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    Albrecht et al. demonstrate that phosphorylation and methylation of the desmosomal protein desmoplakin is required for the proper assembly of intercellular adhesions. A mutation linked to arrhythmogenic cardiomyopathy abolishes one of desmoplakin’s methylation sites, and a version of the protein carrying this mutation (green) shows increased association with keratin intermediate filaments (red), thereby delaying its assembly into intercellular junctions. DNA is labeled blue.
    Image © 2015 Albrecht et al.
    See page 597.

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ISSN 0021-9525
EISSN 1540-8140
In this Issue

In This Issue

In Focus

Studies reveal mechanisms that reverse and then reactivate replication forks.

People & Ideas

Horwitz is leading the Allen Institute for Cell Science in its quest to comprehend the cell.

From the Archive

In 1981, Pollard and Mooseker used electron microscopy to measure the rate of actin polymerization.


Beyond the cell


Sall4 is important for the activation of ATM-dependent cellular responses to DNA double-stranded breaks (DSBs) in mouse embryonic stem cells and confers resistance to DSB-induced cytotoxicity.

New roles for the N-terminal histone tail and folded core of CENP-A are revealed by monitoring early steps in centromere establishment.

Transcripts encoding polarity factors such as Bni1 and Spa2 are nonrandomly clustered in the cytosol to initiate and maintain sites of polarized growth in the fungus Ashbya gossypii.


Following prolonged genotoxic stress, DNA2 and WRN functionally interact to degrade reversed replication forks and promote replication restart, thereby preventing aberrant processing of unresolved replication intermediates

Genotoxic treatments in human cells consistently induce uncoupling of replication forks and their remodeling into four-way junctions by the RAD51 recombinase.

Recurrent supra-ribosomal building blocks separated by ribosome-free mRNA regions form polysomes and reflect cellular translational activity.

Phosphorylation and methylation of desmoplakin are required for proper junction assembly and adhesion strengthening, and inhibition of these modifications might contribute to skin and heart diseases.

Interaction between K17 and hnRNP K regulates CXCR3 signaling in an RSK-dependent fashion to promote epithelial tumor cell growth and invasion.

DENND2B, in a complex with the Rab13 effector MICAL-L2, activates Rab13 at the cell periphery, promoting the dynamic remodeling of the cell’s leading edge during tumor cell migration both in vitro and in vivo.

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