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Cited by 171

The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.

RIPK-Dependent Necrosis and Its Regulation by Caspases: A Mystery in Five Acts

Open access
Green, Douglas R., Oberst, Andrew, Dillon, Christopher P., Weinlich, Ricardo, Salvesen, Guy S.·2011·Molecular Cell

Abstract

Caspase-8, FADD, and FLIP orchestrate apoptosis in response to death receptor ligation. Mysteriously however, these proteins are also required for normal embryonic development and immune cell proliferation, an observation that has led to their implication in several non-apoptotic processes. While many scenarios have been proposed, recent genetic and biochemical evidence points to unregulated signaling by the receptor interacting protein kinases-1 (RIPK1) and RIPK3 as the lethal defect in caspase-8, FADD and FLIP deficient animals and tissues. The RIPKs are known killers, being responsible for a non-apoptotic form of cell death with features similar to necrosis. However, the mechanism by which caspase-8, FADD, and FLIP prevent runaway RIPK activation is unknown, and the signals that trigger these events during development and immune cell activation remain at large. In this review, we will lay out the evidence as it now stands, reinterpreting earlier observations in light of new clues and considering where the investigation might lead.

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Metadata

Authors
Green, D. R., Oberst, A., Dillon, C. P., Weinlich, R., & Salvesen, G. S.
Venue
Molecular Cell
Publisher
Elsevier BV
Published
2011-10
Volume
44
Issue
1
Pages
9-16
ISSN
1097-2765 (ISSN-L)
OpenAlex
W1979178278
Cited by
171
References
16
FWCI
10.70
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: RIPK-Dependent Necrosis and Its Regulation by Caspases: A Mystery in Five Acts. https://app.cochat.ai/papers/10.1016/j.molcel.2011.09.003
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Green, D. R., Oberst, A., Dillon, C. P., Weinlich, R., & Salvesen, G. S. (2011). RIPK-Dependent Necrosis and Its Regulation by Caspases: A Mystery in Five Acts. Molecular Cell. https://doi.org/10.1016/j.molcel.2011.09.003

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