| First Author | Wu C | Year | 2016 |
| Journal | Exp Cell Res | Volume | 347 |
| Issue | 1 | Pages | 65-73 |
| PubMed ID | 27426725 | Mgi Jnum | J:309791 |
| Mgi Id | MGI:6709225 | Doi | 10.1016/j.yexcr.2016.07.011 |
| Citation | Wu C, et al. (2016) LRRC14 attenuates Toll-like receptor-mediated NF-kappaB signaling through disruption of IKK complex. Exp Cell Res 347(1):65-73 |
| abstractText | Activation of NF-kappaB signaling plays pivotal roles in innate immune responses against pathogens. It requires strict control to avert inflammatory diseases. However, the mechanisms underlying this tight regulation are not completely understood. Here, we identified LRRC14, a novel member of LRR (leucine-rich repeat) protein family, as a negative regulator in TLR signaling. Expression of LRRC14 resulted in decreased activation of NF-kappaB, whereas knockdown of LRRC14 enhanced NF-kappaB activation as well as the production of inflammatory cytokines. Mechanistically, LRRC14 bound to HLH domain of IKKbeta to block its interaction with NEMO and thereby inhibiting the phosphorylation of IKKbeta and NF-kappaB activation. In addition, our data showed that TLR signaling led to lower expression of LRRC14. Together, LRRC14 may function as a checkpoint to prevent overzealous inflammation. |
