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Interference by Huntingtin and Atrophin-1 with CBP-Mediated Transcription Leading to Cellular Toxicity

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What this work says

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

inferredcites →https://doi.org/10.1001/archneur.59.6.1038openalex-snapshot

Glutamine Repeats and Neurodegenerative Diseases: Molecular Aspects

inferredcites →https://doi.org/10.1002/ana.410370309openalex-snapshot

Reduced expression of preproenkephalin in striatal neurons from huntington's disease patients

inferredcites →https://doi.org/10.1006/mcne.1999.0773openalex-snapshot

Nuclear Targeting of Mutant Huntingtin Increases Toxicity

inferredcites →https://doi.org/10.1006/nbdi.1998.0168openalex-snapshot

Intranuclear Neuronal Inclusions in Huntington's Disease and Dentatorubral and Pallidoluysian Atrophy: Correlation between the Density of Inclusions andIT15CAG Triplet Repeat Length

inferredcites →https://doi.org/10.1006/nbdi.1999.0260openalex-snapshot

Mutant Huntingtin Forms in Vivo Complexes with Distinct Context-Dependent Conformations of the Polyglutamine Segment

inferredcites →https://doi.org/10.1016/0378-1119(89)90358-2openalex-snapshot

Site-directed mutagenesis by overlap extension using the polymerase chain reaction

inferredcites →https://doi.org/10.1016/0896-6273(95)90067-5openalex-snapshot

Distinct roles for bFGF and NT-3 in the regulation of cortical neurogenesis

inferredcites →https://doi.org/10.1016/0896-6273(95)90138-8openalex-snapshot

When more is less: Pathogenesis of glutamine repeat neurodegenerative diseases

inferredcites →https://doi.org/10.1016/s0006-8993(00)02237-xopenalex-snapshot

Brain-derived neurotrophic factor in Huntington disease

inferredcites →https://doi.org/10.1016/s0092-8674(00)80513-9openalex-snapshot

Formation of Neuronal Intranuclear Inclusions Underlies the Neurological Dysfunction in Mice Transgenic for the HD Mutation

inferredcites →https://doi.org/10.1016/s0092-8674(00)80514-0openalex-snapshot

Huntingtin-Encoded Polyglutamine Expansions Form Amyloid-like Protein Aggregates In Vitro and In Vivo

inferredcites →https://doi.org/10.1016/s0092-8674(00)81369-0openalex-snapshot

Exon 1 of the HD Gene with an Expanded CAG Repeat Is Sufficient to Cause a Progressive Neurological Phenotype in Transgenic Mice

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

Ataxin-1 Nuclear Localization and Aggregation

inferredcites →https://doi.org/10.1016/s0166-2236(99)01500-3openalex-snapshot

Is CREB a key to neuronal survival?

inferredcites →https://doi.org/10.1016/s0304-3940(99)00758-2openalex-snapshot

Preparation of human cDNAs encoding expanded polyglutamine repeats

inferredcites →https://doi.org/10.1016/s0896-6273(00)80376-1openalex-snapshot

Regulation of Dendritic Growth and Remodeling by Rho, Rac, and Cdc42

inferredcites →https://doi.org/10.1016/s0896-6273(00)80737-0openalex-snapshot

Control of Recruitment and Transcription-Activating Function of CBP Determines Gene Regulation by NMDA Receptors and L-Type Calcium Channels

inferredcites →https://doi.org/10.1016/s0896-6273(00)80738-2openalex-snapshot

Regulation of CBP-Mediated Transcription by Neuronal Calcium Signaling

inferredcites →https://doi.org/10.1016/s0896-6273(00)80839-9openalex-snapshot

Nuclear Accumulation of Truncated Atrophin-1 Fragments in a Transgenic Mouse Model of DRPLA

inferredcites →https://doi.org/10.1016/s0896-6273(00)80943-5openalex-snapshot

Intranuclear Inclusions of Expanded Polyglutamine Protein in Spinocerebellar Ataxia Type 3

inferredcites →https://doi.org/10.1016/s0896-6273(00)81010-7openalex-snapshot

Ca2+ Influx Regulates BDNF Transcription by a CREB Family Transcription Factor-Dependent Mechanism

inferredcites →https://doi.org/10.1016/s0968-0004(98)01350-4openalex-snapshot

Glutamine repeats and neurodegenerative diseases: molecular aspects

inferredcites →https://doi.org/10.1023/b:scam.0000007124.19463.e5openalex-snapshot

