Search results for "Isoform"

showing 10 items of 350 documents

The interleukin (IL)-31/IL-31R axis contributes to tumor growth in human follicular lymphoma

2014

Interleukin (IL)-31A binds to an heterodimer composed of IL-31 receptor A (IL-31RA) and Oncostatin M Receptor (OSMR). The IL-31/IL-31R complex is involved in the pathogenesis of various skin diseases, including cutaneous T-cell lymphoma. No information is available on the relations between the IL-31/IL-31R complex and B-cell lymphoma. Here we have addressed this issue in follicular lymphoma (FL), a prototypic germinal center(GC)-derived B-cell malignancy. IL-31 enhanced primary FL cell proliferation through IL-31R-driven signal transducer and activator of transcription factor 1/3 (STAT1/3), extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt phosphorylation. In contrast, GC B cells d…

MaleSTAT3 Transcription Factormedicine.medical_specialtyCancer ResearchPrimary Cell CultureFollicular lymphomaBiologyParacrine signallingCytosolCell-Derived MicroparticlesInternal medicinemedicineHumansProtein IsoformsPhosphorylationAutocrine signallingLymphoma FollicularCell ProliferationMitogen-Activated Protein Kinase 1B-LymphocytesMitogen-Activated Protein Kinase 3Gene Expression Regulation LeukemicInterleukinsMicrovesicleMedicine (all)Cell MembraneB-LymphocyteGerminal centerOncostatin M receptorInterleukinProtein IsoformReceptors InterleukinHematologyInterleukinMiddle Agedmedicine.diseaseGerminal CenterMolecular biologyCell-Derived MicroparticleEndocrinologySTAT1 Transcription FactorAnesthesiology and Pain MedicineOncologyFemaleSignal transductionNeoplasm GradingProto-Oncogene Proteins c-aktHumanSignal Transduction
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IQSEC2-related encephalopathy in males and females: a comparative study including 37 novel patients.

2019

Variants in IQSEC2, escaping X inactivation, cause X-linked intellectual disability with frequent epilepsy in males and females. We aimed to investigate sex-specific differences.

0301 basic medicineMaleGénétique clinique[SDV]Life Sciences [q-bio]MedizinPhysiology030105 genetics & hereditySeizures/epidemiologyEpilepsyBrain Diseases/epidemiologyX-linked inheritanceIntellectual disabilityGuanine Nucleotide Exchange FactorsProtein IsoformsMissense mutationGenetics(clinical)10. No inequalityNon-U.S. Gov'tGenetics (clinical)X-linked recessive inheritanceComputingMilieux_MISCELLANEOUSBrain DiseasesSex CharacteristicsResearch Support Non-U.S. Gov'tBrainSciences bio-médicales et agricoles3. Good healthPedigreePhenotypeintellectual disabilityFemaleBrain/growth & developmentSex characteristicsGénétique moléculaireGuanine Nucleotide Exchange Factors/geneticsEncephalopathyResearch SupportX-inactivationArticle03 medical and health sciencesSeizuresProtein Isoforms/geneticsmedicineJournal ArticleIQSEC2HumansIntellectual Disability/epidemiology[SDV.GEN]Life Sciences [q-bio]/Geneticsbusiness.industryInfant NewbornisoformsCorrectionInfantmedicine.diseaseNewbornHuman genetics030104 developmental biologyMutationepilepsyHuman medicinebusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Biallelic mutations in neurofascin cause neurodevelopmental impairment and peripheral demyelination

2019

See Karakaya and Wirth (doi:10.1093/brain/awz273) for a scientific commentary on this article. Neurofascin (NFASC) isoforms are immunoglobulin cell adhesion molecules involved in node of Ranvier assembly. Efthymiou et al. identify biallelic NFASC variants in ten unrelated patients with a neurodevelopmental disorder characterized by variable degrees of central and peripheral involvement. Abnormal expression of Nfasc155 is accompanied by severe loss of myelinated fibres.

Male[SDV]Life Sciences [q-bio][SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyNerve Fibers MyelinatedGene FrequencyNeurodevelopmental Disorder[SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]Nerve Growth FactorProtein IsoformsChildComputingMilieux_MISCELLANEOUSMyelin Sheathneurofascin; neurodevelopment; peripheral demyelinationAlleleneurodevelopmentDemyelinating DiseaseGenomicsneurodevelopment neurofascin peripheral demyelinationSettore MED/39 - Neuropsichiatria InfantilePedigree[SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunologyChild PreschoolPeripheral Nerve[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Femaleneurodevelopment; neurofascin; peripheral demyelinationNeurogliaHumanAdultAdolescentNervous System MalformationsGuillain-Barre SyndromeAxonNervous System MalformationneurofascinRanvier's NodesHumansNerve Growth FactorsPeripheral NervesAllelesAutoantibodiesperipheral demyelinationInfantProtein IsoformOriginal ArticlesAxonsnervous systemNeurodevelopmental DisordersCell Adhesion MoleculeMutationCell Adhesion MoleculesDemyelinating Diseases
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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
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Cellular stress induces cap-independent alpha-enolase/MBP-1 translation.

