Search results for "MUTATION"

showing 10 items of 2830 documents

Multiply Transitive Permutation Groups

1982

Since the beginnings of finite group theory, the multiply transitive permutation groups have exercised a certain fascination. This is mainly due to the fact that apart from the symmetric and alternating groups not many of them were known. Only very recently final results about multiply transitive permutation groups have been proved, using the classification of all finite simple groups (see 7.5).

Base (group theory)CombinatoricsTransitive relationFinite group theoryPermutation graphClassification of finite simple groupsPermutation groupCyclic permutationMathematics
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On finite products of totally permutable groups

1996

In this paper the structure of finite groups which are the product of two totally permutable subgroups is studied. In fact we can obtain the -residual, where is a formation, -projectors and -normalisers, where is a saturated formation, of the group from the corresponding subgroups of the factor subgroups.

Base (group theory)Pure mathematicsGroup (mathematics)Symmetric groupGeneral MathematicsProduct (mathematics)Structure (category theory)Permutable primeCyclic permutationMathematicsBulletin of the Australian Mathematical Society
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Beckwith–Wiedemann syndrome: multiple molecular mechanisms

2006

Beckwith–Wiedemann syndrome (BWS) is a congenital overgrowth condition with an increased risk of developing embryonic tumours, such as Wilms' tumour. The cardinal features are abdominal wall defects, macroglossia and gigantism. BWS is generally sporadic; only 10–15% of cases are familial. A variety of molecular aberrations have been associated with BWS. The only mutations within a gene are loss-of-function mutations in the CDKN1C gene, which codes for an imprinted cell-cycle regulator. CDKN1C mutations appear to be particularly associated with umbilical abnormalities, but not with increased predisposition to Wilms' tumour. In the remaining BWS subgroups, a disturbance of the tight epigeneti…

Beckwith-Wiedemann SyndromeGenotypeTranscription GeneticBeckwith–Wiedemann syndromeBioinformaticsModels BiologicalEpigenesis GeneticGenomic ImprintingGenotypeMacroglossiaAnimalsHumansMedicineEpigeneticsCyclin-Dependent Kinase Inhibitor p57Molecular BiologyModels Geneticbusiness.industryDNA Methylationmedicine.diseasePhenotypeGigantismPhenotypeMutationDNA methylationMolecular Medicinemedicine.symptombusinessGenomic imprintingExpert Reviews in Molecular Medicine
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β-Catenin Activation Regulates Tissue Growth Non–Cell Autonomously in the Hair Stem Cell Niche

2014

Coordinated Hair Growth Wnt/β-catenin signaling is a key pathway that plays a conserved role in regulating stem cell function during adult tissue regeneration. Using time-lapse imaging of live mice, Deschene et al. (p. 1353 ) show that genetic activation of β-catenin within hair follicle stem cells generates axes of hair growth by coordinated cell divisions and cell movements, even when the normal niches—the dermal papillae—are laser-ablated. Activated β-catenin enhances Wnt ligand secretion, and these ligands can then activate Wnt signaling in adjacent cells that do not have activated β-catenin, indicating how activated stem cells could influence neighboring cells during normal growth and …

Beta-cateninWnt ProteinCellular differentiationLigandBiologyLigandsModels BiologicalArticleMiceStem CellmedicineAnimalsStem Cell NicheAnimals; Cell Differentiation; Cell Division; Hair; Hair Follicle; Ligands; Mice; Models Biological; Mutation; Stem Cell Niche; Stem Cells; Tamoxifen; Up-Regulation; Wnt Proteins; beta Catenin; Wnt Signaling Pathway; Medicine (all); MultidisciplinaryWnt Signaling Pathwaybeta CateninMultidisciplinaryintegumentary systemAnimalStem CellsMedicine (all)Regeneration (biology)Mesenchymal stem cellWnt signaling pathwayCell DifferentiationHair follicleUp-RegulationCell biologyWnt ProteinsTamoxifenmedicine.anatomical_structureCateninMutationbiology.proteinStem cellHair FollicleCell DivisionHairScience
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Elusive amines and cluster headache: mutational analysis of trace amine receptor cluster on chromosome 6q23.

