| First Author | Jiang L | Year | 2018 |
| Journal | J Exp Med | Volume | 215 |
| Issue | 5 | Pages | 1337-1347 |
| PubMed ID | 29669741 | Mgi Jnum | J:261594 |
| Mgi Id | MGI:6155801 | Doi | 10.1084/jem.20171477 |
| Citation | Jiang L, et al. (2018) SHP-1 regulates hematopoietic stem cell quiescence by coordinating TGF-beta signaling. J Exp Med 215(5):1337-1347 |
| abstractText | Cell cycle quiescence is critical for hematopoietic stem cell (HSC) maintenance. TGF-beta signaling in bone marrow niche has been identified in regulating HSC quiescence; however, the intrinsic regulatory mechanisms remain unclear. This study reports that Shp-1 knockout HSCs have attenuated quiescence and impaired long-term self-renewal. SHP-1-activated HSCs are surrounded by megakaryocytes, which regulate HSC quiescence by producing TGF-beta1. Mechanistically, SHP-1 interacts with the immunoreceptor tyrosine-based inhibition motif on TGF-beta receptor 1 and is critical for TGF-beta signaling activation in HSCs. Functionally, Shp-1 knockout HSCs do not respond to TGF-beta-enforced HSC quiescence regulation, both in vitro and in vivo. Therefore, we identify TGF-beta-SHP-1 as a novel intrinsic regulatory mechanism for HSC quiescence maintenance. |
