Search results for "Nuclear proteins"

showing 10 items of 295 documents

Expression inactivation of SMARCA4 by microRNAs in lung tumors

2014

SMARCA4 is the catalytic subunit of the SWI/SNF chromatin-remodeling complex, which alters the interactions between DNA and histones and modifies the availability of the DNA for transcription. The latest deep sequencing of tumor genomes has reinforced the important and ubiquitous tumor suppressor role of the SWI/SNF complex in cancer. However, although SWI/SNF complex plays a key role in gene expression, the regulation of this complex itself is poorly understood. Significantly, an understanding of the regulation of SMARCA4 expression has gained in importance due to recent proposals incorporating it in therapeutic strategies that use synthetic lethal interactions between SMARCA4-MAX and SMAR…

Lung NeoplasmsDeep sequencingHistonesTranscription (biology)Catalytic DomainCell Line TumorGene expressionmicroRNAGeneticsHumansCloning MolecularMolecular BiologyTranscription factorGenetics (clinical)Cell ProliferationCell NucleusRegulation of gene expressionGeneticsbiologyDNA HelicasesHigh-Throughput Nucleotide SequencingNuclear ProteinsReproducibility of ResultsArticlesGeneral MedicineChromatin Assembly and DisassemblyPrognosisUp-RegulationCell biologyGene Expression Regulation NeoplasticMicroRNAsHistonebiology.proteinSMARCA4HeLa CellsTranscription FactorsHuman Molecular Genetics
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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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Symplekin, a polyadenylation factor, prevents MOZ and MLL activity on HOXA9 in hematopoietic cells

2013

International audience; MOZ and MLL encoding a histone acetyltransferase and a histone methyltransferase, respectively, are targets for recurrent chromosomal translocations found in acute myeloblastic or lymphoblastic leukemia. We have previously shown that MOZ and MLL cooperate to activate HOXA9 gene expression in hematopoietic stem/progenitors cells. To dissect the mechanism of action of this complex, we decided to identify new proteins interacting with MOZ. We found that the scaffold protein Symplekin that supports the assembly of polyadenylation machinery was identified by mass spectrometry. Symplekin interacts and co-localizes with both MOZ and MLL in immature hematopoietic cells. Its …

MLLScaffold proteinPolyadenylationHematopoietic System[SDV]Life Sciences [q-bio]PolyadenylationCell Line03 medical and health scienceschemistry.chemical_compound0302 clinical medicinehemic and lymphatic diseasesGene expressionTranscriptional regulationHumansRNA MessengerPromoter Regions GeneticSymplekinHSF1neoplasmsMolecular BiologyHistone Acetyltransferases030304 developmental biologyHomeodomain ProteinsmRNA Cleavage and Polyadenylation Factors0303 health sciences[ SDV ] Life Sciences [q-bio]biologyNuclear ProteinsHistone-Lysine N-MethyltransferaseHOXA9Transcription regulationCell BiologyHistone acetyltransferaseMOZCell biology[SDV] Life Sciences [q-bio]Protein TransportRUNX1chemistry030220 oncology & carcinogenesisHistone methyltransferaseCancer researchbiology.proteinMyeloid-Lymphoid Leukemia ProteinProtein BindingBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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Fine-tuning nucleophosmin in macrophage differentiation and activation

2011

Abstract M-CSF–driven differentiation of peripheral blood monocytes is one of the sources of tissue macrophages. In humans and mice, the differentiation process involves the activation of caspases that cleave a limited number of proteins. One of these proteins is nucleophosmin (NPM1), a multifunctional and ubiquitous protein. Here, we show that caspases activated in monocytes exposed to M-CSF cleave NPM1 at D213 to generate a 30-kDa N-terminal fragment. The protein is further cleaved into a 20-kDa fragment, which involves cathepsin B. NPM1 fragments contribute to the limited motility, migration, and phagocytosis capabilities of resting macrophages. Their activation with lipopolysaccharides …

Macrophage colony-stimulating factorLipopolysaccharidesCellular differentiationImmunologyBiochemistryProinflammatory cytokine03 medical and health sciencesPhagocytes Granulocytes and MyelopoiesisMice0302 clinical medicineAnimalsHumansNuclear proteinCaspaseCells Cultured030304 developmental biologyMice Knockout0303 health sciencesNucleophosminbiologyMacrophage Colony-Stimulating FactorMacrophagesNuclear ProteinsCell DifferentiationCell BiologyHematologyMacrophage ActivationNFKB1Molecular biologyCathepsinsCell biologyProtein Structure TertiaryCXCL1Mice Inbred C57BL030220 oncology & carcinogenesisCaspasesbiology.proteinNucleophosminProtein Processing Post-TranslationalBlood
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TBL1XR1 mutations in Pierpont syndrome are not restricted to the recurrent p.Tyr446Cys mutation