2004

Cluster headache (CH) is characterised by unilateral pain and ipsilateral autonomic features. To date, no molecular genetic evidence has been shown for CH. Small pedigrees and low penetrance render the identification of the CH-gene quite difficult. Nonetheless the association of CH and migraine to a new class of amine, namely trace or elusive amines such as tyramine, octopamine and synephrine, has recently been demonstrated. In particular, in comparison to healthy control subjects, all these neurotransmitters have been found to be greatly elevated in CH sufferers in plasma and platelets both in active and remission periods. A cluster of gene-encoding G-protein-coupled receptors that bind an…

Biogenic AminesGenetic LinkageDNA Mutational AnalysisCluster HeadacheDermatologymedicine.disease_causeReceptors G-Protein-Coupledchemistry.chemical_compoundTar (tobacco residue)Genetic linkageReceptors Biogenic AminemedicineHumansReceptorTrace amineMutationGeneral MedicineTyraminePenetrancePsychiatry and Mental healthchemistryBiochemistryMultigene FamilyOctopamine (neurotransmitter)Chromosomes Human Pair 6Neurology (clinical)Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
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Homozygous deletions localize novel tumor suppressor genes in B-cell lymphomas

2007

AbstractIntegrative genomic and gene-expression analyses have identified amplified oncogenes in B-cell non-Hodgkin lymphoma (B-NHL), but the capability of such technologies to localize tumor suppressor genes within homozygous deletions remains unexplored. Array-based comparative genomic hybridization (CGH) and gene-expression microarray analysis of 48 cell lines derived from patients with different B-NHLs delineated 20 homozygous deletions at 7 chromosome areas, all of which contained tumor suppressor gene targets. Further investigation revealed that only a fraction of primary biopsies presented inactivation of these genes by point mutation or intragenic deletion, but instead some of them w…

BiopsyDNA Mutational AnalysisGene DosageVesicular Transport ProteinsApoptosisBiochemistryEpigenesis Geneticimmune system diseaseshemic and lymphatic diseasesChromosomes HumanGenes Tumor SuppressorPromoter Regions GeneticSorting NexinsOligonucleotide Array Sequence AnalysisSequence DeletionBcl-2-Like Protein 11HomozygoteChromosome MappingNuclear ProteinsNucleic Acid HybridizationRNA-Binding ProteinsHematologyDNA NeoplasmBCL10Gene Expression Regulation Neoplasticmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2DNA methylationLymphoma B-CellTumor suppressor geneImmunologyBiologyGene dosageCell Line TumorProto-Oncogene ProteinsmedicineCyclin-Dependent Kinase Inhibitor p18HumansPoint MutationGene SilencingB cellAdaptor Proteins Signal TransducingHomeodomain ProteinsMembrane ProteinsCell BiologyDNA Methylationmedicine.diseaseMolecular biologyLymphomaCancer researchMantle cell lymphomaApoptosis Regulatory ProteinsCarrier ProteinsDiffuse large B-cell lymphomaTranscription Factors
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Recessive mutations in EPG5 cause Vici syndrome, a multisystem disorder with defective autophagy

2013

Vici syndrome is a recessively inherited multisystem disorder characterized by callosal agenesis, cataracts, cardiomyopathy, combined immunodeficiency and hypopigmentation. To investigate the molecular basis of Vici syndrome, we carried out exome and Sanger sequence analysis in a cohort of 18 affected individuals. We identified recessive mutations in EPG5 (previously KIAA1632), indicating a causative role in Vici syndrome. EPG5 is the human homolog of the metazoan-specific autophagy gene epg-5, encoding a key autophagy regulator (ectopic P-granules autophagy protein 5) implicated in the formation of autolysosomes. Further studies showed a severe block in autophagosomal clearance in muscle a…

BiopsyVesicular Transport ProteinsAutophagy-Related ProteinsGenes RecessiveConsanguinityBiologymedicine.disease_causeArticleCataract03 medical and health sciencesConsanguinity0302 clinical medicineCataractsAntigens NeoplasmGeneticsmedicineAutophagyHumansVici syndromeExomeFamilyMuscle SkeletalExomeImmunodeficiency030304 developmental biologyGenetics0303 health sciencesMutationAutophagyIntracellular Signaling Peptides and ProteinsLysosome-Associated Membrane GlycoproteinsProteinsmedicine.diseaseMutationAutophagy Protein 5Agenesis of Corpus CallosumLysosomes030217 neurology & neurosurgeryNature genetics
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αv-Class integrin binding to fibronectin is solely mediated by RGD and unaffected by an RGE mutation.

