Iuliia Vitko

Functional characterization and neuronal modeling of the effects of childhood absence epilepsy variants of CACNA1H, a T-type calcium channel.

Transfer of beta subunit regulation from high to low voltage-gated Ca2+ channels.

The I-II loop controls plasma membrane expression and gating of Ca(v)3.2 T-type Ca2+ channels: a paradigm for childhood absence epilepsy mutations.

Reducing agents sensitize C-type nociceptors by relieving high-affinity zinc inhibition of T-type calcium channels.

Characterization of the gating brake in the I-II loop of Ca(v)3.2 T-type Ca(2+) channels.

I-II loop structural determinants in the gating and surface expression of low voltage-activated calcium channels.

Alternative splicing within the I-II loop controls surface expression of T-type Ca(v)3.1 calcium channels.

Orientation of the calcium channel beta relative to the alpha(1)2.2 subunit is critical for its regulation of channel activity.

Molecular pharmacology of human Cav3.2 T-type Ca2+ channels: block by antihypertensives, antiarrhythmics, and their analogs.

Molecular mechanisms of lipoic acid modulation of T-type calcium channels in pain pathway.

Orientation of palmitoylated CaVbeta2a relative to CaV2.2 is critical for slow pathway modulation of N-type Ca2+ current by tachykinin receptor activation.

Structural determinants of the high affinity extracellular zinc binding site on Cav3.2 T-type calcium channels.

Molecular and biophysical basis of glutamate and trace metal modulation of voltage-gated Ca(v)2.3 calcium channels.

Mechanisms by which a CACNA1H mutation in epilepsy patients increases seizure susceptibility.

A potassium leak channel silences hyperactive neurons and ameliorates status epilepticus.

Central Mechanisms Mediating Thrombospondin-4-induced Pain States.

Characterization of kindled VGAT-Cre mice as a new animal model of temporal lobe epilepsy.