2018

IF 2.264; International audience; Pierpont syndrome is a rare and sporadic syndrome, including developmental delay, facial characteristics, and abnormal extremities. Recently, a recurrent de novo TBL1XR1 variant (c.1337A > G; p.Tyr446Cys) has been identified in eight patients by whole‐exome sequencing. A dominant‐negative effect of this mutation is strongly suspected, since patients with TBL1XR1 deletion and other variants predicting loss of function do not share the same phenotype. We report two patients with typical Pierpont‐like syndrome features. Exome sequencing allowed identifying a de novo heterozygous missense TBL1XR1 variant in both patients, different from those already reported: …

Male0301 basic medicineAdolescentGenotypeReceptors Cytoplasmic and NuclearBiology03 medical and health sciences0302 clinical medicinePIERPONT SYNDROMEGeneticsHumansTBL1XR1Missense mutationAbnormalities MultipleRecurrent mutationGenetic TestingAllelesGenetics (clinical)Exome sequencingLoss functionUltrasonographyGeneticsComparative Genomic Hybridization[SDV.GEN]Life Sciences [q-bio]/GeneticsBrainFaciesNuclear ProteinsSyndromeMagnetic Resonance ImagingPhenotype3. Good healthRepressor ProteinsPhenotype030104 developmental biologyAmino Acid Substitution030220 oncology & carcinogenesisMutationMutation (genetic algorithm)Pierpont syndromeAmerican Journal of Medical Genetics Part A
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Disruption of the ATXN1-CIC complex causes a spectrum of neurobehavioral phenotypes in mice and humans

2017

International audience; Gain-of-function mutations in some genes underlie neurodegenerative conditions, whereas loss-of-function mutations in the same genes have distinct phenotypes. This appears to be the case with the protein ataxin 1 (ATXN1), which forms a transcriptional repressor complex with capicua (CIC). Gain of function of the complex leads to neurodegeneration, but ATXN1-CIC is also essential for survival. We set out to understand the functions of the ATXN1-CIC complex in the developing forebrain and found that losing this complex results in hyperactivity, impaired learning and memory, and abnormal maturation and maintenance of upper-layer cortical neurons. We also found that CIC …

Male0301 basic medicineAutism Spectrum DisorderAtaxin 1neuronsautismNerve Tissue Proteinsattention-deficit/hyperactivity disorderAmygdalaArticleMice03 medical and health sciencesTranscriptional repressor complexataxin-1Cerebellum[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineAnimalsHumansAttention deficit hyperactivity disorderInterpersonal Relationssca1 neuropathologybiologysocial-behaviorNeurodegenerationcag repeatNuclear ProteinsNeurodegenerative Diseasesmedicine.diseasePhenotypeRepressor ProteinsPhenotype030104 developmental biologymedicine.anatomical_structureAutism spectrum disorderintellectual disabilitybiology.proteinAutismFemaleNeurosciencetime pcr datarepressor capicua[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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The genetic tumor background is an important determinant for heterogeneous MYCN ‐amplified neuroblastoma

2016

Amplification of MYCN is the signature genetic aberration of 20–25% of neuroblastoma and a stratifying marker associated with aggressive tumor behavior. The detection of heterogeneous MYCN amplification (hetMNA) poses a diagnostic dilemma due to the uncertainty of its relevance to tumor behavior. Here, we aimed to shed light on the genomic background which permits hetMNA in neuroblastoma and tied the occurrence to other stratifying markers and disease outcome. We performed SNP analysis using Affymetrix Cytoscan HD arrays on 63 samples including constitutional DNA, tumor, bone marrow and relapse samples of 26 patients with confirmed hetMNA by MYCN‐FISH. Tumors of patients ≤18m were mostly an…

Male0301 basic medicineCancer ResearchPathologymedicine.medical_specialtyTumor Markers and Signaturesuniparental disomyAdolescentMYCN amplificationAneuploidyBiologyPolymorphism Single NucleotideN-Myc Proto-Oncogene ProteinBenign tumorGenetic HeterogeneityNeuroblastoma03 medical and health sciences0302 clinical medicineNeuroblastomamedicineHumansChildIn Situ Hybridization FluorescenceChromosome AberrationsOncogene ProteinsN-Myc Proto-Oncogene ProteinGenetic heterogeneityGene AmplificationInfantNuclear ProteinsAneuploidymedicine.diseaseUniparental disomy030104 developmental biologyOncologyChild Preschool030220 oncology & carcinogenesisintratumoral heterogeneityCancer researchFemaleChromosome DeletionTrisomySNP arrayInternational Journal of Cancer
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Deregulation of ARID1A, CDH1, cMET and PIK3CA and target-related microRNA expression in gastric cancer.

