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Pathogenic Mechanisms of a Polyglutamine-mediated Neurodegenerative Disease, Spinocerebellar Ataxia Type 1

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What this work says

Outgoing claims: the papers this work cites, builds on, or argues with.

inferredcites →https://doi.org/10.1016/0092-8674(95)90273-2openalex-snapshot

SCA1 transgenic mice: A model for neurodegeneration caused by an expanded CAG trinucleotide repeat

inferredcites →https://doi.org/10.1016/j.cell.2005.06.012openalex-snapshot

The AXH Domain of Ataxin-1 Mediates Neurodegeneration through Its Interaction with Gfi-1/Senseless Proteins

inferredcites →https://doi.org/10.1016/j.cell.2006.04.026openalex-snapshot

Cleavage at the Caspase-6 Site Is Required for Neuronal Dysfunction and Degeneration Due to Mutant Huntingtin

inferredcites →https://doi.org/10.1016/j.cell.2006.09.036openalex-snapshot

RORα-Mediated Purkinje Cell Development Determines Disease Severity in Adult SCA1 Mice

inferredcites →https://doi.org/10.1016/j.cell.2006.11.038openalex-snapshot

ATAXIN-1 Interacts with the Repressor Capicua in Its Native Complex to Cause SCA1 Neuropathology

inferredcites →https://doi.org/10.1016/j.neuron.2006.05.022openalex-snapshot

Increased App Expression in a Mouse Model of Down's Syndrome Disrupts NGF Transport and Causes Cholinergic Neuron Degeneration

inferredcites →https://doi.org/10.1016/s0014-5793(03)00818-4openalex-snapshot

The AXH module: an independently folded domain common to ataxin‐1 and HBP1

inferredcites →https://doi.org/10.1016/s0092-8674(00)80623-6openalex-snapshot

Reversal of Neuropathology and Motor Dysfunction in a Conditional Model of Huntington's Disease

inferredcites →https://doi.org/10.1016/s0092-8674(00)81781-xopenalex-snapshot

Ataxin-1 Nuclear Localization and Aggregation

inferredcites →https://doi.org/10.1016/s0092-8674(03)00349-0openalex-snapshot

Interaction of Akt-Phosphorylated Ataxin-1 with 14-3-3 Mediates Neurodegeneration in Spinocerebellar Ataxia Type 1

inferredcites →https://doi.org/10.1016/s0165-3806(01)00095-5openalex-snapshot

Progressive atrophy of cerebellar Purkinje cell dendrites during aging of the heterozygous staggerer mouse (Rora+/sg)

inferredcites →https://doi.org/10.1016/s0166-2236(98)01318-6openalex-snapshot

The anatomy of the cerebellum

inferredcites →https://doi.org/10.1016/s0896-6273(00)81035-1openalex-snapshot

Mutation of the E6-AP Ubiquitin Ligase Reduces Nuclear Inclusion Frequency While Accelerating Polyglutamine-Induced Pathology in SCA1 Mice

inferredcites →https://doi.org/10.1016/s0896-6273(02)00733-xopenalex-snapshot

A Long CAG Repeat in the Mouse Sca1 Locus Replicates SCA1 Features and Reveals the Impact of Protein Solubility on Selective Neurodegeneration

inferredcites →https://doi.org/10.1016/s0896-6273(02)00834-6openalex-snapshot

Testosterone Reduction Prevents Phenotypic Expression in a Transgenic Mouse Model of Spinal and Bulbar Muscular Atrophy

inferredcites →https://doi.org/10.1016/s0896-6273(02)01190-xopenalex-snapshot

SCA7 Knockin Mice Model Human SCA7 and Reveal Gradual Accumulation of Mutant Ataxin-7 in Neurons and Abnormalities in Short-Term Plasticity

inferredcites →https://doi.org/10.1016/s0896-6273(03)00258-7openalex-snapshot

Serine 776 of Ataxin-1 Is Critical for Polyglutamine-Induced Disease in SCA1 Transgenic Mice

inferredcites →https://doi.org/10.1016/s0896-6273(03)00769-4openalex-snapshot

RORα Coordinates Reciprocal Signaling in Cerebellar Development through Sonic hedgehog and Calcium-Dependent Pathways

inferredcites →https://doi.org/10.1016/s0925-4773(97)00187-1openalex-snapshot

Orphan nuclear receptor RORα-deficient mice display the cerebellar defects of staggerer

inferredcites →https://doi.org/10.1038/35040584openalex-snapshot

Identification of genes that modify ataxin-1-induced neurodegeneration

inferredcites →https://doi.org/10.1038/379736a0openalex-snapshot

Disruption of the nuclear hormone receptor RORα in staggerer mice

inferredcites →https://doi.org/10.1038/502openalex-snapshot

Chaperone suppression of aggregation and altered subcellular proteasome localization imply protein misfolding in SCA1

inferredcites →https://doi.org/10.1038/nature02998openalex-snapshot

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

inferredcites →https://doi.org/10.1038/nature06731openalex-snapshot

Opposing effects of polyglutamine expansion on native protein complexes contribute to SCA1

inferredcites →https://doi.org/10.1038/ng0595-94openalex-snapshot

Expression analysis of the ataxin–1 protein in tissues from normal and spinocerebellar ataxia type 1 individuals

inferredcites →https://doi.org/10.1038/ng0793-221openalex-snapshot

Expansion of an unstable trinucleotide CAG repeat in spinocerebellar ataxia type 1

inferredcites →https://doi.org/10.1038/ng1193-254openalex-snapshot

Evidence for a mechanism predisposing to intergenerational CAG repeat instability in spinocerebellar ataxia type I

inferredcites →https://doi.org/10.1038/ng1977openalex-snapshot

Duplication of Atxn1l suppresses SCA1 neuropathology by decreasing incorporation of polyglutamine-expanded ataxin-1 into native complexes

