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PubMed_Structured_Abstracts

Id Subject Object Predicate Lexical cue
T1 114-837 BACKGROUND 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. 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. 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.
T2 851-1737 METHODS 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. 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. 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. Similar to IKKβ, IKKα contributes to the phosphorylation of IκBα on serines 32 and 36, and to its degradation. 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.
T3 1751-2078 CONCLUSIONS denotes Taken together, these results demonstrate the unexpected role of IKKα in the canonical NF-κB pathway triggered by peptidoglycan recognition during bacterial infection. 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.

Inflammaging

Id Subject Object Predicate Lexical cue
T1 0-101 Sentence denotes IKKα contributes to canonical NF-κB activation downstream of Nod1-mediated peptidoglycan recognition.
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.
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.
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.
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.
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.
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.
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.
T1 0-101 Sentence denotes IKKα contributes to canonical NF-κB activation downstream of Nod1-mediated peptidoglycan recognition.
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.
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.
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.
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.
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.
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.
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.

Allie

Id Subject Object Predicate Lexical cue
SS1_20976174_3_0 468-490 expanded denotes nuclear factor-kappa B
SS2_20976174_3_0 492-497 abbr denotes NF-κB
SS1_20976174_4_0 704-722 expanded denotes Inhibitor of NF-κB
SS2_20976174_4_0 724-727 abbr denotes IκB
SS1_20976174_4_1 754-766 expanded denotes IκB kinase β
SS2_20976174_4_1 768-772 abbr denotes IKKβ
SS1_20976174_6_0 873-889 expanded denotes RNA interference
SS2_20976174_6_0 891-895 abbr denotes RNAi
AE1_20976174_3_0 SS1_20976174_3_0 SS2_20976174_3_0 abbreviatedTo nuclear factor-kappa B,NF-κB
AE1_20976174_4_0 SS1_20976174_4_0 SS2_20976174_4_0 abbreviatedTo Inhibitor of NF-κB,IκB
AE1_20976174_4_1 SS1_20976174_4_1 SS2_20976174_4_1 abbreviatedTo IκB kinase β,IKKβ
AE1_20976174_6_0 SS1_20976174_6_0 SS2_20976174_6_0 abbreviatedTo RNA interference,RNAi