conversely, the inactivation of ESCRT-II had no impact on VLP and virion egress. By analyzing the effects of individual ESCRT-III knockdowns, VLP and virion releas…

0301 basic medicineMLV; VLPs; retroviral budding; viral late domain; ESCRT; MVB pathway; CHMP1AEndosomevirusesGenetic Vectorslcsh:QR1-502CHMP1AGene ExpressionGene Products gagMLVmacromolecular substanceslcsh:MicrobiologyArticleESCRTCell LineESCRTMice03 medical and health sciencesviral late domainMVB pathwayVirologyGene OrderMurine leukemia virusAnimalsHumansVLPsTSG101Viral sheddingVirus Releaseretroviral buddingGammaretrovirusBuddingEndosomal Sorting Complexes Required for Transportbiologybiochemical phenomena metabolism and nutritionbiology.organism_classificationVirologyVirus ReleaseLeukemia Virus Murine030104 developmental biologyInfectious DiseasesGene Knockdown TechniquesRetroviridae InfectionsViruses
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Sclerostin and antisclerostin antibody serum levels predict the presence of axial spondyloarthritis in patients with inflammatory bowel disease

2018

Objective.The early diagnosis of inflammatory bowel disease (IBD)-associated spondyloarthritis (SpA/IBD) in patients affected by IBD represents a major topic in clinical practice; in particular, to date there are no available serum biomarkers revealing the presence of joint inflammation in these patients. Sclerostin (SOST), an antagonist of the Wnt/β-catenin pathway, and antisclerostin-immunoglobulin G (anti-SOST–IgG) have been recently studied in patients with ankylosing spondylitis (AS) as a putative marker of disease activity.Methods.SOST and anti-SOST-IgG serum levels were assayed in 125 patients with IBD, 85 with axial or peripheral SpA, and in control groups (patients with AS and rheu…

0301 basic medicineMaleAntibodieAntigen-Antibody ComplexInflammatory bowel diseaseGastroenterologyPathogenesischemistry.chemical_compound0302 clinical medicineGenetic MarkerImmunology and AllergyProspective StudiesMultivariate AnalysibiologyWnt signaling pathwayMiddle AgedRheumatoid arthritisBone Morphogenetic ProteinsRegression AnalysisFemalemedicine.symptomAntibodyHumanGenetic MarkersAdultmedicine.medical_specialtySclerostinImmunologyInflammationAntibodiesRegression AnalysiStatistics Nonparametric03 medical and health sciencesRheumatologyInternal medicineSpondyloarthritismedicineHumansSpondylitis AnkylosingAdaptor Proteins Signal TransducingAntisclerostin Antibodie030203 arthritis & rheumatologyAnkylosing spondylitisbusiness.industryBone Morphogenetic ProteinInflammatory Bowel DiseaseBiomarkerInflammatory Bowel Diseasesmedicine.diseaseProspective StudieSettore MED/16 - Reumatologia030104 developmental biologychemistryROC CurveImmunoglobulin GMultivariate Analysisbiology.proteinSclerostinSpondyloarthritibusinessBiomarkers
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Muscle and serum metabolomes are dysregulated in colon-26 tumor-bearing mice despite amelioration of cachexia with activin receptor type 2B ligand bl…

2019

Cancer-associated cachexia reduces survival, which has been attenuated by blocking the activin receptor type 2B (ACVR2B) ligands in mice. The purpose of this study was to unravel the underlying physiology and novel cachexia biomarkers by use of the colon-26 (C26) carcinoma model of cancer cachexia. Male BALB/c mice were subcutaneously inoculated with C26 cancer cells or vehicle control. Tumor-bearing mice were treated with vehicle (C26+PBS) or soluble ACVR2B either before (C26+sACVR/b) or before and after (C26+sACVR/c) tumor formation. Skeletal muscle and serum metabolomics analysis was conducted by gas chromatography-mass spectrometry. Cancer altered various biologically functional groups …

0301 basic medicineMaleCachexiaPhysiologyEndocrinology Diabetes and MetabolismActivin Receptors Type IIlihaksetMyostatinMice0302 clinical medicineAmino Acidsta315Activin Receptor Type-2BbiologyOrganophosphatesRecombinant Proteins3. Good healthmedicine.anatomical_structureribosome030220 oncology & carcinogenesismyostatinColonic NeoplasmsMetabolomesyöpätauditC26Metabolic Networks and Pathwaysmedicine.medical_specialtyPhenylalanineCachexia03 medical and health sciencesribosomitPhysiology (medical)Internal medicineCell Line TumormedicineAnimalsskeletal muscleMuscle SkeletalPI3K/AKT/mTOR pathwaybusiness.industrySkeletal muscleCancermedicine.diseaseta3122BlockadeImmunoglobulin Fc Fragments030104 developmental biologyEndocrinologyProtein Biosynthesisbiology.proteinaineenvaihduntatuotteetPyrimidine NucleotidesproteiinitbusinesslihassurkastumasairaudetACVR2BAmerican journal of physiology. Endocrinology and metabolism
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Somatic copy number alterations are associated with EGFR amplification and shortened survival in patients with primary glioblastoma.

