Mice that lack the autism- and schizophrenia-linked gene MEF2C in cortical neurons have an imbalance of excitatory and inhibitory synapses, and impaired social and cognitive abilities.

The transcription factor, MEF2C, mediates a change in approximately one half of the expressed frontal cortical transcriptome controlling cellular metabolism and synaptic strength in response to acute loss of sleep.

Generation and validation of a new mouse strain as a tool to demonstrate the implication of p38γ/p38δ in inflammation through the regulation of the transcription factor MEF2D’s activity.

Increasing periods of neuronal activity progressively weaken and then eliminate synapses through the activation of specific transcription factors and genes.

In Drosophila, the loss of Frataxin causes iron accumulation in the nervous system, which in turn enhances sphingolipid synthesis and activation of PDK1 and Mef2, which leads to neurodegeneration.

The iron/sphingolipid/PDK1/Mef2 pathway is activated in mammals upon loss of Frataxin.

Within populations, there is standing variation in paralog expression levels, paralog expression levels are heritable, and variation in paralog expression can modify the phenotypes associated with mutation of one of the paralogs.

Mer2 interacts directly with meiotic chromatin, axial proteins, and the DNA break forming machinery to facilitate the formation of meiotic double-strand breaks.

An ensemble of cryo-EM structures reveals how eukaryotic elongation factor 2 positions the first codon of a viral mRNA for translation.

The regulatory programs governing skeletal muscle regeneration that are controlled by Klf5 in cooperation with MyoD and Mef2 provide a potential avenue for intervention into muscle regeneration through modulation of Klf5.