| First Author | Putz EM | Year | 2013 |
| Journal | Cell Rep | Volume | 4 |
| Issue | 3 | Pages | 437-44 |
| PubMed ID | 23933255 | Mgi Jnum | J:201893 |
| Mgi Id | MGI:5516137 | Doi | 10.1016/j.celrep.2013.07.012 |
| Citation | Putz EM, et al. (2013) CDK8-mediated STAT1-S727 phosphorylation restrains NK cell cytotoxicity and tumor surveillance. Cell Rep 4(3):437-44 |
| abstractText | The transcription factor STAT1 is important in natural killer (NK) cells, which provide immediate defense against tumor and virally infected cells. We show that mutation of a single phosphorylation site (Stat1-S727A) enhances NK cell cytotoxicity against a range of tumor cells, accompanied by increased expression of perforin and granzyme B. Stat1-S727A mice display significantly delayed disease onset in NK cell-surveilled tumor models including melanoma, leukemia, and metastasizing breast cancer. Constitutive phosphorylation of S727 depends on cyclin-dependent kinase 8 (CDK8). Inhibition of CDK8-mediated STAT1-S727 phosphorylation may thus represent a therapeutic strategy for stimulating NK cell-mediated tumor surveillance. |
