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The DOI matches its Crossref record; 59 of the 59 references it cites were found in a registry or an index.

RIPK1 and RIPK3 Kinases Promote Cell-Death-Independent Inflammation by Toll-like Receptor 4

Open access
Najjar, Malek, Saleh, Danish, Zelic, Matija, Nogusa, Shoko, Shah, Saumil, Tai, Albert, Finger, Joshua N., Polykratis, Apostolos, Gough, Peter J., Bertin, John, Whalen, Michael J., Pasparakis, Manolis, Balachandran, Siddharth, Kelliher, Michelle, Poltorak, Alexander, Degterev, Alexei·2016·Immunity

Abstract

Summary Macrophages are a crucial component of the innate immune system in sensing pathogens and promoting local and systemic inflammation. RIPK1 and RIPK3 are homologous kinases, previously linked to activation of necroptotic death. In this study we have described roles for these kinases as master regulators of pro-inflammatory gene expression induced by lipopolysaccharide, independent of their well-documented cell death functions. In primary macrophages, this regulation was elicited in the absence of caspase-8 activity, required the adaptor molecule TRIF, and proceeded in a cell autonomous manner. RIPK1 and RIPK3 kinases promoted sustained activation of Erk, cFos and NFκB, which were required for inflammatory changes. Utilizing genetic and pharmacologic tools, we showed that RIPK1 and RIPK3 account for acute inflammatory responses induced by lipopolysaccharide in vivo; notably, this regulation did not require exogenous manipulation of caspases. These findings identified a new pharmacologically accessible pathway that may be relevant to inflammatory pathologies.

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Crossref · 10.1016/j.immuni.2016.06.007

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Metadata

Authors
Najjar, M., Saleh, D., Zelic, M., Nogusa, S., Shah, S., Tai, A., Finger, J. N., Polykratis, A., Gough, P. J., Bertin, J., Whalen, M. J., Pasparakis, M., Balachandran, S., Kelliher, M., Poltorak, A., & Degterev, A.
Venue
Immunity
Publisher
Elsevier BV
Published
2016-07
Volume
45
Issue
1
Pages
46-59
ISSN
1074-7613 (ISSN-L)
OpenAlex
W2467178923
Cited by
284
References
59
FWCI
15.65
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: RIPK1 and RIPK3 Kinases Promote Cell-Death-Independent Inflammation by Toll-like Receptor 4. https://app.cochat.ai/papers/10.1016/j.immuni.2016.06.007
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Najjar, M., Saleh, D., Zelic, M., Nogusa, S., Shah, S., Tai, A., Finger, J. N., Polykratis, A., Gough, P. J., Bertin, J., Whalen, M. J., Pasparakis, M., Balachandran, S., Kelliher, M., Poltorak, A., & Degterev, A. (2016). RIPK1 and RIPK3 Kinases Promote Cell-Death-Independent Inflammation by Toll-like Receptor 4. Immunity. https://doi.org/10.1016/j.immuni.2016.06.007

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.