inferredcites →https://doi.org/10.1038/nrn1474openalex-snapshot

Pathways to motor incoordination: the inherited ataxias

inferredcites →https://doi.org/10.1038/sj.emboj.7600785openalex-snapshot

Boat, an AXH domain protein, suppresses the cytotoxicity of mutant ataxin‐1

inferredcites →https://doi.org/10.1038/sj.onc.1207415openalex-snapshot

SUMO: a regulator of gene expression and genome integrity

inferredcites →https://doi.org/10.1073/pnas.95.7.3960openalex-snapshot

staggerer phenotype in retinoid-related orphan receptor α-deficient mice

inferredcites →https://doi.org/10.1074/jbc.m309817200openalex-snapshot

The Structure of the AXH Domain of Spinocerebellar Ataxin-1

inferredcites →https://doi.org/10.1074/jbc.m501677200openalex-snapshot

SUMOylation of the Polyglutamine Repeat Protein, Ataxin-1, Is Dependent on a Functional Nuclear Localization Signal

inferredcites →https://doi.org/10.1093/hmg/10.1.25openalex-snapshot

The spinocerebellar ataxia type 1 protein, ataxin-1, has RNA-binding activity that is inversely affected by the length of its polyglutamine tract

inferredcites →https://doi.org/10.1093/hmg/ddn063openalex-snapshot

Biological effects of CCS in the absence of SOD1 enzyme activation: implications for disease in a mouse model for ALS

inferredcites →https://doi.org/10.1126/science.1090278openalex-snapshot

α-Synuclein Locus Triplication Causes Parkinson's Disease

inferredcites →https://doi.org/10.1126/science.1113694openalex-snapshot

Tau Suppression in a Neurodegenerative Mouse Model Improves Memory Function

inferredcites →https://doi.org/10.1146/annurev.neuro.29.051605.113042openalex-snapshot

Trinucleotide Repeat Disorders

inferredcites →https://doi.org/10.1523/jneurosci.0808-04.2004openalex-snapshot

Castration Restores Function and Neurofilament Alterations of Aged Symptomatic Males in a Transgenic Mouse Model of Spinal and Bulbar Muscular Atrophy

inferredcites →https://doi.org/10.1523/jneurosci.18-14-05508.1998openalex-snapshot

Mice Lacking Ataxin-1 Display Learning Deficits and Decreased Hippocampal Paired-Pulse Facilitation

inferredcites →https://doi.org/10.1523/jneurosci.2978-04.2004openalex-snapshot

Recovery from Polyglutamine-Induced Neurodegeneration in Conditional SCA1 Transgenic Mice

What points at this work

Incoming claims: where this work appears in other papers’ reference lists and arguments.

inferred← citeshttps://doi.org/10.2139/ssrn.3155885openalex-extracted

Loss of Ataxin-1 Elevates BACE1 Expression and Impairs Axonal Targeting in the Cerebrum

inferred← citeshttps://doi.org/10.1001/jamaneurol.2014.3953openalex-snapshot

Modulation of GluN3A Expression in Huntington Disease

inferred← citeshttps://doi.org/10.1002/9780470015902.a0021486.pub2openalex-snapshot

Pathogenesis of Polyglutamine Diseases

inferred← citeshttps://doi.org/10.1002/9781119432463.ch20openalex-snapshot

TRIAD (Transcriptional Repression‐Induced Atypical Death)

inferred← citeshttps://doi.org/10.1002/9781119746843.ch8openalex-snapshot

Antioxidant Nutraceuticals as Novel Neuroprotective Agents

inferred← citeshttps://doi.org/10.1002/bit.27220openalex-snapshot

“Trim”ming PolyQ proteins with engineered PML

inferred← citeshttps://doi.org/10.1002/cbic.200900666openalex-snapshot

Strategies for the Inhibition of Protein Aggregation in Human Diseases

inferred← citeshttps://doi.org/10.1002/glia.23451openalex-snapshot

Astroglia contribute to the pathogenesis of spinocerebellar ataxia Type 1 (SCA1) in a biphasic, stage‐of‐disease specific manner

inferred← citeshttps://doi.org/10.1002/jnr.23197openalex-snapshot

Organization and maintenance of molecular domains in myelinated axons

inferred← citeshttps://doi.org/10.1002/jnr.24263openalex-snapshot

Purkinje cell COX deficiency and mtDNA depletion in an animal model of spinocerebellar ataxia type 1

inferred← citeshttps://doi.org/10.1002/prot.24954openalex-snapshot

Conformational fluctuations of the AXH monomer of Ataxin-1

inferred← citeshttps://doi.org/10.1002/prot.25017openalex-snapshot

Characterization of the AXH domain of Ataxin‐1 using enhanced sampling and functional mode analysis

inferred← citeshttps://doi.org/10.1007/978-1-4419-7104-3_11openalex-snapshot

Trinucleotide-Expansion Diseases

inferred← citeshttps://doi.org/10.1007/978-1-4939-1221-6_10openalex-snapshot

RNA-Binding Protein Misregulation in Microsatellite Expansion Disorders

inferred← citeshttps://doi.org/10.1007/978-1-60327-426-5_97openalex-snapshot

Cerebellar Ataxia Type 1

inferred← citeshttps://doi.org/10.1007/978-3-030-23810-0_101openalex-snapshot

Autosomal Dominant Spinocerebellar Ataxias and Episodic Ataxias

inferred← citeshttps://doi.org/10.1007/978-3-030-75817-2_24openalex-snapshot

Molecular Dissection and Therapeutic Application of SCA1 Pathologies Revealed by Comprehensive Approaches

