USP22 controls necroptosis by regulating receptor-interacting protein kinase 3 ubiquitination.
RIPK1
cancer
mixed lineage kinase domain-like
post-translational modifications
ubiquitin hydrolase
Journal
EMBO reports
ISSN: 1469-3178
Titre abrégé: EMBO Rep
Pays: England
ID NLM: 100963049
Informations de publication
Date de publication:
03 02 2021
03 02 2021
Historique:
received:
06
02
2020
revised:
21
10
2020
accepted:
03
11
2020
pubmed:
29
12
2020
medline:
1
6
2021
entrez:
28
12
2020
Statut:
ppublish
Résumé
Dynamic control of ubiquitination by deubiquitinating enzymes is essential for almost all biological processes. Ubiquitin-specific peptidase 22 (USP22) is part of the SAGA complex and catalyzes the removal of mono-ubiquitination from histones H2A and H2B, thereby regulating gene transcription. However, novel roles for USP22 have emerged recently, such as tumor development and cell death. Apart from apoptosis, the relevance of USP22 in other programmed cell death pathways still remains unclear. Here, we describe a novel role for USP22 in controlling necroptotic cell death in human tumor cell lines. Loss of USP22 expression significantly delays TNFα/Smac mimetic/zVAD.fmk (TBZ)-induced necroptosis, without affecting TNFα-mediated NF-κB activation or extrinsic apoptosis. Ubiquitin remnant profiling identified receptor-interacting protein kinase 3 (RIPK3) lysines 42, 351, and 518 as novel, USP22-regulated ubiquitination sites during necroptosis. Importantly, mutation of RIPK3 K518 reduced necroptosis-associated RIPK3 ubiquitination and amplified necrosome formation and necroptotic cell death. In conclusion, we identify a novel role of USP22 in necroptosis and further elucidate the relevance of RIPK3 ubiquitination as crucial regulator of necroptotic cell death.
Identifiants
pubmed: 33369872
doi: 10.15252/embr.202050163
pmc: PMC7857539
doi:
Substances chimiques
NF-kappa B
0
RIPK3 protein, human
EC 2.7.11.1
Receptor-Interacting Protein Serine-Threonine Kinases
EC 2.7.11.1
Ubiquitin Thiolesterase
EC 3.4.19.12
Usp22 protein, human
EC 3.4.19.12
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e50163Informations de copyright
© 2020 The Authors. Published under the terms of the CC BY 4.0 license.
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