Search results for "TRANSCRIPTION FACTORS"

showing 10 items of 848 documents

Deficiency of the autoimmune regulator AIRE in thymomas is insufficient to elicit autoimmune polyendocrinopathy syndrome type 1 (APS‐1)

2007

Thymomas are thymic epithelial neoplasms, associated with a variety of autoimmune disorders (especially myasthenia gravis), that apparently result from aberrant intra-tumourous thymopoiesis and export of inefficiently tolerized T-cells to the periphery. The autoimmune regulator (AIRE) drives the expression of self-antigens in the thymic medulla and plays an essential role in ‘central’ tolerance in both humans and mice. However, while inactivating AIRE mutations result in the ‘autoimmune polyendocrinopathy syndrome type 1’ (APS-1), its major features are not well reproduced in AIRE-knock-out mice. Therefore, alternative human disease scenarios with concomitant AIRE deficiency may be valuable…

AdultMaleThymomaAdolescentThymomaAntibodies NeoplasmThymus Glandmedicine.disease_causeAutoantigensAutoimmune DiseasesPathology and Forensic MedicineAutoimmunity03 medical and health sciences0302 clinical medicineAntigens NeoplasmInterferonMyasthenia GravismedicineHumansPolyendocrinopathies AutoimmuneAgedAutoantibodies030304 developmental biologyAged 80 and over0303 health sciencesbiologybusiness.industryAutoantibodyThymus NeoplasmsMiddle AgedAutoimmune regulatormedicine.diseaseImmunohistochemistryMyasthenia gravisNeoplasm Proteins3. Good healthThymic Tissue030220 oncology & carcinogenesisInterferon Type IImmunologybiology.proteinCytokinesFemaleAntibodybusinessTranscription Factorsmedicine.drugThe Journal of Pathology
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Genotypic and phenotypic spectrum in tricho-rhino-phalangeal syndrome types I and III

2000

Tricho-rhino-phalangeal syndrome (TRPS) is characterized by craniofacial and skeletal abnormalities. Three subtypes have been described: TRPS I, caused by mutations in the TRPS1 gene on chromosome 8; TRPS II, a microdeletion syndrome affecting the TRPS1 and EXT1 genes; and TRPS III, a form with severe brachydactyly, due to short metacarpals, and severe short stature, but without exostoses. To investigate whether TRPS III is caused by TRPS1 mutations and to establish a genotype-phenotype correlation in TRPS, we performed extensive mutation analysis and evaluated the height and degree of brachydactyly in patients with TRPS I or TRPS III. We found 35 different mutations in 44 of 51 unrelated p…

AdultMaleanimal structuresAdolescentGenotypeDNA Mutational AnalysisMolecular Sequence DataLimb Deformities CongenitalBiologyOsteochondrodysplasiasPolymorphism Single NucleotideShort statureLanger–Giedion syndromeGeneticsmedicineHumansMissense mutationTricho–rhino–phalangeal syndromeGenetics(clinical)Amino Acid SequenceChildGenetics (clinical)GeneticsAnthropometryBase SequenceBrachydactylyInfantZinc FingersExonsSyndromeArticlesMiddle AgedMicrodeletion syndromemedicine.diseasePenetranceBody HeightPedigreeDNA-Binding ProteinsRadiographyPhenotypeChild PreschoolMutationTrichorhinophalangeal Syndrome Type IErythroid-Specific DNA-Binding FactorsFemalemedicine.symptomChromosomes Human Pair 8Transcription Factors
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Ten novel mutations found in Aniridia.