Amyloid Formation by Mutant Huntingtin: Threshold, Progressivity and Recruitment of Normal Polyglutamine Proteins

inferredcites →https://doi.org/10.1038/2830openalex-snapshot

Stimulation of cAMP response element (CRE)-mediated transcription during contextual learning

inferredcites →https://doi.org/10.1038/365855a0openalex-snapshot

Phosphorylated CREB binds specifically to the nuclear protein CBP

inferredcites →https://doi.org/10.1038/79139openalex-snapshot

Expanded polyglutamine stretches interact with TAFII130, interfering with CREB-dependent transcription

inferredcites →https://doi.org/10.1038/ng0298-150openalex-snapshot

Length of huntingtin and its polyglutamine tract influences localization and frequency of intracellular aggregates

inferredcites →https://doi.org/10.1038/ng0595-3openalex-snapshot

Gain of glutamines, gain of function?

inferredcites →https://doi.org/10.1073/pnas.100110097openalex-snapshot

The Huntington's disease protein interacts with p53 and CREB-binding protein and represses transcription

inferredcites →https://doi.org/10.1073/pnas.91.12.5355openalex-snapshot

Glutamine repeats as polar zippers: their possible role in inherited neurodegenerative diseases.

inferredcites →https://doi.org/10.1073/pnas.96.20.11404openalex-snapshot

Insoluble detergent-resistant aggregates form between pathological and nonpathological lengths of polyglutamine in mammalian cells

inferredcites →https://doi.org/10.1093/hmg/7.5.783openalex-snapshot

Truncated N-terminal fragments of huntingtin with expanded glutamine repeats form nuclear and cytoplasmic aggregates in cell culture

inferredcites →https://doi.org/10.1093/hmg/8.3.397openalex-snapshot

Intranuclear inclusions and neuritic aggregates in transgenic mice expressing a mutant N-terminal fragment of huntingtin [published erratum appears in Hum Mol Genet 1999 May;8(5):943]

inferredcites →https://doi.org/10.1093/hmg/9.14.2197openalex-snapshot

CREB-binding protein sequestration by expanded polyglutamine

inferredcites →https://doi.org/10.1093/hmg/9.9.1259openalex-snapshot

Decreased expression of striatal signaling genes in a mouse model of Huntington's disease

inferredcites →https://doi.org/10.1097/00005792-199709000-00001openalex-snapshot

Huntington Disease and the Related Disorder, Dentatorubral-Pallidoluysian Atrophy (DRPLA)

inferredcites →https://doi.org/10.1098/rstb.1999.0455openalex-snapshot

Evidence for a recruitment and sequestration mechanism in Huntington'sdisease

inferredcites →https://doi.org/10.1126/science.277.5334.1990openalex-snapshot

Aggregation of Huntingtin in Neuronal Intranuclear Inclusions and Dystrophic Neurites in Brain

inferredcites →https://doi.org/10.1126/science.281.5382.1505openalex-snapshot

CBP: A Signal-Regulated Transcriptional Coactivator Controlled by Nuclear Calcium and CaM Kinase IV

inferredcites →https://doi.org/10.1126/science.286.5443.1358openalex-snapshot

Cell Survival Promoted by the Ras-MAPK Signaling Pathway by Transcription-Dependent and -Independent Mechanisms

inferredcites →https://doi.org/10.1126/science.286.5448.2358openalex-snapshot

Mediation by a CREB Family Transcription Factor of NGF-Dependent Survival of Sympathetic Neurons

inferredcites →https://doi.org/10.1146/annurev.med.47.1.201openalex-snapshot

TRINUCLEOTIDE INSTABILITY: A Repeating Theme in Human Inherited Disorders

inferredcites →https://doi.org/10.1146/annurev.ne.19.030196.000455openalex-snapshot

Trinucleotide Repeats in Neurogenetic Disorders

inferredcites →https://doi.org/10.1523/jneurosci.18-06-02040.1998openalex-snapshot

Manganese Superoxide Dismutase Protects nNOS Neurons from NMDA and Nitric Oxide-Mediated Neurotoxicity

What points at this work

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

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Lysine (K)-Deacetylase Inhibitors: The Real Next Step To Neuropsychiatric And Neurodegenerative Disorders?

