Search results for "COMB"

showing 10 items of 7115 documents

Functional display of an alpha2 integrin-specific motif (RKK) on the surface of baculovirus particles.

2005

The use of baculovirus vectors shows promise as a tool for gene delivery into mammalian cells. These insect viruses have been shown to transduce a variety of mammalian cell lines, and gene transfer has also been demonstrated in vivo. In this study, we generated two recombinant baculovirus vectors displaying an integrin-specific motif, RKK, as a part of two different loops of the green fluorescent protein (GFP) fused with the major envelope protein gp64 of Autographa californica M nucleopolyhedrovirus. By enzyme linked immunosorbent assays, these viruses were shown to bind a peptide representing the receptor binding site of an α2 integrin, the α2I-domain. However, the interaction was not st…

0301 basic medicineModels MolecularCancer ResearchInsectavirusesmedia_common.quotation_subjectAmino Acid MotifsGreen Fluorescent ProteinsIntegrin alpha2PeptideEnzyme-Linked Immunosorbent AssayCHO CellsBiologyGene deliveryGreen fluorescent proteinCell Line03 medical and health sciences0302 clinical medicineCricetinaeAnimalsCloning MolecularInternalizationmedia_commonchemistry.chemical_classificationMicroscopy ConfocalPhospholipase CWild typeGene Transfer Techniquesbiology.organism_classificationFlow CytometryMolecular biologyRecombinant ProteinsProtein Structure TertiaryAutographa californica030104 developmental biologyEnzymeOncologychemistryMicroscopy FluorescenceMutagenesis030220 oncology & carcinogenesisType C PhospholipasesElectrophoresis Polyacrylamide GelPeptidesBaculoviridaeViral Fusion ProteinsPlasmidsProtein BindingTechnology in cancer researchtreatment
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High-Pressure-Driven Reversible Dissociation of α-Synuclein Fibrils Reveals Structural Hierarchy

2017

The analysis of the α-synuclein (aS) aggregation process, which is involved in Parkinson's disease etiopathogenesis, and of the structural feature of the resulting amyloid fibrils may shed light on the relationship between the structure of aS aggregates and their toxicity. This may be considered a paradigm of the ground work needed to tackle the molecular basis of all the protein-aggregation-related diseases. With this aim, we used chemical and physical dissociation methods to explore the structural organization of wild-type aS fibrils. High pressure (in the kbar range) and alkaline pH were used to disassemble fibrils to collect information on the hierarchic pathway by which distinct β-sh…

0301 basic medicineModels MolecularCircular dichroismAmyloidProtein FoldingProtein domainBeta sheetBiophysicsFibrilMicroscopy Atomic ForceSpectrum Analysis RamanDissociation (chemistry)03 medical and health sciences0302 clinical medicineProtein structureMicroscopy Electron TransmissionProtein DomainsSpectroscopy Fourier Transform InfraredEscherichia coliPressureChemistryCircular DichroismEnergy landscapeProteinsalpha synuclein amyloid recombinant proteinHydrogen-Ion ConcentrationRecombinant ProteinsCrystallography030104 developmental biologyMutationalpha-SynucleinProtein foldingProtein Conformation beta-StrandProtein Multimerization030217 neurology & neurosurgery
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Recombinant anthrax protective antigen: Observation of aggregation phenomena by TEM reveals specific effects of sterols.

2017

Abstract Negatively stained transmission electron microscope images are presented that depict the aggregation of recombinant anthrax protective antigen (rPA83 monomer and the PA63 prepore oligomer) under varying in vitro biochemical conditions. Heat treatment (50 °C) of rPA83 produced clumped fibrils, but following heating the PA63 prepore formed disordered aggregates. Freeze-thaw treatment of the PA63 prepore generated linear flexuous aggregates of the heptameric oligomers. Aqueous suspensions of cholesterol microcrystals were shown to bind small rPA83 aggregates at the edges of the planar bilayers. With PA63 a more discrete binding of the prepores to the crystalline cholesterol bilayer ed…

