TMEM2 Modulates ER Stress in a Non-canonical Manner

Cell Metab. 2019 Dec 3;30(6):999-1001. doi: 10.1016/j.cmet.2019.11.008.


Cells utilize multiple mechanisms to support endoplasmic reticulum (ER) function. The unfolded protein response, UPRER, 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 UPRER and linked this path to nematode longevity.

Publication types

  • Research Support, N.I.H., Extramural
  • Comment

MeSH terms

  • Apoptosis
  • Endoplasmic Reticulum
  • Endoplasmic Reticulum Stress
  • Homeostasis
  • Hyaluronoglucosaminidase*
  • Longevity*
  • Signal Transduction
  • Unfolded Protein Response


  • Hyaluronoglucosaminidase