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10.1016/j.bbrc.2014.06.074

http://scihub22266oqcxt.onion/10.1016/j.bbrc.2014.06.074
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C4107148!4107148!24971542
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suck abstract from ncbi


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pmid24971542      Biochem+Biophys+Res+Commun 2014 ; 450 (1): 851-6
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  • HMGB1-DNA Complex-induced Autophagy Limits AIM2 Inflammasome Activation through RAGE #MMPMID24971542
  • Liu L; Yang M; Kang R; Yu Y; Dai Y; Gao F; Wang H; Sun X; Li X; Li J; Wang H; Cao L; Tang D
  • Biochem Biophys Res Commun 2014[Jul]; 450 (1): 851-6 PMID24971542show ga
  • High mobility group box 1 (HMGB1) is a prototype damage-associated molecular pattern (DAMP) that can induce inflammatory and immune responses alone as well as in combination with other molecules such as DNA. However, the intricate molecular mechanisms underlying HMGB1-DNA complex-mediated innate immune response remains largely elusive. In this study, we demonstrated that HMGB1-DNA complex initially induced absent in melanoma 2 (AIM2)-dependent inflammasome activation, and promoted rapid release of inflammasome-dependent early proinflammatory cytokines such as interleukin 1? (IL-1?). Subsequently, HMGB1-DNA complex stimulated an ATG5-dependent cellular degradation process, autophagy, which was paralleled by a cessation of AIM2 inflammasome activation and IL-1? release. These HMGB1-DNA complex-induced inflammasome activation and autophagy were both dependent on the receptor for advanced glycation endproducts (RAGE) that recognizes a wide array of ligands (including HMGB1 and DNA). Thus, autophagy may function as a negative counter-regulatory mechanism for HMGB1-DNA complex-induced inflammasome activation, and provide a checkpoint to limit the development of inflammation.
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