Search results for "mutant"

showing 10 items of 670 documents

Role of secondary metabolites in the biocontrol activity of Pseudomonas corrugata and Pseudomonas mediterranea

2017

In this study, the Pseudomonas corrugata strain CFBP 5454 and the P. mediterranea strain CFBP 5447 were shown to produce diffusible compounds that inhibit the in vitro growth of plant pathogenic fungi and bacteria and antifungal volatile compounds. In addition, both bacterial strains were found to produce cyanide. Mutant derivatives in LuxR transcriptional regulators, i.e. P. corrugata GL2 (pcoR mutant) and GLRFIA (rfiA mutant), and P. mediterranea PSMER (pmeR mutant) and PSRFIA (rfiA mutant) impaired in cyclic lipopeptide (CLP) production, showed a diffusible compound-mediated reduced activity, depending on the biocontrol strain, challenge microorganism and culture medium. The volatile com…

0301 basic medicineCyclic lipopeptidPseudomonas mediterranea030106 microbiologyMutantHydrogen cyanideeHydrogen cyanidePlant ScienceAntimicrobial activityHorticulturePseudomonaMicrobiology03 medical and health scienceschemistry.chemical_compoundPseudomonasBotrytis cinereabiologyLuxR transcriptional regulatorPseudomonasStructural geneSettore AGR/12 - Patologia Vegetalebiology.organism_classificationAntimicrobial activity; Cyclic lipopeptid; eHydrogen cyanide; LuxR transcriptional regulator; PseudomonasCyclic lipopeptidePseudomonas corrugataBiochemistrychemistryHydrogen cyanideAgronomy and Crop ScienceBacteriaEuropean Journal of Plant Pathology
researchProduct

Hog1p activation by marasmic acid through inhibition of the histidine kinase Sln1p

2016

BACKGROUND The histidine kinase (HK) MoHik1p within the high-osmolarity glycerol (HOG) pathway is known to be the target of the fungicide fludioxonil. Treatment of the fungus with fludioxonil causes an uncontrolled hyperactivation of the pathway and cell death. In this study, we used a target-based in vivo test system with mutant strains of the rice blast fungus Magnaporthe oryzae to search for new fungicidal compounds having various target locations within the HOG pathway. Mutants with inactivated HOG signalling are resistant to fungicides having the target located in the HOG pathway. RESULTS The HK MoSln1p was identified as being involved in the new antifungal mode of action of marasmic a…

0301 basic medicineFungal proteinMagnaporthebiologyMutantHistidine kinaseGeneral MedicineFludioxonilbiology.organism_classificationMicrobiology03 medical and health sciencesMetabolic pathway030104 developmental biologyBiochemistryInsect SciencePhosphorylationMode of actionAgronomy and Crop SciencePest Management Science
researchProduct

The Amino-Terminal Domain of GRK5 Inhibits Cardiac Hypertrophy through the Regulation of Calcium-Calmodulin Dependent Transcription Factors.

2018

We have recently demonstrated that the amino-terminal domain of G protein coupled receptor kinase (GRK) type 5, (GRK5-NT) inhibits NFκB activity in cardiac cells leading to a significant amelioration of LVH. Since GRK5-NT is known to bind calmodulin, this study aimed to evaluate the functional role of GRK5-NT in the regulation of calcium-calmodulin-dependent transcription factors. We found that the overexpression of GRK5-NT in cardiomyoblasts significantly reduced the activation and the nuclear translocation of NFAT and its cofactor GATA-4 in response to phenylephrine (PE). These results were confirmed in vivo in spontaneously hypertensive rats (SHR), in which intramyocardial adenovirus-med…