2020

Fibronectin (FN) is an essential glycoprotein of the extracellular matrix; binds integrins, syndecans, collagens, and growth factors; and is assembled by cells into complex fibrillar networks. The RGD motif in FN facilitates cell binding and fibrillogenesis through binding to α5β1 and αv-class integrins. However, whether RGD is the sole binding site for αv-class integrins is unclear. Most notably, substituting aspartate with glutamate (RGE) was shown to eliminate integrin binding in vitro, while mouse genetics revealed that FNRGE preserves αv-class integrin binding and fibrillogenesis. To address this conflict, we employed single-cell force spectroscopy, engineered cells, and RGD motif–defi…

BioquímicaBiologiaIntegrin02 engineering and technologyBiologyBiochemistryArticleFocal adhesion03 medical and health sciencesMiceAnimalsReceptors VitronectinBinding siteCell adhesion030304 developmental biologyIntegrin bindingRGD motif0303 health sciencesCorrectionFibrillogenesisCell Biology021001 nanoscience & nanotechnologyMice Mutant StrainsCell biologyFibronectinMutationAdhesionbiology.protein0210 nano-technologyOligopeptidesThe Journal of cell biology
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Lack of Cry1Fa binding to the midgut brush border membrane in a resistant colony of Plutella xylostella moths with a mutaton in the ABCC2 locus

2012

ABSTRACT Previous studies reported “mode 1” Bacillus thuringiensis resistance in a colony of diamondback moths (NO-QA), and recently, this resistance has been mapped to an ABC transporter ( ABCC2 ) locus. We report the lack of binding of Cry1Fa to insects derived from this colony and compare our data with those from other insects with ABCC2 -associated resistance.

BioquímicaBrush borderBiotecnologia agrícolaDrug ResistanceResistència als plaguicidesLocus (genetics)ATP-binding cassette transporterDrug resistanceApplied Microbiology and BiotechnologyLepidoptera genitaliaHemolysin ProteinsPlagues ControlBacterial ProteinsBacillus thuringiensisInvertebrate MicrobiologyAnimalsGeneticsBacillus thuringiensis ToxinsMicrovilliEcologybiologyfungiPlutellaMidgutbiology.organism_classificationMultidrug Resistance-Associated Protein 2EndotoxinsLepidopteraMutationMultidrug Resistance-Associated ProteinsProtein BindingFood ScienceBiotechnology
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Topoisomerase II regulates yeast genes with singular chromatin architectures

2013

Eukaryotic topoisomerase II (topo II) is the essential decatenase of newly replicated chromosomes and the main relaxase of nucleosomal DNA. Apart from these general tasks, topo II participates in more specialized functions. In mammals, topo IIa interacts with specific RNA polymerases and chromatin-remodeling complexes, whereas topo IIb regulates developmental genes in conjunction with chromatin remodeling and heterochromatin transitions. Here we show that in budding yeast, topo II regulates the expression of specific gene subsets. To uncover this, we carried out a genomic transcription run-on shortly after the thermal inactivation of topo II. We identified a modest number of genes not invol…

BioquímicaHeterochromatinADNSaccharomyces cerevisiaeGene Regulation Chromatin and EpigeneticsGenètica molecularChromatin remodelingHistonesCromatina03 medical and health sciencesGene Expression Regulation FungalGeneticsNucleosomeDNA FungalPromoter Regions GeneticTranscription factor030304 developmental biologyGenetics0303 health sciencesbiologyPolyamine transport030302 biochemistry & molecular biologyPromoterExpressió gènicaChromatinChromatinNucleosomesHistoneDNA Topoisomerases Type IIMutationbiology.proteinGenèticaTranscription FactorsNucleic Acids Research
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