Search results for "glutamine"

showing 10 items of 122 documents

Glutamine Codon Usage and polyQ Evolution in Primates Depend on the Q Stretch Length

2018

Abstract Amino acid usage in a proteome depends mostly on its taxonomy, as it does the codon usage in transcriptomes. Here, we explore the level of variation in the codon usage of a specific amino acid, glutamine, in relation to the number of consecutive glutamine residues. We show that CAG triplets are consistently more abundant in short glutamine homorepeats (polyQ, four to eight residues) than in shorter glutamine stretches (one to three residues), leading to the evolutionary growth of the repeat region in a CAG-dependent manner. The length of orthologous polyQ regions is mostly stable in primates, particularly the short ones. Interestingly, given a short polyQ the CAG usage is higher in…

Primatescongenital hereditary and neonatal diseases and abnormalitiescodon usageProteomeGlutaminehomorepeatEvolution MolecularAnimalsHumansglutamine stretchCodonPeptidespolyQ-associated diseasesResearch ArticleGenome Biology and Evolution
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Italian familial defective apolipoprotein B patients share a unique haplotype with other Caucasian patients.

2001

Familial defective apolipoprotein (apo) B-100 together with familial hypercholesterolemia are the two common genetic conditions that cause hypercholesterolemia. Familial defective apolipoprotein B-100 is due to mutations around codon 3500 of the apo B gene. The most-characterized mutation is a G>A transition at nucleotide 10,708 that results in the substitution of arginine by glutamine at codon 3500 (Apo B Arg3500Gln). Two other mutations are caused by a C>T transition, one at nucleotide 10,800 (Apo B Arg3531Cys) and the other at nucleotide 10,707 (apo B Arg3500Trp). In the present study we describe three new Italian cases of familial defective apolipoprotein B-100 (Apo B Arg3500Gln), one f…

ProbandChinaSettore MED/09 - Medicina InternaApolipoprotein BGlutamineEuropean Continental Ancestry GroupHypercholesterolemiaFamilial hypercholesterolemiamedicine.disease_causeArgininePolymorphism Single NucleotideGeneral Biochemistry Genetics and Molecular BiologyWhite PeopleHaplotypemedicineHumansCysteineAlleleCodonGeneApolipoproteins BGeneticsMutationbiologyTransition (genetics)HaplotypeGeneral Medicinemedicine.diseaseEuropeSettore MED/03 - Genetica MedicaAmino Acid SubstitutionHaplotypesItalyApolipoprotein B-100Mutationbiology.proteinlipids (amino acids peptides and proteins)HumanClinical and experimental medicine
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Polyglutamine toxicity induces rod photoreceptor division, morphological transformation or death in Spinocerebellar ataxia 7 mouse retina

2010

In neurodegenerative disorders caused by polyglutamine (polyQ) expansion, polyQ toxicity is thought to trigger a linear cascade of successive degenerative events leading to neuronal death. To understand how neurons cope with polyQ toxicity, we studied a Spinocerebellar ataxia 7 (SCA7) mouse which expresses polyQ-expanded ATXN7 only in rod photoreceptors. We show that in response to polyQ toxicity, SCA7 rods go through a range of radically different cell fates, including apoptotic and non-apoptotic cell death, cell migration, morphological transformation into a round cell or, most remarkably, cell division. The temporal profile of retinal remodeling indicates that some degenerative pathways …

Programmed cell deathCell divisionProliferationPopulationMice TransgenicNerve Tissue ProteinsBiologylcsh:RC321-571Mice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell MovementRetinal Rod Photoreceptor CellsmedicineAnimalsSpinocerebellar AtaxiasNeurodegenerationeducationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryCell ShapeComputingMilieux_MISCELLANEOUSSpinocerebellar ataxia 7030304 developmental biologyAtaxin-7Mice Knockout0303 health sciencesRetinaeducation.field_of_studyPhotoreceptorCell DeathRetinal DegenerationNeurodegenerationRetinalmedicine.diseaseRemodelingMice Inbred C57BLmedicine.anatomical_structureNeurologyProteotoxicitychemistryNerve DegenerationSpinocerebellar ataxia[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Apoptosis Regulatory ProteinsPeptidesPolyglutamineNeuroscience030217 neurology & neurosurgery
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Insulin and IGFs induce apoptosis in chick embryo retinas deprived of L-glutamine

1999

In chick embryo retinas, cultured in serum-free medium lacking L-glutamine, IGF-I, IGF-II and insulin induced apoptotic DNA fragmentation and cell death, IGF-I being the most efficacious compound. The apoptotic effect, which was particularly evident in retinas removed from 7-day-old chick embryos, declined with the age of the embryos and disappeared after day 11. Apoptosis appeared after a time lag of 8 h and then increased with time up to 16 h. Cycloheximide, an inhibitor of protein synthesis, was capable of entirely abolishing apoptotic cell death. The effect induced by IGFs or insulin was suppressed by the addition of glutamine. Cytokine-mediated apoptosis was also observed after withdra…

