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

JNK signaling is active in developing Drosophila tissues and is required for achieving proper organ size.

A common mechanism might regulate the communal death of cells in flies and mammals.

Plant viruses enhance their replication in vector insects by activating the vector's JNK pathway, and inhibition of this pathway may be a useful strategy for controlling transmission of plant viruses.

NOVA pre-mRNA spacing factors suppress adipose tissue energy expenditure.

The ligand-binding pocket of the Dishevelled PDZ domain can be occupied by Dishevelled's own highly conserved C-terminus, inducing a closed conformation that is ‘opened’ when Wnt signaling stimulates interaction between Frizzled and Dishevelled.

Rab5 and Rab11 regulate hematopoietic homeostasis in Drosophila, and this process involves the JNK, Toll, and Ras/EGFR signaling pathways and autophagy.

The CtBP protein stabilizes cell fates in regenerating tissue.

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

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