Search results for "alpha Subunit"

showing 10 items of 126 documents

Interleukin-12 and -23 Control Plasticity of CD127(+) Group 1 and Group 3 Innate Lymphoid Cells in the Intestinal Lamina Propria.

2015

Human group 1 ILCs consist of at least three phenotypically distinct subsets, including NK cells, CD127(+) ILC1, and intraepithelial CD103(+) ILC1. In inflamed intestinal tissues from Crohn's disease patients, numbers of CD127(+) ILC1 increased at the cost of ILC3. Here we found that differentiation of ILC3 to CD127(+) ILC1 is reversible in vitro and in vivo. CD127(+) ILC1 differentiated to ILC3 in the presence of interleukin-2 (IL-2), IL-23, and IL-1β dependent on the transcription factor RORγt, and this process was enhanced in the presence of retinoic acid. Furthermore, we observed in resection specimen from Crohn's disease patients a higher proportion of CD14(+) dendritic cells (DC), whi…

Interleukin 2Receptors Retinoic AcidCellular differentiationCD14ImmunologyInterleukin-1betaRetinoic acidLipopolysaccharide Receptorschemical and pharmacologic phenomenaTretinoinMice SCIDBiologyInterleukin-12 Subunit p35Interleukin-7 Receptor alpha Subunitchemistry.chemical_compoundMiceIntestinal mucosaCrohn DiseaseMice Inbred NODmedicineImmunology and AllergyAnimalsHumansRetinoid X Receptor gammaLymphocytesIntestinal MucosaInterleukin-7 receptorCells CulturedMice KnockoutRetinoic Acid Receptor alphaInnate lymphoid cellvirus diseaseshemic and immune systemsCell DifferentiationDendritic CellsNuclear Receptor Subfamily 1 Group F Member 3Molecular biologyKiller Cells NaturalMice Inbred C57BLInfectious DiseaseschemistryLymphocyte TransfusionImmunologyInterleukin 12Interleukin-23 Subunit p19Interleukin-2medicine.drugImmunity
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Insulin-dependent leptin expression in breast cancer cells.

2008

Abstract Pathologic conditions associated with hyperinsulinemia, such as obesity, metabolic syndrome, and diabetes, seem to increase the risk of breast cancer. Here, we studied molecular mechanisms by which insulin activates the expression of leptin, an obesity hormone that has been shown to promote breast cancer progression in an autocrine or paracrine way. Using MDA-MB-231 breast cancer cells, we found that (a) insulin stimulated leptin mRNA and protein expression, which was associated with increased activation of the leptin gene promoter; (b) insulin increased nuclear accumulation of transcription factors hypoxia inducible factor (HIF)-1α and Sp1 and their loading on the leptin promoter;…

LeptinTranscriptional ActivationCancer Researchmedicine.medical_specialtySmall interfering RNAChromatin ImmunoprecipitationSp1 Transcription FactorBlotting WesternFluorescent Antibody TechniqueBreast NeoplasmsEnzyme-Linked Immunosorbent AssayBiologyParacrine signallingPhosphatidylinositol 3-Kinasesbreast cancerInternal medicinemedicineHyperinsulinemiaTumor Cells CulturedHumansHypoglycemic AgentsInsulinRNA MessengerRNA Small InterferingAutocrine signallingLuciferasesPromoter Regions GeneticTranscription factorCell NucleusMitogen-Activated Protein Kinase 1Gene knockdownLeptin receptorMitogen-Activated Protein Kinase 3Reverse Transcriptase Polymerase Chain ReactionLeptinmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaEndocrinologyOncologyCancer researchFemalehormones hormone substitutes and hormone antagonistsCancer research
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Hypoxia-inducible factor 1 alpha expression increases during colorectal carcinogenesis and tumor progression

2008

Abstract Background Hypoxia-inducible factor 1 alpha (HIF-1α) is involved in processes promoting carcinogenesis of many tumors. However, its role in the development of colorectal cancer is unknown. To investigate the significance of HIF-1α during colorectal carcinogenesis and progression we examined its expression in precursor lesions constituting the conventional and serrated pathways, as well as in non-metastatic and metastatic adenocarcinomas. Methods Immunohistochemistry and Western blot is used to analyse HIF-1α expression in normal colonic mucosa, hyperplastic polyps (HPP), sessile serrated adenomas (SSA), low-grade (TA-LGD) and high-grade (TA-HGD) traditional adenomas as well as in n…

