Featured
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Article |
Mutations that prevent caspase cleavage of RIPK1 cause autoinflammatory disease
Heterozygous mutateons in the caspase-8 cleavage site of RIPK1 cause a range of autoinflammatory symptoms in humans, and caspase-8 cleavage of RIPK1 in a mouse model limits TNF-induced cell death and inflammation.
- Najoua Lalaoui
- , Steven E. Boyden
- & John Silke
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Letter |
Tumour-cell-induced endothelial cell necroptosis via death receptor 6 promotes metastasis
Human and murine tumour cells induce programmed necrosis (necroptosis) of endothelial cells, which promotes tumour cell extravasation and metastasis.
- Boris Strilic
- , Lida Yang
- & Stefan Offermanns
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Brief Communications Arising |
Is SIRT2 required for necroptosis?
- Kim Newton
- , Joanne M. Hildebrand
- & John Silke
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News & Views |
Death by deacetylation
Necrosis is associated with various diseases, yet it is arguably the least-understood form of programmed cell death. It emerges that a sirtuin protein regulates one form of necrosis through a deacetylation reaction. See Article p.199
- Wen Zhou
- & Junying Yuan
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Article |
The NAD-dependent deacetylase SIRT2 is required for programmed necrosis
Here it is shown that the NAD-dependent deacetylase SIRT2 is an essential component of necrosis, and that mouse hearts that do not contain SIRT2 or that are treated with a pharmacological inhibitor of SIRT2 are largely protected from ischaemic injury.
- Nisha Narayan
- , In Hye Lee
- & Toren Finkel
Gut stem cell necroptosis by genome instability triggers bowel inflammation