0301 basic medicineModels MolecularHot TemperatureBacterial ToxinsGeneral Physics and AstronomyFibrilOligomerNegative Staining03 medical and health scienceschemistry.chemical_compoundProtein AggregatesMicroscopy Electron TransmissionStructural BiologyFreezingGeneral Materials ScienceAntigens BacterialAqueous solutionChemistryBilayerCell BiologyHydrogen-Ion ConcentrationNegative stainSterolRecombinant ProteinsCrystallographySterols030104 developmental biologyMonomerCholesterolTransmission electron microscopyCrystallizationDeoxycholic AcidMicron (Oxford, England : 1993)
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rbFOX1/MBNL1 competition for CCUG RNA repeats binding contributes to myotonic dystrophy type 1/type 2 differences

2018

Myotonic dystrophy type 1 and type 2 (DM1, DM2) are caused by expansions of CTG and CCTG repeats, respectively. RNAs containing expanded CUG or CCUG repeats interfere with the metabolism of other RNAs through titration of the Muscleblind-like (MBNL) RNA binding proteins. DM2 follows a more favorable clinical course than DM1, suggesting that specific modifiers may modulate DM severity. Here, we report that the rbFOX1 RNA binding protein binds to expanded CCUG RNA repeats, but not to expanded CUG RNA repeats. Interestingly, rbFOX1 competes with MBNL1 for binding to CCUG expanded repeats and overexpression of rbFOX1 partly releases MBNL1 from sequestration within CCUG RNA foci in DM2 muscle ce…

0301 basic medicineModels MolecularProtein Conformation alpha-Helical[SDV]Life Sciences [q-bio]General Physics and AstronomyGene ExpressionRNA-binding proteinCrystallography X-Raychemistry.chemical_compoundMOLECULAR-BASISGene expressionMBNL1Myotonic DystrophyComputingMilieux_MISCELLANEOUSMultidisciplinaryCHLORIDE CHANNELQRNA-Binding ProteinsRecombinant Proteins3. Good healthCell biologyCONGENITAL HEART-DISEASEDrosophila melanogasterThermodynamicsSKELETAL-MUSCLERNA Splicing FactorsCUG REPEATSProtein BindingRNA Splicing Factorsmusculoskeletal diseasesSTEADY-STATEcongenital hereditary and neonatal diseases and abnormalitiesScienceRBFOX1BiologyMyotonic dystrophyBinding CompetitiveGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesmedicineEscherichia coliAnimalsHumansProtein Interaction Domains and MotifsBinding siteNucleotide MotifsMuscle SkeletalSPLICING REGULATOR RBFOX2MUSCLEBLIND PROTEINSBinding SitesPRE-MESSENGER-RNARNAGeneral Chemistrymedicine.diseaseDisease Models AnimalKinetics030104 developmental biologychemistryTRIPLET REPEATRNAProtein Conformation beta-Strand3111 Biomedicine
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1,3,5-Triazines: A promising scaffold for anticancer drugs development

2017

This review covering literature reports from the beginning of this century to 2016 describes the synthetic pathways, the antitumor activity, the structure-activity relationship and, whenever reported, the possible mechanism of action of 1,3,5-triazine derivatives as well as of their hetero-fused compounds. Many 1,3,5-triazine derivatives, both uncondensed and hetero-fused, have shown remarkable antitumor activities and some of them reached clinical development.

0301 basic medicineModels MolecularScaffold31Disubstituted 135-triazineTrisubstituted 135-triazineAntineoplastic AgentsChemistry Techniques Synthetic01 natural sciences03 medical and health sciencesStructure-Activity RelationshipNeoplasmsDrug DiscoverymedicineAnimalsHumans5-TriazinesTrisubstituted 1Disubstituted 1Antitumor activityPharmacologyHeterofused 135-triazine010405 organic chemistryChemistryTriazinesNitrogen heterocyclesDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryGeneral MedicineHeterofused 1Combinatorial chemistry135-Triazine0104 chemical sciences030104 developmental biologyNitrogen heterocycleMechanism of action1; 3; 5-Triazines; Antitumor activity; Disubstituted 1; 3; 5-triazines; Heterofused 1; 3; 5-triazines; Nitrogen heterocycles; Trisubstituted 1; 3; 5-triazines; Pharmacology; Drug Discovery3003 Pharmaceutical Science; Organic Chemistrymedicine.symptomAntitumor activity
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Investigation on Quantitative Structure-Activity Relationships of 1,3,4-Oxadiazole Derivatives as Potential Telomerase Inhibitors.

