Felicia F. Chen

TL;DR: 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.

TL;DR: 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.

TL;DR: The proximity of RICK, RIP, and IKK complexes may play an important role for NF-kappaB activation during Nod1 oligomerization or trimerization of the tumor necrosis factor alpha receptor.

TL;DR: It is shown that bacterial lipopolysaccharides, but not other pathogen components tested, induced TLR4- and MyD88-independent NF-κB activation in human embryonic kidney 293T cells expressing trace amounts of Nod 1, suggesting that Nod1 and Nod2 are mammalian counterparts of plant disease-resistant gene products that may function as cytosolic receptors for pathogen component derived from invading bacteria.

TL;DR: A role for NOD2 in the regulation of Paneth cell mediated responses against intestinal bacteria is suggested and a plausible mechanism to explain the selective association of N OD2 mutations with ileal disease is suggested.