AI Article Synopsis
- - The transcription factor STAT1 is crucial for natural killer (NK) cells, which act as the body's first line of defense against tumors and viral infections.
- - A specific mutation in STAT1 called Stat1-S727A boosts NK cell effectiveness against various tumors by increasing levels of perforin and granzyme B.
- - Targeting the phosphorylation process of STAT1 by inhibiting cyclin-dependent kinase 8 (CDK8) could be a new way to enhance NK cell tumor-fighting abilities.
Article Abstract
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.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3748339 | PMC |
| http://dx.doi.org/10.1016/j.celrep.2013.07.012 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!