Emily T. Johnson

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Excessive demands on the protein folding capacity of the endoplasmic reticulum (ER) cause irremediable ER stress and contribute to cell loss in a number of cell degenerative diseases, including type 2 diabetes and neurodegeneration 1,2. The signals communicating catastrophic ER damage to the mitochondrial apoptotic machinery remain poorly understood 3-6. We(More)
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