Expression of expanded CAG transcripts triggers nucleolar stress in Huntington's disease.
about
RNA-Binding Proteins in the Regulation of miRNA Activity: A Focus on Neuronal FunctionsRAN translation and frameshifting as translational challenges at simple repeats of human neurodegenerative disordersMechanisms of RNA-induced toxicity in CAG repeat disordersp53 and mitochondrial dysfunction: novel insight of neurodegenerative diseasesNon-coding RNA in neural function, disease, and agingInsights into the regulation of neuronal viability by nucleophosmin/B23RNA-mediated pathogenic mechanisms in polyglutamine diseases and amyotrophic lateral sclerosisRole of the nucleolus in neurodegenerative diseases with particular reference to the retina: a review.Nucleolar stress with and without p53.Structural Insights Reveal the Dynamics of the Repeating r(CAG) Transcript Found in Huntington's Disease (HD) and Spinocerebellar Ataxias (SCAs)Requirement of Neuronal Ribosome Synthesis for Growth and Maintenance of the Dendritic TreeIdentifying proteins that bind to specific RNAs - focus on simple repeat expansion diseases.Invited review: decoding the pathophysiological mechanisms that underlie RNA dysregulation in neurodegenerative disorders: a review of the current state of the art.Targeting CAG repeat RNAs reduces Huntington's disease phenotype independently of huntingtin levels.Post-Translational Modifications (PTMs), Identified on Endogenous Huntingtin, Cluster within Proteolytic Domains between HEAT Repeats.Cytomegalovirus Late Protein pUL31 Alters Pre-rRNA Expression and Nuclear Organization during Infection.RNA toxicity induced by expanded CAG repeats in Huntington's disease.Regulation of mRNA Translation by MID1: A Common Mechanism of Expanded CAG Repeat RNAs.Protein sequestration as a normal function of long noncoding RNAs and a pathogenic mechanism of RNAs containing nucleotide repeat expansions.Assessing a peptidylic inhibitor-based therapeutic approach that simultaneously suppresses polyglutamine RNA- and protein-mediated toxicities in patient cells and Drosophila.Regulation of Neuronal Survival by Nucleophosmin 1 (NPM1) Is Dependent on Its Expression Level, Subcellular Localization, and Oligomerization Status.Quantitative Proteomic Analysis Reveals Similarities between Huntington's Disease (HD) and Huntington's Disease-Like 2 (HDL2) Human Brains.A brain-targeting lipidated peptide for neutralizing RNA-mediated toxicity in Polyglutamine Diseases.A recurrent de novo missense mutation in UBTF causes developmental neuroregression.A peptidylic inhibitor for neutralizing expanded CAG RNA-induced nucleolar stress in polyglutamine diseases.Ultrastructural Localization and Molecular Associations of HCV Capsid Protein in Jurkat T Cells.Proapoptotic Requirement of Ribosomal Protein L11 in Ribosomal Stress-Challenged Cortical Neurons.
P2860
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P2860
Expression of expanded CAG transcripts triggers nucleolar stress in Huntington's disease.
description
2013 nî lūn-bûn
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2013年の論文
@ja
2013年学术文章
@wuu
2013年学术文章
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2013年学术文章
@zh-cn
2013年学术文章
@zh-hans
2013年学术文章
@zh-my
2013年学术文章
@zh-sg
2013年學術文章
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2013年學術文章
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name
Expression of expanded CAG transcripts triggers nucleolar stress in Huntington's disease.
@en
Expression of expanded CAG transcripts triggers nucleolar stress in Huntington's disease.
@nl
type
label
Expression of expanded CAG transcripts triggers nucleolar stress in Huntington's disease.
@en
Expression of expanded CAG transcripts triggers nucleolar stress in Huntington's disease.
@nl
prefLabel
Expression of expanded CAG transcripts triggers nucleolar stress in Huntington's disease.
@en
Expression of expanded CAG transcripts triggers nucleolar stress in Huntington's disease.
@nl
P2860
P1433
P1476
Expression of expanded CAG transcripts triggers nucleolar stress in Huntington's disease
@en
P2093
P2860
P2888
P304
P356
10.1007/S12311-012-0447-6
P50
P577
2013-06-01T00:00:00Z
P6179
1043469772