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A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease
TLDR
It is shown that a frameshift mutation caused by a cytosine insertion, 3020insC, which is expected to encode a truncated NOD2 protein, is associated with Crohn's disease, and a link between an innate immune response to bacterial components and development of disease is suggested.
Sterile inflammation: sensing and reacting to damage
TLDR
The triggers and receptor pathways that result in sterile inflammation and its impact on human health are reviewed.
Interleukin-3-induced phosphorylation of BAD through the protein kinase Akt.
TLDR
The proapoptotic function of BAD is regulated by the PI 3-kinase-Akt pathway, and active, but not inactive, forms of Akt were found to phosphorylate BAD in vivo and in vitro at the same residues that are phosphorylated in response to IL-3.
NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals
TLDR
This corrects the article to show that the method used to derive the H2O2 “spatially aggregating force” is a two-step process, not a single step, like in the previous version of this paper.
Host Recognition of Bacterial Muramyl Dipeptide Mediated through NOD2
TLDR
NOD2 mediates the host response to bacterial muropeptides derived from peptidoglycan, an activity that is important for protection against Crohn's disease and has implications for understanding adjuvant function and effective vaccine development.
The inflammasome: a caspase-1-activation platform that regulates immune responses and disease pathogenesis
TLDR
Members of the Nod-like receptor family, including NLRP1, NLRP3 and NLRC4, and the adaptor ASC are critical components of the inflammasome that link microbial and endogenous 'danger' signals to caspase-1 activation.
Nod2-Dependent Regulation of Innate and Adaptive Immunity in the Intestinal Tract
TLDR
It is shown that protective immunity mediated by Nod2 recognition of bacterial muramyl dipeptide is abolished in Nod1-deficient mice, providing a possible mechanism for Nod 2 mutations in CD.
Nod2, a Nod1/Apaf-1 Family Member That Is Restricted to Monocytes and Activates NF-κB*
TLDR
A subfamily of Apaf-1-like proteins that function through RICK to activate a NF-κB signaling pathway is defined, which contains a caspase recruitment domain linked to a nucleotide-binding domain and multiple C-terminal leucine-rich repeats.
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