2015

AbstractMyc promoter-binding protein-1 (MBP-1) is a shorter protein variant of the glycolytic enzyme alpha-enolase. Although several lines of evidence indicate that MBP-1 acts as a tumor suppressor, the cellular mechanisms and signaling pathways underlying MBP-1 expression still remain largely elusive. To dissect these pathways, we used the SkBr3 breast cancer cell line and non-tumorigenic HEK293T cells ectopically overexpressing alpha-enolase/MBP-1. Here, we demonstrate that induced cell stresses promote MBP-1 expression through the AKT/PERK/eIF2α signaling axis. Our results contribute to shedding light on the molecular mechanisms underlying MBP-1 expression in non-tumorigenic and cancer c…

Alpha-enolaseCellEukaryotic Initiation Factor-2Alternative translationBiochemistryeIF-2 KinaseBreast cancerHEK293 CellStructural BiologyProtein IsoformsbiologyMedicine (all)Translation (biology)Recombinant ProteinEndoplasmic Reticulum StressRecombinant ProteinsNeoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureFemaleSignal transductionMyc promoter-binding protein-1Breast NeoplasmHumanSignal TransductionCell SurvivalDNA-Binding ProteinRecombinant Fusion ProteinsBiophysicsBreast NeoplasmsNeoplasm ProteinGeneticCell Line TumorEndoplasmic reticulum streGeneticsmedicineBiomarkers TumorHumansGene SilencingMolecular BiologyProtein kinase BTumor Suppressor ProteinTumor Suppressor ProteinsHEK 293 cellsProtein IsoformCell BiologySettore BIO/18 - GeneticaHEK293 CellsBiophysicGene Expression RegulationPhosphopyruvate HydrataseCancer cellbiology.proteinUnfolded protein responseCancer researchProto-Oncogene Proteins c-aktRecombinant Fusion ProteinFEBS letters
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Nfatc1/Αa and Blimp-1 Support the Follicular and Effector Phenotype of Tregs

2021

CD4 + CXCR5 + Foxp3 + T follicular regulatory (T FR ) cells control the germinal center responses. Like follicular helper T-cells, they express high levels of N uclear F actor of A ctivated T -cells c1 , predominantly its short isoform NFATc1/αA. Ablation of NFATc1 in Tregs prevents upregulation of CXCR5 and migration of T FR cells into B-cell follicles. By contrast, constitutive active NFATc1/αA defines the surface density of CXCR5, whose level determines how deep a T FR migrates into the GC and how effectively it controls antibody production. NFATc1/αA is necessary to overcome T FR -expressed B l ymphocyte- i nduced m aturation p rotein (Blimp-1), which can directly repress Cxcr5. Blimp-1…

Gene isoformTransactivationintegumentary systemDownregulation and upregulationChemistryEffectorGerminal centerFOXP3PhenotypeCXCR5Cell biologySSRN Electronic Journal
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Usher syndrome: molecular links of pathogenesis, proteins and pathways.

2006

Contains fulltext : 50437.pdf (Publisher’s version ) (Closed access) Usher syndrome is the most common form of deaf-blindness. The syndrome is both clinically and genetically heterogeneous, and to date, eight causative genes have been identified. The proteins encoded by these genes are part of a dynamic protein complex that is present in hair cells of the inner ear and in photoreceptor cells of the retina. The localization of the Usher proteins and the phenotype in animal models indicate that the Usher protein complex is essential in the morphogenesis of the stereocilia bundle in hair cells and in the calycal processes of photoreceptor cells. In addition, the Usher proteins are important in…

Genetics and epigenetic pathways of disease [NCMLS 6]Usher syndromeCell Cycle ProteinsNerve Tissue ProteinsBiologyRetinaAdherens junctionMiceHair Cells AuditoryCell polarityGeneticsmedicineotorhinolaryngologic diseasesNeurosensory disorders [UMCN 3.3]AnimalsHumansProtein IsoformsCell Cycle ProteinMolecular BiologyGenetics (clinical)Renal disorder [IGMD 9]Adaptor Proteins Signal TransducingStereociliumMembrane ProteinsSignal transducing adaptor proteinGeneral MedicineActin cytoskeletonmedicine.diseaseeye diseasesCell biologyCytoskeletal ProteinsGenetic defects of metabolism [UMCN 5.1]Ear InnerMultiprotein ComplexesCateninSynapsessense organsUsher SyndromesPhotoreceptor Cells Vertebrate
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Isolation and characterization of two T-box genes from sponges, the phylogenetically oldest metazoan taxon

