Associated Papers
SNAP-25 disease variants affect synaptic transmission by destabilizing SNARE complexes within a multimeric SNARE ring.
Vold VA et al.
Cell Reports, 2026
Vesicle trafficking with snares: a perspective for autism.
Özdemir Ç et al.
Molecular Biology Reports, 2022
Energetics, kinetics, and pathways of SNARE assembly in membrane fusion.
Zhang Y et al.
Critical Reviews in Biochemistry and Molecular Biology, 2022
SNAP25 mutation disrupts metabolic homeostasis, steroid hormone production and central neurobehavior.
Hao X et al.
Biochimica Et Biophysica Acta. Molecular Basis of Disease, 2022
Chaperoning SNARE Folding and Assembly.
Zhang Y et al.
Annual Review of Biochemistry, 2021
Presynaptic dysfunction in neurodevelopmental disorders: Insights from the synaptic vesicle life cycle.
Bonnycastle K et al.
Journal of Neurochemistry, 2021
Neuronal SNARE complex: A protein folding system with intricate protein-protein interactions, and its common neuropathological hallmark, SNAP25.
Karmakar S et al.
Neurochemistry International, 2019
Two Disease-Causing SNAP-25B Mutations Selectively Impair SNARE C-terminal Assembly.
Rebane AA et al.
Journal of Molecular Biology, 2018
Mutant SNAP25B causes myasthenia, cortical hyperexcitability, ataxia, and intellectual disability.
Shen XM et al.
Neurology, 2014
Mutation in SNAP25 as a novel genetic cause of epilepsy and intellectual disability.
Rohena L et al.
Rare Diseases (austin, Tex.), 2013
Interaction between environmental and genetic factors modulates schizophrenic endophenotypes in the Snap-25 mouse mutant blind-drunk.
Oliver PL et al.
Human Molecular Genetics, 2009
SNAP-25 in neuropsychiatric disorders.
Corradini I et al.
Annals of the New York Academy of Sciences, 2009
A dominant mutation in Snap25 causes impaired vesicle trafficking, sensorimotor gating, and ataxia in the blind-drunk mouse.
Jeans AF et al.
Proceedings of the National Academy of Sciences of the United States of America, 2007
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