inferred← citeshttps://doi.org/10.1007/978-3-031-52573-5_13openalex-snapshot

Ataxia

inferred← citeshttps://doi.org/10.1007/978-3-319-17223-1_11openalex-snapshot

Genetics of Dominant Ataxias

inferred← citeshttps://doi.org/10.1007/978-3-319-33555-1_9openalex-snapshot

Magnetic Resonance Spectroscopy in Ataxias

inferred← citeshttps://doi.org/10.1007/978-81-322-2035-0openalex-snapshot

Free Radicals in Human Health and Disease

inferred← citeshttps://doi.org/10.1007/978-81-322-2035-0_11openalex-snapshot

Free Radicals and Oxidative Stress in Neurodegenerative Disorders

inferred← citeshttps://doi.org/10.1007/978-94-007-0893-8_5openalex-snapshot

Polyglutamine Diseases and Neurodegeneration: The Example of Ataxin-1

inferred← citeshttps://doi.org/10.1007/978-94-007-1333-8_101openalex-snapshot

Autosomal Dominant Spinocerebellar Ataxias and Episodic Ataxias

inferred← citeshttps://doi.org/10.1007/978-94-007-2774-8_14openalex-snapshot

Strategies for Inhibiting Protein Aggregation: Therapeutic Approaches to Protein-Aggregation Diseases

inferred← citeshttps://doi.org/10.1007/978-981-10-7506-3_15openalex-snapshot

Neurodegenerative Disease Conditions and Genomic Treatment for Better Health

inferred← citeshttps://doi.org/10.1007/s00018-012-1201-4openalex-snapshot

Membrane trafficking in neuronal maintenance and degeneration

inferred← citeshttps://doi.org/10.1007/s00018-020-03520-zopenalex-snapshot

Pathogenic mechanisms underlying spinocerebellar ataxia type 1

inferred← citeshttps://doi.org/10.1007/s00018-022-04419-7openalex-snapshot

The extra-cerebellar effects of spinocerebellar ataxia type 1 (SCA1): looking beyond the cerebellum

inferred← citeshttps://doi.org/10.1007/s00429-009-0237-1openalex-snapshot

Transgenic zebrafish models of neurodegenerative diseases

inferred← citeshttps://doi.org/10.1007/s10048-026-00929-9openalex-snapshot

Hereditary neurodegenerative disorders with spastic-ataxic manifestations: genetic and clinical insights into previously reported variants

inferred← citeshttps://doi.org/10.1007/s10059-009-0095-yopenalex-snapshot

Molecular Pathogenesis of Spinocerebellar Ataxia Type 1 Disease

inferred← citeshttps://doi.org/10.1007/s10815-024-03105-wopenalex-snapshot

PGT-M for spinocerebellar ataxia type 1: development of a STR panel and a report of two clinical cases

inferred← citeshttps://doi.org/10.1007/s11064-010-0393-yopenalex-snapshot

Role of Inositol 1,4,5-Trishosphate Receptors in Pathogenesis of Huntington’s Disease and Spinocerebellar Ataxias

inferred← citeshttps://doi.org/10.1007/s12031-015-0676-5openalex-snapshot

Targeted Molecular Therapies for SBMA

inferred← citeshttps://doi.org/10.1007/s12031-021-01944-1openalex-snapshot

Intercellular Propagation and Aggregate Seeding of Mutant Ataxin-1

inferred← citeshttps://doi.org/10.1007/s12031-025-02425-5openalex-snapshot

Spinocerebellar Ataxia Type 1 (SCA1) Cell Models Display Widespread Mitochondrial and Extra-Nuclear Alterations

inferred← citeshttps://doi.org/10.1007/s12035-012-8322-5openalex-snapshot

Neuroinflammation and Proteostasis are Modulated by Endogenously Biosynthesized Neuroprotectin D1

inferred← citeshttps://doi.org/10.1007/s12035-014-8703-zopenalex-snapshot

Beyond the Glutamine Expansion: Influence of Posttranslational Modifications of Ataxin-1 in the Pathogenesis of Spinocerebellar Ataxia Type 1

inferred← citeshttps://doi.org/10.1007/s12104-013-9509-zopenalex-snapshot

Chemical shift assignment of the ataxin-1 AXH domain in complex with a CIC ligand peptide

inferred← citeshttps://doi.org/10.1007/s12311-010-0182-9openalex-snapshot

Deranged Calcium Signaling in Purkinje Cells and Pathogenesis in Spinocerebellar Ataxia 2 (SCA2) and Other Ataxias

inferred← citeshttps://doi.org/10.1007/s12311-010-0213-6openalex-snapshot

Distinct Neurochemical Profiles of Spinocerebellar Ataxias 1, 2, 6, and Cerebellar Multiple System Atrophy

inferred← citeshttps://doi.org/10.1007/s12311-012-0399-xopenalex-snapshot

Assessing the Efficacy of Specific Cerebellomodulatory Drugs for Use as Therapy for Spinocerebellar Ataxia Type 1

inferred← citeshttps://doi.org/10.1007/s12311-016-0762-4openalex-snapshot

Atxn2 Knockout and CAG42-Knock-in Cerebellum Shows Similarly Dysregulated Expression in Calcium Homeostasis Pathway

inferred← citeshttps://doi.org/10.1007/s12311-020-01226-3openalex-snapshot

Post-symptomatic Delivery of Brain-Derived Neurotrophic Factor (BDNF) Ameliorates Spinocerebellar Ataxia Type 1 (SCA1) Pathogenesis

inferred← citeshttps://doi.org/10.1007/s13311-019-00763-yopenalex-snapshot

Moving Towards Therapy in SCA1: Insights from Molecular Mechanisms, Identification of Novel Targets, and Planning for Human Trials

inferred← citeshttps://doi.org/10.1016/b978-0-12-382032-7.10014-1openalex-snapshot

Reproductive and developmental toxicity models in relation to neurodegenerative diseases

inferred← citeshttps://doi.org/10.1016/b978-0-12-386041-5.00004-2openalex-snapshot

SUMO and Its Role in Human Diseases

inferred← citeshttps://doi.org/10.1016/b978-0-12-801238-3.11517-xopenalex-snapshot

ROS and Redox Mechanism in Neurodegenerative Diseases

inferred← citeshttps://doi.org/10.1016/b978-0-323-31071-0.00020-2openalex-snapshot

Ataxia

inferred← citeshttps://doi.org/10.1016/b978-0-444-51892-7.00025-5openalex-snapshot

