Search results for "Repressor Proteins"

showing 10 items of 169 documents

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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Amplification of ETS2 oncogene in acute nonlymphoblastic leukemia with t(6;21;18).

1992

Cytogenetic and molecular studies in a case of acute nonlymphoblastic leukemia (ANLL) are reported in this paper. Bone marrow blasts carried a hypodiploid karyotype with a complex t(6;18;21)(6qter----6p21::21q22----21qter;18qter ----18p11::6p22----6pter; 21pter----21q22::6p21----6p22::18p11----18pte r) and other numerical and structural changes. We studied the organization and the expression of the ETS2 gene which is located on chromosome 21 in order to investigate its possible involvement in the disease. DNA analysis showed a 20-fold amplification of ETS2 sequences; an increase of 3- to 4-fold in the mRNAs level compared to normal was shown by Northern hybridization.

MaleCancer ResearchChromosomes Human Pair 21Chromosomal translocationBiologyTranslocation GeneticProto-Oncogene Protein c-ets-2Proto-Oncogene ProteinsGene duplicationGeneticsmedicineHumansNorthern blotMolecular BiologySouthern blotAgedChromosome AberrationsOncogeneGene AmplificationKaryotypeProtein-Tyrosine KinasesBlotting NorthernMolecular biologyDNA-Binding ProteinsRepressor ProteinsBlotting SouthernLeukemia Myeloid Acutemedicine.anatomical_structureCancer researchTrans-ActivatorsChromosomes Human Pair 6Bone marrowChromosome 21Chromosomes Human Pair 18Transcription FactorsCancer genetics and cytogenetics
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A genome scan for developmental dyslexia confirms linkage to chromosome 2p11 and suggests a new locus on 7q32

2003

Developmental dyslexia is a distinct learning disability with unexpected difficulty in learning to read despite adequate intelligence, education, and environment, and normal senses. The genetic aetiology of dyslexia is heterogeneous and loci on chromosomes 2, 3, 6, 15, and 18 have been repeatedly linked to it. We have conducted a genome scan with 376 markers in 11 families with 38 dyslexic subjects ascertained in Finland. Linkage of dyslexia to the vicinity of DYX3 on 2p was confirmed with a non-parametric linkage (NPL) score of 2.55 and a lod score of 3.01 for a dominant model, and a novel locus on 7q32 close to the SPCH1 locus was suggested with an NPL score of 2.77. The SPCH1 locus has p…

MaleCandidate geneGenotypeDNA Mutational AnalysisShort ReportLocus (genetics)BiologyDyslexia03 medical and health sciences0302 clinical medicineCommunication disorderDCDC2mental disordersGeneticsmedicineHumansLanguage disorderFinlandGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesGenome HumanDyslexiaChromosome MappingForkhead Transcription FactorsFOXP2medicine.diseasePedigreeRepressor ProteinsChromosomes Human Pair 2Learning disabilityFemaleLod Scoremedicine.symptomChromosomes Human Pair 7030217 neurology & neurosurgeryTranscription FactorsJournal of Medical Genetics
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Gene expression in mouse spermatogenesis during ontogenesis

2006

In this study, we evaluated the expression of genes probably involved in spermatogenesis in the mouse. We examined cytosolic chaperonin theta subunit (CCTtheta), Ngg1 interacting factor 3 like 1 binding protein 1 (NIF3L1 BP1) and apolipoprotein H (ApoH) expression during mouse onto-geny using RT-PCR. Testicular tissue was obtained from mice 3, 6, 8, 10, 12, 14, 18, 20 and 40 (adult) days after birth. For each mouse, one testis was used for histological examination, whereas RNA was extracted from the controlateral testis for expression analysis. RT-PCR analysis showed that CCTtheta gene expression was low until day 10, but increased drastically afterwards. At this age, spermatocytes started …

MaleChaperoninsSpermiogenesisMouse testis ontogenesisBiologyMiceGene expressionTestisGeneticsmedicineAnimalsRNA MessengerSpermatogenesisGeneGene expression; Mouse testis ontogenesis; SpermatogenesisGlycoproteinsReverse Transcriptase Polymerase Chain ReactionGene Expression Regulation DevelopmentalProteinsGeneral MedicineCell cycleMolecular biologyCell biologyChromatinmedicine.anatomical_structurebeta 2-Glycoprotein IGene expressionSpermatogenesisApolipoprotein HCo-Repressor ProteinsGerm cell: gene expression mouse testis ontogenesis spermatogenesisChaperonin Containing TCP-1Transcription Factors
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Dppa3 expression is critical for generation of fully reprogrammed iPS cells and maintenance of Dlk1-Dio3 imprinting.

