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Steadily growing cells prepare for conditions that demand increased translation by producing excess ribosomes, at the expense of lower steady-state growth rate.

Calcium overload in cardiomyocytes disrupts sarcomere integrity, by stimulating transcriptional upregulation of the E3 ubiquitin ligase MuRF1.

Localized feedback on Fa4-Ds1 boundary complexes underlies polarized distribution of Fat4 and Ds1 and gives rise to planar cell polarity.

Proteins of the reticulon and REEP families, homologous to the products of human Hereditary Spastic Paraplegia disease genes, contribute to shaping and continuity of the axonal endoplasmic reticulum network in Drosophila.

PTEN organizes multicellular architecture by non-catalytic scaffolding of spatially localized β-Arrestin1/ARHGAP21/Cdc42 protein complexes to control mitotic spindle orientation, multicellular configuration and lumen formation.

GDE3 is a transmembrane GPI-specific phospholipase C that sheds the urokinase receptor (uPAR) from the cell surface resulting in loss of uPAR function in breast cancer cells and reduced tumor growth.

Signal-peptide cleavage of HIV-1 envelope glycoprotein is delayed because of alpha-helical structure covering the cleavage site, effecting early cleavage alters the folding pathway and resulting in localized misfolding and reduced viral fitness.

Global transcriptome changes, particularly alternative splicing, are highly dynamic the first 2 weeks after birth, and the example of calcineurin A splicing exemplifies the importance of alternative splicing during skeletal muscle development.

In mGlu heterodimers, an oriented asymmetrical activation revealed complex allosteric interaction between subunits.

Leukemia-Related Protein 16 (LRP16), a member of the macro domain family, plays a crucial role in orchestrating genotoxicity-initiated NF-κB signaling in the colon and the pathophysiological relevance of NF-κB activation induced by LRP16 in colonic cell survival/recovery from extrinsic DNA damage.