| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
69-258 |
DRI_Background |
denotes |
This study examines the role of the signal transducer and activator of transcription 1 (STAT1) in induction of lipopolysaccharide (LPS)-stimulated gene expression both in vitro and in vivo. |
| T2 |
259-304 |
DRI_Outcome |
denotes |
LPS-induced expression of an interferon (IFN) |
| T3 |
322-610 |
DRI_Outcome |
denotes |
protein (IP-10), IFN regulatory factor-1 (IRF-1), and inducible nitric oxide synthase (iNOS) mRNAs was severely impaired in macrophages prepared from Stat1-/- mice, whereas levels of tumor necrosis factor alpha and KC (a C-X-C chemokine) mRNA in LPS-treated cell cultures were unaffected. |
| T4 |
611-717 |
DRI_Background |
denotes |
A similar deficiency in LPS-induced gene expression was observed in livers and spleens from Stat1-/- mice. |
| T5 |
718-856 |
DRI_Outcome |
denotes |
The reduced LPS-stimulated gene expression seen in Stat1-/- macrophages was not the result of reduced activation of nuclear factor kappaB. |
| T6 |
857-1020 |
DRI_Outcome |
denotes |
LPS stimulated the delayed activation of both IFN-stimulated response element and IFN-gamma-activated sequence binding activity in macrophages from wild-type mice. |
| T7 |
1021-1148 |
DRI_Approach |
denotes |
Activation of these STAT1-containing transcription factors was mediated by the intermediate induction of type I IFNs, since the |
| T8 |
1166-1327 |
DRI_Approach |
denotes |
, IRF-1, and iNOS mRNA expression was markedly reduced in macrophages from IFN-alpha/betaR-/- mice and blocked by cotreatment with antibodies against type I IFN. |
| T9 |
1328-1594 |
DRI_Outcome |
denotes |
These results indicate that indirect activation of STAT1 by LPS-induced type I IFN participates in promoting optimal expression of LPS-inducible genes, and they suggest that STAT1 may play a critical role in innate immunity against gram-negative bacterial infection. |
