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Cited by 166

The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.

Nuclear RIPK3 and MLKL contribute to cytosolic necrosome formation and necroptosis

Open access
Weber, Kathrin, Roelandt, Ria, Bruggeman, Inge, Estornes, Yann, Vandenabeele, Peter·2018·Communications Biology

Abstract

Necroptotic signaling converges in the assembly of a cytosolic signaling platform, the necrosome, with the activation of its downstream effector, MLKL. RIPK1 and RIPK3, key components of the necrosome, act as signaling intermediates for the activation of MLKL. We report that RIPK3 and MLKL continuously shuttle between the nucleus and the cytoplasm, whereas RIPK1 is constitutively present in both compartments. During TNF-induced necroptosis, nuclear RIPK1 becomes ubiquitinated, after which nuclear MLKL becomes phosphorylated and oligomerized. Pharmacological inhibition of the nuclear export machinery leads to retention of RIPK3 and MLKL in the nucleus, prevents the nucleation of cytosolic RIPK3/MLKL oligomerization, and reduces cell death. Our results suggest that passage of necroptotic signaling components through the nucleus is a mechanism for regulating cytosolic necrosome formation and consequently necroptotic cell death.

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Metadata

Authors
Weber, K., Roelandt, R., Bruggeman, I., Estornes, Y., & Vandenabeele, P.
Venue
Communications Biology
Published
2018-01-22
Volume
1
Issue
1
Pages
6-6
ISSN
2399-3642 (ISSN-L)
OpenAlex
W2782643375
Cited by
166
References
15
FWCI
5.34
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: Nuclear RIPK3 and MLKL contribute to cytosolic necrosome formation and necroptosis. https://app.cochat.ai/papers/10.1038/s42003-017-0007-1
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Weber, K., Roelandt, R., Bruggeman, I., Estornes, Y., & Vandenabeele, P. (2018). Nuclear RIPK3 and MLKL contribute to cytosolic necrosome formation and necroptosis. Communications Biology. https://doi.org/10.1038/s42003-017-0007-1

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