Programmed cell deathChemistryInsulinmedicine.medical_treatmentApoptotic DNA fragmentationEmbryoRetinalCell BiologyAnatomyCycloheximideCell biologyGlutaminechemistry.chemical_compoundApoptosismedicineInsulin apoptosis chick embryo retina development growth factorsMolecular Biology
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A proteomic approach to studying plant response to crenate broomrape (Orobanche crenata) in pea (Pisum sativum)

2004

Abstract Crenate broomrape ( Orobanche crenata ) is a parasitic plant that threatens legume production in Mediterranean areas. Pea ( Pisum sativum ) is severely affected, and only moderate levels of genetic resistance have so far been identified. In the present work we selected the most resistant accession available (Ps 624) and compared it with a susceptible (Messire) cultivar. Experiments were performed by using pot and Petri dish bioassays, showing little differences in the percentage of broomrape seed germination induced by both genotypes, but a significant hamper in the number of successfully installed tubercles and their developmental stage in the Ps 624 compared to Messire. The prote…

Proteomics0106 biological sciencesSilver StainingGenotypeParasitic plantNitrogen assimilationGene ExpressionPlant ScienceHorticultureOrobanche crenataPeptide MappingPlant Roots01 natural sciencesBiochemistryFructokinasePisum03 medical and health sciencesSativumGlutamine synthetaseElectrophoresis Gel Two-DimensionalDatabases ProteinMolecular Biology[SDV.BV.PEP] Life Sciences [q-bio]/Vegetal Biology/Phytopathology and phytopharmacyComputingMilieux_MISCELLANEOUSPlant Proteins030304 developmental biologyPathogenesis-related protein2. Zero hunger0303 health sciencesbiologyOrobanchePeasGeneral Medicinebiology.organism_classification[SDV.BV.PEP]Life Sciences [q-bio]/Vegetal Biology/Phytopathology and phytopharmacyBiochemistrySpectrometry Mass Matrix-Assisted Laser Desorption-IonizationElectrophoresis Polyacrylamide Gel010606 plant biology & botany
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Amyloid-Beta Induces Different Expression Pattern of Tissue Transglutaminase and Its Isoforms on Olfactory Ensheathing Cells: Modulatory Effect of In…

2021

Abstract Alzhèimer Disease (AD) is characterized by protein aggregates in the brain, including amyloid-beta (Aβ), a substrate for tissue transglutaminase (TG2). We assessed the effect of full native peptide of Aβ (1–42), the fragments (25–35 and 35–25) on TG2 expression and its isoforms (Long and Short) on mouse Olfactory Ensheathing Cells (OECs). The levels of cytoskeletal proteins, Vimentin and Glial Fibrillary Acid Protein, were also studied. The effect of the pre-treatment with Indicaxanthin on cell viability, total Reactive Oxygen Species, superoxide anion and apoptotic pathway activation was assessed. Since Nestin is co-expressed in pluripotent stem cells with cyclin D1, their levels …

Pyridinestissue transglutaminase; olfactory ensheathing cells; amyloid-beta; oxidative stress; Indicaxanthin; self-renewalApoptosisAmyloid‐betaIndicaxanthinVimentinself-renewallcsh:ChemistryNestinMicechemistry.chemical_compoundProtein IsoformsCyclin D1lcsh:QH301-705.5SpectroscopybiologySuperoxideOpuntiaCell DifferentiationGeneral MedicineOlfactory Bulbamyloid-betaBetaxanthinsComputer Science ApplicationsCell biologyIndicaxanthinAmyloid betaTissue transglutaminase; Olfactory Ensheathing Cells; Amyloid-Beta; oxidative stress; In-dicaxanthin; self-renewalArticleGene Expression Regulation EnzymologicCatalysisInorganic ChemistryCyclin D1Alzheimer DiseaseGTP-Binding ProteinsGlial Fibrillary Acidic ProteinAnimalsHumansVimentinProtein Glutamine gamma Glutamyltransferase 2Viability assayPhysical and Theoretical ChemistryMolecular BiologyAmyloid beta-PeptidesTransglutaminasesOrganic ChemistryTissue transglutaminaseNestinSelf‐renewalNerve Regenerationlcsh:Biology (General)lcsh:QD1-999chemistryOxidative stressOlfactory ensheathing cellsbiology.proteinOlfactory ensheathing gliaReactive Oxygen SpeciesInternational Journal of Molecular Sciences
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A Comparative Study on Nickel Binding to Hpn-like Polypeptides from Two Helicobacter pylori Strains

2021

Combined potentiometric titration and isothermal titration calorimetry (ITC) methods were used to study the interactions of nickel(II) ions with the N-terminal fragments and histidine-rich fragments of Hpn-like protein from two Helicobacter pylori strains (11637 and 26695). The ITC measurements were performed at various temperatures and buffers in order to extract proton-independent reaction enthalpies of nickel binding to each of the studied protein fragments. We bring up the problem of ITC results of nickel binding to the Hpn-like protein being not always compatible with those from potentiometry and MS regarding the stoichiometry and affinity. The roles of the ATCUN motif and multiple His…

