Characteristic ERK1/2 signaling dynamics distinguishes necroptosis from apoptosis.
Biological sciences
Biomolecular engineering
Cell biology
Journal
iScience
ISSN: 2589-0042
Titre abrégé: iScience
Pays: United States
ID NLM: 101724038
Informations de publication
Date de publication:
24 Sep 2021
24 Sep 2021
Historique:
received:
18
12
2020
revised:
21
05
2021
accepted:
30
08
2021
entrez:
27
9
2021
pubmed:
28
9
2021
medline:
28
9
2021
Statut:
epublish
Résumé
ERK1/2 involvement in cell death remains unclear, although many studies have demonstrated the importance of ERK1/2 dynamics in determining cellular responses. To untangle how ERK1/2 contributes to two cell death programs, we investigated ERK1/2 signaling dynamics during hFasL-induced apoptosis and TNF-induced necroptosis in L929 cells. We observed that ERK1/2 inhibition sensitizes cells to apoptosis while delaying necroptosis. By monitoring ERK1/2 activity by live-cell imaging using an improved ERK1/2 biosensor (EKAR4.0), we reported differential ERK1/2 signaling dynamics between cell survival, apoptosis, and necroptosis. We also decrypted a temporally shifted amplitude- and frequency-modulated (AM/FM) ERK1/2 activity profile in necroptosis versus apoptosis. ERK1/2 inhibition, which disrupted ERK1/2 signaling dynamics, prevented TNF and IL-6 gene expression increase during TNF-induced necroptosis. Using an inducible cell line for activated MLKL, the final executioner of necroptosis, we showed ERK1/2 and its distinctive necroptotic ERK1/2 activity dynamics to be positioned downstream of MLKL.
Identifiants
pubmed: 34568795
doi: 10.1016/j.isci.2021.103074
pii: S2589-0042(21)01042-7
pmc: PMC8449238
doi:
Types de publication
Journal Article
Langues
eng
Pagination
103074Informations de copyright
© 2021 The Author(s).
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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