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The Yale Undergraduate Research Journal

Abstract

Tail-anchored (TA) membrane proteins are critical for protein translocation, intracellular trafficking, and programmed cell death. TA proteins contain hydrophobic transmembrane domains and traverse through the cytosol to post-translationally insert into cellular membranes. It is unclear how this post-translational insertion is affected by Endoplasmic Reticulum (ER) stress. Here, we find that TA protein insertion is significantly reduced with ER stress inducer thapsigargin (Tg), a calcium pump inhibitor that blocks the import of calcium into the ER causing ER stress, but not when treated with other ER stress inducers. Interestingly, out data suggests that increased calcium in the cytosol may decrease TA protein insertion rather than ER stress. One potential mechanism for this is the calciumdependent activation of chaperone, calmodulin, which acts like a trap for TA proteins under certain physiological conditions.

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