Adrian Israelson

A chemical chaperone-based drug candidate is effective in a mouse model of amyotrophic lateral sclerosis (ALS).

In self-defence: hexokinase promotes voltage-dependent anion channel closure and prevents mitochondria-mediated apoptotic cell death.

Oligomeric states of the voltage-dependent anion channel and cytochrome c release from mitochondria.

Fluoxetine (Prozac) interaction with the mitochondrial voltage-dependent anion channel and protection against apoptotic cell death.

A photoactivable probe for calcium binding proteins.

Localization of the voltage-dependent anion channel-1 Ca2+-binding sites.

Azido ruthenium: a new photoreactive probe for calcium-binding proteins.

Mapping the ruthenium red-binding site of the voltage-dependent anion channel-1.

Hexokinase-I protection against apoptotic cell death is mediated via interaction with the voltage-dependent anion channel-1: mapping the site of binding.

The VDAC1 N-terminus is essential both for apoptosis and the protective effect of anti-apoptotic proteins.

Misfolded mutant SOD1 directly inhibits VDAC1 conductance in a mouse model of inherited ALS.

ALS-linked mutant superoxide dismutase 1 (SOD1) alters mitochondrial protein composition and decreases protein import.

New fluorescent reagents specific for Ca(2+)-binding proteins.

Why lithium studies for ALS treatment should not be halted prematurely.

Macrophage migration inhibitory factor as a chaperone inhibiting accumulation of misfolded SOD1.

Macrophage migration inhibitory factor as a component of selective vulnerability of motor neurons in ALS.

Superoxide Dismutase 1 (SOD1)-Derived Peptide Inhibits Amyloid Aggregation of Familial Amyotrophic Lateral Sclerosis SOD1 Mutants.

Endogenous macrophage migration inhibitory factor reduces the accumulation and toxicity of misfolded SOD1 in a mouse model of ALS.