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

The BMAL1-REV-ERB axis controls expression of complement C4b expression and microglial synaptic phagoctyosis, providing a link between cellular circadian clock function and synaptic regulation.

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

Understudied atypical MAPK, ERK3 controls epithelial secretome and chemotaxis.

The aged human auditory cortex shows preserved tonotopy, but temporal modulations are represented with a markedly broader tuning, highlighting decreased temporal selectivity as a hallmark of the aging auditory cortex.

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

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.

Genetic analyses reveal that neuroanatomical areas that are developmentally related co-evolve with one another.

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

The transcription factor ERG recruits the PRMT5 enzyme to methylate the androgen receptor, presenting a post-translational regulatory mechanism that could be therapeutically exploited to control cell proliferation.