Identification of a Molecular Signaling Network that Regulates a Cellular Necrotic Cell Death Pathway
Open accessAbstract
Stimulation of death receptors by agonists such as FasL and TNFalpha activates apoptotic cell death in apoptotic-competent conditions or a type of necrotic cell death dependent on RIP1 kinase, termed necroptosis, in apoptotic-deficient conditions. In a genome-wide siRNA screen for regulators of necroptosis, we identify a set of 432 genes that regulate necroptosis, a subset of 32 genes that act downstream and/or as regulators of RIP1 kinase, 32 genes required for death-receptor-mediated apoptosis, and 7 genes involved in both necroptosis and apoptosis. We show that the expression of subsets of the 432 genes is enriched in the immune and nervous systems, and cellular sensitivity to necroptosis is regulated by an extensive signaling network mediating innate immunity. Interestingly, Bmf, a BH3-only Bcl-2 family member, is required for death-receptor-induced necroptosis. Our study defines a cellular signaling network that regulates necroptosis and the molecular bifurcation that controls apoptosis and necroptosis.
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In presence of SMAC mimetics, RIPK1 is deubiquitinated by CYLD, favoring release from complex I and association with FADD and CASP8 in cytosol to form complex II, which drives extrinsic apoptosis.
“Conversely, in the presence of so-called “SMAC mimetics” (which de facto operate as IAP inhibitors) [337], RIPK1 is deubiquitinated by CYLD lysine 63 deubiquitinase (CYLD), favoring its release from complex I and its association with FADD and CASP8 in the cytosol to form complex II, which drives extrinsic apoptosis [338].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [338]
Necroptosis relies on deubiquitinating activity of CYLD, which is also proteolytic target of CASP8.
“Accordingly, necroptosis relies on the deubiquitinating activity of CYLD [338], which is also a proteolytic target of CASP8 [494–496].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [338]
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- Authors
- Hitomi, J., Christofferson, D. E., Ng, A., Yao, J., Degterev, A., Xavier, R. J., & Yuan, J.
- Affiliations
- Harvard University (US)
- Corresponding author
- Yuan, Junying
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2008-12
- Volume
- 135
- Issue
- 7
- Pages
- 1311-1323
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC2621059
- OpenAlex
- W2161830466
- Cited by
- 989
- References
- 46
- Citations by year
- 2026: 12 · 2025: 26 · 2024: 29 · 2023: 43 · 2022: 54 · 2021: 43 · 2020: 42 · 2019: 55 · 2018: 64 · 2017: 51 · 2016: 68 · 2015: 54 · 2014: 83 · 2013: 86 · 2012: 79
- FWCI
- 27.26
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1689 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Uehara Memorial Foundation
- Pharmaceutical Society of Japan
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- National Institutes of Health (DP1OD000580)
- National Institute on Aging (R37AG012859, R01AG012859)
- National Institute of Allergy and Infectious Diseases (AI 062773, R01AI062773)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 43351, P30DK043351, P30DK040561)
- National Institute of Neurological Disorders and Stroke (U01NS050560)
- 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
- necroptosis, RIP1 kinase, apoptosis, death receptor signaling, Fas ligand, TNF-α, BMF, BH3-only proteins, Bcl-2 family proteins, innate immunity, signaling networks, siRNA screen
- MeSH terms
- Animals, Cell Line, Humans, Necrosis, Oncogenes, Transcription, Genetic, Protein Biosynthesis, Signal Transduction, Genome, Apoptosis, Gene Expression Profiling, Protein Interaction Mapping, Adaptor Proteins, Signal Transducing, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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