MRE11 mobilizes CGAS and drives ZBP1-dependent necroptosis  

作　　者：Manuel Beltrán-Visiedo Siddharth Balachandran Lorenzo Galluzzi 

机构地区：[1]Department of Radiation Oncology,Weill Cornell Medicine,New York,NY,USA. [2]Center for Immunology,Fox Chase Cancer Center,Philadelphia,PA,USA. [3]Sandra and Edward Meyer Cancer Center,New York,NY,USA. [4]Caryl and Israel Englander Institute for Precision Medicine,New York,NY,USA.

出　　处：《Cell Research》2024年第7期477-478,共2页细胞研究（英文版）

摘　　要：Recent data from Cho et al.demonstrate that the DNA repair protein MRE11 liberates CGAS from nucleosomes to license type I interferon secretion upon oncogenic stress and ionizing radiation.MRE11-mediated CGAS activation culminates in ZBP1-driven necroptosis,which is essential for limiting mammary oncogenesis.Mammalian cells are endowed with numerous systems that detect infectious threats,including(but not limited to)a variety of receptors that react to exogenous and/or ectopic nucleic acids by promoting cellular and organismal defense responses,which often involve the secretion of antimicrobial and pro-inflammatory cytokines like type I interferon(IFN).1 While these systems have emerged as part of the pathogen-host co-evolution,abundant preclinical and clinical findings demonstrate that the recognition of immunogenic endogenous RNA and DNA species that are formed(or change subcellular localization)in response to stress is paramount for the preservation of organismal homeostasis,especially in the context of malignant transformation.

关 键 词：INTERFERON HOMEOSTASIS ENDOGENOUS 

分 类 号：Q2[生物学—细胞生物学]