| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
119-313 |
DRI_Approach |
denotes |
Detection of cytosolic DNA by the enzyme cGAS triggers the production of cGAMP, a second messenger that binds and activates the adaptor protein STING, which leads to interferon (IFN) production. |
| T2 |
314-463 |
DRI_Approach |
denotes |
Here, we found that in vivo natural killer (NK) cell killing of tumor cells, but not of normal cells, depends on STING expression in non-tumor cells. |
| T3 |
464-634 |
DRI_Background |
denotes |
Experiments using transplantable tumor models in STING- and cGAS-deficient mice revealed that cGAS expression by tumor cells was critical for tumor rejection by NK cells. |
| T4 |
635-710 |
DRI_Background |
denotes |
In contrast, cGAS expression by host cells was dispensable, suggesting that |
| T5 |
731-791 |
DRI_Background |
denotes |
is transferred to non-tumor cells, where it activates STING. |
| T6 |
792-907 |
DRI_Approach |
denotes |
cGAMP administration triggered STING activation and IFN-β production in myeloid cells and B cells but not NK cells. |
| T7 |
908-1087 |
DRI_Outcome |
denotes |
Our results reveal that the anti-tumor response of NK cells critically depends on the cytosolic DNA sensing pathway, similar to its role in defense against pathogens, and identify |
| T8 |
1108-1198 |
DRI_Outcome |
denotes |
as a major determinant of tumor immunogenicity with implications for cancer immunotherapy. |