Spinocerebellar ataxia type 1

inferred← citeshttps://doi.org/10.1016/b978-1-4377-2369-4.00021-4openalex-snapshot

Ataxia

inferred← citeshttps://doi.org/10.1016/j.arr.2021.101543openalex-snapshot

The protective role of exercise against age-related neurodegeneration

inferred← citeshttps://doi.org/10.1016/j.bbadis.2012.01.016openalex-snapshot

Toxic effects of expanded ataxin-1 involve mechanical instability of the nuclear membrane

inferred← citeshttps://doi.org/10.1016/j.bbapap.2015.01.012openalex-snapshot

A key lysine residue in the AXH domain of ataxin-1 is essential for its ubiquitylation

inferred← citeshttps://doi.org/10.1016/j.bbrc.2018.05.178openalex-snapshot

Dual-specificity phosphatase 18 modulates the SUMOylation and aggregation of Ataxin-1

inferred← citeshttps://doi.org/10.1016/j.bihy.2008.12.006openalex-snapshot

Glial response to polyglutamine-mediated stress

inferred← citeshttps://doi.org/10.1016/j.biochi.2012.09.013openalex-snapshot

WITHDRAWN: Protein sumoylation and human diseases

inferred← citeshttps://doi.org/10.1016/j.bpj.2013.01.048openalex-snapshot

Self-Assembly and Conformational Heterogeneity of the AXH Domain of Ataxin-1: An Unusual Example of a Chameleon Fold

inferred← citeshttps://doi.org/10.1016/j.bpj.2017.11.025openalex-snapshot

Destabilizing the AXH Tetramer by Mutations: Mechanisms and Potential Antiaggregation Strategies

inferred← citeshttps://doi.org/10.1016/j.bpj.2022.10.021openalex-snapshot

Toward the design and development of peptidomimetic inhibitors of the Ataxin-1 aggregation pathway

inferred← citeshttps://doi.org/10.1016/j.brainres.2016.02.037openalex-snapshot

Prion-like domains as epigenetic regulators, scaffolds for subcellular organization, and drivers of neurodegenerative disease

inferred← citeshttps://doi.org/10.1016/j.cell.2015.02.012openalex-snapshot

Pumilio1 Haploinsufficiency Leads to SCA1-like Neurodegeneration by Increasing Wild-Type Ataxin1 Levels

inferred← citeshttps://doi.org/10.1016/j.cell.2019.07.043openalex-snapshot

Loss of Ataxin-1 Potentiates Alzheimer’s Pathogenesis by Elevating Cerebral BACE1 Transcription

inferred← citeshttps://doi.org/10.1016/j.celrep.2014.06.037openalex-snapshot

The SAGA Histone Deubiquitinase Module Controls Yeast Replicative Lifespan via Sir2 Interaction

inferred← citeshttps://doi.org/10.1016/j.celrep.2015.08.060openalex-snapshot

Large Polyglutamine Repeats Cause Muscle Degeneration in SCA17 Mice

inferred← citeshttps://doi.org/10.1016/j.dnarep.2013.04.019openalex-snapshot

Bidirectional transcription of trinucleotide repeats: Roles for excision repair

inferred← citeshttps://doi.org/10.1016/j.expneurol.2015.08.002openalex-snapshot

Studying polyglutamine diseases in Drosophila

inferred← citeshttps://doi.org/10.1016/j.freeradbiomed.2016.07.005openalex-snapshot

Mitochondrial impairments contribute to Spinocerebellar ataxia type 1 progression and can be ameliorated by the mitochondria-targeted antioxidant MitoQ

inferred← citeshttps://doi.org/10.1016/j.ijbiomac.2019.02.148openalex-snapshot

Molecular chaperones biochemistry and role in neurodegenerative diseases

inferred← citeshttps://doi.org/10.1016/j.jmb.2021.167174openalex-snapshot

A Structural Study of the Cytoplasmic Chaperone Effect of 14-3-3 Proteins on Ataxin-1

inferred← citeshttps://doi.org/10.1016/j.jns.2023.120828openalex-snapshot

Lysine 117 on ataxin-3 modulates toxicity in Drosophila models of Spinocerebellar Ataxia Type 3

inferred← citeshttps://doi.org/10.1016/j.molcel.2011.05.036openalex-snapshot

Ube2w and Ataxin-3 Coordinately Regulate the Ubiquitin Ligase CHIP

inferred← citeshttps://doi.org/10.1016/j.nbd.2013.01.019openalex-snapshot

Altered Purkinje cell miRNA expression and SCA1 pathogenesis

inferred← citeshttps://doi.org/10.1016/j.nbd.2014.10.006openalex-snapshot

Deficiency of the miR-29a/b-1 cluster leads to ataxic features and cerebellar alterations in mice

inferred← citeshttps://doi.org/10.1016/j.nbd.2014.11.011openalex-snapshot

Assessing recovery from neurodegeneration in spinocerebellar ataxia 1: Comparison of in vivo magnetic resonance spectroscopy with motor testing, gene expression and histology

inferred← citeshttps://doi.org/10.1016/j.nbd.2019.104535openalex-snapshot

Differential toxicity of ataxin-3 isoforms in Drosophila models of Spinocerebellar Ataxia Type 3

inferred← citeshttps://doi.org/10.1016/j.nbd.2019.104564openalex-snapshot

5′UTR-mediated regulation of Ataxin-1 expression

inferred← citeshttps://doi.org/10.1016/j.nbd.2021.105516openalex-snapshot

Targeting the VCP-binding motif of ataxin-3 improves phenotypes in Drosophila models of Spinocerebellar Ataxia Type 3

inferred← citeshttps://doi.org/10.1016/j.nbd.2023.106023openalex-snapshot

BDNF is altered in a brain-region specific manner and rescues deficits in Spinocerebellar Ataxia Type 1

