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dc.contributor.authorHu, Bo
dc.contributor.authorJin, Chengcheng
dc.contributor.authorLi, Hua-Bing
dc.contributor.authorTong, Jiyu
dc.contributor.authorOuyang, Xinshou
dc.contributor.authorCetinbas, Naniye Malli
dc.contributor.authorZhu, Shu
dc.contributor.authorStrowig, Till
dc.contributor.authorLam, Fred C
dc.contributor.authorZhao, Chen
dc.contributor.authorHenao-Mejia, Jorge
dc.contributor.authorYilmaz, Omer
dc.contributor.authorFitzgerald, Katherine A
dc.contributor.authorEisenbarth, Stephanie C
dc.contributor.authorElinav, Eran
dc.contributor.authorFlavell, Richard A
dc.date.accessioned2018-02-08T15:48:26Z
dc.date.available2018-02-08T15:48:26Z
dc.date.issued2016
dc.identifier.citationThe DNA-sensing AIM2 inflammasome controls radiation-induced cell death and tissue injury. 2016, 354 (6313):765-768 Scienceen
dc.identifier.issn1095-9203
dc.identifier.pmid27846608
dc.identifier.doi10.1126/science.aaf7532
dc.identifier.urihttp://hdl.handle.net/10033/621270
dc.description.abstractAcute exposure to ionizing radiation induces massive cell death and severe damage to tissues containing actively proliferating cells, including bone marrow and the gastrointestinal tract. However, the cellular and molecular mechanisms underlying this pathology remain controversial. Here, we show that mice deficient in the double-stranded DNA sensor AIM2 are protected from both subtotal body irradiation-induced gastrointestinal syndrome and total body irradiation-induced hematopoietic failure. AIM2 mediates the caspase-1-dependent death of intestinal epithelial cells and bone marrow cells in response to double-strand DNA breaks caused by ionizing radiation and chemotherapeutic agents. Mechanistically, we found that AIM2 senses radiation-induced DNA damage in the nucleus to mediate inflammasome activation and cell death. Our results suggest that AIM2 may be a new therapeutic target for ionizing radiation exposure.
dc.language.isoenen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.source.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5640175/
dc.subject.meshAnimalsen
dc.subject.meshApoptosisen
dc.subject.meshBone Marrowen
dc.subject.meshCaspase 1en
dc.subject.meshDNAen
dc.subject.meshDNA Breaks, Double-Strandeden
dc.subject.meshDNA-Binding Proteinsen
dc.subject.meshHematopoiesisen
dc.subject.meshInflammasomesen
dc.subject.meshIntestinal Mucosaen
dc.subject.meshMiceen
dc.subject.meshMice, Inbred C57BLen
dc.subject.meshMice, Knockouten
dc.subject.meshRadiation Injuriesen
dc.subject.meshRadiation, Ionizingen
dc.subject.meshWhole-Body Irradiationen
dc.titleThe DNA-sensing AIM2 inflammasome controls radiation-induced cell death and tissue injury.en
dc.typeArticleen
dc.contributor.departmentHelmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7, 38124 Braunschweig, Germany.en
dc.identifier.journalScience (New York, N.Y.)en
refterms.dateFOA2018-06-13T05:25:23Z
html.description.abstractAcute exposure to ionizing radiation induces massive cell death and severe damage to tissues containing actively proliferating cells, including bone marrow and the gastrointestinal tract. However, the cellular and molecular mechanisms underlying this pathology remain controversial. Here, we show that mice deficient in the double-stranded DNA sensor AIM2 are protected from both subtotal body irradiation-induced gastrointestinal syndrome and total body irradiation-induced hematopoietic failure. AIM2 mediates the caspase-1-dependent death of intestinal epithelial cells and bone marrow cells in response to double-strand DNA breaks caused by ionizing radiation and chemotherapeutic agents. Mechanistically, we found that AIM2 senses radiation-induced DNA damage in the nucleus to mediate inflammasome activation and cell death. Our results suggest that AIM2 may be a new therapeutic target for ionizing radiation exposure.


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