Two zebrafish Keap1-paralogs are equally adept at electrophile-sensing but manifest divergent and co-regulatory electrophile-signaling behaviors.

Comprehensive transcriptomic analyses describe the underlying tumorigenic gene expression state in the invasive Drosophila follicle cells following the loss of epithelial cell polarity and identify a non-canonical role of Keap1-Nrf2 signaling in regulating collective cell invasion.

Inactivation of KAP1 by mTOR-mediated phosphorylation releases human cytomegalovirus from latency, and has the potential to be used as a therapy to purge the virus from transplant organs.

A new zebrafish RBC aggregation model is developed to explore the dynamic process and the underlying regulatory mechanisms in blood clot formation.

Loss of KEAP1 modulates sensitivity to targeted therapies in lung cancer.

By increasing intracellular cysteine levels, NRF2 engages a tumor suppressive metabolic pathway mediated by cysteine dioxygenase 1.

Cyclin D1 protein stability is regulated by ubiquitin-proteasome mechanism mediated by multiple E3 ligases, including newly identified Keap1, DDB2, and WSB2.

Variably methylated retrotransposons have an underlying sequence that allows them to escape KAP1-mediated silencing and recruit ZF-CxxC proteins.