er-stress; inflammation; type I interferon; kinases; Endoplasmic reticulum; unfolded protein response; signaling
Hu Zehan, Yan Chuangye, Liu Peiyuan, Huang Zhiwei, Ma Rui, Zhang Chenlu, Wang Ruiyong, Zhang Yueteng, Martinon Fabio, Miao Di, Deng Haiteng, Wang Jiawei, Chang Junbiao, Chai Jijie (2013), Crystal structure of NLRC4 reveals its autoinhibition mechanism., in Science (New York, N.Y.)
, 341(6142), 172-5.
Martinon Fabio, van der Goot F Gisou (2013), Did cholera toxin finally get caught?, in Cell host & microbe
, 13(5), 501-3.
Martinon F (2012), Dangerous Liaisons: Mitochondrial DNA Meets the NLRP3 Inflammasome, in IMMUNITY
, 36(3), 313-315.
Martinon Fabio (2012), The endoplasmic reticulum: a sensor of cellular stress that modulates immune responses., in Microbes and infection / Institut Pasteur
, 14(14), 1293-300.
Glimcher Laurie H, Martinon Fabio, Modlin Robert L (2011), Editorial overview., in Current opinion in immunology
, 23(1), 1-2.
Kroemer G, Martinon F, Lippens S, Green DR, Knight R, Vandenabeele P, Piacentini M, Nagata S, Borner C, Simon HU, Krammer P, Melino G (2011), Jurg Tschopp-1951-2011-an immortal contribution Obituary
, 18(7), 18(7).
Fabio Martinon and Laurie H Glimcher (2011), Regulation of innate immunity by signaling pathways emerging from the endoplasmic reticulum., in Curr Opin Immunol
, 23(1), 35-40.
Virginie Pétrilli Isabelle Couillin Fabio Martinon (2011), The Inflammasomes
, Birkhauser, Basel.
Hetz C, Martinon F, Rodriguez D, Glimcher LH (2011), The unfolded protein response: integrating stress signals through the stress sensor IRE1α, in PHYSIOLOGICAL REVIEWS
, 91(4), 1219-1243.
Martinon Fabio, Targeting endoplasmic reticulum signaling pathways in cancer., in Acta oncologica (Stockholm, Sweden)
Martinon Fabio, The endoplasmic reticulum: a sensor of cellular stress that modulates immune responses., in Microbes and infection / Institut Pasteur
The endoplasmic reticulum (ER) serves many general functions, including the facilitation of protein folding and the transport of synthesized proteins, but it also has an important role in sensing cellular stress. ER-stress identifies a group of signals that induce a transcriptional program enabling cells to survive protein overload and injury in the ER. This highly coordinated response involves three parallel signaling branches localized at the ER, namely IRE1, ATF6 and PERK. New findings suggest that these signaling pathways can initiate inflammation and, in specialized cells and tissues, may be involved in the pathogenesis of inflammatory and infectious diseases. However, this is an emerging field of research and little is known on the specific nature of these signaling pathways and their function in regulating immunity.The long term goals of this proposal are: to elucidate the molecular mechanisms and pathways emerging from the ER and regulating innate immune responses, and to address the physiological role of ER-stress in inflammation. Two complementary research sub-projects were designed to provide a comprehensive study of molecular mechanisms and to address the physiological role of ER stress in regulating immune responses. The first sub-project will investigate the molecular nature of inflammatory ER-stress responses, by focusing on the biochemical characterization of signaling pathways emerging from the ER-associated kinases IRE1 and PERK as well as on how these signals affect innate immune and inflammatory responses. The second sub-project is aimed at identifying physiologically relevant signals that may promote inflammation by causing ER-stress. The knowledge gained from this study will provide a better understanding of regulatory pathways controlling immune responses and will aid in the development of therapies aimed at improving the outcome of diseases characterized by inflammation and ER-stress.