Search results for "Intracellular Signaling Peptides and Protein"

showing 10 items of 140 documents

On the roles of Notch, Delta, kuzbanian, and inscuteable during the development of Drosophila embryonic neuroblast lineages

2009

AbstractThe generation of cellular diversity in the nervous system involves the mechanism of asymmetric cell division. Besides an array of molecules, including the Par protein cassette, a heterotrimeric G protein signalling complex, Inscuteable plays a major role in controlling asymmetric cell division, which ultimately leads to differential activation of the Notch signalling pathway and correct specification of the two daughter cells. In this context, Notch is required to be active in one sibling and inactive in the other. Here, we investigated the requirement of genes previously known to play key roles in sibling cell fate specification such as members of the Notch signalling pathway, e.g…

Lineage (genetic)Embryo NonmammalianNotchCell divisionCell fate specificationDisintegrinsNeurogenesisContext (language use)BiologyCell fate determinationPolymerase Chain Reaction03 medical and health sciences0302 clinical medicineNeuroblastAsymmetric cell divisionAnimalsDrosophila ProteinsCell LineageMolecular Biology030304 developmental biologyDNA PrimersGeneticsNeurons0303 health sciencesBase SequenceReceptors NotchNeurogenesisIntracellular Signaling Peptides and ProteinsMembrane ProteinsMetalloendopeptidasesCell BiologyEmbryonic stem cellImmunohistochemistryCytoskeletal ProteinsAsymmetric cell divisionDrosophilakuzbanian030217 neurology & neurosurgerySignal TransductionDevelopmental BiologyDevelopmental Biology
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pp32/PHAPI determines the apoptosis response of non-small-cell lung cancer

2007

During malignant transformation, cancer cells have to evade cell-intrinsic tumor suppressor mechanisms including apoptosis, thus acquiring a phenotype that is relatively resistant to clinically applied anticancer therapies. Molecular characterization of apoptotic signal transduction defects may help to identify prognostic markers and to develop novel therapeutic strategies. To this end we have undertaken functional analyses of drug-induced apoptosis in human non-small cell-lung cancer (NSCLC) cells. We found that primary drug resistance correlated with defects in apoptosome-dependent caspase activation in vitro. While cytochrome c-induced apoptosome formation was maintained, the subsequent …

Lung NeoplasmsTransplantation HeterologousAntineoplastic AgentsApoptosisMice SCIDBiologyMalignant transformationMiceProstate cancerIn vivoCarcinoma Non-Small-Cell LungmedicineAnimalsHumansLung cancerMolecular BiologyIntracellular Signaling Peptides and ProteinsNuclear ProteinsRNA-Binding ProteinsCancerCell Biologymedicine.diseaseCell biologyEnzyme ActivationApoptosisCaspasesCancer cellCancer researchSignal transductionNeoplasm TransplantationCell Death & Differentiation
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Three-dimensional invasion of human glioblastoma cells remains unchanged by X-ray and carbon ion irradiation in vitro.

2012

Purpose Cell invasion represents one of the major determinants that treatment has failed for patients suffering from glioblastoma. Contrary findings have been reported for cell migration upon exposure to ionizing radiation. Here, the migration and invasion capability of glioblastoma cells on and in collagen type I were evaluated upon irradiation with X-rays or carbon ions. Methods and Materials Migration on and invasion in collagen type I were evaluated in four established human glioblastoma cell lines exposed to either X-rays or carbon ions. Furthermore, clonogenic radiation survival, proliferation (5-bromo-2-deoxyuridine positivity), DNA double-strand breaks (γH2AX/53BP1-positive foci), a…

MAPK/ERK pathwayCancer ResearchCell signalingMMP2MAP Kinase Kinase 4p38 Mitogen-Activated Protein KinasesCollagen Type IExtracellular matrixHistonesPhosphatidylinositol 3-KinasesCell MovementMedicineHumansRadiology Nuclear Medicine and imagingDNA Breaks Double-StrandedNeoplasm InvasivenessClonogenic assayPI3K/AKT/mTOR pathwayCell ProliferationRadiationbusiness.industryCell growthBrain NeoplasmsIntegrin beta1Intracellular Signaling Peptides and ProteinsCell migrationCarbonOncologyBromodeoxyuridineImmunologyCancer researchbusinessCell Migration AssaysGlioblastomaTumor Suppressor p53-Binding Protein 1International journal of radiation oncology, biology, physics
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p42 MAPK phosphorylates 80 kDa MARCKS at Ser-113.

