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Neurological disease: UPS stops delivering!
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scholarly article
1 reference
stated in
Europe PubMed Central
PubMed ID
12498726
retrieved
5 August 2017
review article
1 reference
stated in
Europe PubMed Central
title
Neurological disease: UPS stops delivering!
(English)
1 reference
stated in
Europe PubMed Central
PubMed ID
12498726
retrieved
5 August 2017
author name string
Richard J Miller
series ordinal
1
1 reference
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Europe PubMed Central
PubMed ID
12498726
retrieved
5 August 2017
Scott M Wilson
series ordinal
2
1 reference
stated in
Europe PubMed Central
PubMed ID
12498726
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5 August 2017
publication date
1 January 2003
1 reference
stated in
Europe PubMed Central
PubMed ID
12498726
retrieved
5 August 2017
published in
Trends in Pharmacological Sciences
1 reference
stated in
Europe PubMed Central
PubMed ID
12498726
retrieved
5 August 2017
volume
24
1 reference
stated in
Europe PubMed Central
PubMed ID
12498726
retrieved
5 August 2017
page(s)
18-23
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stated in
Europe PubMed Central
PubMed ID
12498726
retrieved
5 August 2017
issue
1
1 reference
stated in
Europe PubMed Central
PubMed ID
12498726
retrieved
5 August 2017
cites work
The ubiquitin system
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Ubiquitin--more than just a signal for protein degradation.
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GABA(A) receptor cell surface number and subunit stability are regulated by the ubiquitin-like protein Plic-1
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Aggregates in neurodegenerative disease: crowds and power?
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Ubiquitin, cellular inclusions and their role in neurodegeneration
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Impairment of the ubiquitin-proteasome system by protein aggregation
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Deadly encounter: ubiquitin meets apoptosis
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Frameshift mutants of beta amyloid precursor protein and ubiquitin-B in Alzheimer's and Down patients
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Inhibition of the ubiquitin-proteasome system in Alzheimer's disease.
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Mutant ubiquitin expressed in Alzheimer's disease causes neuronal death.
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Mutant ubiquitin found in neurodegenerative disorders is a ubiquitin fusion degradation substrate that blocks proteasomal degradation
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Impaired proteasome function in Alzheimer's disease
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7 January 2021
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Endoproteolytic cleavage and proteasomal degradation of presenilin 2 in transfected cells
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Cellular defenses against unfolded proteins: a cell biologist thinks about neurodegenerative diseases
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7 January 2021
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Expanding our understanding of polyglutamine diseases through mouse models
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Glutamine repeats and neurodegeneration
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The selective vulnerability of striatopallidal neurons
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7 January 2021
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Mutation of the E6-AP ubiquitin ligase reduces nuclear inclusion frequency while accelerating polyglutamine-induced pathology in SCA1 mice.
1 reference
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Imprinted expression of the murine Angelman syndrome gene, Ube3a, in hippocampal and Purkinje neurons.
1 reference
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7 January 2021
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Mutation of the Angelman ubiquitin ligase in mice causes increased cytoplasmic p53 and deficits of contextual learning and long-term potentiation.
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https://api.crossref.org/works/10.1016%2FS0165-6147%2802%2900011-1
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Huntingtin acts in the nucleus to induce apoptosis but death does not correlate with the formation of intranuclear inclusions.
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A long CAG repeat in the mouse Sca1 locus replicates SCA1 features and reveals the impact of protein solubility on selective neurodegeneration.
1 reference
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Crossref
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https://api.crossref.org/works/10.1016%2FS0165-6147%2802%2900011-1
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Identification of genes that modify ataxin-1-induced neurodegeneration.
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https://api.crossref.org/works/10.1016%2FS0165-6147%2802%2900011-1
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Parkin and the molecular pathways of Parkinson's disease
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https://api.crossref.org/works/10.1016%2FS0165-6147%2802%2900011-1
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Alpha-synuclein in Lewy bodies
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The synucleins: a family of proteins involved in synaptic function, plasticity, neurodegeneration and disease.
