Volume 23, No 2, Feb 2013
ISSN: 1001-0602
EISSN: 1748-7838 2018
impact factor 17.848*
(Clarivate Analytics, 2019)
Volume 23 Issue 2, February 2013: 168-170
RESEARCH HIGHLIGHTS
PKR stirs up inflammasomes
H James Stunden1 and Eicke Latz1,2,3
1Institute of Innate Immunity, Biomedical Center, University Hospitals Bonn, Sigmund-Freud-Str. 25, Bonn 53127, Germany
2University of Massachusetts Medical School, Division of Infectious Diseases & Immunology, 364 Plantation Street LRB 370M, Worcester, MA 01605, USA
3Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), Sigmund-Freud-Str. 25, Bonn 53127, Germany
Correspondence: Eicke Latz(eicke.latz@uni-bonn.de)
Inflammasomes are multiprotein complexes that detect and respond to foreign and endogenous danger signals by activating caspase-1; active caspase-1, in turn, matures the pro-inflammatory IL-1β family cytokines by cleaving their pro-forms into the biologically active cytokines. The upstream mechanisms leading to inflammasome activation, in particular for the NRLP3 inflammasome, remain poorly understood. Lu and colleagues identify a new function of Protein Kinase R (PKR) for activating the NLRP1, NLRP3, NLRC4 and AIM2 inflammasomes, thus identifying a potential new target for treating inflammasome-mediated diseases.
Cell Research (2013) 23:168–170; doi:10.1038/cr.2012.125; published online 4 September 2012
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