2014

Reprogramming of mouse somatic cells into induced pluripotent stem cells (iPSCs) often generates partially reprogrammed iPSCs (pre-iPSCs), low-grade chimera forming iPSCs (lg-iPSCs) and fully reprogrammed, high-grade chimera production competent iPSCs (hg-iPSCs). Lg-iPSC transcriptome analysis revealed misregulated Dlk1-Dio3 cluster gene expression and subsequently the imprinting defect at the Dlk1-Dio3 locus. Here, we show that germ-cell marker Dppa3 is present only in lg-iPSCs and hg-iPSCs, and that induction with exogenous Dppa3 enhances reprogramming kinetics, generating all hg-iPSCs, similar to vitamin C (Vc). Conversely, Dppa3-null fibroblasts show reprogramming block at pre-iPSCs sta…

MaleChromosomal Proteins Non-HistoneGreen Fluorescent ProteinsInduced Pluripotent Stem CellsMice TransgenicAscorbic AcidIodide PeroxidaseArticleGenomic ImprintingMiceAnimalsCrosses GeneticMice KnockoutGene Expression ProfilingCalcium-Binding ProteinsDNA MethylationFibroblastsMice Inbred C57BLRepressor ProteinsKineticsGerm CellsRetroviridaeGene Expression RegulationIntercellular Signaling Peptides and ProteinsFemaleProtein BindingNature communications
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Delineation of a new chromosome 20q11.2 duplication syndrome including the ASXL1 gene.

2013

We report on three males with de novo overlapping 7.5, 9.8, and 10 Mb duplication of chromosome 20q11.2. Together with another patient previously published in the literature with overlapping 20q11 microduplication, we show that such patients display common clinical features including metopic ridging/trigonocephaly, developmental delay, epicanthal folds, and short hands. The duplication comprised the ASXL1 gene, in which de novo heterozygous nonsense or truncating mutations have recently been reported in patients with Borhing-Opitz syndrome. Because of craniofacial features in common with Borhing-Opitz syndrome, in particular metopic ridging/trigonocephaly, we suggest that duplication of ASX…

MaleHeterozygotemedia_common.quotation_subjectDevelopmental DisabilitiesNonsenseChromosomes Human Pair 20TrigonocephalyTrisomyBiologymedicine.disease_causeCraniosynostosesPregnancyIntellectual DisabilityGene duplicationGeneticsmedicineHumansCraniofacialChildGenetics (clinical)media_commonGeneticsMutationMosaicismChromosomeInfantHeterozygote advantageSyndromemedicine.diseasePhenotypeRepressor ProteinsChild PreschoolMutationFemaleHand Deformities CongenitalAmerican journal of medical genetics. Part A
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Androgen receptor activation by polychlorinated biphenyls

2013

The exposure to environmental endocrine disrupting compounds (EDC), as polychlorinated biphenyls (PCBs), widely diffused in the environment may produce epigenetic changes that affect the endocrine system. We found that PCBs activate AR transcriptional activity and that this effect is potentiated by the demethylase Jarid1b, a histone demethylase that catalyzes the removal of trimethylation of lysine 4 on histone H3 (H3K4me3), induced by PCB. The aim of the present study was to investigate the effect of the treatment of cultured cells (HEK293) with a mixture of the most diffused environmental PCBs and, also with dihydrotestosterone (DHT), on the functional interaction between AR and Jarid1b. …

MaleJumonji Domain-Containing Histone DemethylasesJarid1bpolychlorinated biphenylsNuclear ProteinsEndocrine DisruptorsEpigenesis GeneticHistonesRepressor ProteinsReceptors Androgenandrogen receptorTumor Cells CulturedHumanshistone modificationFemaleenvironmentepigeneticResearch PaperEpigenetics
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Mild mutations in the pan neural gene prospero affect male-specific behaviour in Drosophila melanogaster

2004

0376-6357 (Print) Journal Article Research Support, Non-U.S. Gov't; The fruitfly Drosophila melanogaster is one of the most appropriate model organisms to study the genetics of behaviour. Here, we focus on prospero (pros), a key gene for the development of the nervous system which specifies multiple aspects from the early formation of the embryonic central nervous system to the formation of larval and adult sensory organs. We studied the effects on locomotion, courtship and mating behaviour of three mild pros mutations. These newly isolated pros mutations were induced after the incomplete excision of a transposable genomic element that, before excision, caused a lethal phenotype during larv…

