Calcineurin-mediated BAD dephosphorylation activates the caspase-3 apoptotic cascade in traumatic spinal cord injury.

Calcineurin-mediated BAD dephosphorylation activates the caspase-3 apoptotic cascade in traumatic spinal cord injury.

[Anonymous].  2000.  Calcineurin-mediated BAD dephosphorylation activates the caspase-3 apoptotic cascade in traumatic spinal cord injury.. The Journal of neuroscience : the official journal of the Society for Neuroscience. 20(19):7246-51.

Riluzole and methylprednisolone combined treatment improves functional recovery in traumatic spinal cord injury.

Caspase-3 apoptotic signaling following injury to the central nervous system.

Overexpression of GDNF induces and maintains hyperinnervation of muscle fibers and multiple end-plate formation.

NBQX treatment improves mitochondrial function and reduces oxidative events after spinal cord injury.

Assessment of the relative contribution of COX-1 and COX-2 isoforms to ischemia-induced oxidative damage and neurodegeneration following transient global cerebral ischemia.

Assessment of the relative contribution of COX-1 and COX-2 isoforms to ischemia-induced oxidative damage and neurodegeneration following transient global cerebral ischemia.

[Anonymous].  2003.  Assessment of the relative contribution of COX-1 and COX-2 isoforms to ischemia-induced oxidative damage and neurodegeneration following transient global cerebral ischemia.. Journal of neurochemistry. 86(3):545-55.

Temporal and spatial distribution of activated caspase-3 after subdural kainic acid infusions in rat spinal cord.

Apoptosis of spinal cord neurons by preventing depletion nicotine attenuates arachidonic acid-induced of neurotrophic factors.

Mitochondrial uncoupling as a therapeutic target following neuronal injury.

Mitochondrial permeability transition in CNS trauma: cause or effect of neuronal cell death?