2020

Background:Telomerase, a reverse transcriptase, maintains telomere and chromosomes integrity of dividing cells, while it is inactivated in most somatic cells. In tumor cells, telomerase is highly activated, and works in order to maintain the length of telomeres causing immortality, hence it could be considered as a potential marker to tumorigenesis.A series of 1,3,4-oxadiazole derivatives showed significant broad-spectrum anticancer activity against different cell lines, and demonstrated telomerase inhibition.Methods:This series of 24 N-benzylidene-2-((5-(pyridine-4-yl)-1,3,4-oxadiazol-2yl)thio)acetohydrazide derivatives as telomerase inhibitors has been considered to carry out QSAR studies…

0301 basic medicineModels MolecularTelomeraseQuantitative structure–activity relationship2D descriptorsDatasets as TopicQuantitative Structure-Activity RelationshipAntineoplastic Agents010402 general chemistry01 natural sciencesModels BiologicalAnticancer activityMLR03 medical and health sciencesInhibitory Concentration 50Drug DiscoveryLeast-Squares AnalysisTelomerase134-oxadiazolesOxadiazolesMolecular StructureDrug discoveryChemistryQSARQuantitative structureCombinatorial chemistry0104 chemical sciencesTelomerase inhibitors030104 developmental biology1 3 4 oxadiazole derivativesDrug Screening Assays AntitumorCurrent drug discovery technologies
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Identifying Prognostic SNPs in Clinical Cohorts: Complementing Univariate Analyses by Resampling and Multivariable Modeling

2016

Clinical cohorts with time-to-event endpoints are increasingly characterized by measurements of a number of single nucleotide polymorphisms that is by a magnitude larger than the number of measurements typically considered at the gene level. At the same time, the size of clinical cohorts often is still limited, calling for novel analysis strategies for identifying potentially prognostic SNPs that can help to better characterize disease processes. We propose such a strategy, drawing on univariate testing ideas from epidemiological case-controls studies on the one hand, and multivariable regression techniques as developed for gene expression data on the other hand. In particular, we focus on …

0301 basic medicineMultivariate analysisMicroarraysTest StatisticsGene Expressionlcsh:MedicineBioinformatics01 natural sciencesHematologic Cancers and Related DisordersCohort Studies010104 statistics & probabilityMathematical and Statistical TechniquesResamplingMedicine and Health Scienceslcsh:ScienceStatistical DataUnivariate analysisMultidisciplinarySimulation and ModelingMultivariable calculusRegression analysisHematologyMyeloid LeukemiaPrognosisRegressionBioassays and Physiological AnalysisOncologyResearch DesignPhysical SciencesStatistics (Mathematics)Research ArticleAcute Myeloid LeukemiaPermutationSingle-nucleotide polymorphismComputational biologyBiologyResearch and Analysis MethodsPolymorphism Single Nucleotide03 medical and health sciencesLeukemiasGeneticsHumansStatistical Methods0101 mathematicsDiscrete Mathematicslcsh:RUnivariateCancers and NeoplasmsBiology and Life SciencesModels Theoretical030104 developmental biologyCombinatoricsCase-Control StudiesMultivariate Analysislcsh:QMathematicsPLOS ONE
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Peptide Processing Is Critical for T-Cell Memory Inflation and May Be Optimized to Improve Immune Protection by CMV-Based Vaccine Vectors.

2016

Cytomegalovirus (CMV) elicits long-term T-cell immunity of unparalleled strength, which has allowed the development of highly protective CMV-based vaccine vectors. Counterintuitively, experimental vaccines encoding a single MHC-I restricted epitope offered better immune protection than those expressing entire proteins, including the same epitope. To clarify this conundrum, we generated recombinant murine CMVs (MCMVs) encoding well-characterized MHC-I epitopes at different positions within viral genes and observed strong immune responses and protection against viruses and tumor growth when the epitopes were expressed at the protein C-terminus. We used the M45-encoded conventional epitope HGI…