LipopolysaccharidesCancer ResearchPathologymedicine.medical_specialtyColorectal cancerColonic PolypsMouse model of colorectal and intestinal cancermedicine.disease_causelcsh:RC254-282chemistry.chemical_compoundWestern blotCell Line TumorGeneticsMedicineHumansNeoplasm Metastasismedicine.diagnostic_testbusiness.industrymedicine.diseaseHypoxia-Inducible Factor 1 alpha Subunitlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensImmunohistochemistryVascular endothelial growth factorCell Transformation NeoplasticOncologychemistryHyperplastic PolypTumor progressionDisease ProgressionImmunohistochemistrybusinessCarcinogenesisColorectal NeoplasmsPrecancerous ConditionsResearch ArticleBMC Cancer
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Phenolic-glycolipid-1 and lipoarabinomannan preferentially modulate TCR- and CD28-triggered proximal biochemical events, leading to T-cell unresponsi…

2012

Abstract Background Advanced stages of leprosy show T cell unresponsiveness and lipids of mycobacterial origin are speculated to modulate immune responses in these patients. Present study elucidates the role of phenolicglycolipid (PGL-1) and Mannose-capped lipoarabinomannan (Man-LAM) on TCR- and TCR/CD28- mediated signalling. Results We observed that lipid antigens significantly inhibit proximal early signalling events like Zap-70 phosphorylation and calcium mobilization. Interestingly, these antigens preferentially curtailed TCR-triggered early downstream signalling events like p38 phosphorylation whereas potentiated that of Erk1/2. Further, at later stages inhibition of NFAT binding, IL-2…

LipopolysaccharidesEndocrinology Diabetes and MetabolismT-LymphocytesClinical BiochemistryPGL-1Man-LAMGene ExpressionLymphocyte ActivationJurkat cellsJurkat CellsEndocrinologyT-cell activationIL-2 receptorPhosphorylationExtracellular Signal-Regulated MAP KinasesPromoter Regions Geneticlcsh:RC620-627Protein Kinase CImmunity CellularZAP-70 Protein-Tyrosine KinaseCD28hemic and immune systemsCell biologyMycobacterium lepraelcsh:Nutritional diseases. Deficiency diseasesmedicine.anatomical_structureHost-Pathogen InteractionsProtein BindingMAP Kinase Signaling SystemT cellReceptors Antigen T-Cellchemical and pharmacologic phenomenaBiologyImmune systemCD28 AntigensLeprosymedicineHumansSecretionCalcium SignalingCell ProliferationBiochemistry medicalAntigens BacterialLipoarabinomannanNFATC Transcription FactorsResearchBiochemistry (medical)T-cell receptorInterleukin-2 Receptor alpha SubunitMycobacteriaGene Expression RegulationAnergyImmunologyLeukocytes MononuclearInterleukin-2GlycolipidsLipids in Health and Disease
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Interferon-α Suppresses cAMP to Disarm Human Regulatory T Cells

2013

Abstract IFN-α is an antineoplastic agent in the treatment of several solid and hematologic malignancies that exerts strong immune- and autoimmune-stimulating activity. However, the mechanisms of immune activation by IFN-α remain incompletely understood, particularly with regard to CD4+CD25highFoxp+ regulatory T cells (Treg). Here, we show that IFN-α deactivates the suppressive function of human Treg by downregulating their intracellular cAMP level. IFN-α–mediated Treg inactivation increased CD4+ effector T-cell activation and natural killer cell tumor cytotoxicity. Mechanistically, repression of cAMP in Treg was caused by IFN-α–induced MAP–ERK kinase (MEK)/extracellular signal-regulated ki…

MAPK/ERK pathwayCancer Researchmedicine.medical_treatmentGraft vs Host DiseaseAutoimmunitychemical and pharmacologic phenomenaBiologyLymphocyte ActivationT-Lymphocytes RegulatoryNatural killer cellMiceImmune systemDownregulation and upregulationT-Lymphocyte SubsetsCyclic AMPmedicineAnimalsHumansIL-2 receptorPhosphorylationExtracellular Signal-Regulated MAP KinasesCells CulturedMitogen-Activated Protein Kinase KinasesInterleukin-2 Receptor alpha SubunitInterferon-alphaFOXP3hemic and immune systemsDNA-Binding ProteinsKiller Cells NaturalSTAT Transcription Factorsmedicine.anatomical_structureCytokineOncologyHumanized mouseImmunologyCancer researchCancer Research
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Coupling of endothelin receptors to the ERK/MAP kinase pathway. Roles of palmitoylation and G(alpha)q.

