| First Author | Sheng C | Year | 2018 |
| Journal | Nat Commun | Volume | 9 |
| Issue | 1 | Pages | 4381 |
| PubMed ID | 30348973 | Mgi Jnum | J:268350 |
| Mgi Id | MGI:6267573 | Doi | 10.1038/s41467-018-06756-3 |
| Citation | Sheng C, et al. (2018) Cyclophilin J limits inflammation through the blockage of ubiquitin chain sensing. Nat Commun 9(1):4381 |
| abstractText | 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-kappaB) 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-beta 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-kappaB 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-kappaB signaling pathway, and provide insights for understanding the homeostasis of innate immunity. |