inferred← citeshttps://doi.org/10.1016/j.nbd.2024.106530openalex-snapshot

Cerebellar Heterogeneity and Selective vulnerability in Spinocerebellar Ataxia Type 1 (SCA1)

inferred← citeshttps://doi.org/10.1016/j.nbd.2024.106673openalex-snapshot

Expanded ATXN1 alters transcription and calcium signaling in SCA1 human motor neurons differentiated from induced pluripotent stem cells

inferred← citeshttps://doi.org/10.1016/j.neulet.2012.12.057openalex-snapshot

Impairment of spinal motor neurons in spinocerebellar ataxia type 1-knock-in mice

inferred← citeshttps://doi.org/10.1016/j.neuron.2015.11.033openalex-snapshot

Impaired mTORC1-Dependent Expression of Homer-3 Influences SCA1 Pathophysiology

inferred← citeshttps://doi.org/10.1016/j.neuron.2018.02.013openalex-snapshot

ATXN1-CIC Complex Is the Primary Driver of Cerebellar Pathology in Spinocerebellar Ataxia Type 1 through a Gain-of-Function Mechanism

inferred← citeshttps://doi.org/10.1016/j.neuron.2023.10.039openalex-snapshot

Longitudinal single-cell transcriptional dynamics throughout neurodegeneration in SCA1

inferred← citeshttps://doi.org/10.1016/j.neuropharm.2021.108629openalex-snapshot

mGluR1 signaling in cerebellar Purkinje cells: Subcellular organization and involvement in cerebellar function and disease

inferred← citeshttps://doi.org/10.1016/j.plefa.2012.08.008openalex-snapshot

The docosanoid neuroprotectin D1 induces homeostatic regulation of neuroinflammation and cell survival

inferred← citeshttps://doi.org/10.1016/j.pneurobio.2011.11.006openalex-snapshot

Toward understanding Machado–Joseph disease

inferred← citeshttps://doi.org/10.1016/j.sbi.2015.02.017openalex-snapshot

Found in translation: functions and evolution of a recently discovered alternative proteome

inferred← citeshttps://doi.org/10.1016/j.scr.2026.103987openalex-snapshot

Generation of an isogenic human induced pluripotent stem cell line for spinocerebellar ataxia type 1

inferred← citeshttps://doi.org/10.1016/j.tig.2009.11.005openalex-snapshot

Therapeutic gene silencing strategies for polyglutamine disorders

inferred← citeshttps://doi.org/10.1016/j.tig.2018.02.005openalex-snapshot

Cis- and Trans-Modifiers of Repeat Expansions: Blending Model Systems with Human Genetics

inferred← citeshttps://doi.org/10.1016/j.tins.2014.02.003openalex-snapshot

Kaleidoscopic protein–protein interactions in the life and death of ataxin-1: new strategies against protein aggregation

inferred← citeshttps://doi.org/10.1016/j.trci.2018.06.005openalex-snapshot

Minimotifs dysfunction is pervasive in neurodegenerative disorders

inferred← citeshttps://doi.org/10.1017/erm.2011.1openalex-snapshot

RNA therapy for polyglutamine neurodegenerative diseases

inferred← citeshttps://doi.org/10.1038/cr.2013.96openalex-snapshot

New hope for therapy in neurodegenerative diseases

inferred← citeshttps://doi.org/10.1038/embor.2011.49openalex-snapshot

Ataxin‐1 and Brother of ataxin‐1 are components of the Notch signalling pathway

inferred← citeshttps://doi.org/10.1038/nature12204openalex-snapshot

RAS–MAPK–MSK1 pathway modulates ataxin 1 protein levels and toxicity in SCA1

inferred← citeshttps://doi.org/10.1038/nchembio.1670openalex-snapshot

Energy landscapes of functional proteins are inherently risky

inferred← citeshttps://doi.org/10.1038/s41419-025-08154-2openalex-snapshot

Molecular hallmarks of neurodegeneration in polyglutamine spinocerebellar ataxias

inferred← citeshttps://doi.org/10.1038/s41467-017-01790-zopenalex-snapshot

Developmental YAPdeltaC determines adult pathology in a model of spinocerebellar ataxia type 1

inferred← citeshttps://doi.org/10.1038/s41467-020-14931-8openalex-snapshot

Cerebellum-enriched protein INPP5A contributes to selective neuropathology in mouse model of spinocerebellar ataxias type 17

inferred← citeshttps://doi.org/10.1038/s41531-022-00355-2openalex-snapshot

Parkinson’s disease-associated, sex-specific changes in DNA methylation at PARK7 (DJ-1), SLC17A6 (VGLUT2), PTPRN2 (IA-2β), and NR4A2 (NURR1) in cortical neurons

inferred← citeshttps://doi.org/10.1038/s41582-018-0051-6openalex-snapshot

Spinocerebellar ataxias: prospects and challenges for therapy development

inferred← citeshttps://doi.org/10.1038/s41598-020-57994-9openalex-snapshot

Nuclear bodies formed by polyQ-ataxin-1 protein are liquid RNA/protein droplets with tunable dynamics

inferred← citeshttps://doi.org/10.1038/s41598-020-80664-9openalex-snapshot

Mood alterations in mouse models of Spinocerebellar Ataxia type 1

inferred← citeshttps://doi.org/10.1038/s42003-024-06066-zopenalex-snapshot

Dynamic molecular network analysis of iPSC-Purkinje cells differentiation delineates roles of ISG15 in SCA1 at the earliest stage

inferred← citeshttps://doi.org/10.1038/sdata.2018.262openalex-snapshot

Complementary proteomics strategies capture an ataxin-1 interactome in Neuro-2a cells

inferred← citeshttps://doi.org/10.1038/srep00919openalex-snapshot

The importance of serine 776 in Ataxin-1 partner selection: A FRET Analysis

inferred← citeshttps://doi.org/10.1073/pnas.2003798117openalex-snapshot

Ataxin-1 regulates B cell function and the severity of autoimmune experimental encephalomyelitis