2001

Endothelins are potent mitogens that stimulate extracellular signal-regulated kinases (ERK/MAP kinases) through their cognate G-protein-coupled receptors, ET(A) and ET(B). To address the role of post-translational ET receptor modifications such as acylation on ERK activation and to identify relevant downstream effectors coupling the ET receptor to the ERK signaling cascades we have constructed a panel of palmitoylation-deficient ET receptor mutants with differential G(alpha) protein binding capacity. Endothelin-1 stimulation of wild-type ET(A) or ET(B) induced a fivefold to sixfold increase in ERK in COS-7 and CHO cells whereas full-length nonpalmitoylated ET(A) and ET(B) mutants failed to …

MAPK/ERK pathwayGs alpha subunitInsectaMAP Kinase Signaling SystemBlotting WesternMolecular Sequence DataPalmitic AcidSRC Family Tyrosine KinaseBiochemistryCell LineCricetinaeArrestinTumor Cells CulturedAnimalsHumansAmino Acid SequenceReceptorMitogen-Activated Protein Kinase 1KinaseChemistryReceptors EndothelinCell MembraneHeterotrimeric GTP-Binding ProteinsCell biologyEnzyme ActivationErbB ReceptorsType C PhospholipasesCOS CellsMutationcardiovascular systemMutagenesis Site-DirectedPhosphorylationGTP-Binding Protein alpha Subunits Gq-G11Mitogen-Activated Protein KinasesProto-oncogene tyrosine-protein kinase SrcEuropean journal of biochemistry
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P38 MAP Kinase Signaling Is Required for the Conversion of CD4+CD25− T Cells into iTreg

2008

CD4+CD25+ regulatory T cells (Treg) are important mediators of immune tolerance. A subset of Treg can be generated in the periphery by TGF-beta dependent conversion of conventional CD4+CD25− T cells into induced Treg (iTreg). In chronic viral infection or malignancy, such induced iTreg, which limit the depletion of aberrant or infected cells, may be of pathogenic relevance. To identify potential targets for therapeutic intervention, we investigated the TGF-beta signaling in Treg. In contrast to conventional CD4+ T cells, Treg exhibited marked activation of the p38 MAP kinase pathway. Inhibition of p38 MAP kinase activity prevented the TGF-beta-dependent conversion of CD4+CD25− T cells into …

MAPK/ERK pathwayp38 mitogen-activated protein kinasesImmunologyBlotting WesternImmunology/Immunomodulationlcsh:MedicineImmunology/Autoimmunitychemical and pharmacologic phenomenaBiologyT-Lymphocytes Regulatoryp38 Mitogen-Activated Protein KinasesImmune toleranceImmunology/Leukocyte Signaling and Gene ExpressionMiceAnimalsIL-2 receptorlcsh:ScienceMultidisciplinarylcsh:RInterleukin-2 Receptor alpha SubunitFOXP3hemic and immune systemsFlow CytometryCell biologyMitogen-activated protein kinaseCD4 Antigensbiology.proteinPhosphorylationlcsh:QSignal transductionResearch ArticleSignal TransductionPLoS ONE
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Inflammatory activation and endothelial dysfunction markers in patients with permanent atrial fibrillation: A cross-sectional study

2020

In recent years a growing body of evidence supported the role of inflammation in the initiation, maintenance and outcome of atrial fibrillation (AF). Nevertheless, despite a large amount of information, whether AF or the underlying structural heart disease (SHD) is the cause of the inflammatory process is still under debate. We, therefore, sought to determine if the inflammatory process reflect an underlying disease or the arrhythmia 'per se'. We evaluated plasma levels of soluble Interleukin 2 Receptor Alpha (sIL-2Rα), TNF-α and IL-18 in 100 consecutive patients with permanent AF, (43 with a SHD and 57 without a SHD) compared to 121 age and sex-matched controls which had normal sinus rhyth…

