0000000000053851

AUTHOR

Andreas Kerstan

showing 3 related works from this author

Alternative Polyadenylation Events Contribute to the Induction of NF-ATc in Effector T Cells

1999

Abstract The transcription factor NF-ATc is synthesized in three prominent isoforms. These differ in the length of their C terminal peptides and mode of synthesis. Due to a switch from the use of a 3′ polyA site to a more proximal polyA site, NF-ATc expression switches from the synthesis of the two longer isoforms in naive T cells to that of short isoform A in T effector cells. The relative low binding affinity of cleavage stimulation factor CstF-64 to the proximal polyA site seems to contribute to its neglect in naive T cells. These alternative polyadenylation events ensure the rapid accumulation of high concentrations of NF-ATc necessary to exceed critical threshold levels of NF-ATc for g…

Gene isoformPolyadenylationImmunologyMolecular Sequence DataGene inductionBiologyLymphocyte ActivationTransfectionT-Lymphocytes RegulatoryJurkat CellsMiceGenes ReporterCritical thresholdTumor Cells CulturedImmunology and AllergyAnimalsHumansAmino Acid SequenceCloning MolecularLuciferasesTranscription factormRNA Cleavage and Polyadenylation FactorsCleavage stimulation factorBase SequenceNFATC Transcription FactorsEffectorNuclear ProteinsRNA-Binding ProteinsMolecular biologyDNA-Binding ProteinsInfectious DiseasesPoly ATranscription FactorsImmunity
researchProduct

NFATc1 supports imiquimod-induced skin inflammation by suppressing IL-10 synthesis in B cells

2016

Epicutaneous application of Aldara cream containing the TLR7 agonist imiquimod (IMQ) to mice induces skin inflammation that exhibits many aspects of psoriasis, an inflammatory human skin disease. Here we show that mice depleted of B cells or bearing interleukin (IL)-10-deficient B cells show a fulminant inflammation upon IMQ exposure, whereas ablation of NFATc1 in B cells results in a suppression of Aldara-induced inflammation. In vitro, IMQ induces the proliferation and IL-10 expression by B cells that is blocked by BCR signals inducing NFATc1. By binding to HDAC1, a transcriptional repressor, and to an intronic site of the Il10 gene, NFATc1 suppresses IL-10 expression that dampens the pro…

0301 basic medicineNecrosisScienceGeneral Physics and AstronomyInflammationHuman skinImiquimodBiologyGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesPsoriasismedicineddc:610Multidisciplinaryintegumentary systemQInterleukinGeneral ChemistryTLR7medicine.diseaseInterleukin 10030104 developmental biologyImmunologyCancer researchmedicine.symptommedicine.drugNature Communications
researchProduct

cFLIPL Inhibits Tumor Necrosis Factor-related Apoptosis-inducing Ligand-mediated NF-κB Activation at the Death-inducing Signaling Complex in Human Ke…

2004

Human keratinocytes undergo apoptosis following treatment with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) via surface-expressed TRAIL receptors 1 and 2. In addition, TRAIL triggers nonapoptotic signaling pathways including activation of the transcription factor NF-kappaB, in particular when TRAIL-induced apoptosis is blocked. The intracellular protein cFLIP(L) interferes with TRAIL-induced apoptosis at the death-inducing signaling complex (DISC) in many cell types. To study the role of cFLIP(L) in TRAIL signaling, we established stable HaCaT keratinocyte cell lines expressing varying levels of cFLIP(L). Functional analysis revealed that relative cFLIP(L) levels correlat…

KeratinocytesCytoplasmReceptor complexCell SurvivalCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisCell SeparationBiologyCaspase 8Sensitivity and SpecificityBiochemistryProinflammatory cytokineTNF-Related Apoptosis-Inducing LigandRibonucleasesCell Line TumorHumansEnzyme InhibitorsMolecular BiologyTranscription factorSkinInflammationCaspase 8Membrane GlycoproteinsTumor Necrosis Factor-alphaIntracellular Signaling Peptides and ProteinsNF-kappa BCell BiologyFlow CytometryRecombinant ProteinsCell biologyRetroviridaeApoptosisCaspasesDeath-inducing signaling complexRNATumor necrosis factor alphaSignal transductionApoptosis Regulatory ProteinsPropidiumProtein BindingSignal TransductionJournal of Biological Chemistry
researchProduct