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Clearance of Mutant Proteins as a Therapeutic Target in Neurodegenerative Diseases

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The Phosphodiesterase 10 Positron Emission Tomography Tracer, [18F]MNI-659, as a Novel Biomarker for Early Huntington Disease

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Histone Acetylation and Deacetylation

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Pathogenesis of Polyglutamine Diseases

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Pathogenesis of Polyglutamine Diseases

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Misfolding and Aggregation in Huntington Disease and Other Expanded Polyglutamine Repeat Diseases

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Therapeutic Prospects for Polyglutamine Disease

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Herbal Drugs

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Dentatorubral‐Pallidoluysian Atrophy

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Huntington Disease and Other Genetic Choreas

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Protein Folding and Aggregation in the Expanded Polyglutamine Repeat Diseases

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Polyglutamine Aggregates as a Model for Protein‐misfolding Diseases

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Protein Folding and Aggregation in the Expanded Polyglutamine Repeat Diseases

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Polyglutamine Neuropathies: Animal Models to Molecular Mechanisms

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Oligodendrocytic polyglutamine pathology in dentatorubral‐pallidoluysian atrophy

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A disorder similar to Huntington's disease is associated with a novel CAG repeat expansion

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Can flies help humans treat neurodegenerative diseases?

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Dessert or Poison? The Roles of Glycosylation in Alzheimer's, Parkinson's, Huntington's Disease, and Amyotrophic Lateral Sclerosis

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Expansion of the polyQ repeats in THAP11 forms intranuclear aggregation and causes cell G0/G1 arrest

inferred← citeshttps://doi.org/10.1002/cne.10776openalex-snapshot

Time course of early motor and neuropathological anomalies in a knock‐in mouse model of Huntington's disease with 140 CAG repeats

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Hprt (CAG)146 mice: Age of onset of behavioral abnormalities, time course of neuronal intranuclear inclusion accumulation, neurotransmitter marker alterations, mitochondrial function markers, and susceptibility to 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine

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Chronology of behavioral symptoms and neuropathological sequela in R6/2 Huntington's disease transgenic mice

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Overview of Huntington's Disease Models: Neuropathological, Molecular, and Behavioral Differences

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Non‐apoptotic cell death in Caenorhabditis elegans

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Edible bird's nest inhibits the inflammation and regulates the immunological balance of lung injury mice by SO2

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Protein misfolding inside cells: The case of huntingtin and Huntington's disease

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DeSUMOylating enzymes—SENPs

inferred← citeshttps://doi.org/10.1002/jnr.10233openalex-snapshot

Time course of polyglutamine aggregate body formation and cell death: Enhanced growth in nucleus and an interval for cell death

inferred← citeshttps://doi.org/10.1002/jnr.20534openalex-snapshot

Regulation of the proapoptotic activity of huntingtin interacting protein 1 by Dyrk1 and caspase-3 in hippocampal neuroprogenitor cells

inferred← citeshttps://doi.org/10.1002/jnr.21046openalex-snapshot

Striatal specificity of gene expression dysregulation in Huntington's disease

inferred← citeshttps://doi.org/10.1002/jnr.21817openalex-snapshot

Intracerebral transplantation of neural stem cells combined with trehalose ingestion alleviates pathology in a mouse model of Huntington's disease

inferred← citeshttps://doi.org/10.1002/mco2.674openalex-snapshot

Protein modification in neurodegenerative diseases

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Atrophin‐1 Function and Dysfunction in Dentatorubral–Pallidoluysian Atrophy

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Discovery of Therapeutic Approaches for Polyglutamine Diseases: A Summary of Recent Efforts

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Involvement of calpain in the neuropathogenesis of Alzheimer’s disease

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Juvenile onset Huntington's disease—clinical and research perspectives

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Polyglutamine disease proteins: Commonalities and differences in interaction profiles and pathological effects

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Age‐dependent gene expression profile and protein expression in a transgenic rat model of Huntington's disease

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Challenges of Huntington's disease and quest for therapeutic biomarkers

inferred← citeshttps://doi.org/10.1002/prot.22970openalex-snapshot

An accurate model of polyglutamine

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A Microtiter Plate Assay for Polyglutamine Aggregate Extension

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Amino Acid Sequence Requirements of Peptides That Inhibit Polyglutamine-Protein Aggregation and Cell Death

