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    When the tumor suppressor Lkb1 is inhibited in explants of embryonic pancreas, epithelial structures that resemble precancerous lesions are formed even though cell polarity—indicated by actin (red) and the basolateral marker EpCAM (green)—remains intact. Lo et al. use chemical genetics and ex vivo cultures to identify distinct Lkb1-dependent pathways in tissue morphogenesis and cancer development.
    Image © 2012 Lo et al.
    See page 1117.

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ISSN 0021-9525
EISSN 1540-8140
In this Issue

In This Issue

In Focus

Study uses chemical genetics and embryonic explants to reveal kinase’s tissue-specific functions.

People & Ideas

Tsai studies how Cdk5 activity affects brain development, learning, and memory.

Review

Report

In vivo imaging reveals that CSB and XPC promote the repair of oxidative DNA lesions independent of the canonical nucleotide excision repair process.

Independent of their role in apoptosis, cell engulfment proteins are essential for midbody internalization and degradation after cell division.

The Golgi resident protein Cab45 is required for trans-Golgi network Ca2+ homeostasis and sorting of cargos that are destined for secretion.

Article

The chromatin remodeling enzyme p400 forms a complex with Rad51 and is required for its recruitment to double-strand breaks during DNA repair by homologous recombination.

Cep164 provides a molecular link between the mother centriole and the ciliary membrane biogenesis machinery by interacting with the GEF Rabin8 and the GTPase Rab8.

VEGF causes translocation of Syx from endothelial cell junctions, promoting junction disassembly, whereas Angtiopoietin-1 maintains Syx at the junctions and stabilizes them.

A combination of ex vivo embryonic tissue culture, genetic manipulation, and chemical genetics reveals novel details of Lkb1-mediated regulation of tissue morphogenesis.

Tao initiates morphogenesis of a squamous epithelium by promoting the endocytosis of the adhesion molecule Fasciclin 2 from the lateral membrane.

Plasma membrane calcium ATPases PMCA1 and PMCA4 regulate osteoclast differentiation and survival by regulating NFATc1 and NO.

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