Abstract：
:Receptor-interacting protein kinase (RIPK)-1 is involved in RIPK3-dependent and -independent signaling pathways leading to cell death and/or inflammation. Genetic ablation of ripk1 causes postnatal lethality, which was not prevented by deletion of ripk3, caspase-8, or fadd. However, animals that lack RIPK1, RIPK3, and either caspase-8 or FADD survived weaning and matured normally. RIPK1 functions in vitro to limit caspase-8-dependent, TNFR-induced apoptosis, and animals lacking RIPK1, RIPK3, and TNFR1 survive to adulthood. The role of RIPK3 in promoting lethality in ripk1(-/-) mice suggests that RIPK3 activation is inhibited by RIPK1 postbirth. Whereas TNFR-induced RIPK3-dependent necroptosis requires RIPK1, cells lacking RIPK1 were sensitized to necroptosis triggered by poly I:C or interferons. Disruption of TLR (TRIF) or type I interferon (IFNAR) signaling delayed lethality in ripk1(-/-)tnfr1(-/-) mice. These results clarify the complex roles for RIPK1 in postnatal life and provide insights into the regulation of FADD-caspase-8 and RIPK3-MLKL signaling by RIPK1.
journal_name
Celljournal_title
Cellauthors
Dillon CP,Weinlich R,Rodriguez DA,Cripps JG,Quarato G,Gurung P,Verbist KC,Brewer TL,Llambi F,Gong YN,Janke LJ,Kelliher MA,Kanneganti TD,Green DRdoi
10.1016/j.cell.2014.04.018subject
Has Abstractpub_date
2014-05-22 00:00:00pages
1189-202issue
5eissn
0092-8674issn
1097-4172pii
S0092-8674(14)00536-4journal_volume
157pub_type
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