TMEM2 Modulates ER Stress in a Non-canonical Manner.

TMEM2 Modulates ER Stress in a Non-canonical Manner. Cell Metab. 2019 Dec 03;30(6):999-1001 Authors: Goncalves RLS, Hotamisligil GS 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. PMID: 31801059 [PubMed - in process]

https://www.ncbi.nlm.nih.gov/pubmed/31801059?dopt=Abstract

Source: Cell Metabolism - December 2, 2019 Category: Cytology Authors: Goncalves RLS, Hotamisligil GS Tags: Cell Metab Source Type: research

More News: Cytology | Genetics