TMEM2 Modulates ER Stress in a Non-canonical Manner.
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- Record sourced from PubMed, PMID 31801059.
- Also identified by DOI 10.1016/j.cmet.2019.11.008.
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Abstract
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.
Medical subject headings
- Hyaluronoglucosaminidase
- Longevity