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Polyglutamine aggregation behavior in vitro supports a recruitment mechanism of cytotoxicity

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Inhibition of Polyglutamine Aggregation in R6/2 HD Brain Slices—Complex Dose–Response Profiles

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Striatal and Cortical Neurochemical Changes Induced by Chronic Metabolic Compromise in the 3-Nitropropionic Model of Huntington's Disease

inferred← citeshttps://doi.org/10.1006/nbdi.2002.0539openalex-snapshot

Polyglutamine Repeat Length-Dependent Proteolysis of Huntingtin

inferred← citeshttps://doi.org/10.1006/nbdi.2002.0562openalex-snapshot

Huntington's Disease of the Endocrine Pancreas: Insulin Deficiency and Diabetes Mellitus due to Impaired Insulin Gene Expression

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Sp1 and Huntington’s Disease

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The Androgen Receptor and Spinal and Bulbar Muscular Atrophy

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Transcriptional Dysfunctions as Pathogenic Mechanism of Neurodegenerative Diseases

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Chromatin Acetylation Status in the Manifestation of Neurodegenerative Diseases

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Polyglutamine Disease, the Emerging Role of Transcription Interference

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The Role of Histone Deacetylases in Neurodegenerative Diseases and Small-Molecule Inhibitors as a Potential Therapeutic Approach

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Transgenic Animal Models of Huntington’s Disease

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Huntington's Disease: Unraveling the Pathophysiological Cascade Behind a Singular Gene Defect

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Molecular Pathogenesis of the Polyglutamine Disease: Spinal and Bulbar Muscular Atrophy

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HATs and HDACs

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The Role of Hsp70 and Its Co-Chaperones in Protein Misfolding, Aggregation and Disease

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Huntington's Disease

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CREB-Dependent Transcription and Synaptic Plasticity

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Intrinsic Disorder in Proteins Associated with Neurodegenerative Diseases

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Huntington’s Disease

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Clinical Features and Molecular Mechanisms of Spinal and Bulbar Muscular Atrophy (SBMA)

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Cellular Functions of Calcium Channel Subtypes

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Neurotoxicity in Huntington Disease

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Immunohistochemical Localisation of Tata-Binding Protein in Huntington’s Disease Cortex

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Transcriptional Dysregulation in Huntington’s Disease

inferred← citeshttps://doi.org/10.1007/978-1-4757-3538-3_20openalex-snapshot

Dopamine Neurons are Not Affected by Expanded Polyglutamine Stretches in HD Gene Knock-In Mice

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Cell-Death Mechanisms in Neurodegenerative Diseases

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Potential Role of Androgens and Androgen Receptors in Alzheimer’s Disease

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Huntington’s Disease

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Trinucleotide Repeat Disorders

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The Nuclear Ubiquitin–Proteasome System: Visualization of Proteasomes, Protein Aggregates, and Proteolysis in the Cell Nucleus

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Protein Aggregate Characterization in Models of Neurodegenerative Disease

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Trinucleotide Repeat Protocols

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DRPLA: Recent Advances in Research Using Transgenic Mouse Models

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Psychopharmacotherapy in Patients with Tics and Other Motor Disorders

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Neurotoxicity in Huntington Disease

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Neurotoxicity in Huntington Disease

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Perturbations to Stimulus-Dependent Gene Activity Patterns in Neurodegenerative Disorders

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Gene Regulation by Nuclear Calcium and Its Antagonism by NMDAR/TRPM4 Signaling

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Experimental Models of Polyglutamine Disorders

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The Role of HSP70 and Its Co-chaperones in Protein Misfolding, Aggregation and Disease

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Cardiac Autophagy and Its Regulation by Reversible Protein Acetylation

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Psychopharmacotherapy in Patients with Tics and Other Motor Disorders

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Role of Phosphodiesterases in Huntington’s Disease

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X-Linked Spinal and Bulbar Muscular Atrophy: From Clinical Genetic Features and Molecular Pathology to Mechanisms Underlying Disease Toxicity

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What Is the Role of Adenosine Tone and Adenosine Receptors in Huntington’s Disease?