1998

Aniridia (AN) is a sight-threatening congenital ocular disorder characterized by iris hypoplasia, corneal pannus, foveal and optic nerve hypoplasia, cataract formation, and glaucoma. In two-thirds of the patients, AN is inherited in an autosomal dominant fashion with almost complete penetrance but variable expression. The remaining cases are sporadic. Aniridia has been shown to be associated with mutations in the PAX6 gene, located on chromosome 11p13, telomeric to the Wilms' tumor predisposition gene (WT1). This paper describes 14 mutations in the PAX6 gene in patients with AN. Among these 14 mutations, 10 have been unpublished until now. They result most probably in haploinsufficiency and…

AdultMalegenetic structuresAdolescentPAX6 Transcription FactorDNA Mutational AnalysisMolecular Sequence DataBiologyPolymerase Chain ReactionVariable ExpressionGeneticsmedicineHumansPaired Box Transcription FactorsAmino Acid SequenceChildEye ProteinsGeneAniridiaGenetics (clinical)Polymorphism Single-Stranded ConformationalGeneticsHomeodomain ProteinsOptic nerve hypoplasiaInfantMiddle Agedmedicine.diseasePenetranceeye diseasesDNA-Binding ProteinsRepressor ProteinsAniridiaChild PreschoolMutationHomeoboxFemalesense organsPAX6HaploinsufficiencyTranscription FactorsHuman mutation
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Underexpressed Coactivators PGC1α AND SRC1 Impair Hepatocyte Nuclear Factor 4α Function and Promote Dedifferentiation in Human Hepatoma Cells

2006

Hepatocyte nuclear factor 4alpha (HNF4alpha) plays critical roles during liver development and in the transcriptional regulation of many hepatic genes in adult liver. Here we have demonstrated that in human hepatoma HepG2 cells, HNF4alpha is expressed at levels as high as in human liver but its activity on target genes is very low or absent. We have discovered that the low expression of key coactivators (PGC1alpha, SRC1, SRC2, and PCAF) might account for the lack of function of HNF4alpha in HepG2 cells. Among them, PGC1alpha and SRC1 are the two most important HNF4alpha coactivators as revealed by reporter assays with an Apo-CIII promoter construct. Moreover, the expression of these two coa…

AdultMalemedicine.medical_specialtyCarcinoma HepatocellularDown-RegulationBiologyBiochemistryNuclear Receptor Coactivator 1Cell Line TumorInternal medicinemedicineTranscriptional regulationHomeostasisHumansMolecular BiologyPsychological repressionHeat-Shock ProteinsAgedHistone AcetyltransferasesLiver NeoplasmsCell DifferentiationCell BiologyMiddle AgedPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhenotypeCell biologyNuclear receptor coactivator 1Hepatocyte nuclear factorsEndocrinologyHepatocyte Nuclear Factor 4LiverPCAFCell cultureFemaleHomeostasisTranscription FactorsJournal of Biological Chemistry
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The influence of bone marrow- and synovium-derived mesenchymal stromal cells from osteoarthritis patients on regulatory T cells in co-culture

2013

Summary There is increasing evidence that inflammation in the synovium plays a major role in the progression of osteoarthritis (OA). However, the immunogenic properties of mesenchymal stromal cells (MSCs), which are considered to regulate immunity in various diseases, remain largely unknown in OA. The purpose of this study was to determine the influence of MSCs from OA patients on regulatory T cells (Tregs) in an allogeneic co-culture model. Bone marrow (BM) and synovial membrane (SM) were harvested from hip joints of OA patients and co-cultured with lymphocytes enriched in CD4+CD25+CD127– regulatory T cells (Treg+LC) from healthy donors. Treg proportions and MSC markers were assessed by fl…

AdultMalemedicine.medical_treatmentLymphocyteT cellImmunologyBone Marrow Cellschemical and pharmacologic phenomenaT-Lymphocytes RegulatoryInterleukin-7 Receptor alpha SubunitYoung AdultOsteoarthritisHumansImmunology and AllergyMedicineIL-2 receptorInterleukin-7 receptorAgedAged 80 and overInterleukin-6business.industrySynovial MembraneMesenchymal stem cellForkhead Transcription FactorsMesenchymal Stem CellsMiddle AgedCoculture Techniquesmedicine.anatomical_structureCytokineImmunologyFemaleBone marrowSynovial membranebusinessBiomarkersClinical and Experimental Immunology
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Reprogramming of Pericyte-Derived Cells of the Adult Human Brain into Induced Neuronal Cells

