Search results for "Immediate-Early Proteins"

showing 10 items of 40 documents

The Immune Evasion Paradox: Immunoevasins of Murine Cytomegalovirus Enhance Priming of CD8 T Cells by Preventing Negative Feedback Regulation▿

2008

ABSTRACTCytomegaloviruses express glycoproteins that interfere with antigen presentation to CD8 T cells. Although the molecular modes of action of these “immunoevasins” differ between cytomegalovirus species, the convergent biological outcome is an inhibition of the recognition of infected cells. In murine cytomegalovirus, m152/gp40 retains peptide-loaded major histocompatibility complex class I molecules in acis-Golgi compartment, m06/gp48 mediates their vesicular sorting for lysosomal degradation, and m04/gp34, although not an immunoevasin in its own right, appears to assist in the concerted action of all three molecules. Using the Ld-restricted IE1 epitope YPHFMPTNL in the BALB/c mouse m…

MuromegalovirusImmunologyAntigen presentationPriming (immunology)Genome ViralBiologyCD8-Positive T-LymphocytesMajor histocompatibility complexVirus ReplicationMicrobiologyEpitopeImmediate early proteinImmediate-Early ProteinsEpitopesMiceViral ProteinsImmune systemAntigenVirologyCytotoxic T cellAnimalsAntigen PresentationMice Inbred BALB CHerpesviridae InfectionsKiller Cells NaturalInsect ScienceImmunologybiology.proteinPathogenesis and ImmunityFemaleLymph NodesImmunologic MemorySpleen
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Identification of a Kd-restricted antigenic peptide encoded by murine cytomegalovirus early gene M84

2000

The two sister cytomegaloviruses (CMVs), human and murine CMV, have both evolved immune evasion functions that interfere with the major histocompatibility complex class I (MHC-I) pathway of antigen processing and presentation and are effectual in the early (E) phase of virus gene expression. However, studies on murine CMV have shown that E-phase immune evasion is leaky. An E-phase protein involved in immune evasion, namely m04-gp34, was found to simultaneously account for an antigenic peptide presented by the MHC-I molecule Dd. Recent work has demonstrated the induction of protective immunity specific for the E-phase protein M84-p65, one of two murine CMV homologues of the human CMV matrix …

MuromegalovirusPeptideBiologyMajor histocompatibility complexImmediate-Early ProteinsMiceOpen Reading FramesImmune systemVirologyAnimalsAmino Acid SequenceLymphocyte CountAntigens ViralGenes Immediate-EarlyGeneAntigenic peptidechemistry.chemical_classificationMice Inbred BALB CViral matrix proteinAntigen processingH-2 AntigensVirologyMolecular biologyPeptide FragmentschemistryCytomegalovirus earlybiology.proteinImmunologic MemoryT-Lymphocytes CytotoxicJournal of General Virology
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Early gene m18, a novel player in the immune response to murine cytomegalovirus

2002

The identification of all antigenic peptides encoded by a pathogen, its T cell ‘immunome’, is a research aim for rational vaccine design. Screening of proteome-spanning peptide libraries or computational prediction is used to identify antigenic peptides recognized by CD8 T cells. Based on their high coding capacity, cytomegaloviruses (CMVs) could specify numerous antigenic peptides. Yet, current evidence indicates that the memory CD8 T cell response in a given haplotype is actually focused on a few viral proteins. CMVs actively interfere with antigen processing and presentation by the expression of immune evasion proteins. In the case of murine CMV (mCMV), these proteins are effectual in th…

MuromegalovirusT cellMolecular Sequence DataCD8-Positive T-LymphocytesBiologyVirus ReplicationVirusImmediate-Early ProteinsMiceImmune systemVirologymedicineAntigenic variationAnimalsCytotoxic T cellAntigens ViralGeneCells CulturedBase SequenceAntigen processingFibroblastsVirologymedicine.anatomical_structureViral replicationPeptidesImmunologic MemoryJournal of General Virology
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Glucocorticoids inhibit MAP kinase via increased expression and decreased degradation of MKP-1

2001

Glucocorticoids inhibit the proinflammatory activities of transcription factors such as AP-1 and NF-kappa B as well as that of diverse cellular signaling molecules. One of these signaling molecules is the extracellular signal-regulated kinase (Erk-1/2) that controls the release of allergic mediators and the induction of proinflammatory cytokine gene expression in mast cells. The mechanism of inhibition of Erk-1/2 activity by glucocorticoids is unknown. Here we report a novel dual action of glucocorticoids for this inhibition. Glucocorticoids increase the expression of the MAP kinase phosphatase-1 (MKP-1) gene at the promoter level, and attenuate proteasomal degradation of MKP-1, which we re…