MaleMutantPoint Mutation/*geneticsSexual Behavior AnimalBehavioral NeuroscienceAnimal/*physiologyDrosophila ProteinsGeneticsBehavior AnimalbiologyReproductionHomozygoteNuclear ProteinsGeneral MedicinePhenotypeNerve Tissue Proteins/*geneticshumanitiesDNA Transposable Elements/geneticsDrosophila melanogasterLocomotion/physiologyFemaleDrosophila melanogasterLocomotionHeterozygoteFertility/physiologySexual BehavioreducationNerve Tissue ProteinsTranscription Factors/*geneticsAnimal/physiologyDrosophilidaeNuclear Proteins/*geneticsPoint MutationAnimalsAlleleGeneDrosophilaReproduction/physiologyAllelesBehaviorfungiDrosophila Proteins/*geneticsHeterozygote advantageRepressor Proteins/*geneticsbiology.organism_classificationRepressor ProteinsFertilityDNA Transposable ElementsAnimal Science and ZoologyTranscription Factors
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Myelodysplastic syndromes with 20q deletion: incidence, prognostic value and impact on response to azacitidine of ASXL1 chromosomal deletion and gene…

2021

In myelodysplastic syndromes (MDS), the 20q deletion [del(20q)] may cause deletion of the ASXL1 gene. We studied 153 patients with MDS and del(20q) to assess the incidence, prognostic value and impact on response to azacitidine (AZA) of ASXL1 chromosomal alterations and genetic mutations. Additionally, in vitro assay of the response to AZA in HAP1 (HAP1(WT)) and HAP1 ASXL1 knockout (HAP1(KN)) cells was performed. ASXL1 chromosomal alterations were detected in 44 patients (28 center dot 5%): 34 patients (22%) with a gene deletion (ASXL1(DEL)) and 10 patients (6 center dot 5%) with additional gene copies. ASXL1(DEL) was associated with a lower platelet count. The most frequently mutated genes…

MaleOncologyAntimetabolites Antineoplasticazacitidinemedicine.medical_specialtyAzacitidineASXL1Gene mutationInternal medicinemedicineHumansGeneChromosomal DeletionAged20q deletiongene mutationsAged 80 and overbusiness.industryIncidenceMyelodysplastic syndromesIncidence (epidemiology)Hazard ratioHematologyMiddle AgedPrognosismedicine.diseasemyelodysplastic syndromesConfidence intervalRepressor ProteinsMyelodysplastic SyndromesMutationAzacitidineFemaleChromosome Deletionbusinessmedicine.drugBritish Journal of Haematology
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Delineation of the 3p14.1p13 microdeletion associated with syndromic distal limb contractures

2014

International audience; Distal limb contractures (DLC) represent a heterogeneous clinical and genetic condition. Overall, 20–25% of the DLC are caused by mutations in genes encoding the muscle contractile apparatus. Large interstitial deletions of the 3p have already been diagnosed by standard chromosomal analysis, but not associated with a specific phenotype. We report on four patients with syndromic DLC presenting with a de novo 3p14.1p13 micro-deletion. The clinical features associated multiple contractures, feeding problems, developmental delay, and intellectual disability. Facial dysmorphism was constant with low-set posteriorly rotated ears and blepharophimosis. Review of previously r…

MalePathologymedicine.medical_specialtyContracture[SDV]Life Sciences [q-bio]Locus (genetics)FOXP1BiologyMicedistal limb contracturessymbols.namesakeExonEIF4E3Intellectual disabilityGeneticsmedicineAnimalsHumans[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]3p141p13 microdeletionGenetics (clinical)ArthrogryposisChromosome AberrationsMice KnockoutSanger sequencingGeneticsComparative Genomic Hybridization[ SDV ] Life Sciences [q-bio]ExtremitiesForkhead Transcription FactorsSyndromeFOXP1Microdeletion syndromemedicine.diseaseBlepharophimosisPhenotypeRepressor Proteins[SDV] Life Sciences [q-bio]array-CGH[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]symbolsFemale[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Chromosomes Human Pair 3FranceCarrier Proteinsintronic regulatory sequenceAmerican Journal of Medical Genetics Part A
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