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Mutational inactivation of the JNK signaling pathway causes genomic instability and breast cancer development.

A diverse group of modifier genes, including the proto-oncogene Src, cooperate with Notch specifically to control cell proliferation.

A gain-of-function in a new chemical defense resulted in no trade-offs and and independent evolution between novel and ancestral defenses, suggesting low redundancy among different defensive chemicals.

Hey together with LaminC continuously supervise nuclear organisation and differentiated enterocyte identity, a regulation that is lost upon ageing, resulting in loss of gut homeostasis.

The kinase JNK is required in endothelial cells for the development of native collateral arteries.

EPO/JAK2/PKA signaling cascade via AKAP10 relocalization to the outer mitochondrial membrane results in the phosphorylation of the terminal heme synthesis enzyme ferrochelatase, which contributes to heme production in red cells.

LRH-1/NR5A2 responds to ER stress by inducing a novel pathway that is required for stress resolution in mice and can be targeted by LRH-1 agonists.

The retarding effect of a ribosome-bound internal ribosome entry site on eukaryotic protein synthesis is largely overcome following translocation of tripeptidyl-tRNA.

Synthetic cytokines engage new signaling programs with therapeutic potential.

A large-scale RNA interference screen uncovers a new transcriptional regulatory program involving the histone H3 demethylase KDM3A, which mediates detachment-induced apoptosis (anoikis) in breast epithelial cells.