| First Author | Xiao S | Year | 2004 |
| Journal | J Immunol | Volume | 173 |
| Issue | 8 | Pages | 5095-102 |
| PubMed ID | 15470053 | Mgi Jnum | J:93704 |
| Mgi Id | MGI:3505600 | Doi | 10.4049/jimmunol.173.8.5095 |
| Citation | Xiao S, et al. (2004) Novel negative regulator of expression in Fas ligand (CD178) cytoplasmic tail: evidence for translational regulation and against Fas ligand retention in secretory lysosomes. J Immunol 173(8):5095-102 |
| abstractText | Fas ligand ((FasL) CD178), a type II transmembrane protein, induces apoptosis of cells expressing the Fas receptor. It possesses a unique cytoplasmic tail (FasLCyt) of 80 aa. As a type II transmembrane protein, the early synthesis of FasLCyt could affect FasL translation by impacting FasL endoplasmic reticulum translocation and/or endoplasmic reticulum retention. Previous studies suggest that the proline-rich domain (aa 43-70) in FasLCyt (FasLPRD) inhibits FasL membrane expression by retaining FasL in the secretory lysosomes. This report shows that deletion of aa 2-33 of FasLCyt dramatically increased total FasL levels and FasL cell surface expression. This negative regulator of FasL expression is dominant despite the presence of FasLPRD. In addition, retention of proline-rich domain-containing FasL in the cytoplasm was not observed. Moreover, we demonstrated that FasLCyt regulates FasL expression by controlling the rate of de novo synthesis of FasL. Our study demonstrated a novel negative regulator of FasL expression in the FasLCyt region and its mechanism of action. |