0301 basic medicineG-Protein-Coupled Receptor Kinase 5MalecalmodulinMutantWistarPlasma protein binding030204 cardiovascular system & hematologyCatalysilcsh:ChemistryPhenylephrine0302 clinical medicineRats Inbred SHRMyocytes Cardiaclcsh:QH301-705.5SpectroscopybiologyChemistrycardiac hypertrophyNFATComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineLeft VentricularComputer Science ApplicationsCell biologycardiac hypertrophy; transcription factors; calmodulin; GRKGRKHypertrophy Left VentricularCardiacProtein BindingInbred SHRCalmodulinCalmodulin; Cardiac hypertrophy; GRK; Transcription factors; Animals; Binding Sites; Calmodulin; Cell Line; G-Protein-Coupled Receptor Kinase 5; GATA4 Transcription Factor; Hypertrophy Left Ventricular; Male; Myocytes Cardiac; NFATC Transcription Factors; Phenylephrine; Protein Binding; Rats; Rats Inbred SHR; Rats Wistar; Catalysis; Molecular Biology; Spectroscopy; Computer Science Applications1707 Computer Vision and Pattern Recognition; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic ChemistryCatalysisArticleCell LineInorganic Chemistry03 medical and health sciencesG-Protein-Coupled Receptor Kinase 5transcription factorsAnimalsPhysical and Theoretical ChemistryRats WistarTranscription factorMolecular BiologyG protein-coupled receptor kinaseMyocytesBinding SitesNFATC Transcription FactorsOrganic ChemistryHypertrophyNFATC Transcription FactorsGATA4 Transcription FactorRats030104 developmental biologylcsh:Biology (General)lcsh:QD1-999biology.proteinTranscription factorInternational journal of molecular sciences
researchProduct

NOX2ko Mice Show Largely Increased Expression of a Mutated NOX2 mRNA Encoding an Inactive NOX2 Protein

2020

Background: The superoxide-generating enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2 or gp91phox, the phagocytic isoform) was reported as a major source of oxidative stress in various human diseases. Genetic deletion is widely used to study the impact of NOX2-derived reactive oxygen species (ROS) on disease development and progression in various animal models. Here, we investigate why NOX2 knockout mice show no NOX2 activity but express NOX2 mRNA and protein. Methods and Results: Oxidative burst (NOX2-dependent formation of ROS) was measured by L-012-based chemiluminescence and was largely absent in whole blood of NOX2 knockout mice. Protein expression was still de…

0301 basic medicineGene isoformPhysiologyClinical Biochemistrynext generation sequencing (NGS)030204 cardiovascular system & hematologymedicine.disease_causeBiochemistryArticlenicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2) knockout mice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineWestern blotmedicineMolecular BiologyGeneMessenger RNAmedicine.diagnostic_testurogenital systemCell BiologyMolecular biologyRespiratory burst030104 developmental biologychemistryKnockout mousecardiovascular systemoxidative stress related diseasetruncated and inactive mutanthormones hormone substitutes and hormone antagonistsOxidative stressNicotinamide adenine dinucleotide phosphatecirculatory and respiratory physiologyAntioxidants
researchProduct

Comparison of CRISPR and Marker-Based Methods for the Engineering of Phage T7

2020

This article belongs to the Section Bacterial Viruses.

0301 basic medicineGenetic Markersviruses030106 microbiologyMutantlcsh:QR1-502t7Computational biologyGenome ViralBiologyGenomeArticlelcsh:MicrobiologyBacteriophage03 medical and health sciencesbacteriophageVirologyBacteriophage T7CRISPRClustered Regularly Interspaced Short Palindromic RepeatsGenomescrisprBacteriophageGeneSelection (genetic algorithm)Gene EditingQHT7Viral Tail Proteinsbiology.organism_classificationBacteriòfags3. Good healthQRtail fibres030104 developmental biologyInfectious DiseasesLytic cycleCRISPRMutationTail fibresCRISPR-Cas SystemsHomologous recombinationGenèticaViruses
researchProduct

Identification and Successful Negotiation of a Metabolic Checkpoint in Direct Neuronal Reprogramming

2016

Despite the widespread interest in direct neuronal reprogramming, the mechanisms underpinning fate conversion remain largely unknown. Our study revealed a critical time point after which cells either successfully convert into neurons or succumb to cell death. Co-transduction with Bcl-2 greatly improved negotiation of this critical point by faster neuronal differentiation. Surprisingly, mutants with reduced or no affinity for Bax demonstrated that Bcl-2 exerts this effect by an apoptosis-independent mechanism. Consistent with a caspase-independent role, ferroptosis inhibitors potently increased neuronal reprogramming by inhibiting lipid peroxidation occurring during fate conversion. Genome-w…

0301 basic medicineGeneticsProgrammed cell deathCell typeCellular Reprogramming TechniquesMutantCell BiologyBiologyIn vitroCell biology03 medical and health sciencesTransduction (genetics)030104 developmental biologyIn vivoGeneticsMolecular MedicineReprogrammingCell Stem Cell
researchProduct

