| First Author | Choi HK | Year | 2013 |
| Journal | Cell Res | Volume | 23 |
| Issue | 4 | Pages | 524-36 |
| PubMed ID | 23478294 | Mgi Jnum | J:334006 |
| Mgi Id | MGI:7444879 | Doi | 10.1038/cr.2013.33 |
| Citation | Choi HK, et al. (2013) Early estrogen-induced gene 1, a novel RANK signaling component, is essential for osteoclastogenesis. Cell Res 23(4):524-36 |
| abstractText | The receptor activator of NF-kappaB (RANK) and immunoreceptor tyrosine-based activation motif (ITAM)-containing adaptors are essential factors involved in regulating osteoclast formation and bone remodeling. Here, we identify early estrogen-induced gene 1 (EEIG1) as a novel RANK ligand (RANKL)-inducible protein that physically interacts with RANK and further associates with Gab2, PLCgamma2 and Tec/Btk kinases upon RANKL stimulation. EEIG1 positively regulates RANKL-induced osteoclast formation, likely due to its ability to facilitate RANKL-stimulated PLCgamma2 phosphorylation and NFATc1 induction. In addition, an inhibitory peptide designed to block RANK-EEIG1 interaction inhibited RANKL-induced bone destruction by reducing osteoclast formation. Together, our results identify EEIG1 as a novel RANK signaling component controlling RANK-mediated osteoclast formation, and suggest that targeting EEIG1 might represent a new therapeutic strategy for the treatment of pathological bone resorption. |
