期刊
CELL CYCLE
卷 9, 期 15, 页码 3072-3077出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.9.15.12459
关键词
anthracyclines; apoptosis; calreticulin receptor; ER stress
类别
资金
- Ligue Nationale contre le Cancer (Equipes labellisee)
- Agence Nationale pour la Recherche (ANR)
- European Commission
- Fondation pour la Recherche Medicale (FRM)
- Institut National du Cancer (INCa)
- Canceropole Ile-de-France
- INSERM
- Cancerfonden
- Barncancerfonden
- Swedish Royal Academy of Sciences
- Ake Wiberg Stiftelse
- Ligue Nationale contre le Cancer
In response to immunogenic cell death inducers, calreticulin (CRT) translocates from its orthotopic localization in the lumen of the endoplasmic reticulum (ER) to the surface of the plasma membrane where it serves as an engulfment signal for antigen-presenting cells. 1 Here, we report that yet another ER protein, the lysyl-tRNA synthetase (KARS), was exposed on the surface of stressed cells, on which KARS co-localized with CRT in lipid rafts. Depletion of KARS with small interfering RNAs suppressed CRT exposure induced by anthracyclines or UVC light. In contrast to CRT, KARS was also found in the supernatant of stressed cells. Recombinant KARS protein was unable to influence the binding of recombinant CRT to the cell surface. Moreover, recombinant KARS protein was unable to stimulate macrophages in vitro. These results underscore the contribution of KARS to the emission of (one of) the principal signal(s) of immunogenic cell death, CRT exposure.
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