Department of Molecular Biosciences, LaMontagne Center for Infectious Disease, Institute for Cellular and Molecular Biology, University of Texas at Austin, Austin, TX 78712, USA.
Department of Microbiology, Immunology, & Molecular Genetics, University of Texas Health Sciences Center at San Antonio, San Antonio, TX 78229, USA.
Cell Host Microbe. 2017 Mar 8;21(3):290-293. doi: 10.1016/j.chom.2017.01.016.
Interrogation of murine cytomegalovirus (MCMV)-encoded cell-death suppressors revealed that necroptosis functions as a trap door to eliminate virally infected cells. This crucial host defense pathway is orchestrated by the sensing of infection by DAI/ZBP-1, engagement of the kinase RIPK3, and subsequent membrane permeablization by the pseudokinase MLKL.
对鼠巨细胞病毒（MCMV）编码的细胞死亡抑制剂的研究表明，细胞坏死是一种消除病毒感染细胞的“活板门”。这种关键的宿主防御途径是通过 DAI/ZBP-1 对感染的感知、激酶 RIPK3 的参与以及随后伪激酶 MLKL 的膜通透性来协调的。
