TMEM2 Modulates ER Stress in a Non-canonical Manner

Cells utilize multiple mechanisms to support endoplasmic reticulum (ER) function. The unfolded protein response, UPR^ER, is engaged during proteotoxic challenges to either mitigate ER stress or promote apoptosis. In a CRISPR-based genetic screen, Schinzel et al. (2019) identified TMEM2 as a mediator of ER stress tolerance independent of the individual branches of the canonical UPR^ER and linked this path to nematode longevity.