During an action potential, Ca 2+ entering a presynaptic terminal triggers synaptic vesicle
exocytosis and neurotransmitter release in less than a millisecond. How does Ca 2+ …

SNARE proteins and Sec1/Munc18 (SM) proteins constitute the core molecular engine that
drives nearly all intracellular membrane fusion and exocytosis. While SNAREs are known to …

Tau (MAPT) drives neuronal dysfunction in Alzheimer disease (AD) and other tauopathies.
To dissect the underlying mechanisms, we combined an engineered ascorbic acid …

The two universally required components of the intracellular membrane fusion machinery,
SNARE and SM (Sec1/Munc18-like) proteins, play complementary roles in fusion. Vesicular …

Most neuronal communication relies upon the synchronous release of neurotransmitters,
which occurs through synaptic vesicle exocytosis triggered by action potential invasion of a …

Extensive research has yielded crucial insights into the mechanism of neurotransmitter
release, and working models for the functions of key proteins involved in release. The …

Presynaptic nerve terminals release neurotransmitters by synaptic vesicle exocytosis.
Membrane fusion mediating synaptic exocytosis and other intracellular membrane traffic is …

Research for three decades and major recent advances have provided crucial insights into
how neurotransmitters are released by Ca2+‐triggered synaptic vesicle exocytosis, leading …

Intracellular membrane fusion is mediated in most cases by membrane-bridging complexes
of soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) …

Neurotransmitter release depends critically on Munc18-1, Munc13, the Ca2+ sensor
synaptotagmin-1, and the soluble N-ethylmaleimide–sensitive factor (NSF) attachment …