Erin R. Cullen

De novo Design of a Peptide Modulator to Reverse Sodium Channel Dysfunction Linked to Cardiac Arrhythmias and Epilepsy

This study designs a de novo peptide modulator, ELIXIR, that inhibits pathogenic late sodium current in NaV channels, reversing dysfunction in cardiac arrhythmias and epilepsy models.

Hyperactivity of mTORC1 and mTORC2-dependent signaling mediate epilepsy downstream of somatic PTEN loss.

This study shows that both mTORC1 and mTORC2 hyperactivity contribute to epilepsy caused by somatic PTEN loss, and that inhibiting both complexes can normalize brain activity.

The paradoxical effects of K+ channel gain-of-function are mediated by GABAergic neuron hypoexcitability and hyperconnectivity.

The paper investigates how a gain-of-function K+ channel variant causes seizures by reducing inhibitory neuron excitability and increasing network hyperconnectivity.

mTORC1 and mTORC2 regulate distinct aspects of glutamatergic synaptic transmission.

This study investigates the distinct roles of mTORC1 and mTORC2 in glutamatergic synaptic transmission by genetically inactivating each complex in mouse neurons, revealing their specific effects on presynaptic and postsynaptic functions.