2015

Genetic and epigenetic alterations play an important role in gastric cancer (GC) pathogenesis. Aberrations of the phosphatidylinositol-3-kinase signaling pathway are well described. However, emerging genes have been described such as, the chromatin remodeling gene ARID1A. Our aim was to determine the expression levels of four GC-related genes, ARID1A, CDH1, cMET and PIK3CA, and 14 target-related microRNAs (miRNAs). We compared mRNA and miRNA expression levels among 66 gastric tumor and normal adjacent mucosa samples using quantitative real-time reverse transcription PCR. Moreover, ARID1A, cMET and PIK3CA protein levels were assessed by immunohistochemistry (IHC). Finally, gene and miRNAs as…

MaleARID1AClass I Phosphatidylinositol 3-KinasesReal-Time Polymerase Chain ReactionCDH1Epigenesis GeneticPhosphatidylinositol 3-KinasesAntigens CDStomach NeoplasmsGene expressionmicroRNAmedicineBiomarkers TumorHumansRNA MessengerAgedbiologyReverse Transcriptase Polymerase Chain ReactionGene Expression Profilinggastric cancerCancerNuclear ProteinsbiomarkersMiddle AgedProto-Oncogene Proteins c-metmedicine.diseaseCadherinsMolecular biologyImmunohistochemistryChromatinGene expression profilingReverse transcription polymerase chain reactionDNA-Binding ProteinsGene Expression Regulation NeoplasticMicroRNAsReal-time polymerase chain reactionmicrorna expressionOncologyGastric Mucosabiology.proteingene expressionFemaleTranscription FactorsResearch PaperOncotarget
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Prospero mutants induce precocious sexual behavior in Drosophila males.

2007

0001-8244 (Print) Journal Article Research Support, Non-U.S. Gov't; Brain maturation, a developmental process influenced by both endogenous and environmental factors, can affect sexual behavior. In vertebrates and invertebrates, sexual maturation is under the influence of hormones and neuromodulators, but the role of developmental genes in this process is still poorly understood. We report that prospero (pros), a gene crucial for nervous system development, can change the age of onset of sexual behavior in Drosophila melanogaster males: adult males carrying a single copy of several pros mutations court females and mate at a younger age than control males. However, these pros mutations had n…

MaleAgingmedia_common.quotation_subjectSexual BehavioreducationNerve Tissue ProteinsTranscription Factors/*geneticsCrossesmedicine.disease_causeCourtship03 medical and health sciencesSexual Behavior Animal0302 clinical medicineGeneticGeneticsmedicineNuclear Proteins/*geneticsAnimal/*physiologySexual maturityAnimalsDrosophila ProteinsMatingHydrocarbons/analysisGenetics (clinical)Ecology Evolution Behavior and SystematicsCrosses Genetic030304 developmental biologymedia_commonGenetics0303 health sciencesMutationbiologyDrosophila Proteins/*geneticsNuclear ProteinsProsperobiology.organism_classificationPhenotypeNerve Tissue Proteins/*geneticshumanitiesHydrocarbonsDrosophila melanogasterPhenotypeMutationFemaleDrosophila melanogasterAge of onset030217 neurology & neurosurgeryDrosophila melanogaster/cytology/*genetics/growth & development/physiologyTranscription FactorsBehavior genetics
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Expression of serologically identified tumor antigens in acute leukemias.

2003

Cancer/testis antigens (CTA) are an expanding family of immunogenic proteins selectively expressed in human neoplasms. As little is known about the expression of serologically identified CTA in leukemias so far, we investigated the expression of 5 CT genes (SSX-1, HOM-MEL-40/SSX-2, HOM-TES-14/SCP-1, SCP-3 and NY-ESO-1) in leukemic blood samples obtained from patients with either acute lymphatic leukemias (ALL) or myelocytic leukemia (AML). RT-PCR-analyses showed no expression of any of the CT-genes in the leukemia samples of 19 patients with AML, whereas frequent expression was found in ALL. In the 17 ALL cases studied, SCP3a, SSX-1, HOM-MEL-40/SXX-2 and HOM-TES-14/SCP-1 were expressed in 4…

MaleCancer ResearchCell Cycle ProteinsSerologyAntigenTesticular NeoplasmsAntigens Neoplasmhemic and lymphatic diseasesBiomarkers TumorMedicineHumansRNA MessengerGeneDNA Primersbusiness.industryGene Expression Regulation LeukemicReverse Transcriptase Polymerase Chain ReactionCancerMembrane ProteinsNuclear ProteinsProteinsHematologyPrecursor Cell Lymphoblastic Leukemia-Lymphomamedicine.diseaseNeoplasm ProteinsDNA-Binding ProteinsRepressor ProteinsLeukemiaLeukemia Myeloid AcuteLymphatic systemOncologyImmunologyCancer/testis antigensMyelocytic leukemiabusinessLeukemia research
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