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In Focus

A component of the nuclear envelope–spanning LINC complex maintains the integrity of epidermal cell adhesions.

People & Ideas

Schwille’s group breaks down cell phenomena into their simplest parts.




The Nek5 protein kinase contributes not only to uncoupling of the centrosome linker but also to integrity of the pericentriolar material and centrosomal microtubule nucleation, which together ensure the timely separation of centrosomes during early mitosis.

Hsp72 is a novel mitotic substrate of Nek6, and, together, these proteins play an essential role in assembly of robust mitotic spindles capable of efficient chromosome congression through K-fiber recruitment of the ch-TOG and TACC3 complex.

Myo2p is regulated by a head-to-tail interaction and defects in this regulatory mechanism lead to a host of cellular problems in vivo, including impaired cargo capture and delayed motor recycling

Rac1 promotes the rapid and dynamic localization of Formin-like 2 (FMNL2) to adherens junctions, where it promotes actin assembly.

Late endosome-loaded dynein–snapin complexes drive amphisome retrograde transport upon fusion of autophagosomes with late endosomes in distal axons.


During anaphase B, Imp1-mediated transport of the AAA-ATPase Cdc48 protein at the membrane domain surrounding the mitotic spindle midzone promotes spindle midzone dissolution in fission yeast.

The LINC complex component SUN2 contributes to the mechanical integrity of intercellular adhesions between mammalian epidermal keratinocytes.

Tau ablation, knockdown, and reconstitution studies in primary mouse neurons show that tau enables amyloid β oligomers to inhibit axonal transport through activation of GSK3β and through functions of tau that do not depend on its microtubule binding activity.

Rab27a controls the recruitment of phosphatidylinositol 4-kinase type 2α from endosomes to the plasma membrane, which promotes high levels of PI(4)P, fuels PI(4,5)P2 production, and favors the recruitment of Pr55Gag and HIV-1 assembly.

An alternative pathway triggering enhanced platelet release from bone marrow megakaryocytes via a rupture-based mechanism is regulated by IL-1α in response to acute platelet requirements.


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