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Peptidoglycan-derived muramyl dipeptide (MDP) activates innate immunity via the host sensor NOD2. Although MDP is N-acetylated in most bacteria, mycobacteria and related Actinomycetes convert their MDP to an N-glycolylated form through the action of N-acetyl muramic acid hydroxylase (NamH). We used a combination of bacterial genetics and synthetic chemistry(More)
Primarily used in military communications in the past, code division multiple access (CDMA) is recently found to be attractive for personal communications as well. As a large number of mobile hosts are supported within a cell and a wide range of services are provided, one of the most important issues in a CDMA personal communication network is how to(More)
While the recognition of microbial infection often occurs at the cell surface via Toll-like receptors, the cytosol of the cell is also under surveillance for microbial products that breach the cell membrane. An important outcome of cytosolic recognition is the induction of IFNalpha and IFNbeta, which are critical mediators of immunity against both bacteria(More)
The Rip2 kinase contains a caspase recruitment domain and has been implicated in the activation of the transcriptional factor NF-kappaB downstream of Toll-like receptors, Nod-like receptors, and the T cell receptor. Although Rip2 has been linked to Nod signaling, how Nod-Rip2 proteins mediate NF-kappaB activation has remained unclear. We find Rip2 required(More)
This paper presents a novel scheme of low-density-parity-check (LDPC) coded modulation system called bit-expand-interleaved coded modulation with iterative decoding and demapping (BEICM-ID) over Rayleigh fading channels. In traditional bit-interleaved coded modulation (BICM) schemes and its iterative version, BICM-ID, each bit node is mapped into one single(More)
Pathological activation of the Toll-like receptor signaling adaptor protein MYD88 underlies many autoimmune and inflammatory disease states. In the activated B cell-like (ABC) subtype of diffuse large B cell lymphoma (DLBCL), the oncogenic MYD88 L265P mutation occurs in 29% of cases, making it the most prevalent activating mutation in this malignancy. IRAK4(More)