A combination of genetic, electrophysiological, and modeling approaches reveals that presynaptic Rac1 is a key molecule that controls synaptic strength and plasticity by regulating the synaptic vesicle cycle steps controlling the number of fusion competent synaptic vesicles.

Asc1/RACK1 promotes the translation of mRNAs associated with the translational closed loop complex, which have short open reading frames and encode proteins required for core metabolic processes.

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.

The GLS2 enzyme suppresses cancer metastasis by interacting with the small GTPase Rac1 and inhibiting its activity.

Rings of actin polymerisation that form around PIP3/Ras patches in the cell membrane drive the formation of macropinocytic cups.

HIPK4 is a male germ cell-enriched kinase that regulates cytoskeletal rearrangements in spermatids during spermiogenesis and is required for male fertility in mice.

At gastrulation, mesoderm arises as a migratory germ layer that will participate to both foetal and placental development through region-dependant adaptation of cytoskeleton composition, cell shape and migration mode.

The cryo-electron microscopy structure of an assembly of the WAVE Regulatory Complex and its activator, the Rac GTPase, plus complementary biochemistry and biophysics, reveal a novel activation mechanism involving two distinct Rac binding sites.

An individual extracellular signal regulates multiple cellular actions through differences in the temporal dynamics of spatially distinct populations of the central signaling enzyme, extracellular-signal regulated kinase.

Non-core RAG regions, especially RAG1, maintain V(D)J recombination accuracy and genomic stability, reducing malignant characteristics and off-target recombination in BCR-ABL1⁺ B-cell acute lymphoblastic leukemia.