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The PYRIN domain-only protein POP2 inhibits inflammasome priming and activation
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Journal Article
The PYRIN domain-only protein POP2 inhibits inflammasome priming and activation
2017
Overview
Inflammasomes are protein platforms linking recognition of microbe, pathogen-associated and damage-associated molecular patterns by cytosolic sensory proteins to caspase-1 activation. Caspase-1 promotes pyroptotic cell death and the maturation and secretion of interleukin (IL)-1β and IL-18, which trigger inflammatory responses to clear infections and initiate wound-healing; however, excessive responses cause inflammatory disease. Inflammasome assembly requires the PYRIN domain (PYD)-containing adaptor ASC, and depends on PYD–PYD interactions. Here we show that the PYD-only protein POP2 inhibits inflammasome assembly by binding to ASC and interfering with the recruitment of ASC to upstream sensors, which prevents caspase-1 activation and cytokine release. POP2 also impairs macrophage priming by inhibiting the activation of non-canonical IκB kinase ɛ and IκBα, and consequently protects from excessive inflammation and acute shock
in vivo
. Our findings advance our understanding of the complex regulatory mechanisms that maintain a balanced inflammatory response and highlight important differences between individual POP members.
Excessive inflammasome activation leads to inflammatory diseases, but how inflammasomes are regulated by PYD-only adaptors is unclear. Here the authors show that the PYD-only protein POP2 inhibits both inflammasome priming and assembly by interfering, respectively, with IκBα activation and NLRP3-ASC interaction.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/106
/ 13/109
/ 13/21
/ 13/31
/ 13/51
/ 13/89
/ 13/95
/ 38/109
/ 38/22
/ 38/35
/ 38/39
/ 38/77
/ 38/88
/ 59/5
/ 64/110
/ 64/60
/ 82/83
/ Adaptor Proteins, Signal Transducing - metabolism
/ Animals
/ Disease
/ Genomes
/ Humanities and Social Sciences
/ Humans
/ I-kappa B Kinase - metabolism
/ Interleukin-1beta - metabolism
/ Kinases
/ Medicine
/ Mice
/ Nuclear Proteins - metabolism
/ Proteins
/ Science
