First Author | Cui Y | Year | 2016 |
Journal | Cell Rep | Volume | 15 |
Issue | 2 | Pages | 256-63 |
PubMed ID | 27050515 | Mgi Jnum | J:234945 |
Mgi Id | MGI:5792466 | Doi | 10.1016/j.celrep.2016.03.016 |
Citation | Cui Y, et al. (2016) Uhrf1 Controls iNKT Cell Survival and Differentiation through the Akt-mTOR Axis. Cell Rep 15(2):256-63 |
abstractText | Uhrf1 (also known as Np95) is a regulator of DNA methylation and histone ubiquitination and plays an important role in embryogenesis and tumorigenesis. Here, we report that Uhrf1 is essential for invariant natural killer T (iNKT) cell development. We found that Uhrf1 was significantly upregulated in stage 1 iNKT cells. Targeted disruption of Uhrf1 resulted in stage 1-specific transition defects as observed by not only increased apoptosis, but also aberrant effector differentiation, which eventually led to the impaired generation of iNKT cells in Uhrf1-deficient mice. Notably, Uhrf1 deficiency resulted in attenuated activation of Akt-mTOR signaling in stage 1 iNKT cells and overexpression of active Akt rescued iNKT cell developmental defects. Collectively, our results suggest that Uhrf1 regulation of the Akt-mTOR signaling pathway is required for iNKT cell development. |