Id |
Subject |
Object |
Predicate |
Lexical cue |
T1 |
0-101 |
Sentence |
denotes |
IKKα contributes to canonical NF-κB activation downstream of Nod1-mediated peptidoglycan recognition. |
T1 |
0-101 |
Sentence |
denotes |
IKKα contributes to canonical NF-κB activation downstream of Nod1-mediated peptidoglycan recognition. |
T2 |
102-113 |
Sentence |
denotes |
BACKGROUND: |
T2 |
102-113 |
Sentence |
denotes |
BACKGROUND: |
T3 |
114-338 |
Sentence |
denotes |
During pathogen infection, innate immunity is initiated via the recognition of microbial products by pattern recognition receptors and the subsequent activation of transcription factors that upregulate proinflammatory genes. |
T3 |
114-338 |
Sentence |
denotes |
During pathogen infection, innate immunity is initiated via the recognition of microbial products by pattern recognition receptors and the subsequent activation of transcription factors that upregulate proinflammatory genes. |
T4 |
339-538 |
Sentence |
denotes |
By controlling the expression of cytokines, chemokines, anti-bacterial peptides and adhesion molecules, the transcription factor nuclear factor-kappa B (NF-κB) has a central function in this process. |
T4 |
339-538 |
Sentence |
denotes |
By controlling the expression of cytokines, chemokines, anti-bacterial peptides and adhesion molecules, the transcription factor nuclear factor-kappa B (NF-κB) has a central function in this process. |
T5 |
539-837 |
Sentence |
denotes |
In a typical model of NF-κB activation, the recognition of pathogen associated molecules triggers the canonical NF-κB pathway that depends on the phosphorylation of Inhibitor of NF-κB (IκB) by the catalytic subunit IκB kinase β (IKKβ), its degradation and the nuclear translocation of NF-κB dimers. |
T5 |
539-837 |
Sentence |
denotes |
In a typical model of NF-κB activation, the recognition of pathogen associated molecules triggers the canonical NF-κB pathway that depends on the phosphorylation of Inhibitor of NF-κB (IκB) by the catalytic subunit IκB kinase β (IKKβ), its degradation and the nuclear translocation of NF-κB dimers. |
T6 |
838-850 |
Sentence |
denotes |
METHODOLOGY: |
T6 |
838-850 |
Sentence |
denotes |
METHODOLOGY: |
T7 |
851-1071 |
Sentence |
denotes |
Here, we performed an RNA interference (RNAi) screen on Shigella flexneri-induced NF-κB activation to identify new factors involved in the regulation of NF-κB following infection of epithelial cells by invasive bacteria. |
T7 |
851-1071 |
Sentence |
denotes |
Here, we performed an RNA interference (RNAi) screen on Shigella flexneri-induced NF-κB activation to identify new factors involved in the regulation of NF-κB following infection of epithelial cells by invasive bacteria. |
T8 |
1072-1232 |
Sentence |
denotes |
By targeting a subset of the human signaling proteome, we found that the catalytic subunit IKKα is also required for complete NF-κB activation during infection. |
T8 |
1072-1232 |
Sentence |
denotes |
By targeting a subset of the human signaling proteome, we found that the catalytic subunit IKKα is also required for complete NF-κB activation during infection. |
T9 |
1233-1417 |
Sentence |
denotes |
Depletion of IKKα by RNAi strongly reduces the nuclear translocation of NF-κB p65 during S. flexneri infection as well as the expression of the proinflammatory chemokine interleukin-8. |
T9 |
1233-1417 |
Sentence |
denotes |
Depletion of IKKα by RNAi strongly reduces the nuclear translocation of NF-κB p65 during S. flexneri infection as well as the expression of the proinflammatory chemokine interleukin-8. |
T10 |
1418-1528 |
Sentence |
denotes |
Similar to IKKβ, IKKα contributes to the phosphorylation of IκBα on serines 32 and 36, and to its degradation. |
T10 |
1418-1528 |
Sentence |
denotes |
Similar to IKKβ, IKKα contributes to the phosphorylation of IκBα on serines 32 and 36, and to its degradation. |
T11 |
1529-1737 |
Sentence |
denotes |
Experiments performed with the synthetic Nod1 ligand L-Ala-D-γ-Glu-meso-diaminopimelic acid confirmed that IKKα is involved in NF-κB activation triggered downstream of Nod1-mediated peptidoglycan recognition. |
T11 |
1529-1737 |
Sentence |
denotes |
Experiments performed with the synthetic Nod1 ligand L-Ala-D-γ-Glu-meso-diaminopimelic acid confirmed that IKKα is involved in NF-κB activation triggered downstream of Nod1-mediated peptidoglycan recognition. |
T12 |
1738-1750 |
Sentence |
denotes |
CONCLUSIONS: |
T12 |
1738-1750 |
Sentence |
denotes |
CONCLUSIONS: |
T13 |
1751-1918 |
Sentence |
denotes |
Taken together, these results demonstrate the unexpected role of IKKα in the canonical NF-κB pathway triggered by peptidoglycan recognition during bacterial infection. |
T13 |
1751-1918 |
Sentence |
denotes |
Taken together, these results demonstrate the unexpected role of IKKα in the canonical NF-κB pathway triggered by peptidoglycan recognition during bacterial infection. |
T14 |
1919-2078 |
Sentence |
denotes |
In addition, they suggest that IKKα may be an important drug target for the development of treatments that aim at limiting inflammation in bacterial infection. |
T14 |
1919-2078 |
Sentence |
denotes |
In addition, they suggest that IKKα may be an important drug target for the development of treatments that aim at limiting inflammation in bacterial infection. |