The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.
RIP3: a molecular switch for necrosis and inflammation
Open accessAbstract
The receptor-interacting protein kinase 3 (RIP3/RIPK3) has emerged as a critical regulator of programmed necrosis/necroptosis, an inflammatory form of cell death with important functions in pathogen-induced and sterile inflammation. RIP3 activation is tightly regulated by phosphorylation, ubiquitination, and caspase-mediated cleavage. These post-translational modifications coordinately regulate the assembly of a macromolecular signaling complex termed the necrosome. Recently, several reports indicate that RIP3 can promote inflammation independent of its pronecrotic activity. Here, we review our current understanding of the mechanisms that drive RIP3-dependent necrosis and its role in different inflammatory diseases.
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Cites
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Cited by
Glutaminolysis and transferrin regulate ferroptosis
Gao, M., Monian, P., Quadri, N., Ramasamy, R., & Jiang, X. (2015) · Molecular Cell · doi:10.1016/j.molcel.2015.06.011 · Cited by 2,069
Ferroptosis is an autophagic cell death process
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CaMKII is a RIP3 substrate mediating ischemia- and oxidative stress–induced myocardial necroptosis
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Metadata
- Authors
- Moriwaki, K., & Chan, F. K.-M.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2013-08-01
- Volume
- 27
- Issue
- 15
- Pages
- 1640-1649
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- OpenAlex
- W2104028914
- Cited by
- 355
- References
- 23
- Type
- posted content
- Language
- en
- Open access
- diamond
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