2019

Glioblastoma (GBM) is the most common malignant primary tumor of the central nervous system. With no effective therapy, the prognosis for patients is terrible poor. It is highly heterogeneous and EGFR amplification is its most frequent molecular alteration. In this light, we aimed to examine the genetic heterogeneity of GBM and to correlate it with the clinical characteristics of the patients. For that purpose, we analyzed the status of EGFR and the somatic copy number alterations (CNAs) of a set of tumor suppressor genes and oncogenes. Thus, we found GBMs with high level of EGFR amplification, low level and with no EGFR amplification. Highly amplified tumors showed histological features of…

0301 basic medicineMaleCancer ResearchBiopsyL-amp GB EGFR-low amplified glioblastomamedicine.disease_causewt wildtypeMYBPC3 myosin-binding protein C0302 clinical medicineHIC1 hypermethylated in cancer 1Gene duplicationIn Situ Hybridization FluorescenceIDH2 isocitrate dehydrogenase 2MutationRB-pat RB signaling pathwayEGFRvIII epidermal growth factor receptor variant number IIIPAH phenylalanine hydroxylaseGBM glioblastoma IDH-wildtype (glioblastoma multiforme primary glioblastoma).ANOVA ANalysis Of VArianceN-amp GB EGFR-no amplified glioblastomaMiddle AgedCDKN2A cyclin-dependent kinase inhibitor 2Alcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisPrimary tumorImmunohistochemistryH-amp GB EGFR-high amplified glioblastomaErbB ReceptorsTKR-pat tyrosine-kinase receptors signaling pathway030220 oncology & carcinogenesisDisease ProgressionCDK6 cyclin-dependent kinase 6CDH1 Cadherin 1FemaleCREM cAMP response element modulatorIHC immunohistochemistryAdultOriginal articleDNA Copy Number VariationsCDKN1B cyclin-dependent kinase inhibitor 1BBiologyRARB retinoic acid receptor betaCNS central nervous systemlcsh:RC254-282IDH1 isocitrate dehydrogenase 1BCL2 B-cell cll/ lymphoma 2CNAs copy number algerationsWHO World Health Organization03 medical and health sciencesYoung Adultp53-pat p53 signaling pathwaymedicineBiomarkers TumorTMA tissue microarrayPTENHumansProtein kinase BPI3K/AKT/mTOR pathwaySurvival analysisAgedGenetic heterogeneityGene AmplificationGFAP glial fibrillary acidic proteinMLPA multiplex ligation-dependent probe amplificationmedicine.diseaseFISH fluorescence in situ hibridizationSurvival AnalysisCDKN2B cyclin-dependent kinase inhibitor 2BPTEN phosphatase and tensin homologEGFR epidermal growth factor receptorCNV-load load of copy number variations030104 developmental biologyMutationPARK2 parkinCancer researchbiology.proteinTCGA The Cancer Genome AtlasLARGE1 acetylglucosaminyltransferase-like protein 1GlioblastomaCHD7 Chromodomain Helicase DNA Binding Protein 7DAPI 4′6-diamidino-2-phenylindoleNeoplasia (New York, N.Y.)
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BRG1/SMARCA4 is essential for neuroblastoma cell viability through modulation of cell death and survival pathways.

2016

Neuroblastoma (NB) is a neoplasm of the sympathetic nervous system, and is the most common solid tumor of infancy. NBs are very heterogeneous, with a clinical course ranging from spontaneous regression to resistance to all current forms of treatment. High-risk patients need intense chemotherapy, and only 30-40% will be cured. Relapsed or metastatic tumors acquire multi-drug resistance, raising the need for alternative treatments. Owing to the diverse mechanisms that are responsible of NB chemoresistance, we aimed to target epigenetic factors that control multiple pathways to bypass therapy resistance. We found that the SWI/SNF-related, matrix-associated, actin-dependent regulator of chromat…

0301 basic medicineMaleCancer ResearchCombination therapyCell SurvivalBiologyMolecular oncologyTranscriptome03 medical and health sciencesNeuroblastomaPhosphatidylinositol 3-Kinases0302 clinical medicineGrowth factor receptorNeuroblastomaCell Line TumorGeneticsmedicineHumansMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCell ProliferationCell DeathDNA HelicasesNuclear ProteinsCell cyclemedicine.diseaseGene Expression Regulation Neoplastic030104 developmental biologyProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisImmunologyCancer researchFemaleTranscriptomeSignal TransductionTranscription FactorsOncogene
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Exome-wide somatic mutation characterization of small bowel adenocarcinoma

