| First Author | Zhao X | Year | 2018 |
| Journal | Front Med | Volume | 12 |
| Issue | 5 | Pages | 559-565 |
| PubMed ID | 29247407 | Mgi Jnum | J:302014 |
| Mgi Id | MGI:6507463 | Doi | 10.1007/s11684-017-0562-3 |
| Citation | Zhao X, et al. (2018) Zfyve16 regulates the proliferation of B-lymphoid cells. Front Med 12(5):559-565 |
| abstractText | Zfyve16 (a.k.a. endofin or endosome-associated FYVE-domain protein), a member of the FYVE-domain protein family, is involved in endosomal trafficking and in TGF-beta, BMP, and EGFR signaling. The FYVE protein SARA regulates the TGF-beta signaling pathway by recruiting Smad2/3 and accelerating their phosphorylation, thereby altering their susceptibility to TGF-beta-mediated T cell suppression. Zfyve16 binds to Smad4 and their binding affects the formation of Smad2/3-Smad4 complex in TGF-beta signaling. However, the in vivo function of Zfyve16 remains unknown. In this study, we generated a Zfyve16 knockout mouse strain (Zfyve16(KO)) and examined its hematopoietic phenotypes and hematopoietic reconstruction ability. The proportion of Tcells in the peripheral blood of Zfyve16(KO) mice increases compared with that in wild-type mice. This finding is consistent with the role of Zfyve16 in facilitating TGF-beta signaling. Unpredictably, B cell proliferation is inhibited in Zfyve16(KO) mice. The proliferation potential of Zfyve16(KO) B-lymphoid cells also significantly decreases in vitro. These results suggest that Zfyve16 inhibits the proliferation of T cells, possibly through the TGF-beta signaling, but upregulates the proliferation of B-lymphoid cells. |
