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STAC2 negatively regulates osteoclast formation by targeting the RANK signaling complex
- Title
- STAC2 negatively regulates osteoclast formation by targeting the RANK signaling complex
- Authors
- Jeong, Eutteum; Choi, Han Kyoung; Park, Jin Hee; Lee, Soo Young
- Ewha Authors
- 이수영
- SCOPUS Author ID
- 이수영
- Issue Date
- 2018
- Journal Title
- CELL DEATH AND DIFFERENTIATION
- ISSN
- 1350-9047
1476-5403
- Citation
- CELL DEATH AND DIFFERENTIATION vol. 25, no. 8, pp. 1364 - 1374
- Publisher
- NATURE PUBLISHING GROUP
- Indexed
- SCIE; SCOPUS
- Document Type
- Article
- Abstract
- The receptor activator of nuclear factor-kappa B (RANK) protein activates various protein kinase signaling cascades, including those involving NF-kappa B, mitogen-activated protein kinase (MAPK), and Bruton tyrosine kinase (Btk)/tyrosine-protein kinase Tec. However, the mechanism underlying the negative regulation of RANK by downstream signaling molecules remains unclear. Here, we report that Src homology 3 domain and cysteine-rich domain-containing protein 2 (STAC2) is a novel RANK ligand-inducible protein that negatively regulates RANK-mediated osteoclast formation. STAC2 physically interacts with RANK and inhibits the formation of the RANK signaling complex, which contains Grb-2-associated binder 2 (Gab2) and phospholipase C gamma 2 (PLC gamma 2), thus leading to the suppression of RANK-mediated NF-kappa B and MAPK activation. Furthermore, STAC2 overexpression limits Btk/Tec-mediated PLC gamma 2 phosphorylation via the interaction between STAC2 and Btk/Tec. Taken together, our results reveal a novel mechanism whereby RANK signaling is restricted by its physical interaction with STAC2.
- DOI
- 10.1038/s41418-017-0048-5
- Appears in Collections:
- 자연과학대학 > 생명과학전공 > Journal papers
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