Different RhoA and Rac1 dynamics at the cell front and rear are coordinated through periodic GTPase waves, which define the minimal autonomous biochemical machinery necessary and sufficient for cell migration.

Glycosylation of flagellins with pseudaminic acid in the bacterial cytoplasm governed by an unknown type of modular glycosyltransferase harboring an N-terminal substrate binding domain and a C-terminal glycosyltransferase domain.

Presynaptic Rac1 inhibition in the hippocampus impairs spatial working memory, potentially by modulating the synaptic cytoskeleton and kinase-mediated phosphorylation of key synaptic vesicle proteins.

SNARE protein tomosyn differentially affects two main secretory pathways in mammalian neurons.

In vivo analysis of endogenously tagged Ca²⁺ channel subunits reveals unexpected differences in subunit composition and synapse-specific relationships between channel abundance and synaptic strength.

Doc2B functions in two distinct vesicle priming steps; membrane localization occludes upstream Ca2+-dependent priming, whereas Ca2+-binding and interaction with synaptotagmin-1, SNAREs, and Munc13-2 are involved in downstream priming, which makes vesicles readily releasable.

The SNAP-25 linker acts as a functional component of SNARE complexes, initially facilitating SNARE interactions and later promoting fusion triggering and pore evolution by local membrane contacts.

SNAP25 disease mutations within the synaptotagmin interface impair vesicle priming and cause uncontrolled spontaneous release due to enhanced SNARE:SNARE interactions, whereas a mutation within the SNARE-bundle increases the fusion energy barrier.

Neurodevelopmental critical periods act to integrate activity to encode homeostatic set points that remain fixed thereafter.

The amount of secreted Pgk1 is sharply decreased in Rtn4al/NogoA-overexpressed muscle cells, leading to various manifestations of neurodegenerative disease, including denervated neuromuscular junction and failed neurite outgrowth of motoneurons.