Proteasome Endopeptidase ComplexCell signalingMitogen-Activated Protein Kinase 3Cell Cycle ProteinsBiologyDexamethasoneGene Expression Regulation EnzymologicArticleGeneral Biochemistry Genetics and Molecular BiologyCell LineImmediate-Early ProteinsProinflammatory cytokineMiceGlucocorticoid receptorMultienzyme ComplexesProtein Phosphatase 1Phosphoprotein PhosphatasesAnimalsEnzyme InhibitorsPhosphorylationMolecular BiologyTranscription factorDNA PrimersMitogen-Activated Protein Kinase 1Regulation of gene expressionMitogen-Activated Protein Kinase 3Base SequenceGeneral Immunology and MicrobiologyKinaseHydrolysisGeneral NeuroscienceDual Specificity Phosphatase 1Cell biologyMice Inbred C57BLCysteine EndopeptidasesMitogen-activated protein kinasebiology.proteinMitogen-Activated Protein KinasesProtein Tyrosine PhosphatasesThe EMBO Journal
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Exogenous introduction of an immunodominant peptide from the non-structural IE1 protein of human cytomegalovirus into the MHC class I presentation pa…

2008

Exogenous introduction of particle-associated proteins of human cytomegalovirus (HCMV) into the major histocompatibility complex (MHC) class I presentation pathway by subviral dense bodies (DB) is an effective way to sensitize cells against CD8 T-cell (CTL) recognition and killing. Consequently, these particles have been proposed as a platform for vaccine development. We have developed a strategy to refine the antigenic composition of DB. For proof of principle, an HCMV recombinant (RV-VM3) was generated that encoded the immunodominant CTL determinant IE1TMY from the IE1 protein in fusion with the major constituent of DB, the tegument protein pp65. To generate RV-VM3, a bacterial artificial…

Recombinant Fusion ProteinsvirusesCytomegalovirusImmunodominanceMajor histocompatibility complexImmediate-Early Proteinslaw.inventionViral ProteinsAntigenlawVirologyMHC class IHumansAntigen PresentationbiologyHistocompatibility Antigens Class IVirionvirus diseasesViral VaccinesGenetic TherapyFusion proteinVirologyPeptide FragmentsCTL*Cytomegalovirus Infectionsbiology.proteinRecombinant DNACD8T-Lymphocytes CytotoxicJournal of General Virology
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CD8 T Cells Control Cytomegalovirus Latency by Epitope-Specific Sensing of Transcriptional Reactivation

2006

ABSTRACT During murine cytomegalovirus (mCMV) latency in the lungs, most of the viral genomes are transcriptionally silent at the major immediate-early locus, but rare and stochastic episodes of desilencing lead to the expression of IE1 transcripts. This low-frequency but perpetual expression is accompanied by an activation of lung-resident effector-memory CD8 T cells specific for the antigenic peptide 168-YPHFMPTNL-176, which is derivedfrom the IE1 protein. These molecular and immunological findings were combined in the “silencing/desilencing and immune sensing hypothesis” of cytomegalovirus latency and reactivation. This hypothesis proposes that IE1 gene expression proceeds to cell surfac…

Transcriptional ActivationMuromegalovirusvirusesImmunologyAntigen presentationCD8-Positive T-LymphocytesVirus ReplicationMajor histocompatibility complexModels BiologicalMicrobiologyEpitopeImmediate-Early ProteinsEpitopesImmunocompromised HostMiceAntigenVirologyMHC class IVirus latencymedicineAnimalsGene silencingCytotoxic T cellAmino Acid SequenceAntigens ViralLungBone Marrow TransplantationMice Inbred BALB CBase Sequencebiologyvirus diseasesHerpesviridae Infectionsbiochemical phenomena metabolism and nutritionmedicine.diseaseVirologyMolecular biologyVirus LatencyVirus-Cell InteractionsPhenotypeAmino Acid SubstitutionInsect ScienceDNA ViralMutagenesis Site-DirectedTrans-Activatorsbiology.proteinFemaleJournal of Virology
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Transactivation of cellular genes involved in nucleotide metabolism by the regulatory IE1 protein of murine cytomegalovirus is not critical for viral…

2008

ABSTRACT Despite its high coding capacity, murine CMV (mCMV) does not encode functional enzymes for nucleotide biosynthesis. It thus depends on cellular enzymes, such as ribonucleotide reductase (RNR) and thymidylate synthase (TS), to be supplied with deoxynucleoside triphosphates (dNTPs) for its DNA replication. Viral transactivation of these cellular genes in quiescent cells of host tissues is therefore a parameter of viral fitness relevant to pathogenicity. Previous work has shown that the IE1, but not the IE3, protein of mCMV transactivates RNR and TS gene promoters and has revealed an in vivo attenuation of the mutant virus mCMV-ΔIE1. It was attractive to propose the hypothesis that la…