MaleAgingmedicine.medical_specialtyHeart diseaseAlpha (ethology)InflammationDiseaseSystemic inflammationendothelial dysfunctionInternal medicineAtrial FibrillationmedicineHumansEndothelial dysfunctionReactive hyperemiaAgedAged 80 and overInflammationTumor Necrosis Factor-alphabusiness.industryInterleukin-18Interleukin-2 Receptor alpha SubunitAtrial fibrillationAtrial fibrillation Cytokines Endothelial dysfunction Inflammation Structural heart diseaseCell BiologyMiddle Agedmedicine.diseasestructural heart diseasecytokinesCross-Sectional StudiesLogistic ModelsROC CurveCase-Control StudiesCardiologyFemaleEndothelium Vascularmedicine.symptombusinessBiomarkersResearch Paper
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De novo loss-of-function KCNMA1 variants are associated with a new multiple malformation syndrome and a broad spectrum of developmental and neurologi…

2019

Abstract KCNMA1 encodes the large-conductance Ca2+- and voltage-activated K+ (BK) potassium channel α-subunit, and pathogenic gain-of-function variants in this gene have been associated with a dominant form of generalized epilepsy and paroxysmal dyskinesia. Here, we genetically and functionally characterize eight novel loss-of-function (LoF) variants of KCNMA1. Genome or exome sequencing and the participation in the international Matchmaker Exchange effort allowed for the identification of novel KCNMA1 variants. Patch clamping was used to assess functionality of mutant BK channels. The KCNMA1 variants p.(Ser351Tyr), p.(Gly356Arg), p.(Gly375Arg), p.(Asn449fs) and p.(Ile663Val) abolished the …

MaleAtaxiaGenotypeDevelopmental DisabilitiesMutation MissenseBiology03 medical and health sciences0302 clinical medicineNeurodevelopmental disorderProtein DomainsLoss of Function MutationGeneticsmedicineHumansMissense mutationAbnormalities MultipleGenetic Predisposition to DiseaseProtein Interaction Domains and MotifsAlleleLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMolecular BiologyAllelesGenetic Association StudiesGenetics (clinical)Loss functionExome sequencing030304 developmental biologyGenetics0303 health sciencesInfant NewbornGeneral MedicineParoxysmal dyskinesiamedicine.diseaseElectrophysiological PhenomenaPedigreePhenotypeAmino Acid SubstitutionSpeech delayFemaleGeneral Articlemedicine.symptom030217 neurology & neurosurgeryHuman Molecular Genetics
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Altered receptor subtypes in the forebrain of GABAA receptor δ subunit-deficient mice: recruitment of γ2 subunits

2002

A GABA(A) receptor delta subunit-deficient mouse line was created by homologous recombination in embryonic stem cells to investigate the role of the subunit in the brain GABA(A) receptors. High-affinity [(3)H]muscimol binding to GABA sites as studied by ligand autoradiography was reduced in various brain regions of delta(-/-) animals. [(3)H]Ro 15-4513 binding to benzodiazepine sites was increased in delta(-/-) animals, partly due to an increment of diazepam-insensitive receptors, indicating an augmented forebrain assembly of gamma 2 subunits with alpha 4 subunits. In the western blots of forebrain membranes of delta(-/-) animals, the level of gamma 2 subunit was increased and that of alpha …

MaleAzidesProtein subunitBiologyTritiumSynaptic TransmissionIon ChannelsGABAA-rho receptorInterleukin 10 receptor alpha subunitBenzodiazepinesMiceRadioligand Assaychemistry.chemical_compoundAnimalsReceptorGABA Agonistsgamma-Aminobutyric AcidMice KnockoutNeuronsBinding SitesMuscimolGABAA receptorGeneral NeuroscienceBrainAffinity LabelsNeural InhibitionReceptors GABA-AMolecular biologynervous systemMuscimolchemistryMutationForebrainFemaleCys-loop receptorsNeuroscience
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