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Toxic RNA in the Nucleus: Unstable Microsatellite Expression in Neuromuscular Disease

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HDACs in Skeletal Muscle Remodeling and Neuromuscular Disease

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Huntington’s Disease

inferred← citeshttps://doi.org/10.1007/978-3-642-55543-5_6openalex-snapshot

Neurodegenerative Diseases: Insights from Drosophila and Mouse Models

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Therapeutics in Huntington’s Disease

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Dentatorubral-pallidoluysian atrophy (DRPLA)

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Therapeutics for Polyglutamine Diseases Through Protein Degradation Pathway: Targeting the Nucleus

inferred← citeshttps://doi.org/10.1007/978-4-431-55852-1_11openalex-snapshot

HSF Inhibits the Progression of Age-Related Neurodegenerative Diseases

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

Free Radicals in Human Health and Disease

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Free Radicals and Oxidative Stress in Neurodegenerative Disorders

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/10.1007/978-94-007-5416-4_15openalex-snapshot

Modeling the Polyglutamine Aggregation Pathway in Huntington’s Disease: From Basic Studies to Clinical Applications

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

Neurodegenerative Disease Conditions and Genomic Treatment for Better Health

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Post-translational Modifications: A Mystery to Unravel Huntington’s Disease Prognosis

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Therapeutic Potential of HDAC Inhibitors in Neurodegenerative Diseases

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Protein Metabolism: Critical Factors Implicated in Neurodegenerative Diseases

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The roles of proteolysis and nuclear localisation in the toxicity of the polyglutamine diseases. A review

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Polyglutamine diseases: a transcription disorder?

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Synaptic dysfunction in Huntington’s disease: a new perspective

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Rubinstein-Taybi syndrome: molecular findings and therapeutic approaches to improve cognitive dysfunction

inferred← citeshttps://doi.org/10.1007/s00018-006-6242-0openalex-snapshot

Huntington’s disease: from huntingtin function and dysfunction to therapeutic strategies

inferred← citeshttps://doi.org/10.1007/s00018-007-7035-9openalex-snapshot

Histone deacetylases: Focus on the nervous system

inferred← citeshttps://doi.org/10.1007/s00018-008-8403-9openalex-snapshot

Atrophins’ emerging roles in development and neurodegenerative disease

inferred← citeshttps://doi.org/10.1007/s00018-018-2854-4openalex-snapshot

Mechanisms of protein toxicity in neurodegenerative diseases

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

Pathogenic mechanisms underlying spinocerebellar ataxia type 1

inferred← citeshttps://doi.org/10.1007/s00109-004-0530-7openalex-snapshot

Spinal and bulbar muscular atrophy: ligand-dependent pathogenesis and therapeutic perspectives

inferred← citeshttps://doi.org/10.1007/s00109-004-0632-2openalex-snapshot

A novel therapeutic strategy for polyglutamine diseases by stabilizing aggregation-prone proteins with small molecules

inferred← citeshttps://doi.org/10.1007/s00109-015-1344-5openalex-snapshot

Connectivity mapping uncovers small molecules that modulate neurodegeneration in Huntington’s disease models

inferred← citeshttps://doi.org/10.1007/s00401-007-0306-6openalex-snapshot

Huntington disease models and human neuropathology: similarities and differences

inferred← citeshttps://doi.org/10.1007/s00401-008-0437-4openalex-snapshot

NSF, Unc-18-1, dynamin-1 and HSP90 are inclusion body components in neuronal intranuclear inclusion disease identified by anti-SUMO-1-immunocapture

inferred← citeshttps://doi.org/10.1007/s00401-017-1732-8openalex-snapshot

Remodeling of heterochromatin structure slows neuropathological progression and prolongs survival in an animal model of Huntington’s disease

inferred← citeshttps://doi.org/10.1007/s00439-023-02607-4openalex-snapshot

Functional implications of paralog genes in polyglutamine spinocerebellar ataxias

inferred← citeshttps://doi.org/10.1007/s004390100548openalex-snapshot

Glutamine repeats and neurodegenerative diseases: molecular aspects

inferred← citeshttps://doi.org/10.1007/s10038-006-0001-9openalex-snapshot

Exclusion of mutations in the PRNP, JPH3, TBP, ATN1, CREBBP, POU3F2 and FTL genes as a cause of disease in Portuguese patients with a Huntington-like phenotype

inferred← citeshttps://doi.org/10.1007/s10072-013-1515-5openalex-snapshot

Nuclear localization of huntingtin during spermatogenesis

inferred← citeshttps://doi.org/10.1007/s10571-012-9836-0openalex-snapshot

Mapping Molecular Memory: Navigating the Cellular Pathways of Learning

inferred← citeshttps://doi.org/10.1007/s11064-023-03889-wopenalex-snapshot

Modulation of Synaptic Plasticity Genes Associated to DNA Damage in a Model of Huntington’s Disease