1996

Abstract It is demonstrated here that p42 MAPKinase (p42 MAPK) phosphorylates the M yristoylated A lanine- R ich C - K inase S ubstrate (MARCKS) at Ser-113. In permeabilised Swiss 3T3 cells activation of protein kinase C (PKC) leads to p42 MAPK activation, but only the protein kinase C sites in MARCKS become phosphorylated and not Ser-113. The mitogen platelet-derived growth factor (PDGF) elicits the same response. These results demonstrate that while Ser-113 is a substrate for p42 MAPK in vitro and can be phosphorylated in vivo as shown by Taniguchi et al. [(1994) J. Biol. Chem. 269, 18299–18302], its phosphorylation is not subject to acute regulation by p42 MAPK in Swiss 3T3 cells.

MAPK/ERK pathwayMARCKSmedicine.medical_treatmentMitogen-activated protein kinase kinaseBiochemistryenvironment and public healthSubstrate SpecificityMiceStructural BiologySerinep42MAPKinasePhosphorylationMyristoylated Alanine-Rich C Kinase SubstrateCells CulturedProtein Kinase CMitogen-Activated Protein Kinase 1Platelet-Derived Growth FactorbiologyChemistryIntracellular Signaling Peptides and Proteins3T3 CellsProtein-Tyrosine KinasesCell biologyBiochemistryMitogen-activated protein kinasePhosphorylationTetradecanoylphorbol Acetatebiological phenomena cell phenomena and immunityPlatelet-derived growth factor receptorhormones hormone substitutes and hormone antagonistsendocrine systemRecombinant Fusion ProteinsMolecular Sequence DataBiophysicsGeneticsmedicineAnimalsAmino Acid SequenceMARCKSMolecular BiologyProtein kinase CGrowth factorMembrane ProteinsProteinsCell BiologyPeptide FragmentsEnzyme ActivationMolecular Weightenzymes and coenzymes (carbohydrates)Calcium-Calmodulin-Dependent Protein Kinasesbiology.proteinMutagenesis Site-DirectedMitogensFEBS letters
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Activation of MAP kinase p38 is critical for the cell-cycle–controlled suppressor function of regulatory T cells

2007

AbstractRegulatory T cells play an essential role in the control of self-tolerance and processes of adaptive immunity. Tolerogenic IL-10–modulated human dendritic cells (IL-10DCs) induce anergic T cells with strong suppressive properties (iTregs) that inhibit the activation of effector T cells. In this study, we evaluated the interaction between cell-cycle regulation and intracellular signaling in these iTregs. Analysis of signal transduction events revealed a down-regulation of the mitogen-activated protein kinases (MAPKs) Jun N-terminal kinase (JNK) and a nonactivation of extracellular-signal–regulated kinase (ERK) in contrast to a marked activation of p38 MAPK and the p38 effector MAPK-a…

MAPK/ERK pathwayp38 mitogen-activated protein kinasesImmunologyIn Vitro TechniquesProtein Serine-Threonine KinasesBiologyT-Lymphocytes Regulatoryp38 Mitogen-Activated Protein KinasesBiochemistryAldesleukinHumansProtein kinase AMitogen-Activated Protein Kinase KinasesKinaseCell CycleIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesCell BiologyHematologyAcquired immune systemInterleukin-10Cell biologyMitogen-activated protein kinasebiology.proteinSignal transductionCyclin-Dependent Kinase Inhibitor p27Blood
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Mapping candidate genes for Drosophila melanogaster resistance to the parasitoid wasp Leptopilina boulardi.

