Title : ER Protein Processing Under Oxidative Stress: Implications and Prevention.

Pub. Date : 2016 Jun

PMID : 26983927






1 Functional Relationships(s)
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1 Using a model system to mimic mitochondrial oxidative and nitrosative stress, we demonstrate a PDI-independent mechanism whereby reactive oxygen species (ROS) compromise regeneration rates of disulfide bond-containing ER-processed proteins. Disulfides prolyl 4-hydroxylase subunit beta Homo sapiens