inferred← citeshttps://doi.org/10.1007/s11064-024-04167-zopenalex-snapshot

Epigenetic Orchestration of Neurodegenerative Disorders: A Possible Target for Curcumin as a Therapeutic

inferred← citeshttps://doi.org/10.1007/s11910-002-0072-8openalex-snapshot

The spinocerebellar ataxias: Order emerges from chaos

inferred← citeshttps://doi.org/10.1007/s12013-013-9628-2openalex-snapshot

Regulating the Ubiquitin/Proteasome Pathway Via cAMP-signaling: Neuroprotective Potential

inferred← citeshttps://doi.org/10.1007/s12017-013-8219-0openalex-snapshot

Increased 5-Methylcytosine and Decreased 5-Hydroxymethylcytosine Levels are Associated with Reduced Striatal A2AR Levels in Huntington’s Disease

inferred← citeshttps://doi.org/10.1007/s12031-012-9739-zopenalex-snapshot

Sp1 Regulates Human Huntingtin Gene Expression

inferred← citeshttps://doi.org/10.1007/s12035-010-8156-yopenalex-snapshot

The Role of PML in the Nervous System

inferred← citeshttps://doi.org/10.1007/s12035-012-8316-3openalex-snapshot

Mouse Models of Polyglutamine Diseases in Therapeutic Approaches: Review and Data Table. Part II

inferred← citeshttps://doi.org/10.1007/s12035-015-9601-8openalex-snapshot

Induced Pluripotent Stem Cells in Huntington’s Disease: Disease Modeling and the Potential for Cell-Based Therapy

inferred← citeshttps://doi.org/10.1007/s12035-016-0010-4openalex-snapshot

Genome-wide Analysis of RARβ Transcriptional Targets in Mouse Striatum Links Retinoic Acid Signaling with Huntington’s Disease and Other Neurodegenerative Disorders

inferred← citeshttps://doi.org/10.1007/s12035-017-0707-zopenalex-snapshot

Glycoprotein NMB: an Emerging Role in Neurodegenerative Disease

inferred← citeshttps://doi.org/10.1007/s12035-018-1160-3openalex-snapshot

Tissue-Specific Upregulation of Drosophila Insulin Receptor (InR) Mitigates Poly(Q)-Mediated Neurotoxicity by Restoration of Cellular Transcription Machinery

inferred← citeshttps://doi.org/10.1007/s12035-019-01847-8openalex-snapshot

Neuroprotective Effects of Doxycycline in the R6/2 Mouse Model of Huntington’s Disease

inferred← citeshttps://doi.org/10.1007/s12038-008-0047-2openalex-snapshot

Non-coding RNAs in polyglutamine disorders: friend or foe?

inferred← citeshttps://doi.org/10.1007/s12038-019-9974-3openalex-snapshot

Regulation of epigenetic state by non-histone chromatin proteins and transcription factors: Implications in disease

inferred← citeshttps://doi.org/10.1007/s12041-010-0072-4openalex-snapshot

Modifiers and mechanisms of multi-system polyglutamine neurodegenerative disorders: lessons from fly models

inferred← citeshttps://doi.org/10.1007/s12311-008-0026-zopenalex-snapshot

Spinocerebellar ataxias caused by polyglutamine expansions: A review of therapeutic strategies

inferred← citeshttps://doi.org/10.1007/s12311-008-0027-yopenalex-snapshot

Molecular pathogenesis and cellular pathology of spinocerebellar ataxia type 7 neurodegeneration

inferred← citeshttps://doi.org/10.1007/s12311-012-0430-2openalex-snapshot

Altered Expression of Carbonic Anhydrase-Related Protein XI in Neuronal Cells Expressing Mutant Ataxin-3

inferred← citeshttps://doi.org/10.1007/s12640-010-9227-6openalex-snapshot

Modulation of Mutant Huntingtin N-Terminal Cleavage and Its Effect on Aggregation and Cell Death

inferred← citeshttps://doi.org/10.1007/s13148-011-0025-7openalex-snapshot

Targeting Huntington’s disease through histone deacetylases

inferred← citeshttps://doi.org/10.1007/s13311-012-0112-2openalex-snapshot

Huntington's Disease and the Striatal Medium Spiny Neuron: Cell-Autonomous and Non-Cell-Autonomous Mechanisms of Disease

inferred← citeshttps://doi.org/10.1007/s13311-013-0206-5openalex-snapshot

Epigenetic Mechanisms of Neurodegeneration in Huntington's Disease

inferred← citeshttps://doi.org/10.1007/s13311-013-0244-zopenalex-snapshot

Treatment of Huntington's Disease

inferred← citeshttps://doi.org/10.1016/b978-0-12-374105-9.00303-8openalex-snapshot

