H
Haibing Zhang
Researcher at Chinese Academy of Sciences
Publications - 52
Citations - 1420
Haibing Zhang is an academic researcher from Chinese Academy of Sciences. The author has contributed to research in topics: Necroptosis & Programmed cell death. The author has an hindex of 18, co-authored 35 publications receiving 1027 citations. Previous affiliations of Haibing Zhang include Nanjing University of Science and Technology & Shanghai Jiao Tong University.
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Journal ArticleDOI
Functional complementation between FADD and RIP1 in embryos and lymphocytes
Haibing Zhang,Xiaohui Zhou,Xiaohui Zhou,Thomas McQuade,Jinghe Li,Francis Ka-Ming Chan,Jianke Zhang +6 more
TL;DR: It is shown that Fadd−/− embryos contain raised levels of RIP1 and exhibit massive necrosis, and an unexpected cell-type-specific interplay between FADD and RIP1 is critical for the regulation of apoptosis and necrosis during embryogenesis and lymphocyte function.
Journal ArticleDOI
RIP1-dependent and independent effects of necrostatin-1 in necrosis and T cell activation.
TL;DR: The results reveal that besides RIP1, Nec-1 also targets other factors crucial for necrosis induction in L929 cells, and high doses of Nec- 1 inhibit other signal transduction pathways such as that for T cell receptor activation.
Journal ArticleDOI
Gut epithelial TSC1/mTOR controls RIPK3-dependent necroptosis in intestinal inflammation and cancer
Yadong Xie,Yadong Xie,Yifan Zhao,Lei Shi,Wei Li,Kun Chen,Min Li,Xia Chen,Haiwei Zhang,Tiantian Li,Yu Matsuzawa-Ishimoto,Xiaomin Yao,Dianhui Shao,Zunfu Ke,Jian Li,Chen Yan,Xiaoming Zhang,Jun Cui,Shuzhong Cui,Qibin Leng,Ken Cadwell,Xiaoxia Li,Hong Wei,Haibing Zhang,Huabin Li,Huabin Li,Hui Xiao +26 more
TL;DR: The results uncovered a critical role for TSC1-mTOR in restraining the expression and activation of RIPK3 in the gut epithelium through Trim11-mediated ubiquitination and autophagy-dependent degradation and identify the mTOR-RIPK3-necroptosis axis as a driving force for intestinal inflammation and cancer.
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MLKL and FADD Are Critical for Suppressing Progressive Lymphoproliferative Disease and Activating the NLRP3 Inflammasome
Xixi Zhang,Cunxian Fan,Haiwei Zhang,Qun Zhao,Yongbo Liu,Chengxian Xu,Qun Xie,Qun Xie,Xiaoxia Wu,Xianjun Yu,Xianjun Yu,Jianke Zhang,Haibing Zhang +12 more
TL;DR: It is shown that genetic deletion of Mlkl rescues the developmental defect in Fadd-deficient mice and that Fadd (-/-)Mlkl(-/-) mice are viable and fertile and play critical roles in preventing lymphoproliferative disease and activating the NLRP3 inflammasome.
Journal ArticleDOI
LNK/SH2B3 regulates IL-7 receptor signaling in normal and malignant B-progenitors
Ying Cheng,Kudakwashe R. Chikwava,Chao Wu,Haibing Zhang,Anchit Bhagat,Dehua Pei,John K. Choi,Wei Tong +7 more
TL;DR: The results suggest that LNK suppresses IL-7R/JAK/STAT signaling to restrict pro-/pre-B progenitor expansion and leukemia development, providing a pathogenic mechanism and a potential therapeutic approach for B-ALLs with LNK mutations.