Search results for "DELETION"

showing 10 items of 383 documents

Multiplex ligation-dependent probe amplification detection of an unknown large deletion of the CREB-binding protein gene in a patient with Rubinstein…

2013

Rubinstein-Taybi syndrome is a rare autosomal dominant congenital disorder characterized by postnatal growth retardation, psychomotor developmental delay, skeletal anomalies, peculiar facial morphology, and tumorigenesis. Mutations in the gene encoding the cAMP response element-binding protein (CREB, also known as CREBBP or CBP) on chromosome 16p13.3 have been identified. In addition, some patients with low intelligence quotients and autistic features bear large deletions. Based on these observations, we used multiplex ligation-dependent probe amplification to search for large deletions affecting the CREBBP gene in a Rubinstein-Taybi syndrome patient. We identified a novel heterozygote dele…

HeterozygoteCREBExonSettore BIO/13 - Biologia ApplicataGeneticsmedicineHumansMultiplexMultiplex ligation-dependent probe amplificationGenetic TestingCREB-binding proteinMolecular BiologyGeneGeneticsRubinstein-Taybi SyndromeRubinstein–Taybi syndromebiologyMultiplex ligation-dependent probe amplification Comparative multiplex dosage analysis CREB-binding protein Rubinstein-Taybi syndromeHeterozygote advantageGeneral Medicinemedicine.diseaseMolecular biologyCREB-Binding ProteinChild Preschoolbiology.proteinFemaleMultiplex Polymerase Chain ReactionGene Deletion
researchProduct

Loss of heterozygosity at the short arm of chromosome 3 in renal‐cell cancer correlates with the cytological tumour type

1993

A majority of renal-cell tumours retain heterozygosity at the short arm of chromosome 3. To investigate possible histopathological differences between tumours with and without such losses, we compared loss of heterozygosity data from 51 tumours with 1 histological and 2 different cytological classifications of renal-cell tumour. Using the cytological classification of Thoenes et al., we only found tumours with loss of heterozygosity in these authors' clear-cell category. Possibly, only these tumours arise by a mechanism of double loss of a tumour-suppressor gene on 3p, non-clear-cell renal tumours having a different genetic background. Alternatively, deletions may occur in all subtypes, in …

HeterozygoteCancer Researchmedicine.medical_specialtyPathologyMitotic crossoverCARCINOMAChromosome DisordersBiologyMOLECULAR ANALYSISLoss of heterozygosityGene duplicationmedicineHumansCarcinoma Renal CellSequence DeletionChromosome AberrationsDELETIONBreakpointCytogeneticsChromosomeCYTOGENETICSKidney NeoplasmsOncologyChromosome 3Clear cell carcinomaChromosomes Human Pair 3Polymorphism Restriction Fragment LengthInternational Journal of Cancer
researchProduct

p16INK4A (CDKN2A) gene deletion is a frequent genetic event in synovial sarcomas.

2006

We assessed the frequency of genomic deletion of p16 INK4A (CDKN2A) in synovial sarcomas (SSs) and its possible association with immunoexpression of p16 and cyclin D1 and the Ki-67 proliferation index using dualcolor fluorescence in situ hybridization (FISH) on tissue microarray sections of 41 histologically and molecularly confirmed SSs. A heterozygous p16 INK4A gene deletion was identified in 28 (74%) of 38 cases, with 25 (89%) of them showing abnormal p16 protein expression (20 negative and 5 heterogeneous). Of 25 cases, 19 (76%) exhibiting increased cyclin D1 expression also demonstrated heterozygous p16 INK4A deletion. No significant association was observed between p16 INK4A deletion …

HeterozygoteProliferation indexTumor suppressor geneSoft Tissue NeoplasmsBiologySarcoma SynovialCyclin D1CDKN2ACyclin DCyclinsmedicineBiomarkers TumorHumansCDKN2A Gene DeletionCyclin-Dependent Kinase Inhibitor p16In Situ Hybridization FluorescenceCell Nucleusmedicine.diagnostic_testGeneral Medicinemedicine.diseaseImmunohistochemistrySynovial sarcomaKi-67 AntigenTumor progressionTissue Array AnalysisCancer researchGene DeletionFluorescence in situ hybridizationAmerican journal of clinical pathology
researchProduct

The role of the human cytomegalovirus UL111A gene in down-regulating CD4+ T-cell recognition of latently infected cells: implications for virus elimi…

