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In Focus

A biochemical approach reveals that α-actinin-4 and Arp2/3 team up to assemble actin at intercellular adhesions.

People & Ideas

Burridge studies how Rho proteins regulate everything from focal adhesions to leukocyte migration.



A systematic analysis revealed that the nuclear pore complex is extensively modified by ubiquitin and that ubiquitylation of the NPC component Nup159 is required for dynein light chain targeting to the NPC and proper nuclear segregation during mitosis.

PTEN nuclear entry driven by ubiquitination is mediated by the ligase-interacting protein Ndfip1 and is essential for neuronal survival in mice after cerebral ischemia.

Semaphorin 3A-mediated signaling and axonal repulsion in the mouse brain require Synaptobrevin-dependent vesicular traffic.


High-resolution time-lapse imaging of meiosis in C. elegans reveals stage-specific, dynein-driven chromosome motion that accelerates homologue pairing and triggers synapsis.

Drosophila EHBP1 is a novel regulator of Notch signaling that may function as an adaptor protein during the exocytosis and recycling of the Notch ligand Delta.

RAB-6.2, its effector LIN-10, and the retromer complex maintain synaptic strength by recycling postsynaptic glutamate receptors along the retrograde transport pathway.

Septins assemble on the cortex and restore normal cell shape by retracting aberrantly protruding membranes and promoting cortical contraction during amoeboid motility.

α-Actinin-4 plays an important role in coupling actin nucleation to assembly at cadherin-based cell–cell adhesive contacts.

Electron microscopy and crystallography studies of α4β7 integrin reveal the mechanism by which this atypical integrin enables rolling adhesion prior to integrin activation.

Cyclin A2 promotes RhoA activation, which inhibits cytoskeletal rearrangements and cell migration.

Extracellular proteolysis mediated by the uPA/PAI-1 system determines miR-21 expression in fibroblasts, which affects age-associated fibrogenesis and muscle deterioration in a muscular dystrophy model.


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