Atrophin-1

inferred← citeshttps://doi.org/10.1016/b978-0-12-374767-9.00030-5openalex-snapshot

Chromatin Remodeling

inferred← citeshttps://doi.org/10.1016/b978-0-12-381328-2.00014-6openalex-snapshot

Genetics and Neuropathology of Huntington's Disease

inferred← citeshttps://doi.org/10.1016/b978-0-12-381328-2.00015-8openalex-snapshot

Pathogenic Mechanisms in Huntington's Disease

inferred← citeshttps://doi.org/10.1016/b978-0-12-381328-2.00016-xopenalex-snapshot

Experimental Models of HD and Reflection on Therapeutic Strategies

inferred← citeshttps://doi.org/10.1016/b978-0-12-385883-2.00010-2openalex-snapshot

Huntington Disease and the Huntingtin Protein

inferred← citeshttps://doi.org/10.1016/b978-0-12-405195-9.00033-0openalex-snapshot

Modeling Huntington Disease in Yeast and Invertebrates

inferred← citeshttps://doi.org/10.1016/b978-0-12-405195-9.00034-2openalex-snapshot

HDL2 Mouse

inferred← citeshttps://doi.org/10.1016/b978-0-12-417044-5.00050-0openalex-snapshot

Dominantly Inherited Spinocerebellar Syndromes

inferred← citeshttps://doi.org/10.1016/b978-0-12-800681-8.00002-5openalex-snapshot

The Functional Genome

inferred← citeshttps://doi.org/10.1016/b978-0-12-800684-9.00017-4openalex-snapshot

The functional genome: epigenetics and epigenomics

inferred← citeshttps://doi.org/10.1016/b978-0-12-801238-3.65836-1openalex-snapshot

Excitotoxicity

inferred← citeshttps://doi.org/10.1016/b978-0-12-801893-4.00002-xopenalex-snapshot

Mechanisms underlying neurodegeneration in Huntington disease: applications to novel disease-modifying therapies

inferred← citeshttps://doi.org/10.1016/b978-0-12-801899-6.00026-7openalex-snapshot

Chromatin Landscape and Epigenetic Signatures in Neurological Disorders

inferred← citeshttps://doi.org/10.1016/b978-0-12-802206-1.00032-5openalex-snapshot

Epigenetics in Neuropathologies of the Basal Ganglia

inferred← citeshttps://doi.org/10.1016/b978-0-12-802206-1.00045-3openalex-snapshot

Cellular and Molecular Mechanisms of Neuronal Dysfunction in Huntington's Disease

inferred← citeshttps://doi.org/10.1016/b978-0-12-802208-5.00015-1openalex-snapshot

Predicting and Monitoring Responses to Epigenetic Drugs

inferred← citeshttps://doi.org/10.1016/b978-0-12-809324-5.00490-9openalex-snapshot

Expansion of a Polyglutamine Tract Within the Human Atrophin-1 Co-Repressor is Responsible for the DRPLA Disease☆

inferred← citeshttps://doi.org/10.1016/b978-0-12-811304-2.00007-9openalex-snapshot

Huntington’s Disease and Other Polyglutamine Repeat Diseases

inferred← citeshttps://doi.org/10.1016/b978-0-12-813796-3.00004-3openalex-snapshot

Epigenetic mechanisms in Huntington's disease

inferred← citeshttps://doi.org/10.1016/b978-0-12-816422-8.00013-1openalex-snapshot

Epigenetic treatment of neurodegenerative disorders

inferred← citeshttps://doi.org/10.1016/b978-0-12-823928-5.00040-2openalex-snapshot

Experimental approaches toward histone acetyltransferase modulators as therapeutics

inferred← citeshttps://doi.org/10.1016/b978-0-323-31071-0.00013-5openalex-snapshot

