Biologically active molecules that reduce polyglutamine aggregation and toxicity.
about
Phosphorylation of profilin by ROCK1 regulates polyglutamine aggregationHeparan sulfate proteoglycans mediate internalization and propagation of specific proteopathic seedsQuantitative relationships between huntingtin levels, polyglutamine length, inclusion body formation, and neuronal death provide novel insight into huntington's disease molecular pathogenesis.High throughput screening for neurodegeneration and complex disease phenotypes.Monkey hybrid stem cells develop cellular features of Huntington's disease.Probing the metabolic aberrations underlying mutant huntingtin toxicity in yeast and assessing their degree of preservation in humans and mice.Composite primary neuronal high-content screening assay for Huntington's disease incorporating non-cell-autonomous interactions.Oligonucleotide-based strategies to combat polyglutamine diseases.Drosophila melanogaster in the study of human neurodegeneration.An aggregation sensing reporter identifies leflunomide and teriflunomide as polyglutamine aggregate inhibitors.A cell-based fascin bioassay identifies compounds with potential anti-metastasis or cognition-enhancing functions.Functional screening of Alzheimer pathology genome-wide association signals in Drosophila.Human disease models in Drosophila melanogaster and the role of the fly in therapeutic drug discovery.RNAi screening in Drosophila cells identifies new modifiers of mutant huntingtin aggregation.Neuronal store-operated calcium entry pathway as a novel therapeutic target for Huntington's disease treatment.Quantitative characterization of intrinsic disorder in polyglutamine: insights from analysis based on polymer theories.Trans-cellular propagation of Tau aggregation by fibrillar speciesAn N-terminal nuclear export signal regulates trafficking and aggregation of Huntingtin (Htt) protein exon 1.Rho Kinase Pathway Alterations in the Brain and Leukocytes in Huntington's Disease.Novel therapeutic strategies for the treatment of protein-misfolding diseases.Myotonic dystrophy: therapeutic strategies for the future.Polyglutamine diseases: where does toxicity come from? what is toxicity? where are we going?Perspectives on gene therapy in myotonic dystrophy type 1.Using Drosophila models of neurodegenerative diseases for drug discovery.Fruit flies as a powerful model to drive or validate pain genomics efforts.Discovery of Therapeutic Approaches for Polyglutamine Diseases: A Summary of Recent Efforts.ROCK and PRK-2 mediate the inhibitory effect of Y-27632 on polyglutamine aggregation.The Aggregation of Huntingtin and α-Synuclein.Linking model systems to cancer therapeutics: the case of MastermindWhy mammalian wound-healing researchers may wish to turn to Drosophila as a model.
P2860
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P2860
Biologically active molecules that reduce polyglutamine aggregation and toxicity.
description
2006 nî lūn-bûn
@nan
2006 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
2006 թվականի մայիսին հրատարակված գիտական հոդված
@hy
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
name
Biologically active molecules that reduce polyglutamine aggregation and toxicity.
@ast
Biologically active molecules that reduce polyglutamine aggregation and toxicity.
@en
type
label
Biologically active molecules that reduce polyglutamine aggregation and toxicity.
@ast
Biologically active molecules that reduce polyglutamine aggregation and toxicity.
@en
prefLabel
Biologically active molecules that reduce polyglutamine aggregation and toxicity.
@ast
Biologically active molecules that reduce polyglutamine aggregation and toxicity.
@en
P2093
P356
P1476
Biologically active molecules that reduce polyglutamine aggregation and toxicity.
@en
P2093
Aye Aye K Ma
Brent R Stockwell
J Lawrence Marsh
Judit Pallos
Leslie Michels Thompson
Marc I Diamond
Urvee A Desai
P304
P356
10.1093/HMG/DDL135
P577
2006-05-23T00:00:00Z