| First Author | Guo Z | Year | 2016 |
| Journal | Nat Commun | Volume | 7 |
| Pages | 10307 | PubMed ID | 26728942 |
| Mgi Jnum | J:235820 | Mgi Id | MGI:5803756 |
| Doi | 10.1038/ncomms10307 | Citation | Guo Z, et al. (2016) DCAF1 controls T-cell function via p53-dependent and -independent mechanisms. Nat Commun 7:10307 |
| abstractText | On activation, naive T cells grow in size and enter cell cycle to mount immune response. How the fundamental processes of T-cell growth and cell cycle entry are regulated is poorly understood. Here we report that DCAF1 (Ddb1-cullin4-associated-factor 1) is essential for these processes. The deletion of DCAF1 in T cells impairs their peripheral homeostasis. DCAF1 is upregulated on T-cell receptor activation and critical for activation-induced T-cell growth, cell cycle entry and proliferation. In addition, DCAF1 is required for T-cell expansion and function during anti-viral and autoimmune responses in vivo. DCAF1 deletion leads to a drastic stabilization of p53 protein, which can be attributed to a requirement of DCAF1 for MDM2-mediated p53 poly-ubiquitination. Importantly, p53 deletion rescues the cell cycle entry defect but not the growth defect of DCAF1-deficient cells. Therefore, DCAF1 is vital for T-cell function through p53-dependent and -independent mechanisms. |
