chen_dicty_2007 - Immune-like Phagocyte Activity in the...

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DOI: 10.1126/science.1143991 , 678 (2007); 317 Science et al. Guokai Chen, Amoeba Immune-like Phagocyte Activity in the Social (this information is current as of October 13, 2009 ): The following resources related to this article are available online at version of this article at: including high-resolution figures, can be found in the online Updated information and services, can be found at: Supporting Online Material found at: can be related to this article A list of selected additional articles on the Science Web sites , 12 of which can be accessed for free: cites 31 articles This article 16 article(s) on the ISI Web of Science. cited by This article has been 1 articles hosted by HighWire Press; see: cited by This article has been Immunology : subject collections This article appears in the following in whole or in part can be found at: this article permission to reproduce of this article or about obtaining reprints Information about obtaining registered trademark of AAAS. is a Science 2007 by the American Association for the Advancement of Science; all rights reserved. The title Copyright American Association for the Advancement of Science, 1200 New York Avenue NW, Washington, DC 20005. (print ISSN 0036-8075; online ISSN 1095-9203) is published weekly, except the last week in December, by the Science on October 13, 2009 Downloaded from
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moter hyporesponsiveness is the molecular basis of TLR tolerance. Neither Bcl-3 nor p50 alone is sufficient to maintain the tolerant state of gene promoters (Fig. 4) ( 22 ). In the absence of Bcl-3- p50 complex, the loading of NF- k B subunits on target promoters and the subsequent dimer exchange, critical for appropriate gene expres- sion ( 23 , 24 ), are disrupted, leading to aberrant expression of inflammatory cytokines. Thus, TLR tolerance and suppression are dependent on the coordinated action of both the inhibitor p50 and its stabilizer, Bcl-3 (fig. S9 and SOM text). These findings provide important insights into the molecular mechanisms of TLR signaling and suggest that deleterious inflammatory re- sponses can be effectively controlled by targeting the NF- k B p50 ubiquitination pathway. References and Notes 1. S. Akira, K. Takeda, Nat. Rev. Immunol. 4 , 499 (2004). 2. A. Iwasaki, R. Medzhitov,
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This note was uploaded on 11/07/2010 for the course INTEGBI 118 taught by Professor Shapira during the Fall '10 term at Berkeley.

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chen_dicty_2007 - Immune-like Phagocyte Activity in the...

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