Search results for "polyQ"

showing 7 items of 7 documents

The importance of definitions in the study of polyQ regions: A tale of thresholds, impurities and sequence context

2020

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lcsh:BiotechnologyGlutamineBiophysicsContext (language use)Computational biologyBiologyBiochemistrypolyQ03 medical and health sciences0302 clinical medicineStructural Biologylcsh:TP248.13-248.65GeneticsHuman proteome projectComputingMethodologies_COMPUTERGRAPHICS030304 developmental biologySequence (medicine)chemistry.chemical_classificationSequence context0303 health sciencesHomorepeatA proteinComputer Science ApplicationsAmino acidchemistry030220 oncology & carcinogenesisCodon usage biasProteomeCodon usageLength distributionResearch ArticleBiotechnologyComputational and Structural Biotechnology Journal
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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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Nuclear inclusions of pathogenic ataxin-1 induce oxidative stress and perturb the protein synthesis machinery

2020

Spinocerebellar ataxia type-1 (SCA1) is caused by an abnormally expanded polyglutamine (polyQ) tract in ataxin-1. These expansions are responsible for protein misfolding and self-assembly into intranuclear inclusion bodies (IIBs) that are somehow linked to neuronal death. However, owing to lack of a suitable cellular model, the downstream consequences of IIB formation are yet to be resolved. Here, we describe a nuclear protein aggregation model of pathogenic human ataxin-1 and characterize IIB effects. Using an inducible Sleeping Beauty transposon system, we overexpressed the ATXN1(Q82) gene in human mesenchymal stem cells that are resistant to the early cytotoxic effects caused by the expr…

0301 basic medicineSCA1 Spinocerebellar ataxia type-1Intranuclear Inclusion BodiesClinical BiochemistryMSC mesenchymal stem cellProtein aggregationBiochemistry0302 clinical medicineMutant proteinProtein biosynthesisDE differentially expressed genesNuclear proteinlcsh:QH301-705.5FTIR Fourier-transform infrared spectroscopyAtaxin-1lcsh:R5-920biologyChemistryNuclear ProteinspolyQ polyglutamineRibosomeCell biologySB Sleeping BeautyRibosome ; Polyglutamine ; Ataxin-1 ; Oxidative stress ; Transposon ; Sleeping beauty transposon ; Protein networkSpinocerebellar ataxiaProtein foldingCellular modelFunction and Dysfunction of the Nervous Systemlcsh:Medicine (General)Research PaperiPSC induced pluripotent stem cellAtaxin 1Nerve Tissue ProteinsPPI protein-protein interaction03 medical and health sciencesROS reactive oxygen speciesProtein networkSleeping beauty transposonGSEA Gene Set Enrichment AnalysismedicineHumansNPC neural progenitor cellOrganic Chemistrymedicine.diseaseAFM atomic force microscopyOxidative Stress030104 developmental biologylcsh:Biology (General)IIBs intranuclear inclusion bodiesMS mass spectrometryCardiovascular and Metabolic Diseasesbiology.proteinPolyglutamine030217 neurology & neurosurgery
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A new synthetic entry into the tricyclo[3.3.0.03,7] octane skeleton

1987

Abstract A short synthesis of dimethyl tricyclo[3.3.0.03,7] octane-1,5-dicarboxylate, 13 , and its 3,7-dimethyl-derivative, 14 , by iodine oxidation of the bis-enolate derived from the corresponding dimethyl cis -bicyclo[3.3.0] octane-3,7-dicarboxylate, 11 or 12 , is described.

Diketonechemistry.chemical_compoundBicyclic moleculeChemistryOrganic ChemistryDrug DiscoveryOrganic chemistrySkeleton (category theory)BiochemistryPolyquinaneOctane
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Synergistic activation of AMPK prevents from polyglutamine-inducedtoxicity inCaenorhabditis elegans

2020

11 páginas, 4 figuras. Supplementary material related to this article can be found, in the online version, at doi: https://doi.org/10.1016/j.phrs.2020.105105.

0301 basic medicineAMPKProtein subunitMutantEnzyme ActivatorsAMP-Activated Protein KinasesProtein Serine-Threonine KinasesProtein Aggregation PathologicalpolyQ toxicityArticleAnimals Genetically ModifiedProtein Aggregates03 medical and health sciences0302 clinical medicineRNA interferenceAutophagymedicineAnimalsAMPK Caenorhabditis elegans Metformin Salycilate Synergy polyQ toxicityCaenorhabditis elegans ProteinsCaenorhabditis elegansLoss functionCaenorhabditis elegansNeuronsPharmacologybiologyChemistrySalycilateAutophagyAMPKDrug Synergismbiology.organism_classificationSalicylatesMetforminCell biologyMetforminEnzyme ActivationSynergy030104 developmental biology030220 oncology & carcinogenesisMutationProteostasisPeptidesmedicine.drug
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Dynamics of a Protein Interaction Network Associated to the Aggregation of polyQ-Expanded Ataxin-1

2020

Background: Several experimental models of polyglutamine (polyQ) diseases have been previously developed that are useful for studying disease progression in the primarily affected central nervous system. However, there is a missing link between cellular and animal models that would indicate the molecular defects occurring in neurons and are responsible for the disease phenotype in vivo. Methods: Here, we used a computational approach to identify dysregulated pathways shared by an in vitro and an in vivo model of ATXN1(Q82) protein aggregation, the mutant protein that causes the neurodegenerative polyQ disease spinocerebellar ataxia type-1 (SCA1). Results: A set of common dysregulated pathwa…

0301 basic medicinelcsh:QH426-470Ataxin 1Mice TransgenicNerve Tissue ProteinsProtein aggregationBlood–brain barrierblood-brain-barrierArticledrugspolyQ03 medical and health sciences0302 clinical medicineataxin-1Interaction networkIn vivoMutant proteinCerebellumGeneticsmedicineAnimalsGene Regulatory NetworksProtein Interaction MapsGenetics (clinical)NeuronsbiologypathwayGene Expression Profilingmedicine.diseaselcsh:Genetics030104 developmental biologymedicine.anatomical_structureGene Expression Regulationnetworkbiology.proteinSpinocerebellar ataxiaPeptidesNeuroscience030217 neurology & neurosurgeryFunction (biology)Genes
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Dažāda veida mākslīgo asaru ietekme uz sausās acs radītajām pazīmēm un simptomiem

2021

Maģistra darbs ir uzrakstīts angļu valodā uz 5 5 lappaspusēm. Tas satur 13 attēlus, 19 tabulas un 30 atsauces uz literatūras avotiem. Šī pētījuma mērķis ir novērtēt dažādu mākslīgo asaru ietekmi uz sausu acu simptomiem un pazīmēm. Sauso acu slimība (DED) ir hroniska, daudzfaktoru acu virsmas slimība, kas noved pie diskomforta, redzes traucējumiem un asaru plēvītes nestabilitātes, ar iespējamu acu virsmas bojājumu. Vecums un dzimums tiek mi nēts par svarīgākajiem faktoriem, kas izraisa sauso acu slimību, turpretī citi riski bieži netiek ņemti vērā. Lai nozīmētu DED ārstēšanu, jāveic dažādi diagnostikas testi. Mūsdienās ir pieejamas atšķirīgas ārstēšanas metodes, bet mākslīgās asaras ir visbi…

PolyquadDry eyeBAK (benzalkonium chloride)Fizikaartificial teras
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