RIPK1 is required for ZBP1-driven necroptosis in human cells.

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Tác giả: Oluwamuyiwa T Amusan, Siddharth Balachandran, Benjamin Bellenie, Hongyan Guo, Heather S Koehler, Yixun Li, Chang Liu, Pascal Meier, Seyedeh L Poorbaghi, Kim Seong, Yuchen Shen, Tencho Tenev, Jason W Upton, Jian Wang, Shuqi Wang, Rebecca Wilson, Joseph Yates, Chaoran Yin, Ting Zhang

Ngôn ngữ: eng

Ký hiệu phân loại: 946.7 *Eastern Spain and Andorra

Thông tin xuất bản: United States : PLoS biology , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 473307

Necroptosis initiated by the host sensor Z-NA binding protein 1 (ZBP1) is essential for host defense against a growing number of viruses, including herpes simplex virus 1 (HSV-1). Studies with HSV-1 and other necroptogenic stimuli in murine settings have suggested that ZBP1 triggers necroptosis by directly complexing with the kinase RIPK3. Whether this is also the case in human cells, or whether additional co-factors are needed for ZBP1-mediated necroptosis, is unclear. Here, we show that ZBP1-induced necroptosis in human cells requires RIPK1. We have found that RIPK1 is essential for forming a stable and functional ZBP1-RIPK3 complex in human cells, but is dispensable for the formation of the equivalent murine complex. The receptor-interacting protein (RIP) homology interaction motif (RHIM) in RIPK3 is responsible for this difference between the 2 species, because replacing the RHIM in human RIPK3 with the RHIM from murine RIPK3 is sufficient to overcome the requirement for RIPK1 in human cells. These observations describe a critical mechanistic difference between mice and humans in how ZBP1 engages in necroptosis, with important implications for treating human diseases.
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