Huntington disease

inferred← citeshttps://doi.org/10.1016/b978-0-323-95672-7.00006-6openalex-snapshot

Systems biology study of Huntington's disease

inferred← citeshttps://doi.org/10.1016/b978-0-443-07941-2.50018-8openalex-snapshot

Huntington Disease

inferred← citeshttps://doi.org/10.1016/b978-0-444-51892-7.00041-3openalex-snapshot

Dentatorubral–pallidoluysian atrophy

inferred← citeshttps://doi.org/10.1016/b978-0-444-52002-9.00030-9openalex-snapshot

Huntington's disease

inferred← citeshttps://doi.org/10.1016/b978-0-444-52014-2.00002-1openalex-snapshot

Huntington's disease

inferred← citeshttps://doi.org/10.1016/b978-0-444-52014-2.00003-3openalex-snapshot

Molecular biology of Huntington's disease

inferred← citeshttps://doi.org/10.1016/b978-0-444-63233-3.00011-7openalex-snapshot

The CAG–polyglutamine repeat diseases: a clinical, molecular, genetic, and pathophysiologic nosology

inferred← citeshttps://doi.org/10.1016/b978-012088382-0/50009-8openalex-snapshot

Use of C. elegans to Model Human Movement Disorders

inferred← citeshttps://doi.org/10.1016/b978-012088382-0/50027-xopenalex-snapshot

Transgenic Rodent Models of Huntington Disease

inferred← citeshttps://doi.org/10.1016/b978-012088382-0/50056-6openalex-snapshot

SCA7 Mouse Models

inferred← citeshttps://doi.org/10.1016/b978-012369415-7/50023-5openalex-snapshot

Transplants of CNTF-producing Cells for the Treatment of Huntington's Disease

inferred← citeshttps://doi.org/10.1016/b978-012369437-9/50024-4openalex-snapshot

Trafficking Defects in Huntington's Disease

inferred← citeshttps://doi.org/10.1016/b978-012369462-1/50015-6openalex-snapshot

Molecular Pathogenesis and Therapeutic Targets in Huntington's Disease

inferred← citeshttps://doi.org/10.1016/b978-012369462-1/50027-2openalex-snapshot

Pathogenesis of Spinocerebellar Ataxia Type 7: New Insights from Mouse Models and Ataxin-7 Function

inferred← citeshttps://doi.org/10.1016/b978-012369462-1/50028-4openalex-snapshot

Spinocerebellar Ataxia Type 7: Clinical Features to Cellular Pathogenesis

inferred← citeshttps://doi.org/10.1016/b978-012369462-1/50034-xopenalex-snapshot

Polyalanine and Polyglutamine Diseases: Possible Common Mechanisms?

inferred← citeshttps://doi.org/10.1016/b978-012369462-1/50035-1openalex-snapshot

Chemical and Physical Properties of Polyglutamine Repeat Sequences

inferred← citeshttps://doi.org/10.1016/b978-012369509-3.50007-xopenalex-snapshot

Protein Misfolding, Chaperone Networks, and the Heat Shock Response in the Nervous System

inferred← citeshttps://doi.org/10.1016/b978-012369509-3.50019-6openalex-snapshot

Polyglutamine Disorders Including Huntington's Disease

inferred← citeshttps://doi.org/10.1016/b978-012373983-4.50017-1openalex-snapshot

TRANSCRIPTION FACTORS AND HUMAN DISEASE

inferred← citeshttps://doi.org/10.1016/b978-012373994-0.50013-0openalex-snapshot

GENE AND CELLULAR TRANSPLANTATION THERAPIES FOR HUNTINGTON'S DISEASE

inferred← citeshttps://doi.org/10.1016/b978-012437178-1/50015-1openalex-snapshot

Transcription Factors and Human Disease

inferred← citeshttps://doi.org/10.1016/b978-012566652-7/50007-1openalex-snapshot

Spinocerebellar Ataxia 3—Machado-Joseph Disease (SCA3)

inferred← citeshttps://doi.org/10.1016/b978-012566652-7/50018-6openalex-snapshot

Dentatorubral-Pallidoluysian Atrophy (DRPLA)

inferred← citeshttps://doi.org/10.1016/b978-012566652-7/50035-6openalex-snapshot

Molecular Biology of Huntington's Disease (HD) and HD-Like Disorders

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