Zebrafish as a Model for the Study of Chaperonopathies

2016

There is considerable information on the clinical manifestations and mode of inheritance for many genetic chaperonopathies but little is known on the molecular mechanisms underlying the cell and tissue abnormalities that characterize them. This scarcity of knowledge is mostly due to the lack of appropriate animal models that mimic closely the human molecular, cellular, and histological characteristics. In this article we introduce zebrafish as a suitable model to study molecular and cellular mechanisms pertaining to human chaperonopathies. Genetic chaperonopathies manifest themselves from very early in life so it is necessary to examine the impact of mutant chaperone genes during developmen…

0301 basic medicineGeneticsbiologymedicine.diagnostic_testPhysiologyClinical BiochemistryMutantCell BiologyComputational biologybiology.organism_classificationClinical biochemistry03 medical and health sciences030104 developmental biologyChaperone (protein)biology.proteinmedicineGeneZebrafishOrganismGenetic testingZebrafish genomeJournal of Cellular Physiology
researchProduct

Pyomelanin-producingPseudomonas aeruginosaselected during chronic infections have a large chromosomal deletion which confers resistance to pyocins

2016

When bacterial lineages make the transition from free-living to permanent association with hosts, they can undergo massive gene losses, for which the selective forces within host tissues are unknown. We identified here melanogenic clinical isolates of Pseudomonas aeruginosa with large chromosomal deletions (66 to 270 kbp) and characterized them to investigate how they were selected. When compared with their wild-type parents, melanogenic mutants (i) exhibited a lower fitness in growth conditions found in human tissues, such as hyperosmolarity and presence of aminoglycoside antibiotics, (ii) narrowed their metabolic spectrum with a growth disadvantage with particular carbon sources, includin…

0301 basic medicineGeneticseducation.field_of_studyPseudomonas aeruginosamedicine.drug_class030106 microbiologyAntibioticsPopulationMutantDrug resistanceBiologymedicine.disease_causeMicrobiology3. Good healthMicrobiologyBacterial genetics03 medical and health sciences030104 developmental biologymedicineeducationGeneEcology Evolution Behavior and SystematicsChromosomal DeletionEnvironmental Microbiology
researchProduct

L1 syndrome diagnosis complemented with functional analysis of L1CAM variants located to the two N-terminal Ig-like domains

2016

L1CAM gene mutations cause neurodevelopmental disorders collectively termed L1 syndrome. Insufficient information about L1CAM variants complicates clinical prognosis, genetic diagnosis and genetic counseling. We combined clinical data, in silico effect predictions and functional analysis of four L1CAM variants, p.I37N, p.T38M, p.M172I and p.D202Y, located to the two N-terminal Ig-like domains present in five families with symptoms of L1 syndrome. Software tools predicted destabilizing effects of p.I37N and p.D202Y but results for p.T38M and p.M172I were inconsistent. Cell surface expression of mutant proteins L1-T38M, L1-M172I and L1-D202Y was normal. Conversely, L1-I37N accumulated in the …

0301 basic medicineGeneticsmedicine.medical_specialtyL1In silicoEndoplasmic reticulumMutantBiologymedicine.disease03 medical and health sciences030104 developmental biology0302 clinical medicineNeurodevelopmental disorderGeneticsmedicineMedical geneticsProtein foldingProtein maturation030217 neurology & neurosurgeryGenetics (clinical)Clinical Genetics
researchProduct

TheGCA1gene encodes a glycosidase-like protein in the cell wall ofCandida albicans

2016

Candida albicans Gca1p is a putative glucoamylase enzyme which contains 946 amino acids, 11 putative sites for N -glycosylation and 9 for O -glycosylation. Gca1p was identified in β-mercaptoethanol extracts from isolated cell walls of strain C. albicans SC5314 and it is involved in carbohydrate metabolism. The significance and the role of this protein within the cell wall structure were studied in the corresponding mutants. The homozygous mutant showed that GCA1 was not an essential gene for cell viability. Subsequent phenotypic analysis performed in the mutants obtained did not show significant difference in the behavior of mutant when compared with the wild strain SC5314. Zymoliase, Calco…

0301 basic medicineGlycosylationGlycoside HydrolasesGenes Fungal030106 microbiologyMutantCalcofluor-whiteApplied Microbiology and BiotechnologyMicrobiologyCell wallGene Knockout Techniques03 medical and health scienceschemistry.chemical_compoundGlucosidesCell WallCandida albicansCandida albicanschemistry.chemical_classificationMicrobial ViabilitybiologyGeneral Medicinebiology.organism_classificationMolecular biologyEnzyme assayCorpus albicansEnzymechemistryBiochemistrybiology.proteinFEMS Yeast Research
researchProduct