inferred← citeshttps://doi.org/10.1073/pnas.2208513119openalex-snapshot

Differential effects of Wnt-β-catenin signaling in Purkinje cells and Bergmann glia in spinocerebellar ataxia type 1

inferred← citeshttps://doi.org/10.1074/jbc.m109.079079openalex-snapshot

Loss of Function of ATXN1 Increases Amyloid β-Protein Levels by Potentiating β-Secretase Processing of β-Amyloid Precursor Protein

inferred← citeshttps://doi.org/10.1074/jbc.m111.287078openalex-snapshot

Ataxin-1 Poly(Q)-induced Proteotoxic Stress and Apoptosis Are Attenuated in Neural Cells by Docosahexaenoic Acid-derived Neuroprotectin D1

inferred← citeshttps://doi.org/10.1074/jbc.m113.472654openalex-snapshot

An Out-of-frame Overlapping Reading Frame in the Ataxin-1 Coding Sequence Encodes a Novel Ataxin-1 Interacting Protein

inferred← citeshttps://doi.org/10.1080/15384101.2015.1033595openalex-snapshot

PRMT5- mediated symmetric arginine dimethylation is attenuated by mutant huntingtin and is impaired in Huntington's disease (HD)

inferred← citeshttps://doi.org/10.1093/brain/aws069openalex-snapshot

‘Costa da Morte’ ataxia is spinocerebellar ataxia 36: clinical and genetic characterization

inferred← citeshttps://doi.org/10.1093/brain/awv292openalex-snapshot

Broad distribution of ataxin 1 silencing in rhesus cerebella for spinocerebellar ataxia type 1 therapy

inferred← citeshttps://doi.org/10.1093/brain/awv298openalex-snapshot

Re-establishing ataxin-2 downregulates translation of mutant ataxin-3 and alleviates Machado–Joseph disease

inferred← citeshttps://doi.org/10.1093/brain/awz328openalex-snapshot

Antisense oligonucleotide therapeutics in neurodegenerative diseases: the case of polyglutamine disorders

inferred← citeshttps://doi.org/10.1093/database/bay018openalex-snapshot

NDDVD: an integrated and manually curated Neurodegenerative Diseases Variation Database

inferred← citeshttps://doi.org/10.1093/g3journal/jkad180openalex-snapshot

Phenotypic defects from the expression of wild-type and pathogenic TATA-binding proteins in new Drosophila models of Spinocerebellar Ataxia Type 17

inferred← citeshttps://doi.org/10.1093/hmg/ddp534openalex-snapshot

Gain and loss of function of ALS-related mutations of TARDBP (TDP-43) cause motor deficits in vivo

inferred← citeshttps://doi.org/10.1093/hmg/ddq132openalex-snapshot

Partners in crime: bidirectional transcription in unstable microsatellite disease

inferred← citeshttps://doi.org/10.1093/hmg/ddr045openalex-snapshot

Ataxin-2 intermediate-length polyglutamine expansions in European ALS patients

inferred← citeshttps://doi.org/10.1093/hmg/ddr437openalex-snapshot

Retrotransposon activation contributes to fragile X premutation rCGG-mediated neurodegeneration

inferred← citeshttps://doi.org/10.1093/hmg/dds392openalex-snapshot

A conserved eEF2 coding variant in SCA26 leads to loss of translational fidelity and increased susceptibility to proteostatic insult

inferred← citeshttps://doi.org/10.1093/hmg/ddu081openalex-snapshot

The histone deacetylase HDAC3 is essential for Purkinje cell function, potentially complicating the use of HDAC inhibitors in SCA1

inferred← citeshttps://doi.org/10.1093/hmg/ddz265openalex-snapshot

Cerebellar contribution to the cognitive alterations in SCA1: evidence from mouse models

inferred← citeshttps://doi.org/10.1093/jmcb/mjq005openalex-snapshot

Polyglutamine Diseases: Where does Toxicity Come from? What is Toxicity? Where are We Going?

inferred← citeshttps://doi.org/10.1093/molbev/msx183openalex-snapshot

Inference of Causative Genes for Alzheimer’s Disease Due to Dosage Imbalance

inferred← citeshttps://doi.org/10.1093/nar/gkq700openalex-snapshot

Atomic resolution structure of CAG RNA repeats: structural insights and implications for the trinucleotide repeat expansion diseases

inferred← citeshttps://doi.org/10.1093/nar/gkr608openalex-snapshot

CAG repeats mimic CUG repeats in the misregulation of alternative splicing

inferred← citeshttps://doi.org/10.1093/nar/gku536openalex-snapshot

Structural studies of CNG repeats

inferred← citeshttps://doi.org/10.1097/01.nt.0000432687.24042.3fopenalex-snapshot

A New Disease Pathway Is Identified for Spinocerebellar Ataxia — A Screening Strategy That Could Be Used for Other Neurodegenerative Disorders

inferred← citeshttps://doi.org/10.1097/icu.0b013e32833eaf71openalex-snapshot

Ophthalmologic features of the common spinocerebellar ataxias

inferred← citeshttps://doi.org/10.1097/icu.0b013e3283402a34openalex-snapshot

Current World Literature

inferred← citeshttps://doi.org/10.1097/wno0b013e3181b416deopenalex-snapshot

The Spinocerebellar Ataxias

inferred← citeshttps://doi.org/10.1101/2020.07.04.187559openalex-snapshot

CRISPR/Cas9-based silencing of the ATXN1 gene in Spinocerebellar ataxia type 1 (SCA1) fibroblasts

inferred← citeshttps://doi.org/10.1101/2021.09.08.459434openalex-snapshot

Parkinson’s Disease-Associated, Sex-specific Changes in DNA Methylation at PARK7 (DJ-1), ATXN1, SLC17A6, NR4A2 , and PTPRN2 in Cortical Neurons

inferred← citeshttps://doi.org/10.1101/2021.10.21.465333openalex-snapshot

Differential effects of Wnt-β-catenin signaling in Purkinje cells and Bergmann glia in SCA1

