Abstract
Cells are protected from endoplasmic reticulum stress through the unfolded protein response (UPR). In this issue of Cell, Schinzel, Higuchi-Sanabria, Shalem et al., identify a mechanism that helps cells cope with ER stress but is independent of canonical UPR activation, instead involving the extracellular matrix hyaluronidase, TMEM2, as a signaling mediator.
Original language | English |
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Pages (from-to) | 1246-1248 |
Number of pages | 3 |
Journal | Cell |
Volume | 179 |
Issue number | 6 |
DOIs | |
Publication status | Published - 27-Nov-2019 |