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Cardif is an adaptor protein in the RIG-I antiviral pathway and is targeted by hepatitis C virus
TLDR
Cardif is described, a new CARD-containing adaptor protein that interacts with RIG-I and recruits IKKα, IKKβ and IKKɛ kinases by means of its C-terminal region, leading to the activation of NF-κB and IRF3.
Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1
TLDR
Observations indicate that TBK1 and NF-κB signalling are essential in KRAS mutant tumours, and establish a general approach for the rational identification of co-dependent pathways in cancer.
Intracellular pattern recognition receptors in the host response
TLDR
It is apparent that Toll-like receptors, a class of membrane receptors that sense extracellular microbes and trigger anti-pathogen signalling cascades, are likely to have critical roles in health and disease.
RIP1 is an essential mediator of Toll-like receptor 3-induced NF-kappa B activation.
TLDR
This work investigated the 'downstream' signaling events that regulate TLR3-dependent Trif-induced NF-kappa B activation and found that RIP1 mediates Trif’s NF-Kappa Bactivation through its RIP homotypic interaction motif.
RIP1 is an essential mediator of Toll-like receptor 3–induced NF-κB activation
TLDR
This work investigated the 'downstream' signaling events that regulate TLR3-dependent Trif-induced NF-κB activation and found that RIP1 mediates Trif -RIP1–inducedNF-κBs activation.
Requirement for NF-κB signalling in a mouse model of lung adenocarcinoma
TLDR
It is shown that the NF-κB pathway is required for the development of tumours in a mouse model of lung adenocarcinoma and that this requirement depends on p53 status, and that inhibition of the pathway in lung tumouring in vivo resulted in significantly reduced tumour development.
The RIP kinases: crucial integrators of cellular stress.
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