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.