2018

Small bowel adenocarcinoma (SBA) is an aggressive disease with limited treatment options. Despite previous studies, its molecular genetic background has remained somewhat elusive. To comprehensively characterize the mutational landscape of this tumor type, and to identify possible targets of treatment, we conducted the first large exome sequencing study on a population-based set of SBA samples from all three small bowel segments. Archival tissue from 106 primary tumors with appropriate clinical information were available for exome sequencing from a patient series consisting of a majority of confirmed SBA cases diagnosed in Finland between the years 2003–2011. Paired-end exome sequencing was…

0301 basic medicineMaleCancer ResearchMICROSATELLITE INSTABILITYColorectal canceroncogenesReceptor ErbB-2medicine.disease_causeCOLORECTAL-CANCERACTIVATIONCohort Studies0302 clinical medicineAnimal CellsAdenocarcinomasMedicine and Health SciencesExomeFrameshift MutationExomeGenetics (clinical)Exome sequencingAged 80 and overSMALL-INTESTINEeducation.field_of_study1184 Genetics developmental biology physiologyCELIAC-DISEASENonsense MutationMiddle Aged3. Good healthsyöpägeenitOncology030220 oncology & carcinogenesissyöpätauditFemaleSIGNALING PATHWAYKRASCellular TypesResearch ArticleAdultProto-Oncogene Proteins B-raflcsh:QH426-470SEQUENCING DATAImmune CellsNonsense mutationPopulationImmunologyAntigen-Presenting CellsComputational biologysuolistosyövätBiologyAdenocarcinomata3111CarcinomasFrameshift mutation03 medical and health sciencesGermline mutationQUALITY-CONTROLGenetiikka kehitysbiologia fysiologia - Genetics developmental biology physiologySyöpätaudit - CancersIntestinal NeoplasmsmedicineGeneticsPoint MutationHumanseducationMolecular BiologyEcology Evolution Behavior and SystematicsAgedColorectal CancerBiology and Life SciencesCancers and Neoplasmscancerous diseasesCell Biologymedicine.diseaseta3122mutationsCOMPREHENSIVE MOLECULAR CHARACTERIZATIONlcsh:Genetics030104 developmental biologyMutationSomatic Mutationbowel cancer3111 BiomedicinemutaatiotHIGH-RESOLUTIONPLoS Genetics
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Cerebello-cortical network fingerprints differ between essential, Parkinson's and mimicked tremors.

2017

Cerebello-thalamo-cortical loops play a major role in the emergence of pathological tremors and voluntary rhythmic movements. It is unclear whether these loops differ anatomically or functionally in different types of tremor. We compared age- and sex-matched groups of patients with Parkinson's disease or essential tremor and healthy controls (n = 34 per group). High-density 256-channel EEG and multi-channel EMG from extensor and flexor muscles of both wrists were recorded simultaneously while extending the hands against gravity with the forearms supported. Tremor was thereby recorded from patients, and voluntarily mimicked tremor was recorded from healthy controls. Tomographic maps of EEG-E…

0301 basic medicineMaleCerebellumEfferentEssential TremorSensory systemElectroencephalographyPremotor cortex03 medical and health sciences0302 clinical medicineCerebellumNeural PathwaysmedicineImage Processing Computer-AssistedHumansMuscle SkeletalAgedEssential tremorResting state fMRImedicine.diagnostic_testbusiness.industryElectromyographyMotor CortexElectroencephalographyParkinson DiseaseMiddle Agedmedicine.diseaseMagnetic Resonance Imagingnervous system diseases030104 developmental biologymedicine.anatomical_structureNonlinear DynamicsCerebral cortexCase-Control StudiesFemaleNeurology (clinical)businessNeuroscience030217 neurology & neurosurgeryBrain : a journal of neurology
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Activation of Corticothalamic Layer 6 Cells Decreases Angular Tuning in Mouse Barrel Cortex.

2019

In the mouse whisker system, the contribution of L6 corticothalamic cells (L6 CT) to cortical and thalamic processing of the whisker deflection direction was investigated. A genetically defined population of L6 CT cells project to infragranular GABAergic interneurons that hyperpolarize neurons in somatosensory barrel cortex (BC). Optogenetic activation of these neurons switched BC to an adapted mode in which excitatory cells lost their angular tuning. In contrast, however, this was not the case with a general activation of inhibitory interneurons via optogenetic activation of Gad2-expressing cells. The decrease in angular tuning, when L6 CT cells were activated, was due to changes in cortic…

0301 basic medicineMaleCognitive NeurosciencePopulationNeuroscience (miscellaneous)OptogeneticsSomatosensory systemInhibitory postsynaptic potentiallcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineThalamusexcitation inhibition balancedirection selectivitymedicineAnimalsGABAergic Neuronseducationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryOriginal ResearchNeuronseducation.field_of_studyAfferent PathwaysNeocortexGAD2NTSR1ChemistryNeural InhibitionSomatosensory CortexBarrel cortexSensory Systemslayer 6030104 developmental biologymedicine.anatomical_structurenervous systemTouch PerceptionVibrissaeExcitatory postsynaptic potentialGABAergicFemaleNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in neural circuits
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