2012

SummaryReprogramming of somatic cells into neurons provides a new approach toward cell-based therapy of neurodegenerative diseases. A major challenge for the translation of neuronal reprogramming into therapy is whether the adult human brain contains cell populations amenable to direct somatic cell conversion. Here we show that cells from the adult human cerebral cortex expressing pericyte hallmarks can be reprogrammed into neuronal cells by retrovirus-mediated coexpression of the transcription factors Sox2 and Mash1. These induced neuronal cells acquire the ability of repetitive action potential firing and serve as synaptic targets for other neurons, indicating their capability of integrat…

AdultNeurogenesisCellular differentiationInduced Pluripotent Stem CellsAction PotentialsBiologySynaptic TransmissionMiceNeural Stem CellsSOX2Basic Helix-Loop-Helix Transcription FactorsGeneticsmedicineAnimalsHumansInduced pluripotent stem cellCells CulturedCerebral CortexNeuronsSOXB1 Transcription FactorsNeurogenesisCell DifferentiationNeurodegenerative DiseasesCell BiologyCellular ReprogrammingNeural stem cellCell biologyRetroviridaemedicine.anatomical_structureImmunologyMolecular MedicineNeuronPericyteNerve NetPericytesReprogrammingStem Cell TransplantationCell Stem Cell
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The role of recent thymic emigrant-regulatory T-cell (RTE-Treg) differentiation during pregnancy.

2014

During pregnancy, regulatory T cells (Tregs) have a key role in maternal immune tolerance to the semi-allogeneic fetus. Our previous results showed that the naive CD45RA(+)-Treg pool is functionally improved in pregnant women compared with non-pregnant women. Therefore, we examined the thymic output and differentiation of CD45RA(+)CD31(+) recent thymic emigrant (RTE)-Tregs during normal pregnancy and in the presence of preeclampsia. With the onset of pregnancy, the composition of the total CD4(+)CD127(low+/-)FoxP3(+)-Treg pool changed in the way that its percentage of RTE- and CD45RA(-)CD31(+)-memory Tregs decreased strongly, whereas that of the CD45RA(+)CD31(-)-mature naive (MN)-Tregs did …

Adultmedicine.medical_specialtyAdolescentRegulatory T cellImmunologyRecent Thymic Emigrantchemical and pharmacologic phenomenaThymus GlandT-Lymphocytes RegulatoryPreeclampsiaImmune toleranceYoung AdultPre-EclampsiaPregnancyT-Lymphocyte SubsetsInternal medicineImmune ToleranceImmunology and AllergyMedicineAnimalsHumansInterleukin-7 receptorFetusPregnancybusiness.industryFOXP3hemic and immune systemsCell DifferentiationForkhead Transcription FactorsCell BiologyMiddle Agedmedicine.diseasemedicine.anatomical_structureEndocrinologyLeukocyte Common AntigensFemalebusinessImmunologic MemoryImmunology and cell biology
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(Partial) loss of BAF250a (ARID1A) in rectovaginal deep-infiltrating endometriosis, endometriomas and involved pelvic sentinel lymph nodes

2015

study hypothesis: Loss of protein BAF250a (ARID1A) expression is present in women with rectovaginal deep-infiltrating endometriosis (DIE) and endometriosis affecting the pelvic sentinel lymph nodes (PSLN). study finding: Partial loss of protein BAF250a was found in some of our patient samples, comprising all endometriosis entities, including rectovaginal DIE and endometriosis affecting the PSLN. what is known already: Loss of BAF250a (BRG-associated factor 250a)/ARIDIA (AT-rich interactive domain 1A) protein expression was identified among endometriosis-associated ovarian carcinomas and ovarian endometriosis, and this phenomenonwas described as a possible early event in the transformation o…