2006

Drosophila melanogaster resistance against the parasitoid wasp Leptopilina boulardi is under the control of a single gene (Rlb), with two alleles, the resistant one being dominant. Using strains bearing deletions, we previously demonstrated that the 55E2–E6; 55F3 region on chromosome 2R is involved in the resistance phenomenon. In this paper, we first restricted the Rlb containing region by mapping at the molecular level the breakpoints of the Df(2R)Pc66, Df(2R)P34 and Df(2R)Pc4 deficiencies, using both chromosomal in situ hybridization and Southern analyses. The resistance gene was localized in a 100 kb fragment, predicted to contain about 10 different genes. Male recombination genetic exp…

Male0106 biological sciencesCandidate geneWaspsGenes Insect010603 evolutionary biology01 natural sciencesParasitoid wasp03 medical and health sciencesGenes RegulatorGeneticsAnimalsDrosophila Proteins[SDV.BV]Life Sciences [q-bio]/Vegetal BiologyAlleleGeneIn Situ Hybridization030304 developmental biologyRecombination GeneticGenetics0303 health sciences[SDV.GEN]Life Sciences [q-bio]/GeneticsModels GeneticbiologyBreakpointIntracellular Signaling Peptides and ProteinsChromosome MappingMembrane ProteinsChromosomeGeneral MedicineCosmidsbiology.organism_classificationDrosophila melanogasterLarvaDrosophila melanogasterRecombination
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Metabolic Inflammation-Associated IL-17A Causes Non-alcoholic Steatohepatitis and Hepatocellular Carcinoma

2016

Obesity increases hepatocellular carcinoma (HCC) risks via unknown mediators. We report that hepatic unconventional prefoldin RPB5 interactor (URI) couples nutrient surpluses to inflammation and non-alcoholic steatohepatitis (NASH), a common cause of HCC. URI-induced DNA damage in hepatocytes triggers inflammation via T helper 17 (Th17) lymphocytes and interleukin 17A (IL-17A). This induces white adipose tissue neutrophil infiltration mediating insulin resistance (IR) and fatty acid release, stored in liver as triglycerides, causing NASH. NASH and subsequently HCC are prevented by pharmacological suppression of Th17 cell differentiation, IL-17A blocking antibodies, and genetic ablation of t…

Male0301 basic medicineCancer ResearchCarcinoma HepatocellularInflammationWhite adipose tissueDiet High-FatMice03 medical and health sciencesNon-alcoholic Fatty Liver DiseasemedicineAnimalsHumansUnconventional prefoldin RPB5 interactorbiologyInterleukin-17Liver NeoplasmsFatty liverIntracellular Signaling Peptides and ProteinsCell Biologymedicine.diseasedigestive system diseasesGene Expression Regulation NeoplasticRepressor Proteins030104 developmental biologyNeutrophil InfiltrationOncologyHepatocellular carcinomaImmunologybiology.proteinTh17 CellsInterleukin 17SteatosisSteatohepatitismedicine.symptomDNA DamageCancer Cell
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Diagnostic strategy in segmentation defect of the vertebrae: a retrospective study of 73 patients

2018

BackgroundSegmentation defects of the vertebrae (SDV) are non-specific features found in various syndromes. The molecular bases of SDV are not fully elucidated due to the wide range of phenotypes and classification issues. The genes involved are in the Notch signalling pathway, which is a key system in somitogenesis. Here we report on mutations identified in a diagnosis cohort of SDV. We focused on spondylocostal dysostosis (SCD) and the phenotype of these patients in order to establish a diagnostic strategy when confronted with SDV.Patients and methodsWe used DNA samples from a cohort of 73 patients and performed targeted sequencing of the five known SCD-causing genes (DLL3,MESP2,LFNG,HES7…

Male0301 basic medicineOncologymedicine.medical_specialtyCandidate geneAdolescent030105 genetics & heredityspondylocostal dysostosisdiagnostic strategysegmentation defect of the vertebraewhole exome sequencingLFNG03 medical and health sciencesgene panelInternal medicineExome SequencingBasic Helix-Loop-Helix Transcription FactorsGeneticsmedicineHumansFLNBChildGenetics (clinical)Exome sequencingBone Diseases Developmentalbusiness.industryIntracellular Signaling Peptides and ProteinsGlycosyltransferasesInfantMembrane ProteinsRetrospective cohort studymedicine.diseasePhenotypeSpineSpondylocostal dysostosisPedigreePhenotype[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsChild PreschoolMutationCohortFemaleT-Box Domain Proteinsbusiness
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SPRED1, a RAS MAPK pathway inhibitor that causes Legius syndrome, is a tumour suppressor downregulated in paediatric acute myeloblastic leukaemia

