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TRADD mediates the tumor necrosis factor-induced apoptosis of L929 cells in the absence of RIP3
Open accessAbstract
Receptor-interacting protein kinase 3 (RIP3) is a critical initiator in mediating necroptosis induced by tumor necrosis factor alpha (TNFα) in L929 cells, so knockdown of RIP3 inhibits TNFα-induced L929 cell necroptosis. However, RIP3 knockdown was shown to switch TNFα-induced necroptosis to apoptosis in L929 cells in other studies. Therefore, whether RIP3 knockdown blocks the TNFα-induced death of L929 cells is controversial. In this study, TNFα activated caspase pathway and induced cell death in RIP3 knockdown L929 cells, and the RIP3-independent cell death had been blocked by Z-VAD-FMK (pan-caspase inhibitor) or caspase 8 knockdown, demonstrating that RIP3 knockdown switched TNFα-induced necroptosis to caspase-dependent apoptosis. Although both TNF receptor type 1-associated death domain protein (TRADD) and RIP1 have been reported to mediate TNFα-induced apoptosis, the knockdown of TRADD, but not RIP1, suppressed TNFα-induced activation of the caspase pathway and subsequent apoptosis in RIP3 knockdown L929 cells. In addition, TRADD bound and activated caspase 8 during the RIP3-independent apoptosis process, indicating that TRADD initiates RIP3-independent apoptosis by activating the caspase pathway. Collectively, we identified the target and mechanism underlying RIP3-independent apoptosis and elucidated the coordinated roles of RIP3 and TRADD in mediating the programmed cell death of L929 cells following TNFα stimulation.
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TRADD encodes TNFRSF1A-associated death domain and mediates TNF-receptor-activated apoptosis.
“TRADD (FC = −1.26, p = 0.02) encodes TNFRSF1A-associated death domain and is a mediator of the TNF-receptor-activated apoptosis [20].”
From Early onset senescence and cognitive impairment in a murine model of repeated mTBI (2021) · cites this paper as [20]
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Early onset senescence and cognitive impairment in a murine model of repeated mTBI
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Metadata
- Authors
- Chang, X., Wang, L., Wang, Z., Wu, S., Zhu, X., Hu, S., Wang, Y., Yu, J., & Chen, G.
- Affiliations
- Institute of Basic Medical Sciences of the Chinese Academy of Medical Sciences (CN)
- Corresponding author
- Wang, Yu
- Yu, Jiyun
- Chen, Guozhu
- Venue
- Scientific Reports
- Published
- 2017-11-23
- Volume
- 7
- Issue
- 1
- Pages
- 16111-16111
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC5701027
- OpenAlex
- W2770019817
- Cited by
- 13
- References
- 46
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2022: 1 · 2021: 3 · 2020: 4 · 2019: 1
- FWCI
- 0.56
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (31201041, 31371434)
- 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
- TRADD, RIPK3, RIPK1, TNF-α, apoptosis, necroptosis, caspase-8, caspase pathway, L929 fibroblasts, programmed cell death
- MeSH terms
- Animals, Cell Line, Tumor Necrosis Factor-alpha, Signal Transduction, Cell Death, Apoptosis, Mice, Caspase 8, TNF Receptor-Associated Death Domain Protein, Receptor-Interacting Protein Serine-Threonine Kinases
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