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Mutation in the alpha-synuclein gene identified in families with Parkinson's disease
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Glutathione decreases in dopaminergic PC12 cells interfere with the ubiquitin protein degradation pathway: relevance for Parkinson's disease?
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The A53T alpha-synuclein mutation increases iron-dependent aggregation and toxicity
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Induction of alpha-synuclein aggregation by intracellular nitrative insult.
1 reference
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https://api.crossref.org/works/10.1016%2FS0165-6147%2802%2900011-1
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Formation and removal of alpha-synuclein aggregates in cells exposed to mitochondrial inhibitors
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Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism
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Ubiquitination of a new form of alpha-synuclein by parkin from human brain: implications for Parkinson's disease
1 reference
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reference URL
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Parkin ubiquitinates the alpha-synuclein-interacting protein, synphilin-1: implications for Lewy-body formation in Parkinson disease
1 reference
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Crossref
reference URL
https://api.crossref.org/works/10.1016%2FS0165-6147%2802%2900011-1
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An unfolded putative transmembrane polypeptide, which can lead to endoplasmic reticulum stress, is a substrate of Parkin
1 reference
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Crossref
reference URL
https://api.crossref.org/works/10.1016%2FS0165-6147%2802%2900011-1
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7 January 2021
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Parkin localizes to the Lewy bodies of Parkinson disease and dementia with Lewy bodies
1 reference
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Crossref
reference URL
https://api.crossref.org/works/10.1016%2FS0165-6147%2802%2900011-1
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7 January 2021
based on heuristic
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Inducible expression of mutant alpha-synuclein decreases proteasome activity and increases sensitivity to mitochondria-dependent apoptosis
1 reference
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Crossref
reference URL
https://api.crossref.org/works/10.1016%2FS0165-6147%2802%2900011-1
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Rat alpha-synuclein interacts with Tat binding protein 1, a component of the 26S proteasomal complex
1 reference
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Crossref
reference URL
https://api.crossref.org/works/10.1016%2FS0165-6147%2802%2900011-1
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7 January 2021
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Failure of the ubiquitin-proteasome system in Parkinson's disease
1 reference
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Crossref
reference URL
https://api.crossref.org/works/10.1016%2FS0165-6147%2802%2900011-1
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7 January 2021
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The ubiquitin pathway in Parkinson's disease.
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A polymorphic variation of serine to tyrosine at codon 18 in the ubiquitin C-terminal hydrolase-L1 gene is associated with a reduced risk of sporadic Parkinson's disease in a Japanese population
1 reference
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Crossref
reference URL
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Intragenic deletion in the gene encoding ubiquitin carboxy-terminal hydrolase in gad mice
1 reference
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Crossref
reference URL
https://api.crossref.org/works/10.1016%2FS0165-6147%2802%2900011-1
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Loss of Uch-L1 and Uch-L3 leads to neurodegeneration, posterior paralysis and dysphagia
1 reference
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Crossref
reference URL
https://api.crossref.org/works/10.1016%2FS0165-6147%2802%2900011-1
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Calcium channels prove to be a real headache
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Ubiquitination-dependent mechanisms regulate synaptic growth and function.
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Fat facets does a Highwire act at the synapse.
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https://api.crossref.org/works/10.1016%2FS0165-6147%2802%2900011-1
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Synaptic defects in ataxia mice result from a mutation in Usp14, encoding a ubiquitin-specific protease
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+1 Proteins and aging
1 reference
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https://api.crossref.org/works/10.1016%2FS0165-6147%2802%2900011-1
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Polyglutamine pathogenesis: emergence of unifying mechanisms for Huntington's disease and related disorders
1 reference
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https://api.crossref.org/works/10.1016%2FS0165-6147%2802%2900011-1
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7 January 2021
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Identifiers
DOI
10.1016/S0165-6147(02)00011-1
1 reference
stated in
Europe PubMed Central
PubMed ID
12498726
retrieved
5 August 2017
PubMed ID
12498726
1 reference
stated in
Europe PubMed Central
PubMed ID
12498726
retrieved
5 August 2017
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