inferred← citeshttps://doi.org/10.1101/2021.10.28.466301openalex-snapshot

Single-nuclei RNA sequencing uncovers non-cell autonomous changes in cerebellar astrocytes and oligodendrocytes that may contribute to Spinocerebellar Ataxia Type 1 (SCA1) pathogenesis

inferred← citeshttps://doi.org/10.1101/2022.02.24.481789openalex-snapshot

Loss of intracerebellar heterogeneity and selective vulnerability in Spinocerebellar ataxia type 1 neurodegeneration

inferred← citeshttps://doi.org/10.1101/2024.07.30.605685openalex-snapshot

The big tau splice isoform resists Alzheimer’s-related pathological changes

inferred← citeshttps://doi.org/10.1111/bpa.12946openalex-snapshot

Region‐specific preservation of Purkinje cell morphology and motor behavior in the ATXN1[82Q] mouse model of spinocerebellar ataxia 1

inferred← citeshttps://doi.org/10.1111/j.1369-1600.2012.00463.xopenalex-snapshot

Genome‐wide association study of a quantitative disordered gambling trait

inferred← citeshttps://doi.org/10.1111/jnc.70302openalex-snapshot

Oral KDS2010 , a Monoamine Oxidase‐B ( MAO ‐B) Inhibitor, Slows the Deterioration of Motor Coordination in Genetic SCA1 Models by Inhibiting Astrocytic MAO‐B‐Mediated Inflammation

inferred← citeshttps://doi.org/10.1126/science.1212673openalex-snapshot

Exercise and Genetic Rescue of SCA1 via the Transcriptional Repressor Capicua

inferred← citeshttps://doi.org/10.1126/science.1214714openalex-snapshot

Another Reason to Exercise

inferred← citeshttps://doi.org/10.1126/science.abn3263openalex-snapshot

Vocal learning–associated convergent evolution in mammalian proteins and regulatory elements

inferred← citeshttps://doi.org/10.1134/s1022795410030154openalex-snapshot

Simulation of the distribution of spinocerebellar ataxia type 1 in Yakut populations: Description of the model

inferred← citeshttps://doi.org/10.1136/jnnp-2014-308421openalex-snapshot

The autosomal dominant spinocerebellar ataxias: emerging mechanistic themes suggest pervasive Purkinje cell vulnerability

inferred← citeshttps://doi.org/10.1142/9789814350457_0001openalex-snapshot

THE CELLULAR PROCESS OF AUTOPHAGY AND CONTROL OF AUTOPHAGY IN NEURONS

inferred← citeshttps://doi.org/10.1142/9789814350457_0011openalex-snapshot

AUTOPHAGY IN HUNTINGTON’S AND PARKINSON’S DISEASES: PATHOGENIC MECHANISMS AND THERAPEUTIC POTENTIALS

inferred← citeshttps://doi.org/10.1155/2017/2525967openalex-snapshot

Oxidative Stress in Neurodegenerative Diseases: From Molecular Mechanisms to Clinical Applications

inferred← citeshttps://doi.org/10.1172/jci.insight.123193openalex-snapshot

Antisense oligonucleotide–mediated ataxin-1 reduction prolongs survival in SCA1 mice and reveals disease-associated transcriptome profiles

inferred← citeshttps://doi.org/10.1172/jci156616openalex-snapshot

Cross-species genetic screens identify transglutaminase 5 as a regulator of polyglutamine-expanded ataxin-1

inferred← citeshttps://doi.org/10.1177/2514183x18785258openalex-snapshot

Epidemiology of inherited cerebellar ataxias and challenges in clinical research

inferred← citeshttps://doi.org/10.1186/2053-8871-1-7openalex-snapshot

Current understanding of the role of microRNAs in spinocerebellar ataxias

inferred← citeshttps://doi.org/10.1186/gm150openalex-snapshot

Trinucleotide repeats: triggers for genomic disorders?

inferred← citeshttps://doi.org/10.1186/s12920-019-0594-4openalex-snapshot

ATXN1 N-terminal region explains the binding differences of wild-type and expanded forms

inferred← citeshttps://doi.org/10.1186/s12974-017-0880-zopenalex-snapshot

Inhibition of colony-stimulating factor 1 receptor early in disease ameliorates motor deficits in SCA1 mice

inferred← citeshttps://doi.org/10.1186/s12974-025-03450-2openalex-snapshot

An expanded polyglutamine in ATAXIN1 results in a loss-of-function that exacerbates severity of Multiple Sclerosis in an EAE mouse model

inferred← citeshttps://doi.org/10.1186/s40035-019-0166-8openalex-snapshot

Xenografting of human umbilical mesenchymal stem cells from Wharton’s jelly ameliorates mouse spinocerebellar ataxia type 1

inferred← citeshttps://doi.org/10.1186/s40035-021-00240-7openalex-snapshot

Neurodegenerative diseases: a hotbed for splicing defects and the potential therapies

inferred← citeshttps://doi.org/10.1212/wnl.0000000000005690openalex-snapshot

Overlap between age-at-onset and disease-progression determinants in Huntington disease

inferred← citeshttps://doi.org/10.1242/dev.034686openalex-snapshot

Axons find their way in the snow

inferred← citeshttps://doi.org/10.1242/jcs.092965openalex-snapshot

The Capicua repressor – a general sensor of RTK signaling in development and disease

inferred← citeshttps://doi.org/10.1371/journal.pbio.2000733openalex-snapshot

The Machado–Joseph Disease Deubiquitinase Ataxin-3 Regulates the Stability and Apoptotic Function of p53

inferred← citeshttps://doi.org/10.1371/journal.pgen.1002897openalex-snapshot

Identification of Human Proteins That Modify Misfolding and Proteotoxicity of Pathogenic Ataxin-1

inferred← citeshttps://doi.org/10.1371/journal.pone.0008372openalex-snapshot

Phosphorylation of S776 and 14-3-3 Binding Modulate Ataxin-1 Interaction with Splicing Factors

