Understudied atypical MAPK, ERK3 controls epithelial secretome and chemotaxis.

Tight regulation of a central developmental kinase cascade evolved through two key mutations.

Cavin-3 is a tumor suppressor protein that inhibits Akt signaling, suppresses Warburg metabolism, promotes apoptosis, and protects against cachexia.

ERK3 controls actin cytoskeleton.

New ATP-competitive inhibitors show properties of conformation selection when complexed with the MAP kinase, ERK2, altering movements around the activation loop.

ERK/MAPK activity is regulated by the cap-binding protein 4EHP, via translational control of the DUSP6 phosphatase.

ERK activation during induction of long-term synaptic plasticity is enhanced by synergistic interactions among signaling pathways mediated by the synaptically located GTPase-activating protein, and each pathway contributes to different ERK temporal dynamics.

Cancer cells driven by mutations in KRAS or EGFR are dependent on DUSP6 to prevent ERK-induced cell death, creating a novel vulnerability for targeted therapy.

Genetically engineered murine models reveal novel mechanisms of cell identity regulation in lung cancer and provide insights into the complex interplay between lineage specifiers and oncogenic signaling pathways in this disease.

Genetic and biochemical analyses uncover a dichotomy of ERK pathway functions in osteoblasts, whereby ERK activation promotes the early differentiation of osteoblast precursors, but inhibits the subsequent differentiation of committed osteoblasts via mTOR-mediated regulation of mitochondrial function and SGK1.