Tunicamycin-induced mitochondrial ATP in NSC-34 cells

Background information: ER stress occurs when the capacity of the ER to fold proteins becomes saturated. As a consequence, mitochondrial ATP is increased to cope with the unfolded proteins. ER stress and ultimately the accumulation or aggregation of misfolded proteins is the hallmark of a variety of neurodegenerative diseases such as Alzheimer’s disease or ALS. Tunicamycin enhances mitochondrial bioenergetics in NSC-34 cells grown in glucose-free media.

Cells:  NSC-34,  Mouse Motor Neuron-Like Hybrid Cell Line

Damage induction:  0.5mM Tunicamycin, 24h.

Readout:  ATP-Lite and cell viability

Positive control: NE-100 (sigma-1 antagonist)

Compound treatment: Compounds are added to cells 2h before the addition of tunicamycin

Turnaround time:  1 months.