0301 basic medicineMuromegalovirusEpitopes T-LymphocyteCD8-Positive T-LymphocytesLymphocyte ActivationPathology and Laboratory MedicineBiochemistryEpitopeMass SpectrometryMiceWhite Blood Cells0302 clinical medicineAnimal CellsMedicine and Health SciencesCytotoxic T celllcsh:QH301-705.5Antigens ViralImmune ResponseStainingVaccines SyntheticbiologyT CellsCell StainingHerpesviridae InfectionsFlow CytometryRecombinant Proteins3. Good healthmedicine.anatomical_structureMedical MicrobiologyViral PathogensVirusesHuman CytomegalovirusCellular TypesPathogensResearch Articlelcsh:Immunologic diseases. AllergyHerpesvirusesT cellImmune CellsAntigen presentationImmunologyCytotoxic T cellsMajor histocompatibility complexResearch and Analysis MethodsMicrobiology03 medical and health sciencesViral ProteinsImmune systemAntigenVirologyGeneticsmedicineAnimalsAntigen-presenting cellMolecular Biology TechniquesMolecular BiologyMicrobial PathogensBlood CellsImmunodominant EpitopesOrganismsBiology and Life SciencesProteinsViral VaccinesCell BiologyVirology030104 developmental biologylcsh:Biology (General)Specimen Preparation and Treatmentbiology.proteinMutagenesis Site-DirectedParasitologylcsh:RC581-607PeptidesDNA virusesImmunologic Memory030215 immunologyChromatography LiquidCloningPLoS pathogens
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Mechanisms of viral mutation

2016

The remarkable capacity of some viruses to adapt to new hosts and environments is highly dependent on their ability to generate de novo diversity in a short period of time. Rates of spontaneous mutation vary amply among viruses. RNA viruses mutate faster than DNA viruses, single-stranded viruses mutate faster than double-strand virus, and genome size appears to correlate negatively with mutation rate. Viral mutation rates are modulated at different levels, including polymerase fidelity, sequence context, template secondary structure, cellular microenvironment, replication mechanisms, proofreading, and access to post-replicative repair. Additionally, massive numbers of mutations can be intro…

0301 basic medicineMutation rateEvolutionMutation ratevirusesGenome ViralReviewBiologyVirus ReplicationGenetic diversityVirus03 medical and health sciencesCellular and Molecular NeuroscienceMolecular BiologySuppressor mutationRecombination GeneticPharmacologyGeneticsCell BiologyResistance mutationVirologyReplication fidelityVirusPost-replicative repair030104 developmental biologyViral replicationViral evolutionMutationVirusesMutation (genetic algorithm)Dynamic mutationMolecular MedicineHyper-mutationCellular and Molecular Life Sciences
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Impact of BRAF and RAS mutations on first-line efficacy of FOLFIRI plus cetuximab versus FOLFIRI plus bevacizumab: analysis of the FIRE-3 (AIO KRK-03…

2017

Abstract Background RAS and BRAF mutations have been identified as negative prognostic factors in metastatic colorectal cancer. Efficacy of 5-fluorouracil, leucovorin, irinotecan (FOLFIRI) plus bevacizumab in patients with RAS-mutant tumours needs to be further evaluated. Whether to treat patients with BRAF-mutant tumours with either bevacizumab or anti-epidermal growth factor receptor (EGFR) antibodies remains unclear. Methods Patients treated within the FIRE-3 trial were retrospectively tested for BRAF and RAS mutations using formalin fixated paraffin embedded (FFPE) tumour material applying pyrosequencing for KRAS and NRAS exon 2, 3 and 4 mutations as far as for BRAF mutations. Survival …

0301 basic medicineNeuroblastoma RAS viral oncogene homologOncologyMaleProto-Oncogene Proteins B-rafCancer Researchmedicine.medical_specialtyBevacizumabColorectal cancerLeucovorinCetuximabmedicine.disease_causeProto-Oncogene Proteins p21(ras)03 medical and health sciences0302 clinical medicineInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansneoplasmsSurvival analysisAgedRetrospective StudiesCetuximabbusiness.industryLiver NeoplasmsExonsMiddle Agedmedicine.diseasedigestive system diseasesIrinotecanBevacizumab030104 developmental biologyTreatment OutcomeOncology030220 oncology & carcinogenesisMutationFOLFIRICamptothecinFemaleKRASFluorouracilbusinessColorectal Neoplasmsmedicine.drugEuropean journal of cancer (Oxford, England : 1990)
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