A dominant autoinflammatory disease caused by non-cleavable variants of RIPK1

Tao, PF; Sun, JQ; Wu, ZM; Wang, SH; Wang, J; Li, WJ; Pan, HL; Bai, RK; Zhang, JH; Wang, Y; Lee, PY; Ying, WJ; Zhou, QH; Hou, J; Wang, WJ; Sun, BJ; Yang, M; Liu, DR; Fang, R; Han, H; Yang, ZH; Huang, X; Li, HB; Deuitch, N; Zhang, Y; Dissanayake, D; Haude, K; McWalter, K; Roadhouse, C; MacKenzie, JJ; Laxer, RM; Aksentijevich, I; Yu, XM; Wang, XC; Yuan, JY; Zhou, Q

Yu, XM; Zhou, Q (corresponding author), Zhejiang Univ, Inst Life Sci, MOE Key Lab Biosyst Homeostasis & Protect, Hangzhou, Peoples R China.; Wang, XC (corresponding author), Fudan Univ, Childrens Hosp, Dept Clin Immunol, Shanghai, Peoples R China.; Yuan, JY (corresponding author), Harvard Med Sch, Dept Cell Biol, Boston, MA 02115 USA.

NATURE, 2020; 577 (7788): 109

Abstract

Activation of RIPK1 controls TNF-mediated apoptosis, necroptosis and inflammatory pathways(1). Cleavage of human and mouse RIPK1 after residues D324 a......

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