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

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

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

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

Metabolic stress-induced activation of the JNK3 protein regulates excitatory transmission onto AgRP neurons to regulate food consumption.

miR-306 and miR-79 selectively eliminate JNK-activated tumors, providing a new microRNA-based strategy against cancer.

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.

The cancer drug vemurafenib has potent off-target effects on JNK signaling that contribute to the development of squamous cell carcinomas in humans and in mice.

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

T-bet suppresses the expression of immature NK cell-defining genes.