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Mutant VAPB: Culprit or Innocent Bystander of Amyotrophic Lateral Sclerosis?
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- Contact (25152564), 2021, p. 1, doi. 10.1177/25152564211022515
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Mutant VAPB: Culprit or Innocent Bystander of Amyotrophic Lateral Sclerosis?
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- Contact (25152564), 2021, p. 1, doi. 10.1177/25152564211022515
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- Article
Mutant VAPB: Culprit or Innocent Bystander of Amyotrophic Lateral Sclerosis?
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- Contact (25152564), 2021, v. 4, p. 1, doi. 10.1177/25152564211022515
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TMEM30A is a candidate interacting partner for the β-carboxyl-terminal fragment of amyloid-β precursor protein in endosomes.
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- PLoS ONE, 2018, v. 13, n. 8, p. 1, doi. 10.1371/journal.pone.0200988
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- Article
ER Dynamics and Derangement in Neurological Diseases.
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- Frontiers in Neuroscience, 2018, p. 1, doi. 10.3389/fnins.2018.00091
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Intracellular seeded aggregation of mutant Cu,Zn-superoxide dismutase associated with amyotrophic lateral sclerosis.
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- FEBS Letters, 2013, v. 587, n. 16, p. 2500, doi. 10.1016/j.febslet.2013.06.046
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A Functional Null Mutation of SCN1B in a Patient with Dravet Syndrome.
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- Journal of Neuroscience, 2009, v. 29, n. 34, p. 10764, doi. 10.1523/JNEUROSCI.2475-09.2009
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Cross-Seeding Fibrillation of Q/N-Rich Proteins Offers New Pathomechanism of Polyglutamine Diseases.
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- Journal of Neuroscience, 2009, v. 29, n. 16, p. 5153, doi. 10.1523/JNEUROSCI.0783-09.2009
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Deranged Calcium Signaling and Neurodegeneration in Spinocerebellar Ataxia Type 3.
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- Journal of Neuroscience, 2008, v. 28, n. 48, p. 12713, doi. 10.1523/JNEUROSCI.3909-08.2008
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Suppression of Mutant Huntingtin Aggregate Formation by Cdk5/p35 through the Effect on Microtubule Stability.
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- Journal of Neuroscience, 2008, v. 28, n. 35, p. 8747, doi. 10.1523/JNEUROSCI.0973-08.2008
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The pathogenic mechanisms of polyglutamine diseases and current therapeutic strategies.
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- Journal of Neurochemistry, 2009, v. 110, n. 6, p. 1737, doi. 10.1111/j.1471-4159.2009.06302.x
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Induction of chemokines, MCP-1, and KC in the mutant huntingtin expressing neuronal cells because of proteasomal dysfunction.
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- Journal of Neurochemistry, 2009, v. 108, n. 3, p. 787, doi. 10.1111/j.1471-4159.2008.05823.x
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Pael-R transgenic mice crossed with parkin deficient mice displayed progressive and selective catecholaminergic neuronal loss.
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- Journal of Neurochemistry, 2008, v. 107, n. 1, p. 171, doi. 10.1111/j.1471-4159.2008.05607.x
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p45, an ATPase subunit of the 19S proteasome, targets the polyglutamine disease protein ataxin-3 to the proteasome.
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- Journal of Neurochemistry, 2007, v. 101, n. 6, p. 1651, doi. 10.1111/j.1471-4159.2007.04460.x
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Effects of human apolipoprotein E isoforms on the amyloid β-protein concentration and lipid composition in brain low-density membrane domains.
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- Journal of Neurochemistry, 2007, v. 101, n. 4, p. 949, doi. 10.1111/j.1471-4159.2006.04400.x
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Sodium channel β4 subunit: down-regulation and possible involvement in neuritic degeneration in Huntington's disease transgenic mice.
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- Journal of Neurochemistry, 2006, v. 98, n. 2, p. 518, doi. 10.1111/j.1471-4159.2006.03893.x
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Expanded polyglutamines impair synaptic transmission and ubiquitin–proteasome system in Caenorhabditis elegans.
