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The effects of the polyglutamine repeat protein ataxin-1 on the UbL-UBA protein A1UpRORalpha-mediated Purkinje cell development determines disease severity in adult SCA1 micePumilio1 haploinsufficiency leads to SCA1-like neurodegeneration by increasing wild-type Ataxin1 levelsExpression analysis of the ataxin-1 protein in tissues from normal and spinocerebellar ataxia type 1 individualsRNA association and nucleocytoplasmic shuttling by ataxin-1miR-19, miR-101 and miR-130 co-regulate ATXN1 levels to potentially modulate SCA1 pathogenesisPathogenic mechanisms of a polyglutamine-mediated neurodegenerative disease, spinocerebellar ataxia type 1Polyglutamine neurodegeneration: expanded glutamines enhance native functionsMapmodulin/leucine-rich acidic nuclear protein binds the light chain of microtubule-associated protein 1B and modulates neuritogenesisThe AXH domain of Ataxin-1 mediates neurodegeneration through its interaction with Gfi-1/Senseless proteinsOpposing effects of polyglutamine expansion on native protein complexes contribute to SCA1Altered trafficking of membrane proteins in purkinje cells of SCA1 transgenic miceLithium therapy improves neurological function and hippocampal dendritic arborization in a spinocerebellar ataxia type 1 mouse model.Targeted deletion of a single Sca8 ataxia locus allele in mice causes abnormal gait, progressive loss of motor coordination, and Purkinje cell dendritic deficitsThe cerebellar leucine-rich acidic nuclear protein interacts with ataxin-1Trinucleotide Repeat DisordersSCA1-like disease in mice expressing wild-type ataxin-1 with a serine to aspartic acid replacement at residue 776.A cell-based screen for modulators of ataxin-1 phosphorylation.Identification of a novel phosphorylation site in ataxin-1.Interaction of Akt-phosphorylated ataxin-1 with 14-3-3 mediates neurodegeneration in spinocerebellar ataxia type 1.Polyglutamine neurodegenerative diseases and regulation of transcription: assembling the puzzle.RAS-MAPK-MSK1 pathway modulates ataxin 1 protein levels and toxicity in SCA1Polyglutamine diseases: protein cleavage and aggregation.Noninvasive detection of presymptomatic and progressive neurodegeneration in a mouse model of spinocerebellar ataxia type 1.RNA targets of the fragile X protein.Tolerance is established in polyclonal CD4(+) T cells by distinct mechanisms, according to self-peptide expression patterns.Regional rescue of spinocerebellar ataxia type 1 phenotypes by 14-3-3epsilon haploinsufficiency in mice underscores complex pathogenicity in neurodegenerationThe GSK3 beta signaling cascade and neurodegenerative disease.Partial loss of Tip60 slows mid-stage neurodegeneration in a spinocerebellar ataxia type 1 (SCA1) mouse model.Assessing recovery from neurodegeneration in spinocerebellar ataxia 1: Comparison of in vivo magnetic resonance spectroscopy with motor testing, gene expression and histology.Early activation of microglia and astrocytes in mouse models of spinocerebellar ataxia type 1.Abnormalities in the climbing fiber-Purkinje cell circuitry contribute to neuronal dysfunction in ATXN1[82Q] mice14-3-3 Binding to ataxin-1(ATXN1) regulates its dephosphorylation at Ser-776 and transport to the nucleus.In vivo monitoring of recovery from neurodegeneration in conditional transgenic SCA1 miceExercise and genetic rescue of SCA1 via the transcriptional repressor Capicua.A native interactor scaffolds and stabilizes toxic ATAXIN-1 oligomers in SCA1.Visualizing and mapping the cerebellum with serial optical coherence scanner.Ataxin-1 oligomers induce local spread of pathology and decreasing them by passive immunization slows Spinocerebellar ataxia type 1 phenotypes.Purkinje cell ataxin-1 modulates climbing fiber synaptic input in developing and adult mouse cerebellum.Polyglutamine disease toxicity is regulated by Nemo-like kinase in spinocerebellar ataxia type 1.
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