2009

AbstractThe capacity of human cytomegalovirus (HCMV) to establish and maintain a latent infection from which it can later reactivate ensures its widespread distribution in the population, but the mechanisms enabling maintenance of latency in the face of a robust immune system are poorly understood. We examined the role of the HCMV UL111A gene, which encodes homologs of the immunosuppressive cytokine interleukin-10 in the context of latent infection of myeloid progenitor cells. A UL111A deletion virus was able to establish, maintain, and reactivate from experimental latency in a manner comparable with parental virus, but major histocompatibility complex class II levels increased significantl…

Human cytomegalovirusCD4-Positive T-LymphocytesIsoantigensMyeloidGenes Viralmedicine.medical_treatmentImmunologyPopulationCytomegalovirusDown-RegulationBiologyIn Vitro Techniquesmedicine.disease_causeBiochemistryAutoantigensHerpesviridaeVirusImmune systemmedicineHumansProgenitor celleducationMyeloid Progenitor Cellseducation.field_of_studyHistocompatibility Antigens Class IICell BiologyHematologymedicine.diseaseVirologyVirus LatencyCytokinemedicine.anatomical_structureImmunologyCytomegalovirus InfectionsHost-Pathogen InteractionsGene DeletionBlood
researchProduct

Candida albicans adhesin Als3p is dispensable for virulence in the mouse model of disseminated candidiasis

2011

The presence of specific proteins, including Ece1p, Hwp1p and Als3p, distinguishes theCandida albicanshyphal cell wall from that of yeast-form cells. These proteins are thought to be important for the ability ofC. albicanscells to adhere to living and non-living surfaces and for the cell-to-cell adhesion necessary for biofilm formation, and also to be pivotal in mediatingC. albicansinteractions with endothelial cells. Using anin vitroflow adhesion assay, we previously observed that yeast cells bind in greater numbers to human microvascular endothelial cells than do hyphal or pseudohyphal cells. This is consistent with previous observations that, in a murine model of disseminated candidiasis…

HyphaeMicrobiologyMicrobiologyMicrobial PathogenicityFungal ProteinsMiceCandida albicansCell AdhesionAnimalsHumansCandida albicansCell adhesionFungal proteinMice Inbred BALB CbiologyVirulenceBiofilmCandidiasisEndothelial Cellsbiology.organism_classificationDisseminated CandidiasisCorpus albicansBacterial adhesinDisease Models AnimalFemaleHyphal cell wallGene Deletion
researchProduct

Dissection of human papillomavirus type 33 L2 domains involved in nuclear domains (ND) 10 homing and reorganization

2003

Abstract We have recently shown that the minor capsid protein L2 of human papillomavirus type 33 (HPV33) recruits the transcriptional repressor Daxx into nuclear domains (ND) 10 and causes the loss of the transcriptional activator Sp100 from these subnuclear structures (Florin et al., 2002b) . In order to dissect L2 domains involved in nuclear translocation, ND10 homing, loss of Sp100, and recruitment of Daxx, a detailed deletion mutagenesis of L2 was performed. Using immunofluorescence and green fluorescent protein fusions, we have identified two nuclear localization signals (NLS) in the central and C-terminal part of L2, respectively, homologous to previously identified NLS in HPV6B L2 (S…

ImmunoprecipitationRecombinant Fusion ProteinsGreen Fluorescent ProteinsNuclear Localization SignalsActive Transport Cell NucleusFluorescent Antibody TechniqueBiologyImmunofluorescenceAutoantigensGreen fluorescent proteinDeath-associated protein 6DaxxVirologyTumor Cells CulturedmedicineSp100HumansNLSPapillomaviridaeAdaptor Proteins Signal TransducingCell Nucleusmedicine.diagnostic_testIntracellular Signaling Peptides and ProteinsND10Nuclear ProteinsAntigens NuclearL2Oncogene Proteins ViralPapillomavirusbiochemical phenomena metabolism and nutritionMolecular biologyDeletion MutagenesisLuminescent ProteinsCapsidMutagenesisCapsid ProteinsCarrier ProteinsCo-Repressor ProteinsGene DeletionNuclear localization sequenceMolecular ChaperonesVirology
researchProduct

Hypercalciuria and kidney calcifications in terminal 4q deletion syndrome: further evidence for a putative gene on 4q.