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- Journal of Neurochemistry, 2006, v. 98, n. 2, p. 576, doi. 10.1111/j.1471-4159.2006.03895.x
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Decreased expression of hypothalamic neuropeptides in Huntington disease transgenic mice with expanded polyglutamine-EGFP fluorescent aggregates.
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- Journal of Neurochemistry, 2005, v. 93, n. 3, p. 641, doi. 10.1111/j.1471-4159.2005.03035.x
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Reappraisal of VAChT-Cre: Preference in slow motor neurons innervating type I or IIa muscle fibers.
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- Genesis: The Journal of Genetics & Development, 2016, v. 54, n. 11, p. 568, doi. 10.1002/dvg.22979
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Membrane microdomain switching: a regulatory mechanism of amyloid precursor protein processing.
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- Journal of Cell Biology, 2008, v. 183, n. 2, p. 339, doi. 10.1083/jcb.200804075
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Depletion of p62 reduces nuclear inclusions and paradoxically ameliorates disease phenotypes in Huntington’s model mice.
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- Human Molecular Genetics, 2015, v. 24, n. 4, p. 1092, doi. 10.1093/hmg/ddu522
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Nuclear localization of MBNL1: splicing-mediated autoregulation and repression of repeat-derived aberrant proteins.
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- Human Molecular Genetics, 2015, v. 24, n. 3, p. 740, doi. 10.1093/hmg/ddu492
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Dexamethasone induces heat shock response and slows down disease progression in mouse and fly models of Huntington's disease.
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- Human Molecular Genetics, 2014, v. 23, n. 10, p. 2737, doi. 10.1093/hmg/ddt667
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Mutant huntingtin fragment selectively suppresses Brn-2 POU domain transcription factor to mediate hypothalamic cell dysfunction.
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- Human Molecular Genetics, 2010, v. 19, n. 11, p. 2099, doi. 10.1093/hmg/ddq087
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Knock-down of PQBP1 impairs anxiety-related cognition in mouse.
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- Human Molecular Genetics, 2009, v. 18, n. 22, p. 4239, doi. 10.1093/hmg/ddp378
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Mutant SOD1 impairs axonal transport of choline acetyltransferase and acetylcholine release by sequestering KAP3.
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- Human Molecular Genetics, 2009, v. 18, n. 5, p. 942, doi. 10.1093/hmg/ddn422
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Blocking acid-sensing ion channel 1 alleviates Huntington's disease pathology via an ubiquitin-proteasome system-dependent mechanism.
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- Human Molecular Genetics, 2008, v. 17, n. 20, p. 3223, doi. 10.1093/hmg/ddn218
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Autophagy-mediated clearance of aggresomes is not a universal phenomenon.
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- Human Molecular Genetics, 2008, v. 17, n. 16, p. 2570, doi. 10.1093/hmg/ddn157
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Dosage-dependent over-expression of genes in the trisomic region of Ts1Cje mouse model for Down syndrome.
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- Human Molecular Genetics, 2004, v. 13, n. 13, p. 1333, doi. 10.1093/hmg/ddh154
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NF-Y inactivation causes atypical neurodegeneration characterized by ubiquitin and p62 accumulation and endoplasmic reticulum disorganization.
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- Nature Communications, 2014, v. 5, n. 2, p. 3354, doi. 10.1038/ncomms4354
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Multiple system degeneration with basophilic inclusions in Japanese ALS patients with FUS mutation.
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- Acta Neuropathologica, 2010, v. 119, n. 3, p. 355, doi. 10.1007/s00401-009-0621-1
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FUS/TLS deficiency causes behavioral and pathological abnormalities distinct from amyotrophic lateral sclerosis.
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- Acta Neuropathologica Communications, 2015, v. 3, n. 1, p. 1, doi. 10.1186/s40478-015-0202-6
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ROCK-phosphorylated vimentin modifies mutant huntingtin aggregation via sequestration of IRBIT.
