6WVW
Crystal structure of the R59P-SNAP25 containing SNARE complex
Summary for 6WVW
| Entry DOI | 10.2210/pdb6wvw/pdb |
| Descriptor | Vesicle-associated membrane protein 2, Syntaxin-1A, Synaptosomal-associated protein 25, ... (7 entities in total) |
| Functional Keywords | snare complex, synaptic vesicle fusion, exocytosis |
| Biological source | Rattus norvegicus (Rat) More |
| Total number of polymer chains | 8 |
| Total formula weight | 62087.74 |
| Authors | Zhou, Q.,White, K.I.,Brunger, A.T. (deposition date: 2020-05-07, release date: 2021-03-17, Last modification date: 2023-10-18) |
| Primary citation | Alten, B.,Zhou, Q.,Shin, O.H.,Esquivies, L.,Lin, P.Y.,White, K.I.,Sun, R.,Chung, W.K.,Monteggia, L.M.,Brunger, A.T.,Kavalali, E.T. Role of Aberrant Spontaneous Neurotransmission in SNAP25-Associated Encephalopathies. Neuron, 109:59-72.e5, 2021 Cited by PubMed Abstract: SNARE (soluble N-ethylmaleimide sensitive factor attachment protein receptor) complex, composed of synaptobrevin, syntaxin, and SNAP25, forms the essential fusion machinery for neurotransmitter release. Recent studies have reported several mutations in the gene encoding SNAP25 as a causative factor for developmental and epileptic encephalopathies of infancy and childhood with diverse clinical manifestations. However, it remains unclear how SNAP25 mutations give rise to these disorders. Here, we show that although structurally clustered mutations in SNAP25 give rise to related synaptic transmission phenotypes, specific alterations in spontaneous neurotransmitter release are a key factor to account for disease heterogeneity. Importantly, we identified a single mutation that augments spontaneous release without altering evoked release, suggesting that aberrant spontaneous release is sufficient to cause disease in humans. PubMed: 33147442DOI: 10.1016/j.neuron.2020.10.012 PDB entries with the same primary citation |
| Experimental method | X-RAY DIFFRACTION (2.11 Å) |
Structure validation
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