α-Synuclein Promotes SNARE-Complex Assembly in Vivo and in Vitro

By Jacqueline Burré, Manu Sharma, Theodoros Tsetsenis, V. Buchman, M. Etherton, T. Sūdhof. Science, 2010

1,587 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/34252b82057ae53927524418a402ca2e516486f1

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Citations in the corpus

Autophagy and apoptosis dysfunction in neurodegenerative disorders. (2014, positive): “Alpha-syn seems to act as a molecular chaperone for SNARE synaptic proteins (Burre et al., 2010; Chandra et al., 2005).”
A new pathway for mitochondrial quality control: mitochondrial‐derived vesicles (2014, background): “While a functional role for a-synuclein has been proposed in the assembly of presynaptic SNARE complexes (Chandra et al, 2005; Burre et al, 2010; Diao et al, 2013), a-synuclein has also been shown to function at mitochondria.”
Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, positive): “Concerning the mechanism of this functional interaction it has been demonstrated that a -synuclein directly promotes the assembly of SNARE complexes by simultaneous binding to phospholipids via its N-terminal region and to synaptobrevin-2 via its C-terminal domain (Burre et al , 2010; Figure 4).”
Dopamine release in the basal ganglia (2011, result): “These data suggest that synucleins limit vesicular DA release through mechanisms that differ from those indicated for other transmitters in separate studies also using TKOs (e.g., Burre et al., 2010; Greten-Harrison et al., 2010).”
Exogenous α-Synuclein Fibrils Induce Lewy Body Pathology Leading to Synaptic Dysfunction and Neuron Death (2011, positive): “Alterations in the expression and localization of these proteins occurs upon ablation of all three synuclein family members or overexpression of α-syn (Burre et al., 2010; GretenHarrison et al., 2010; Nemani et al., 2010).”
Neurotransmitter Release: The Last Millisecond in the Life of a Synaptic Vesicle (2013, background): “This evidence includes the observation that a-synuclein, which is centrally involved in multiple neurodegenerative disorders including Parkinson’s disease, is a SNARE complex assembly chaperone (Burré et al., 2010), the finding that the SM protein Munc18-1 is frequently mutated in Ohtahara syndrome ”
Oxidative stress in the aging substantia nigra and the etiology of Parkinson's disease (2019, background): “The fusion and clustering of tSNARE‐as‐ sociated vesicles to the presynaptic membrane is also regulated by an interaction of α‐synuclein with VAMP2 in the presynaptic termi‐ nal (Burre et al., 2010), which keeps VAMP2 in close proximity to tSNAREs to regulate neurotransmitter release.”