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.

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.

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

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

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

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

JNK pathway activity induces spermatogonial dedifferentiation under challenging conditions to maintain the germline stem cell pool and to endow it with potentially fitter cells that have increased proliferation.

An insulin-Myc feed-forward loop triggered by transient JNK boosts transcription of genes essential for mitochondrial respiration and biogenesis during early oogenesis to support massive mtDNA replication and inheritance in Drosophila.

Tissue damage induces a reversible cell cycle arrest in G2, which promotes survival and mitogenic signals to facilitate tissue regeneration but drives senescence-like phenotypes under chronic stress conditions.