Cyclophilin J limits inflammation through the blockage of ubiquitin chain sensing

Chunjie Sheng, Chen Yao, Ziyang Wang, Hongyuan Chen, Yu Zhao, Dazhi Xu, Haojie Huang, Wenlin Huang and Shuai Chen ()
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Chunjie Sheng: Collaborative Innovation Center of Cancer Medicine
Chen Yao: Collaborative Innovation Center of Cancer Medicine
Ziyang Wang: Collaborative Innovation Center of Cancer Medicine
Hongyuan Chen: Guangdong Pharmaceutical University
Yu Zhao: Mayo Clinic College of Medicine
Dazhi Xu: Collaborative Innovation Center of Cancer Medicine
Haojie Huang: Mayo Clinic College of Medicine
Wenlin Huang: Collaborative Innovation Center of Cancer Medicine
Shuai Chen: Collaborative Innovation Center of Cancer Medicine

Nature Communications, 2018, vol. 9, issue 1, 1-13

Abstract: Abstract Maintaining innate immune homeostasis is important for individual health. Npl4 zinc finger (NZF) domain-mediated ubiquitin chain sensing is reported to function in the nuclear factor-kappa B (NF-κB) signal pathway, but the regulatory mechanism remains elusive. Here we show that cyclophilin J (CYPJ), a member of the peptidylprolyl isomerase family, is induced by inflammation. CYPJ interacts with the NZF domain of transform growth factor-β activated kinase 1 binding protein 2 and 3 as well as components of the linear ubiquitin chain assembly complex to block the binding of ubiquitin-chain and negatively regulates NF-κB signaling. Mice with Cypj deficiency are susceptible to lipopolysaccharide and heat-killed Listeria monocytogenes-induced sepsis and dextran sulfate sodium-induced colitis. These findings identify CYPJ as a negative feedback regulator of the NF-κB signaling pathway, and provide insights for understanding the homeostasis of innate immunity.

Date: 2018
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DOI: 10.1038/s41467-018-06756-3

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