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.

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

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.

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

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.

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.

Identification and characterization of enhancers for eight key arterial genes reveal transcription factors associated with different aspects of endothelial gene expression specificity and provide a tool for a better understanding of arterial differentiation.

Myelin generation during development and nerve regeneration is guaranteed by responsive backup circuits that coordinate class IIa HDACs to repress the expression of negative regulators of myelination and permit Schwann cell differentiation in response to cAMP.

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.