A potent small molecule inhibits polyglutamine aggregation in Huntington's disease neurons and suppresses neurodegeneration in vivo. - Test2 - elhamkhani - TriplyDB

A potent small molecule inhibits polyglutamine aggregation in Huntington's disease neurons and suppresses neurodegeneration in vivo.

A potent small molecule inhibits polyglutamine aggregation in Huntington's disease neurons and suppresses neurodegeneration in vivo.

http://www.wikidata.org/entity/Q33756277

about

Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson's, Huntington's, Alzheimer's, prions, bactericides, chemical toxicology and others as examples Structural and Genetic Studies Demonstrate Neurologic Dysfunction in Triosephosphate Isomerase Deficiency Is Associated with Impaired Synaptic Vesicle Dynamics High-content chemical and RNAi screens for suppressors of neurotoxicity in a Huntington's disease model Disease-Associated Polyglutamine Stretches in Monomeric Huntingtin Adopt a Compact Structure A genomic screen in yeast implicates kynurenine 3-monooxygenase as a therapeutic target for Huntington disease.Aggresome formation and neurodegenerative diseases: therapeutic implications Protein kinase A regulates molecular chaperone transcription and protein aggregation Extended polyglutamine tracts cause aggregation and structural perturbation of an adjacent beta barrel protein.Therapeutic prospects for spinocerebellar ataxia type 2 and 3.Monoclonal antibodies recognize distinct conformational epitopes formed by polyglutamine in a mutant huntingtin fragment.Effects of 2,4-diaminoquinazoline derivatives on SMN expression and phenotype in a mouse model for spinal muscular atrophy Detection of Mutant Huntingtin Aggregation Conformers and Modulation of SDS-Soluble Fibrillar Oligomers by Small Molecules.Quantitative relationships between huntingtin levels, polyglutamine length, inclusion body formation, and neuronal death provide novel insight into huntington's disease molecular pathogenesis.An engineered viral protease exhibiting substrate specificity for a polyglutamine stretch prevents polyglutamine-induced neuronal cell death.Two approaches to drug discovery in SOD1-mediated ALS.Potency of a tau fibrillization inhibitor is influenced by its aggregation state High throughput screening for neurodegeneration and complex disease phenotypes.Potent inhibitors of Huntingtin protein aggregation in a cell-based assay 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.Modeling Huntington disease in yeast: perspectives and future directions.Development and characterization of 3-(benzylsulfonamido)benzamides as potent and selective SIRT2 inhibitors Therapeutic Strategies in Huntington's Disease Linking amyloid protein aggregation and yeast survival.ASIP Outstanding Investigator Award Lecture. New approaches to the pathology and genetics of neurodegeneration Absence of behavioral abnormalities and neurodegeneration in vivo despite widespread neuronal huntingtin inclusions.An independent study of the preclinical efficacy of C2-8 in the R6/2 transgenic mouse model of Huntington's disease An aggregation sensing reporter identifies leflunomide and teriflunomide as polyglutamine aggregate inhibitors.Neurodegenerative models in Drosophila: polyglutamine disorders, Parkinson disease, and amyotrophic lateral sclerosis.Systemic delivery of P42 peptide: a new weapon to fight Huntington's disease.Huntington's disease: revisiting the aggregation hypothesis in polyglutamine neurodegenerative diseases.Human disease models in Drosophila melanogaster and the role of the fly in therapeutic drug discovery.Role of inositol 1,4,5-trisphosphate receptors in pathogenesis of Huntington's disease and spinocerebellar ataxias Flanking sequences profoundly alter polyglutamine toxicity in yeast.RNAi screening in Drosophila cells identifies new modifiers of mutant huntingtin aggregation.Expanded polyglutamine-binding peptoid as a novel therapeutic agent for treatment of Huntington's disease.Conformational variability of the intracellular domain of Drosophila Notch and its interaction with Suppressor of Hairless 3-(N-arylsulfamoyl)benzamides, inhibitors of human sirtuin type 2 (SIRT2)Quantitative characterization of intrinsic disorder in polyglutamine: insights from analysis based on polymer theories.Endoplasmic Reticulum Stress and Unfolded Protein Response Pathways: Potential for Treating Age-related Retinal Degeneration

P2860

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P2860

A potent small molecule inhibits polyglutamine aggregation in Huntington's disease neurons and suppresses neurodegeneration in vivo.

http://www.wikidata.org/entity/Q33756277

description

2005 nî lūn-bûn

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2005 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2005 թվականի հունվարին հրատարակված գիտական հոդված

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2005年の論文

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2005年論文

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2005年論文

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2005年論文

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2005年論文

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2005年論文

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2005年论文

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name

A potent small molecule inhibi ...... ses neurodegeneration in vivo.

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A potent small molecule inhibi ...... ses neurodegeneration in vivo.

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type

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A potent small molecule inhibi ...... ses neurodegeneration in vivo.

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A potent small molecule inhibi ...... ses neurodegeneration in vivo.

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A potent small molecule inhibi ...... ses neurodegeneration in vivo.

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A potent small molecule inhibi ...... ses neurodegeneration in vivo.

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PNAS.0408936102

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Proceedings of the National Academy of Sciences of the United States of America

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A potent small molecule inhibi ...... ses neurodegeneration in vivo.

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Aleksey G Kazantsev

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Anne B Young

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David E Housman

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Deborah E Russel

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Donna L Smith

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J Lawrence Marsh

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Leslie Michels Thompson

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Margo Roark

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Michele M Maxwell

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Sabine Engemann

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P2860

A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes.

Huntingtin aggregation and toxicity in Huntington's disease

Formation of neuronal intranuclear inclusions underlies the neurological dysfunction in mice transgenic for the HD mutation

More powerful procedures for multiple significance testing

Protein aggregation and neurodegenerative disease

Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death

Reversal of neuropathology and motor dysfunction in a conditional model of Huntington's disease

Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice

Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila

Aggregation of huntingtin in neuronal intranuclear inclusions and dystrophic neurites in brain

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892-897

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10.1073/PNAS.0408936102

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3

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102

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Anatoli B Meriin

Michael Y Sherman

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8088356

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15642944

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Huntington disease

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545525

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