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    On the cover
    Human umbilical vein endothelial cells stained for VE-cadherin (green), F-actin (red), and DNA (blue) align in the direction of fluid flow (left to right). Coon et al. demonstrate that the transmembrane domain of VE-cadherin allows endothelial cells to respond to fluid shear stress by binding to the transmembrane domains of VEGFR2 and VEGFR3, recruiting these proteins into a mechanosensory complex with the adhesion molecule PECAM-1.
    Image © 2015 Coon et al.
    See page 975.

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ISSN 0021-9525
EISSN 1540-8140
In this Issue

In This Issue

In Focus

Study describes how the adhesion molecule’s transmembrane domain helps endothelial cells respond to fluid shear stress.

People & Ideas

Zurzolo studies the trafficking of GPI-anchored proteins and how this links to human disease.

From the Archive

In 2008, Narendra et al. revealed that a protein associated with Parkinson’s disease promotes the turnover of dysfunctional mitochondria.



The mitotic checkpoint protein Spindly is farnesylated in vivo and this modification is required for its interaction with the RZZ complex and its localization to kinetochores.

The formin Fus1 nucleates a novel actin structure in fission yeast, named the actin fusion focus, which consists of an aster of actin filaments whose barbed ends are focalized at a membrane proximal site and serves to focalize cell wall hydrolase delivery for cell fusion.

YB-1, which is upregulated in human sarcomas, controls the availability of the stress granule nucleator G3BP1 and thereby controls stress granule assembly.

Rab8, POSH, and TAK1 regulate synaptic growth responses, which suggests that recycling endosomes are key compartments for synaptic growth regulation in neurodegenerative processes.

Expression of the Gria1-targeting miRNA miR-501-3p is increased locally in dendrites after NMDAR activation and is required for NMDAR-dependent inhibition of GluA1 expression and long-lasting spine shrinkage and elimination.

WISp39 associates with Hsp90, Coronin 1B, and Slingshot phosphatase to regulate Cofilin activation and Arp2/3 complex localization at the leading edge of migrating cells.

VE-cadherin plays a critical role in endothelial shear stress mechanotransduction by interacting with VEGFRs through their transmembrane domains.

CCM2–CCM3 interactions protect CCM2 and CCM3 from proteasomal degradation, and both CCM2 and CCM3 are required for normal endothelial cell network formation.

Targeted domain-specific mutations and cell type–specific rescue experiments show that L1CAM/Neuroglian is required for axon–axon interactions and yield insights into the cellular mechanisms controlling establishment of the complex mushroom body architecture.

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