Transcriptional ActivationMuromegalovirusvirusesImmunologyMutantMolecular Sequence DataBiologyVirus ReplicationMicrobiologyImmediate-Early ProteinsTransactivationMiceVirologyAnimalsPoint MutationAmino Acid SequencePromoter Regions GeneticGeneCells CulturedRegulation of gene expressionMice Inbred BALB CBase SequenceNucleotidesDNA replicationvirus diseasesTransfectionbiochemical phenomena metabolism and nutritionFibroblastsMolecular biologyGenome Replication and Regulation of Viral Gene ExpressionRibonucleotide reductaseViral replicationGene Expression RegulationLiverInsect ScienceNIH 3T3 CellsPeptidesSequence AlignmentJournal of virology
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Involvement of KSRP in the post-transcriptional regulation of human iNOS expression–complex interplay of KSRP with TTP and HuR

2005

We purified the KH-type splicing regulatory protein (KSRP) as a protein interacting with the 3'-untranslated region (3'-UTR) of the human inducible nitric oxide (iNOS) mRNA. Immunodepletion of KSRP enhanced iNOS 3'-UTR RNA stability in in vitro-degradation assays. In DLD-1 cells overexpressing KSRP cytokine-induced iNOS expression was markedly reduced. In accordance, downregulation of KSRP expression increases iNOS expression by stabilizing iNOS mRNA. Co-immunoprecipitations showed interaction of KSRP with the exosome and tristetraprolin (TTP). To analyze the role of KSRP binding to the 3'-UTR we studied iNOS expression in DLD-1 cells overexpressing a non-binding mutant of KSRP. In these ce…

Untranslated regionRNA StabilityTristetraprolinNitric Oxide Synthase Type II610 Medicine & healthRNA-binding proteinBiologyImmediate early proteinArticleGene Expression Regulation EnzymologicELAV-Like Protein 1Immediate-Early ProteinsTristetraprolinCell Line TumorGeneticsHumansRNA Messenger610 Medicine & healthPost-transcriptional regulation3' Untranslated RegionsRegulation of gene expressionMessenger RNAThree prime untranslated regionRNA-Binding ProteinsMolecular biologyDNA-Binding ProteinsELAV ProteinsAntigens SurfaceMutationTrans-ActivatorsCytokinesNitric Oxide SynthaseNucleic Acids Research
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Aplidin® induces JNK-dependent apoptosis in human breast cancer cells via alteration of glutathione homeostasis, Rac1 GTPase activation, and MKP-1 ph…

2006

Aplidin® is an antitumor agent in phase II clinical trials that induces apoptosis through the sustained activation of Jun N-terminal kinase (JNK). We report that Aplidin® alters glutathione homeostasis increasing the ratio of oxidized to reduced forms (GSSG/GSH). Aplidin® generates reactive oxygen species and disrupts the mitochondrial membrane potential. Exogenous GSH inhibits these effects and also JNK activation and cell death. We found two mechanisms by which Aplidin® activates JNK: rapid activation of Rac1 small GTPase and downregulation of MKP-1 phosphatase. Rac1 activation was diminished by GSH and enhanced by L-buthionine (SR)-sulfoximine, which inhibits GSH synthesis. Downregulatio…

rac1 GTP-Binding ProteinProgrammed cell deathSmall interfering RNAGlutathione reductaseDown-RegulationAntineoplastic AgentsApoptosisBreast NeoplasmsCell Cycle ProteinsBiologyPeptides CyclicImmediate-Early ProteinsMembrane Potentialschemistry.chemical_compoundMiceDownregulation and upregulationDepsipeptidesProtein Phosphatase 1Phosphoprotein PhosphatasesAnimalsHomeostasisHumansMolecular Biologychemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidaseGlutathione DisulfideJNK Mitogen-Activated Protein KinasesProtein phosphatase 1Dual Specificity Phosphatase 1Cell BiologyGlutathioneCell biologyEnzyme ActivationOxidative StressGlutathione ReductasechemistryMitochondrial MembranesGlutathione disulfideCalciumProtein Tyrosine PhosphatasesReactive Oxygen SpeciesCopperHeLa CellsCell Death and Differentiation
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Mouse models of cytomegalovirus latency: overview.

2002

Abstract Background: The molecular regulation of viral latency and reactivation is a central unsolved issue in the understanding of cytomegalovirus (CMV) biology. Like human CMV (hCMV), murine CMV (mCMV) can establish a latent infection in cells of the myeloid lineage. Since mCMV genome remains present in various organs after its clearance from hematopoietic cells first in bone marrow and much later in blood, there must exist one or more widely distributed cell type(s) representing the cellular site(s) of enduring mCMV latency in host tissues. Endothelial cells and histiocytes are candidates, but the question is not yet settled. Another long debated problem appears to be solved: mCMV establ…

virusesCytomegalovirusBiologymedicine.disease_causeVirusHerpesviridaeImmediate-Early ProteinsTransactivationMiceViral ProteinsVirologyVirus latencymedicineCytotoxic T cellAnimalsHumansLatency (engineering)GeneMice Inbred BALB Cvirus diseasesmedicine.diseaseVirologyVirus LatencyHaematopoiesisDisease Models AnimalInfectious DiseasesImmunologyCytomegalovirus InfectionsTrans-ActivatorsVirus ActivationJournal of clinical virology : the official publication of the Pan American Society for Clinical Virology
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