CSPα knockout causes neurodegeneration by impairing SNAP-25 function
about
J protein mutations and resulting proteostasis collapseUbiquitin-Synaptobrevin Fusion Protein Causes Degeneration of Presynaptic Motor Terminals in MiceDynamic binding mode of a Synaptotagmin-1-SNARE complex in solutionLatrophilins function as heterophilic cell-adhesion molecules by binding to teneurins: regulation by alternative splicingNeurotransmitter release: the last millisecond in the life of a synaptic vesicleSystematic mutagenesis of α-synuclein reveals distinct sequence requirements for physiological and pathological activitiesSNAP-25, a Known Presynaptic Protein with Emerging Postsynaptic FunctionsExpanding proteostasis by membrane trafficking networksSynaptic vesicle recycling: steps and principlesAPP is cleaved by Bace1 in pre-synaptic vesicles and establishes a pre-synaptic interactome, via its intracellular domain, with molecular complexes that regulate pre-synaptic vesicles functionsActivity-Dependent Degradation of Synaptic Vesicle Proteins Requires Rab35 and the ESCRT PathwayCaenorhabditis elegans dnj-14, the orthologue of the DNAJC5 gene mutated in adult onset neuronal ceroid lipofuscinosis, provides a new platform for neuroprotective drug screening and identifies a SIR-2.1-independent action of resveratrol.Leveraging existing data sets to generate new insights into Alzheimer's disease biology in specific patient subsets.Roles of tau protein in health and disease.Post translational changes to α-synuclein control iron and dopamine trafficking; a concept for neuron vulnerability in Parkinson's disease.Phosphomimetic mutation of cysteine string protein-α increases the rate of regulated exocytosis by modulating fusion pore dynamics in PC12 cells.Oligomerization of Cysteine String Protein alpha mutants causing adult neuronal ceroid lipofuscinosis.Cytotoxicity of botulinum neurotoxins reveals a direct role of syntaxin 1 and SNAP-25 in neuron survival.Septin dynamics are essential for exocytosisReduced expression of the presynaptic co-chaperone cysteine string protein alpha (CSPα) does not exacerbate experimentally-induced ME7 prion diseaseIncreased Expression of the Large Conductance, Calcium-Activated K+ (BK) Channel in Adult-Onset Neuronal Ceroid LipofuscinosisCysteine string protein α: a new role in vesicle recyclingReplacing SNAP-25b with SNAP-25a expression results in metabolic disease.NMNAT2:HSP90 Complex Mediates Proteostasis in Proteinopathies.Expression profile of a Caenorhabditis elegans model of adult neuronal ceroid lipofuscinosis reveals down regulation of ubiquitin E3 ligase components.Clinically early-stage CSPα mutation carrier exhibits remarkable terminal stage neuronal pathology with minimal evidence of synaptic loss.Palmitoylation-induced aggregation of cysteine-string protein mutants that cause neuronal ceroid lipofuscinosisContrasting effects of α-synuclein and γ-synuclein on the phenotype of cysteine string protein α (CSPα) null mutant mice suggest distinct function of these proteins in neuronal synapses.α-Synuclein membrane association is regulated by the Rab3a recycling machinery and presynaptic activity.Lysosomal dysfunction disrupts presynaptic maintenance and restoration of presynaptic function prevents neurodegeneration in lysosomal storage diseases.An extracellular mechanism that can explain the neurotoxic effects of α-synuclein aggregates in the brainThe function of α-synuclein.CSPα-chaperoning presynaptic proteins.The molecular machinery of neurotransmitter release (Nobel lecture).Cysteine string protein (CSP) and its role in preventing neurodegeneration.The evolving spectrum of PRRT2-associated paroxysmal diseases.Primary fibroblasts from CSPα mutation carriers recapitulate hallmarks of the adult onset neuronal ceroid lipofuscinosis.DnaJ/Hsc70 chaperone complexes control the extracellular release of neurodegenerative-associated proteins.SNAP-25 is abundantly expressed in enteric neuronal networks and upregulated by the neurotrophic factor GDNF.In Situ Peroxidase Labeling and Mass-Spectrometry Connects Alpha-Synuclein Directly to Endocytic Trafficking and mRNA Metabolism in Neurons.
P2860
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P2860
CSPα knockout causes neurodegeneration by impairing SNAP-25 function
description
2012 nî lūn-bûn
@nan
2012 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2012 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
name
CSPα knockout causes neurodegeneration by impairing SNAP-25 function
@ast
CSPα knockout causes neurodegeneration by impairing SNAP-25 function
@en
CSPα knockout causes neurodegeneration by impairing SNAP-25 function
@nl
type
label
CSPα knockout causes neurodegeneration by impairing SNAP-25 function
@ast
CSPα knockout causes neurodegeneration by impairing SNAP-25 function
@en
CSPα knockout causes neurodegeneration by impairing SNAP-25 function
@nl
prefLabel
CSPα knockout causes neurodegeneration by impairing SNAP-25 function
@ast
CSPα knockout causes neurodegeneration by impairing SNAP-25 function
@en
CSPα knockout causes neurodegeneration by impairing SNAP-25 function
@nl
P2093
P2860
P3181
P356
P1433
P1476
CSPα knockout causes neurodegeneration by impairing SNAP-25 function
@en
P2093
Manu Sharma
Peter Bronk
Yingsha Zhang
P2860
P304
P3181
P356
10.1038/EMBOJ.2011.467
P407
P577
2012-02-15T00:00:00Z