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"The authors showed that CYLD deubiquitinated RIPK2 in macrophages infected with L. monocytogenes, leading to impaired activation of NF-kappaB, reduced production of proinflammatory cytokines and reactive oxygen and nitrogen species, which ultimately resulted in impaired infection control."
"CYLD-mediated K63 deubiquitination of RIPK2 resulted in an impaired activation of both NF-kappaB and ERK1/2 pathways, reduced production of proinflammatory cytokines interleukin-6 (IL-6), IL-12, anti-listerial reactive oxygen species (ROS) and nitric oxide (NO), and, finally, impaired pathogen control."