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Cited by 599

The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

RIP1 autophosphorylation is promoted by mitochondrial ROS and is essential for RIP3 recruitment into necrosome

Open access
Zhang, Yingying, Su, Sheng Sean, Zhao, Shubo, Yang, Zhentao, Zhong, Chuan-Qi, Chen, Xin, Cai, Qixu, Yang, Zhang-Hua, Huang, Deli, Wu, Rui, Han, Jiahuai·2017·Nature Communications
DOI 10.1038/ncomms14329
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Abstract

Necroptosis is a type of programmed cell death with great significance in many pathological processes. Tumour necrosis factor-α(TNF), a proinflammatory cytokine, is a prototypic trigger of necroptosis. It is known that mitochondrial reactive oxygen species (ROS) promote necroptosis, and that kinase activity of receptor interacting protein 1 (RIP1) is required for TNF-induced necroptosis. However, how ROS function and what RIP1 phosphorylates to promote necroptosis are largely unknown. Here we show that three crucial cysteines in RIP1 are required for sensing ROS, and ROS subsequently activates RIP1 autophosphorylation on serine residue 161 (S161). The major function of RIP1 kinase activity in TNF-induced necroptosis is to autophosphorylate S161. This specific phosphorylation then enables RIP1 to recruit RIP3 and form a functional necrosome, a central controller of necroptosis. Since ROS induction is known to require necrosomal RIP3, ROS therefore function in a positive feedback circuit that ensures effective induction of necroptosis.

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Research works printed but not linked: 38

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Metadata

Authors
Zhang, Y., Su, S. S., Zhao, S., Yang, Z., Zhong, C.-Q., Chen, X., Cai, Q., Yang, Z.-H., Huang, D., Wu, R., & Han, J.
Venue
Nature Communications
Publisher
Springer Science and Business Media LLC
Published
2017-02-08
Volume
8
Issue
1
Pages
14329-14329
ISSN
2041-1723 (ISSN-L)
DOI
10.1038/ncomms14329
OpenAlex
W2586088194
Cited by
599
References
11
FWCI
13.39
Type
journal article
Language
en
Open access
gold
Licence

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CoChat. (2026). Citation check: RIP1 autophosphorylation is promoted by mitochondrial ROS and is essential for RIP3 recruitment into necrosome. https://app.cochat.ai/papers/10.1038/ncomms14329
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Zhang, Y., Su, S. S., Zhao, S., Yang, Z., Zhong, C.-Q., Chen, X., Cai, Q., Yang, Z.-H., Huang, D., Wu, R., & Han, J. (2017). RIP1 autophosphorylation is promoted by mitochondrial ROS and is essential for RIP3 recruitment into necrosome. Nature Communications. https://doi.org/10.1038/ncomms14329

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