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| <div style="padding: .4em .9em .9em">
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| '''Rongcong Wu''' (SM), joint with David Schauer
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| TLR-4 is a typical Toll-like receptor (TLR) that is essential in host defense against bacterial infection. By recognition of specific pathogen-associated molecular patterns (PAMPs) such as lipopolysaccharide (LPS), a conserved structure expressed by gram-negative bacteria, TLR-4 can in tandem initiate a pair of downstream signaling pathways by recruiting two different sets of adaptors to regulate cytokine/chemokine release, endotoxin tolerance and apoptosis, which have been suggested to directly or indirectly participate in the regulation of innate and adaptive immune responses. In contrast, some pathogens also release virulence determinants to disturb these signaling pathways and alter host cell responses to prevent being eliminated by host defenses. Our objective is to develop a systems-level approach to elucidate how these TLR-4-stimulated downstream signaling pathways are coordinated and altered to determine apoptosis in murine macrophages. Data-driven models may eventually be built up and utilized to discover new drug targets.
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