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- Molecular Neurodegeneration, 2012, v. 7, n. 1, p. 43, doi. 10.1186/1750-1326-7-43
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Increased expression of p62 in expanded polyglutamine-expressing cells and its association with polyglutamine inclusions.
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- Journal of Neurochemistry, 2004, v. 91, n. 1, p. 57, doi. 10.1111/j.1471-4159.2004.02692.x
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Pro-apoptotic protein kinase Cδ is associated with intranuclear inclusions in a transgenic model of Huntington's disease.
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- Journal of Neurochemistry, 2003, v. 87, n. 2, p. 395, doi. 10.1046/j.1471-4159.2003.02002.x
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Aggregate formation and the impairment of long-term synaptic facilitation by ectopic expression of mutant huntingtin in Aplysia neurons.
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- Journal of Neurochemistry, 2003, v. 85, n. 1, p. 160, doi. 10.1046/j.1471-4159.2003.01650.x
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α-Synuclein forms a complex with transcription factor Elk-1.
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- Journal of Neurochemistry, 2001, v. 77, n. 1, p. 239, doi. 10.1046/j.1471-4159.2001.00232.x
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The Parkinson’s Disease-Associated Protein Kinase LRRK2 Modulates Notch Signaling through the Endosomal Pathway.
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- PLoS Genetics, 2015, v. 11, n. 9, p. 1, doi. 10.1371/journal.pgen.1005503
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Phosphorylation of Mitochondrial Polyubiquitin by PINK1 Promotes Parkin Mitochondrial Tethering.
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- PLoS Genetics, 2014, v. 10, n. 12, p. 1, doi. 10.1371/journal.pgen.1004861
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Quantum-dot-labeled synuclein seed assay identifies drugs modulating the experimental prion-like transmission.
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- Communications Biology, 2022, v. 5, n. 1, p. 1, doi. 10.1038/s42003-022-03590-8
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Harnessing chaperone-mediated autophagy for the selective degradation of mutant huntingtin protein.
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- Nature Biotechnology, 2010, v. 28, n. 3, p. 256, doi. 10.1038/nbt.1608
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Hornerin deposits in neuronal intranuclear inclusion disease: direct identification of proteins with compositionally biased regions in inclusions.
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- Acta Neuropathologica Communications, 2022, v. 10, n. 1, p. 1, doi. 10.1186/s40478-022-01333-8
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Proteomics-Based Approach Identifies Altered ER Domain Properties by ALS-Linked VAPB Mutation.
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- Scientific Reports, 2020, v. 10, n. 1, p. 1, doi. 10.1038/s41598-020-64517-z
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Large-Scale RNA Interference Screening in Mammalian Cells Identifies Novel Regulators of Mutant Huntingtin Aggregation.
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- PLoS ONE, 2014, v. 9, n. 4, p. 1, doi. 10.1371/journal.pone.0093891
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Loss of aPKCλ in Differentiated Neurons Disrupts the Polarity Complex but Does Not Induce Obvious Neuronal Loss or Disorientation in Mouse Brains.
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- PLoS ONE, 2013, v. 8, n. 12, p. 1, doi. 10.1371/journal.pone.0084036
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RNAi Screening in Drosophila Cells Identifies New Modifiers of Mutant Huntingtin Aggregation.
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- PLoS ONE, 2009, v. 4, n. 9, p. 1, doi. 10.1371/journal.pone.0007275
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Acidic mammalian chitinase is a proteases-resistant glycosidase in mouse digestive system.
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- Scientific Reports, 2016, p. 37756, doi. 10.1038/srep37756
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FUS/TLS acts as an aggregation-dependent modifier of polyglutamine disease model mice.
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- Scientific Reports, 2016, p. 35236, doi. 10.1038/srep35236
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Differential roles of NF-Y transcription factor in ER chaperone expression and neuronal maintenance in the CNS.
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- Scientific Reports, 2016, p. 34575, doi. 10.1038/srep34575
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Structure-based site-directed photo-crosslinking analyses of multimeric cell-adhesive interactions of voltage-gated sodium channel β subunits.
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- Scientific Reports, 2016, p. 26618, doi. 10.1038/srep26618
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