inferred← citeshttps://doi.org/10.1371/journal.pone.0011982openalex-snapshot

The Human Proteins MBD5 and MBD6 Associate with Heterochromatin but They Do Not Bind Methylated DNA

inferred← citeshttps://doi.org/10.1371/journal.pone.0030824openalex-snapshot

Polyglutamine Repeats Are Associated to Specific Sequence Biases That Are Conserved among Eukaryotes

inferred← citeshttps://doi.org/10.1371/journal.pone.0037985openalex-snapshot

FOX-2 Dependent Splicing of Ataxin-2 Transcript Is Affected by Ataxin-1 Overexpression

inferred← citeshttps://doi.org/10.1371/journal.pone.0052665openalex-snapshot

The Vasculome of the Mouse Brain

inferred← citeshttps://doi.org/10.1371/journal.pone.0076456openalex-snapshot

Protein-Protein Interactions as a Strategy towards Protein-Specific Drug Design: The Example of Ataxin-1

inferred← citeshttps://doi.org/10.1371/journal.pone.0163359openalex-snapshot

Polyglutamine Tract Expansion Increases S-Nitrosylation of Huntingtin and Ataxin-1

inferred← citeshttps://doi.org/10.1371/journal.pone.0178333openalex-snapshot

Molecular dynamics analysis of the aggregation propensity of polyglutamine segments

inferred← citeshttps://doi.org/10.1371/journal.pone.0183719openalex-snapshot

TGC repeat expansion in the TCF4 gene increases the risk of Fuchs’ endothelial corneal dystrophy in Australian cases

inferred← citeshttps://doi.org/10.1371/journal.pone.0200013openalex-snapshot

Inhibition of NF-κB signaling in IKKβF/F;LysM Cre mice causes motor deficits but does not alter pathogenesis of Spinocerebellar ataxia type 1

inferred← citeshttps://doi.org/10.1515/revneuro.2010.21.4.251openalex-snapshot

Pathogenic TARDBP Mutations in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia: Disease-Associated Pathways

inferred← citeshttps://doi.org/10.1523/jneurosci.1357-15.2015openalex-snapshot

Neuronal Atrophy Early in Degenerative Ataxia Is a Compensatory Mechanism to Regulate Membrane Excitability

inferred← citeshttps://doi.org/10.15252/embj.2020106106openalex-snapshot

Dual targeting of brain region‐specific kinases potentiates neurological rescue in Spinocerebellar ataxia type 1

inferred← citeshttps://doi.org/10.20944/preprints202508.1517.v1openalex-snapshot

Muscle Mechanics in Metabolic Health and Longevity: The Biochemistry of Training Adaptations

inferred← citeshttps://doi.org/10.2119/molmed.2014.00219openalex-snapshot

A Coding Variant of ANO10, Affecting Volume Regulation of Macrophages, Is Associated with Borrelia Seropositivity

inferred← citeshttps://doi.org/10.2217/fnl.09.69openalex-snapshot

Role of the ubiquitin–proteasome system and autophagy in polyglutamine neurodegenerative diseases

inferred← citeshttps://doi.org/10.32657/10356/75820openalex-snapshot

Roles of activity-dependent transcription factor Mef2c in the synaptic and morphological organization of early postnatal Purkinje neurons

inferred← citeshttps://doi.org/10.3389/fcell.2021.642773openalex-snapshot

Juvenile Huntington’s Disease and Other PolyQ Diseases, Update on Neurodevelopmental Character and Comparative Bioinformatic Review of Transcriptomic and Proteomic Data

inferred← citeshttps://doi.org/10.3389/fncel.2018.00290openalex-snapshot

Roles of Post-translational Modifications in Spinocerebellar Ataxias

inferred← citeshttps://doi.org/10.3389/fncel.2018.00509openalex-snapshot

Brain Derived Neurotrophic Factor (BDNF) Delays Onset of Pathogenesis in Transgenic Mouse Model of Spinocerebellar Ataxia Type 1 (SCA1)

inferred← citeshttps://doi.org/10.3389/fnmol.2023.1280546openalex-snapshot

Intranuclear inclusions of polyQ-expanded ATXN1 sequester RNA molecules

inferred← citeshttps://doi.org/10.3390/biom13050788openalex-snapshot

Therapeutic Strategies for Spinocerebellar Ataxia Type 1

inferred← citeshttps://doi.org/10.3390/brainsci9040080openalex-snapshot

Extracellular S100β Disrupts Bergman Glia Morphology and Synaptic Transmission in Cerebellar Purkinje Cells

inferred← citeshttps://doi.org/10.3390/cells11203323openalex-snapshot

Spatial and Temporal Diversity of Astrocyte Phenotypes in Spinocerebellar Ataxia Type 1 Mice

inferred← citeshttps://doi.org/10.3390/cells12020252openalex-snapshot

Zebrafish: A Model Deciphering the Impact of Flavonoids on Neurodegenerative Disorders

inferred← citeshttps://doi.org/10.3390/ijms21165783openalex-snapshot

Alzheimer’s Disease and Specialized Pro-Resolving Lipid Mediators: Do MaR1, RvD1, and NPD1 Show Promise for Prevention and Treatment?

inferred← citeshttps://doi.org/10.3390/ijms22147351openalex-snapshot

Genetic Modeling of the Neurodegenerative Disease Spinocerebellar Ataxia Type 1 in Zebrafish

inferred← citeshttps://doi.org/10.3390/ijms222111348openalex-snapshot

Structural Analysis and Spatiotemporal Expression of Atxn1 Genes in Zebrafish Embryos and Larvae

inferred← citeshttps://doi.org/10.3390/ijms26062623openalex-snapshot

Sex Differences in a Novel Mouse Model of Spinocerebellar Ataxia Type 1 (SCA1)

inferred← citeshttps://doi.org/10.3390/ijms26104698openalex-snapshot

Fingolimod Prevents Neuroinflammation but Has a Limited Effect on the Development of Ataxia in a Mouse Model for SCA1

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