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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Divergence of bacterial lipopolysaccharide pro-apoptotic signaling downstream of IRAK-1.

The vascular endothelium is a key target of circulating bacterial lipopolysaccharide (LPS). LPS elicits a wide array of endothelial responses, including the up-regulation of cytokines, adhesion molecules, and tissue factor, many of which are dependent on NF-kappa B activation. In addition, LPS has been demonstrated to induce endothelial apoptosis both in vitro and in vivo. Although the mechanism by which LPS activates NF-kappa B has been well elucidated, the signaling pathway(s) involved in LPS-induced apoptosis remains unknown. Using a variety of dominant negative constructs, we have identified a role for MyD88 and interleukin-1 receptor-associated kinase-1 (IRAK-1) in mediating LPS pro-apoptotic signaling in human endothelial cells. We also demonstrate that LPS-induced endothelial NF-kappa B activation and apoptosis occur independent of one another. Together, these data suggest that the proximal signaling molecules involved in LPS-induced NF-kappa B activation have a requisite involvement in LPS- induced apoptosis and that the pathways leading to NF-kappa B activation and apoptosis diverge downstream of IRAK-1.[1]

References

  1. Divergence of bacterial lipopolysaccharide pro-apoptotic signaling downstream of IRAK-1. Bannerman, D.D., Tupper, J.C., Erwert, R.D., Winn, R.K., Harlan, J.M. J. Biol. Chem. (2002) [Pubmed]
 
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