Cited by 2,214Cell death mechanisms and regulationNF-κB Signaling PathwaysDeath, Funerary Practices, and Mourning

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Receptor Interacting Protein Kinase-3 Determines Cellular Necrotic Response to TNF-α

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He, Sudan, Wang, Lai, Miao, Lin, Wang, Tao, Du, Fenghe, Zhao, Liping, Wang, Xiaodong·2009·Cell

DOI 10.1016/j.cell.2009.05.021

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Abstract

Smac mimetics induce apoptosis synergistically with TNF-alpha by triggering the formation of a caspase-8-activating complex containing receptor interacting protein kinase-1 (RIPK1). Caspase inhibitors block this form of apoptosis in many types of cells. However, in several other cell lines, caspase inhibitors switch the apoptotic response to necrosis. A genome wide siRNA screen revealed another member of the RIP kinase family, RIP3, to be required for necrosis. The expression of RIP3 in different cell lines correlates with their responsiveness to necrosis induction. The kinase activity of RIP3 is essential for necrosis execution. Upon induction of necrosis, RIP3 is recruited to RIPK1 to form a necrosis-inducing complex. Embryonic fibroblasts from RIP3 knockout mice are resistant to necrosis and RIP3 knockout animals are devoid of inflammation inflicted tissue damage in an acute pancreatitis model. These data indicate RIP3 as the determinant for cellular necrosis in response to TNF-alpha family of death-inducing cytokines.

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Authors: He, S., Wang, L., Miao, L., Wang, T., Du, F., Zhao, L., & Wang, X.
Affiliations: Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
Howard Hughes Medical Institute (US)
National Institute of Biological Sciences, Beijing (CN)
Corresponding author: Wang, Xiaodong
ORCID: He, Sudan
Wang, Lai
Miao, Lin
Wang, Tao
Du, Fenghe
Zhao, Liping
Wang, Xiaodong
Venue: Cell
Publisher: Elsevier BV
Published: 2009-06
Volume: 137
Issue: 6
Pages: 1100-1111
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/j.cell.2009.05.021
OpenAlex: W2052605153
Cited by: 2,214
References: 35
Citations by year: 2026: 82 · 2025: 118 · 2024: 114 · 2023: 124 · 2022: 158 · 2021: 168 · 2020: 147 · 2019: 136 · 2018: 143 · 2017: 147 · 2016: 171 · 2015: 155 · 2014: 179 · 2013: 101 · 2012: 106
FWCI: 36.20
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 1507 d)
Locations: Cell (publishedVersion)
PubMed (publishedVersion)
Bristol Research (University of Bristol) (submittedVersion)
Funders: National Institutes of Health (5p01ca095471-10)
National Cancer Institute (P01 CA95471)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Social Sciences › Anthropology › Death, Funerary Practices, and Mourning
Keywords: RIPK3, receptor-interacting protein kinase, necrosis, TNF-α, RIPK1, IAP antagonists, caspase-8, kinase activity, acute pancreatitis, inflammation, siRNA screen
MeSH terms: Animals, Ceruletide, Humans, Mutation, Necrosis, Pancreatitis, Tumor Necrosis Factor-alpha, Protein Structure, Tertiary, RNA, Small Interfering, Cell Line, Tumor, Mice, Receptor-Interacting Protein Serine-Threonine Kinases

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Receptor Interacting Protein Kinase-3 Determines Cellular Necrotic Response to TNF-α

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