Elizabeth A. Jonas

Effects of dexpramipexole on brain mitochondrial conductances and cellular bioenergetic efficiency.

BAK alters neuronal excitability and can switch from anti- to pro-death function during postnatal development.

Modulation of mitochondrial function by endogenous Zn2+ pools.

Modulation of synaptic transmission by the BCL-2 family protein BCL-xL.

Proapoptotic N-truncated BCL-xL protein activates endogenous mitochondrial channels in living synaptic terminals.

Exposure to hypoxia rapidly induces mitochondrial channel activity within a living synapse.

Oligomeric Bax is a component of the putative cytochrome c release channel MAC, mitochondrial apoptosis-induced channel.

Actions of BAX on mitochondrial channel activity and on synaptic transmission.

The role of the mitochondrial apoptosis induced channel MAC in cytochrome c release.

Zinc-dependent multi-conductance channel activity in mitochondria isolated from ischemic brain.

Hypoxia increases BK channel activity in the inner mitochondrial membrane.

Expression of the voltage-gated sodium channel NaV1.5 in the macrophage late endosome regulates endosomal acidification.

Bcl-xL inhibitor ABT-737 reveals a dual role for Bcl-xL in synaptic transmission.

Bcl-xL induces Drp1-dependent synapse formation in cultured hippocampal neurons.

PKC-induced intracellular trafficking of Ca(V)2 precedes its rapid recruitment to the plasma membrane.

Ischemic preconditioning blocks BAD translocation, Bcl-xL cleavage, and large channel activity in mitochondria of postischemic hippocampal neurons.

Bcl-x L increases mitochondrial fission, fusion, and biomass in neurons.

Bcl-xL regulates metabolic efficiency of neurons through interaction with the mitochondrial F1FO ATP synthase.

Bcl-xL regulates mitochondrial energetics by stabilizing the inner membrane potential.

N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death.

NAD kinase regulates the size of the NADPH pool and insulin secretion in pancreatic β-cells.

Multipolar functions of BCL-2 proteins link energetics to apoptosis.