QH301-705.5Glutaminenickel bindingCalorimetry<i>H. pylori</i>glutamine-richArticleCatalysisInorganic ChemistryBacterial ProteinsProtein DomainsNickelHistidinenickel binding; <i>H. pylori</i>; Hpn-like; histidine-rich; glutamine-rich; ATCUN motifAmino Acid SequenceBiology (General)Physical and Theoretical ChemistryQD1-999Molecular BiologySpectroscopyHelicobacter pyloriHpn-likeOrganic ChemistryGeneral Medicinehistidine-richATCUN motifComputer Science ApplicationsChemistryPotentiometryPeptidesH. pyloriInternational Journal of Molecular Sciences
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Factors that influence the quality of metabolomics data in in vitro cell toxicity studies: a systematic survey

2021

Abstract REACH (Registration, Evaluation, Authorization and Restriction of Chemicals) is a global strategy and regulation policy of the EU that aims to improve the protection of human health and the environment through the better and earlier identification of the intrinsic properties of chemical substances. It entered into force on 1st June 2007 (EC 1907/2006). REACH and EU policies plead for the use of robust high-throughput "omic" techniques for the in vitro investigation of the toxicity of chemicals that can provide an estimation of their hazards as well as information regarding the underlying mechanisms of toxicity. In agreement with the 3R’s principles, cultured cells are nowadays wide…

Quality ControlHEPATOTOXICITYSciencemedia_common.quotation_subjectDiseasesComputational biologyMETABOLISMBiologyHEPATOCYTESCitric AcidArticleXenobioticsProductes químicschemistry.chemical_compoundMetabolomicsMedical researchCell Line TumorMetabolomeHumansMetabolomicsSPECTROMETRY DATAQuality (business)HEPARG CELLSAcetaminophenmedia_commonBATCH EFFECT CORRECTIONMultidisciplinaryFATTY-ACIDDrug discoveryValproic AcidQRReproducibility of ResultsHep G2 CellsIn vitroBioactive compoundGLUTAMINEMetabolic pathwayLiverchemistryToxicityMetabolomeMedicineCURRENT STATEChemical and Drug Induced Liver InjuryXenobioticMetabolic Networks and PathwaysBiomarkersVALPROATEScientific Reports
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Flanking regions determine the structure of the poly-glutamine homo- repeat in huntingtin through mechanisms common among glutamine-rich human protei…

2020

International audience; The causative agent of Huntington's disease, the poly-Q homo-repeat in the N-terminal region of huntingtin (httex1), is flanked by a 17-residue-long fragment (N17) and a proline-rich region (PRR), which promote and inhibit the aggregation propensity of the protein, respectively, by poorly understood mechanisms. Based on experimental data obtained from site-specifically labeled NMR samples, we derived an ensemble model of httex1 that identified both flanking regions as opposing poly-Q secondary structure promoters. While N17 triggers helicity through a promiscuous hydrogen bond network involving the side chains of the first glutamines in the poly-Q tract, the PRR prom…

Repetitive Sequences Amino AcidHuntingtinAmino Acid Motifs[SDV.BBM.BP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biophysics03 medical and health sciencesHuntington's diseaseStructural BiologyHuman proteome projectmedicineHumans[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]Molecular BiologyHuman proteinsProtein secondary structure[SDV.BBM.BC] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]030304 developmental biology[INFO.INFO-BI] Computer Science [cs]/Bioinformatics [q-bio.QM]Huntingtin Protein0303 health sciencesChemistry030302 biochemistry & molecular biologyPromotermedicine.diseaseCell biologyIntrinsically Disordered ProteinsGlutamine[SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry Molecular Biology/BiophysicsPolyglutamic Acid[INFO.INFO-BI]Computer Science [cs]/Bioinformatics [q-bio.QM]Low Complexity Region
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Inhibition of expression of natural UAG suppressor glutamine tRNA in HIV-infected human H9 cells in vitro by Avarol.

1988

HTLV-IIIB-infected H9 cells are shown to contain a high level of the natural UAG suppressor glutamine tRNA(UmUG Gln); this tRNA has been demonstrated to be required for the synthesis of Moloney murine leukemia virus (Mo-MuLV)-encoded protease. After cultivation of HTLV-IIIB-infected H9 cells with Avarol at a concentration (1 microgram/ml), previously found to protect the cells against the cytopathic effects of HTLV-III, an almost complete inhibition of the synthesis of the tRNA(UmUG Gln) was observed. Moreover, we obtained some evidence that the processing of the HTLV-III precursor protein p53 to p24 is inhibited by Avarol in infected cells, suggesting that the compound interferes with the …

ReticulocytesvirusesGlutamineImmunologyBiologyAntiviral AgentsViruslaw.inventionCell LineSuppression GeneticlawVirologyRNA Transfer GlnGene expressionAnimalsHumansCodonvirus diseasesHIVNucleic Acid HybridizationBiological activitybiochemical phenomena metabolism and nutritionRNA Transfer Amino Acid-SpecificCell Transformation ViralMolecular biologyIn vitroGlutamineTobacco Mosaic VirusInfectious DiseasesCell cultureProtein BiosynthesisTransfer RNASuppressorRNA ViralRabbitsSesquiterpenesAIDS research and human retroviruses
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