Journal
CELL REPORTS
Volume 4, Issue 3, Pages 437-444Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2013.07.012
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Funding
- Austrian Academy of Science DOC-fFORTE fellowship
- Austrian Science Fund FWF grant [SFB F28]
- GEN-AU program Austromouse of the Austrian Federal Ministry of Science and Research
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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.
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