2004

We report a newborn girl with a de novo terminal 4q deletion (q31.3 --> qter) and a characteristic phenotype of minor facial anomalies, cleft palate, congenital heart defect, abnormalities of hands and feet, and postnatal onset of growth deficiency. Laboratory studies showed excessive urinary calcium excretion on standard milk formula and on oral calcium load. Blood measurements of parathyroid hormone, calcitonin, bicarbonate, calcium, phosphorus, magnesium, sodium, chlorine, potassium, and urinary measurements of phosphorus, magnesium, sodium, chlorine, potassium were normal for age. At 2 months of life, ultrasonography showed kidney calcifications. Clinical and laboratory data support the…

Infant NewbornIndiaSyndromecalcificationKidney CalculiKaryotypingHumansAbnormalities MultipleCalciumFemaledeletionChromosome DeletionChromosomes Human Pair 4hypercalciuriaUltrasonographyAmerican journal of medical genetics. Part A
researchProduct

The Drosophila ACP65A cuticle gene: deletion scanning analysis of cis-regulatory sequences and regulation by DHR38

2005

1526-954X (Print) Journal Article Research Support, Non-U.S. Gov't; The regulatory sequences of the Drosophila ACP65A cuticle gene were analyzed in vivo in transgenic flies, using both fusion genes constructs and transposase-mediated deletions within a P element containing ACP65A regulatory sequences fused to the lacZ gene (deletion scanning). The sequences located between -594 and +161 are sufficient to confer both temporal and spatial expression specificities, indicating the presence of tissue-specific enhancers and response elements to hormone-induced factors. In addition, timing of expression and tissue-specificity appear to be controlled by distinct cis-regulatory elements, which sugge…

Insect Proteins/*genetics/metabolismMaleBase SequenceGene Expression Regulation/*physiologyTranscription Factors/*physiologyGenetically ModifiedCytoplasmic and Nuclear/*physiologyCrossesDrosophila/*geneticsGeneticDrosophila Proteins/*genetics/metabolism/physiologyDNA-Binding Proteins/*physiologyPupa/geneticsReceptorsAnimalsFemaleSteroid/physiologyTranscriptionSequence Deletion
researchProduct

Yeast Dun1 Kinase Regulates Ribonucleotide Reductase Inhibitor Sml1 in Response to Iron Deficiency

2014

Iron is an essential micronutrient for all eukaryotic organisms because it participates as a redox-active cofactor in many biological processes, including DNA replication and repair. Eukaryotic ribonucleotide reductases (RNRs) are Fe-dependent enzymes that catalyze deoxyribonucleoside diphosphate (dNDP) synthesis. We show here that the levels of the Sml1 protein, a yeast RNR large-subunit inhibitor, specifically decrease in response to both nutritional and genetic Fe deficiencies in a Dun1-dependent but Mec1/Rad53- and Aft1-independent manner. The decline of Sml1 protein levels upon Fe starvation depends on Dun1 forkhead-associated and kinase domains, the 26S proteasome, and the vacuolar pr…

Iron-Sulfur ProteinsProteasome Endopeptidase ComplexSaccharomyces cerevisiae ProteinsDeoxyribonucleoside triphosphateRibonucleotideIronDeoxyribonucleotidesGenes FungalSaccharomyces cerevisiaeCell Cycle ProteinsSaccharomyces cerevisiaeRibonucleotide reductase inhibitorProtein Serine-Threonine KinasesBiologyProtein degradationchemistry.chemical_compoundTristetraprolinRibonucleotide ReductasesAspartic Acid EndopeptidasesPhosphorylationMolecular BiologyCheckpoint Kinase 2Binding SitesKinaseIntracellular Signaling Peptides and ProteinsArticlesCell Biologybiology.organism_classificationDNA-Binding ProteinsDeoxyribonucleosideCheckpoint Kinase 2chemistryBiochemistryProteolysisGene DeletionTranscription FactorsMolecular and Cellular Biology
researchProduct

Not all KIT 557/558 codons mutations have the same prognostic influence on recurrence-free survival: breaking the exon 11 mutations in gastrointestin…

2021

Background: Although the gastrointestinal stromal tumor (GIST) genotype is not currently included in risk-stratification systems, a growing body of evidence shows that the pathogenic variant (PV) type and codon location hold a strong prognostic influence on recurrence-free survival (RFS). This information has particular relevance in the adjuvant setting, where an accurate prognostication could help to better identify high-risk tumors and guide clinical decision-making. Materials and Methods: Between January 2005 and December 2020, 96 patients with completely resected GISTs harboring a KIT proto-oncogene receptor tyrosine kinase ( KIT) exon 11 PV were included in the study. We analyzed the t…

KIT proto-oncogene receptor tyrosine kinaseGiSTbusiness.industryplatelet-derived growth factor receptor alphaPlatelet-Derived Growth Factor Receptor AlphaNeoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasegastrointestinal stromal tumorExon557/558 deletionOncologyRecurrence free survivalGenotypeCancer researchmedicinePrognostic biomarkerGastrointestinal stromal tumors (GISTs)Stromal tumorprognostic biomarkerbusinessRC254-282Therapeutic Advances in Medical Oncology
researchProduct