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In Focus

Protein network strengthens cell–cell contacts, promoting pluripotency.

People & Ideas

Nachury studies how defective signaling from the cell's antenna causes human disease.


Review series


Arp2/3 actin filament nucleating complex drives circumnavigation of cortical actin clusters during mitosis.

The high-resolution structure of doublecortin-stabilized microtubules provides unprecedented insight into their in vivo architecture.

An automated, image-based RNAi screen for cell shape reveals roles for membrane secretion factors in cell spreading.


CrebA up-regulates expression of both the general protein machinery required in all cells for secretion and genes encoding cell type–specific secreted components.

Localization and activation of Elm1 at the bud neck coordinates SPC activity with mother–daughter polarity during cell division.

Pom121 anchors core structures of the NPC to the membrane through its binding to the β-propeller domains of Nup155 and Nup160.

Orai1 trafficking between the cell membrane and endosomes during meiosis requires caveolin and is important for tuning calcium signaling during oocyte maturation.

Inactivation of the essential autophagy gene Atg5 results in selective accumulation of aggregation-prone proteins independently of substrate ubiquitination.

A temperature-sensitive chimeric transmembrane protein reveals a mechanism for disposing misfolded proteins that make it to the plasma membrane.

Visualization of VASP tetramers interacting with static and growing actin filaments in vitro by TIRF microscopy leads to a new model for VASP-mediated actin filament assembly.

The small GTPase Cdc42 regulates interactions of dynein with microtubules through the polarity protein Dlg1 and the scaffolding protein GKAP.

Posttranslational lipid modifications promote association of Syt VII with the tetraspanin CD63, determining its exit from the Golgi and targeting to lysosomes.

Identification of the pathway by which caveolin-1 is degraded when caveolae assembly is compromised suggests that “caveosomes” may be endosomal accumulations of the protein awaiting degradation.

Nonmuscle myosin IIA and p120-catenin control E-cadherin–mediated cell–cell adhesions essential for hESC pluripotency and long-term survival.

EpCAM confers “invasive” properties to embryonic cells through intracellular signaling.

Inhibition of Cdc42 by dRich induces postsynaptic release of the BMP ligand Glass bottom boat.

Neutrophil elastase escapes azurophilic granules, translocates to the nucleus, and degrades histones to promote chromatin decondensation necessary for NET formation.

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