Adultmedicine.medical_specialtyBAF250a human proteinEmbryologyARID1APelvic sentinel lymph nodePopulationEndometriosisEndometriosisDeep-infiltrating endometriosiEndometriumGastroenterologyMalignant transformation03 medical and health sciencesEndometriumYoung Adult0302 clinical medicineGeneticInternal medicineGeneticsmedicinePTENHumanseducationMolecular BiologyCancerOvarian Neoplasmseducation.field_of_study030219 obstetrics & reproductive medicinebiologyCancerNuclear ProteinsObstetrics and GynecologyCell BiologyMiddle Agedmedicine.diseaseImmunohistochemistryARID1ADNA-Binding Proteinsmedicine.anatomical_structureReproductive Medicine030220 oncology & carcinogenesisOvarian Endometriosisbiology.proteinFemaleSentinel Lymph NodeTranscription FactorsDevelopmental Biology
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The role of regulatory T cell (Treg) subsets in gestational diabetes mellitus.

2014

Physiological changes during normal pregnancy are characterized by an inflammatory immune response and insulin resistance. Therefore, we hypothesize that gestational diabetes mellitus (GDM) may be caused by an inappropriate adaption of the maternal immune system to pregnancy. In this study we examined the role of regulatory T cell (Treg) differentiation for the development of GDM during pregnancy. We used six-colour flow cytometric analysis to demonstrate that the total CD4(+) CD127(low+/-) CD25(+) forkhead box protein 3 (FoxP3(+)) T(reg) pool consists of four different T(reg) subsets: naive CD45RA(+) T(regs), HLA-DR(-) CD45RA(-) memory T(regs) (DR(-) T(regs)) and the highly differentiated …

Adultmedicine.medical_specialtyendocrine system diseasesRegulatory T cellImmunologychemical and pharmacologic phenomenaCell SeparationLymphocyte ActivationT-Lymphocytes RegulatoryImmunophenotypingYoung AdultImmune systemInsulin resistanceimmune system diseasesPregnancyT-Lymphocyte Subsetshemic and lymphatic diseasesInternal medicinemedicineImmune ToleranceImmunology and AllergyHomeostasisHumansIL-2 receptorInterleukin-7 receptorbusiness.industryFOXP3hemic and immune systemsCell DifferentiationForkhead Transcription FactorsT helper cellOriginal Articlesmedicine.diseaseFlow CytometryGestational diabetesDiabetes GestationalEndocrinologymedicine.anatomical_structureImmunologyCD4 AntigensFemalebusinessImmunologic MemoryClinical and experimental immunology
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Repair of oxidatively generated DNA damage in Cockayne syndrome

2013

Defects in the repair of endogenously (especially oxidatively) generated DNA modifications and the resulting genetic instability can potentially explain the clinical symptoms of Cockayne syndrome (CS), a hereditary disease characterized by developmental defects and neurological degeneration. In this review, we describe the evidence for the involvement of CSA and CSB proteins, which are mutated in most of the CS patients, in the repair and processing of DNA damage induced by reactive oxygen species and the implications for the induction of cell death and mutations. Taken together, the data demonstrate that CSA and CSB, in addition to their established role in transcription-coupled nucleotide…

AgingDNA RepairTranscription GeneticDNA damageDNA repairBiologymedicine.disease_causeCockayne syndromemedicineAnimalsHumansCockayne SyndromePoly-ADP-Ribose Binding ProteinsMutationDNA HelicasesBase excision repairmedicine.diseaseMolecular biologyCell biologyDNA Repair EnzymesMitochondrial DNA repairMutationDNA mismatch repairOxidation-ReductionDNA DamageTranscription FactorsDevelopmental BiologyNucleotide excision repairMechanisms of Ageing and Development
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