The end of RIPK1-RIPK3-MLKL–mediated necroptosis in acetaminophen-induced hepatotoxicity?

Hepatology

Volumn 64, Issue 1, 2016, Pages 311-312

  Yang, Xiao ^a,b   Chao, Xiaojuan ^a   Wang, Zheng Tao ^b   Ding, Wen Xing ^a  

^a UNIVERSITY OF KANSAS SCHOOL OF MEDICINE   (United States)

^b SHANGHAI UNIVERSITY OF TRADITIONAL CHINESE MEDICINE   (China)

Author keywords

[No Author keywords available]

Indexed keywords

MLKL PROTEIN; PARACETAMOL; PROTEIN; PROTEIN KINASE; RECEPTOR INTERACTING PROTEIN KINASE 1; RECEPTOR INTERACTING PROTEIN KINASE 3; STRESS ACTIVATED PROTEIN KINASE; UNCLASSIFIED DRUG;

CELL DEATH; INNATE IMMUNITY; LETTER; LIVER INJURY; LIVER TOXICITY; NECROPTOSIS; NONHUMAN; PRIORITY JOURNAL; PROTEIN PROTEIN INTERACTION;

EID: 85028256263     PISSN: 02709139     EISSN: 15273350     Source Type: Journal    
DOI: 10.1002/hep.28263     Document Type: Letter

References (4)

1. Dara L, Johnson H, Suda J, Win S, Gaarde W, Han D, et al. Receptor Interacting protein kinase-1 mediates murine acetaminophen toxicity independent of the necrosome and not through necroptosis. Hepatology 2015;62:1847-1857.
2. Ramachandran A, McGill MR, Xie Y, Ni HM, Ding WX, Jaeschke H. Receptor interacting protein kinase 3 is a critical early mediator of acetaminophen-induced hepatocyte necrosis in mice. Hepatology 2013;58:2099-2108.
3. He S, Wang L, Miao L, Wang T, Du F, Zhao L, et al. Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha. Cell 2009;137:1100-1111.
4. Wu J, Huang Z, Ren J, Zhang Z, He P, Li Y, et al. Mlkl knockout mice demonstrate the indispensable role of Mlkl in necroptosis. Cell Res 2013;23:994-1006.