2013

Constitutional dominant loss-of-function mutations in the SPRED1 gene cause a rare phenotype referred as neurofibromatosis type 1 (NF1)-like syndrome or Legius syndrome, consisted of multiple café-au-lait macules, axillary freckling, learning disabilities and macrocephaly. SPRED1 is a negative regulator of the RAS MAPK pathway and can interact with neurofibromin, the NF1 gene product. Individuals with NF1 have a higher risk of haematological malignancies. SPRED1 is highly expressed in haematopoietic cells and negatively regulates haematopoiesis. SPRED1 seemed to be a good candidate for leukaemia predisposition or transformation. We performed SPRED1 mutation screening and expression status i…

MaleCancer ResearchAdolescentLoss of HeterozygosityFrameshift mutationGene productLoss of heterozygosityPrecursor B-Cell Lymphoblastic Leukemia-Lymphomahemic and lymphatic diseasesGeneticsmedicineHumansGenes Tumor SuppressorNeurofibromatosisChildMolecular BiologyAdaptor Proteins Signal TransducingLegius syndromeNeurofibromin 1biologyCafe-au-Lait SpotsInfant NewbornIntracellular Signaling Peptides and ProteinsMacrocephalyInfantMembrane Proteinsmedicine.diseaseNeurofibromin 1Gene Expression Regulation NeoplasticLeukemia Myeloid AcuteHaematopoiesisGenes rasChild PreschoolMutationCancer researchbiology.proteinFemalemedicine.symptomOncogene
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Integrating genome-wide genetic variations and monocyte expression data reveals trans-regulated gene modules in humans.

2011

One major expectation from the transcriptome in humans is to characterize the biological basis of associations identified by genome-wide association studies. So far, few cis expression quantitative trait loci (eQTLs) have been reliably related to disease susceptibility. Trans-regulating mechanisms may play a more prominent role in disease susceptibility. We analyzed 12,808 genes detected in at least 5% of circulating monocyte samples from a population-based sample of 1,490 European unrelated subjects. We applied a method of extraction of expression patterns—independent component analysis—to identify sets of co-regulated genes. These patterns were then related to 675,350 SNPs to identify maj…

MaleCancer ResearchGene ExpressionGenome-wide association studyGenetic NetworksCoronary Artery Disease[SDV.GEN] Life Sciences [q-bio]/GeneticsCardiovascularMESH: MonocytesMonocytesMESH: HypertensionTranscriptomes0302 clinical medicineMESH: ProteinsMESH: Genetic VariationGenetics (clinical)GeneticsMESH: Aged0303 health scienceseducation.field_of_studyMESH: Middle AgedMESH: Polymorphism Single NucleotideIntracellular Signaling Peptides and ProteinsMESH: Genetic Predisposition to DiseaseGenomicsMESH: Transcription FactorsMiddle AgedMESH: Ribosomal ProteinsMESH: Gene Expression Regulation3. Good healthHypertensionMedicineFemaleMESH: Diabetes Mellitus Type 1Research ArticleAdultRibosomal Proteinslcsh:QH426-470PopulationQuantitative Trait LociLocus (genetics)Single-nucleotide polymorphismBiologyQuantitative trait locusPolymorphism Single Nucleotide03 medical and health sciencesMESH: Gene Expression ProfilingGenome Analysis ToolsGeneticsGenome-Wide Association StudiesHumansGenetic Predisposition to DiseaseGene NetworkseducationMolecular BiologyBiologyEcology Evolution Behavior and SystematicsMESH: Genome Human030304 developmental biologyGenetic associationAdaptor Proteins Signal TransducingAged[SDV.GEN]Life Sciences [q-bio]/GeneticsMESH: HumansGenome HumanGene Expression ProfilingGenetic VariationProteinsHuman GeneticsMESH: AdultAtherosclerosisMESH: MaleMESH: Quantitative Trait LociGene expression profilingCeliac Diseaselcsh:GeneticsDiabetes Mellitus Type 1Gene Expression RegulationExpression quantitative trait lociGenetics of DiseaseMESH: Genome-Wide Association StudyMESH: MuramidaseMuramidaseGenome Expression AnalysisMESH: Female030217 neurology & neurosurgeryMESH: Celiac DiseaseGenome-Wide Association StudyTranscription Factors
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