Variants in FGF13, associated with developmental and epileptic encephalopathies, alter neuronal excitability by affecting inhibitory neurons and by a sodium channel-independent mechanism.

TIM23 core deficiency specifically impacts the oxidative phosphorylation and the mitochondrial ribosome complexes and, unexpectedly, leads to reduction of plasma membrane voltage-dependent potassium channels in neurons.

Loss-of-function variants of human ACK1 and BRK kinase underlie systemic lupus erythematosus in young patients from multiplex families and disrupt the anti-inflammatory response of macrophages to apoptotic cells.

Polyunsaturated fatty acids activate IKs channels by stabilizing a conductive state of the selectivity filter.

In neurons of the Drosophila brain’s memory center, PKCδ relays a post-learning dopamine signal to mitochondria, boosting their metabolic activity and thereby unlocking long-term memory formation.