2003

It is now well established that all metazoan phyla derived from one common ancestor, the hypothetical Urmetazoa. Due to the basal position of Porifera (Demospongiae) in the phylogenetic tree of Metazoa, studies on the mechanisms controlling the development of these animals can provide clues on the understanding of the origin of multicellular animals and on how the first organization of the body plan evolved. In this report we describe the isolation and genomic characterization of two T-box genes from the siliceous sponge Suberites domuncula. The phylogenetic analysis classifies one into the subfamily of Brachyury, Sd-Bra, and the second into the Tbx2 subfamily, Sd-Tbx2. Analyses of the Sd-B…

Siliceous spongeBrachyuryDNA ComplementarySubfamilyMolecular Sequence DataMolecular evolutionPhylogeneticsGeneticsAnimalsProtein IsoformsElectrophoresis Gel Two-DimensionalAmino Acid SequencePhylogenyBase SequencebiologyPhylogenetic treeSequence Analysis DNAAnatomybiology.organism_classificationPoriferaSuberites domunculaAlternative SplicingBody planEvolutionary biologyT-Box Domain ProteinsProtein Processing Post-TranslationalDevelopmental BiologyDevelopment Genes and Evolution
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Altered splicing pattern of TACC1 mRNA in gastric cancer

2002

Abstract Transforming acidic coiled-coil ( TACC ) proteins are centrosome and microtubule-associated proteins that are essential for mitotic spindle function. We identified TACC1 as an immunogenic protein and a potential tumor antigen by applying serological identification of antigens by recombinant expression cloning (SEREX) technique to screen a gastric cancer cDNA library. The 5′RLM-RACE and reverse transcriptase polymerase chain reaction analyses revealed at least six different transcript variants of TACC1 with variable transcription start sites and alternative exon usage (designated TACC1-A–TACC1-F ). All transcripts differ in their 5′ ends but share an identical 3′ region encoding coi…

Fetal ProteinsGene isoformCancer ResearchTranscription GeneticBiologyPolymerase Chain ReactionExonStomach NeoplasmsGene expressionGeneticsmedicineHumansRNA MessengerMolecular BiologyDNA PrimersBase SequencecDNA libraryAlternative splicingGenetic VariationNuclear ProteinsCancermedicine.diseaseMolecular biologyReverse transcriptaseAlternative SplicingRNA splicingMicrotubule-Associated ProteinsCancer Genetics and Cytogenetics
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Usher syndrome and Leber congenital amaurosis are molecularly linked via a novel isoform of the centrosomal ninein-like protein.

2009

Contains fulltext : 80984.pdf (Publisher’s version ) (Closed access) Usher syndrome (USH) and Leber congenital amaurosis (LCA) are autosomal recessive disorders resulting in syndromic and non-syndromic forms of blindness. In order to gain insight into the pathogenic mechanisms underlying retinal degeneration, we searched for interacting proteins of USH2A isoform B (USH2A(isoB)) and the LCA5-encoded protein lebercilin. We identified a novel isoform of the centrosomal ninein-like protein, hereby named Nlp isoform B (Nlp(isoB)), as a common interactor. Although we identified the capacity of this protein to bind calcium with one of its three EF-hand domains, the interacton with USH2A(isoB) did …

Gene isoformRetinal degenerationCandidate geneGenetics and epigenetic pathways of disease [NCMLS 6]Usher syndromeMolecular Sequence DataOptic Atrophy Hereditary LeberBiologyIn Vitro TechniquesNeuroinformatics [DCN 3]CiliopathiesRetinaCell LineMiceCiliogenesisTwo-Hybrid System TechniquesGeneticsmedicineotorhinolaryngologic diseasesAnimalsHumansProtein IsoformsPhotoreceptor CellsAmino Acid SequenceNuclear proteinRats WistarEye ProteinsMolecular BiologyGenetics (clinical)GeneticsExtracellular Matrix ProteinsCiliumNuclear ProteinsGeneral MedicineArticlesmedicine.diseaseRatsMice Inbred C57BLMicrotubule-Associated ProteinsSequence AlignmentUsher SyndromesFunctional Neurogenomics [DCN 2]Protein BindingHuman Molecular Genetics
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