| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-102 |
Sentence |
denotes |
Wiskott-Aldrich syndrome protein regulates autophagy and inflammasome activity in innate immune cells. |
| T1 |
0-102 |
Sentence |
denotes |
Wiskott-Aldrich syndrome protein regulates autophagy and inflammasome activity in innate immune cells. |
| T2 |
103-217 |
Sentence |
denotes |
Dysregulation of autophagy and inflammasome activity contributes to the development of auto-inflammatory diseases. |
| T2 |
103-217 |
Sentence |
denotes |
Dysregulation of autophagy and inflammasome activity contributes to the development of auto-inflammatory diseases. |
| T3 |
218-325 |
Sentence |
denotes |
Emerging evidence highlights the importance of the actin cytoskeleton in modulating inflammatory responses. |
| T3 |
218-325 |
Sentence |
denotes |
Emerging evidence highlights the importance of the actin cytoskeleton in modulating inflammatory responses. |
| T4 |
326-486 |
Sentence |
denotes |
Here we show that deficiency of Wiskott-Aldrich syndrome protein (WASp), which signals to the actin cytoskeleton, modulates autophagy and inflammasome function. |
| T4 |
326-486 |
Sentence |
denotes |
Here we show that deficiency of Wiskott-Aldrich syndrome protein (WASp), which signals to the actin cytoskeleton, modulates autophagy and inflammasome function. |
| T5 |
487-695 |
Sentence |
denotes |
In a model of sterile inflammation utilizing TLR4 ligation followed by ATP or nigericin treatment, inflammasome activation is enhanced in monocytes from WAS patients and in WAS-knockout mouse dendritic cells. |
| T5 |
487-695 |
Sentence |
denotes |
In a model of sterile inflammation utilizing TLR4 ligation followed by ATP or nigericin treatment, inflammasome activation is enhanced in monocytes from WAS patients and in WAS-knockout mouse dendritic cells. |
| T6 |
696-1050 |
Sentence |
denotes |
In ex vivo models of enteropathogenic Escherichia coli and Shigella flexneri infection, WASp deficiency causes defective bacterial clearance, excessive inflammasome activation and host cell death that are associated with dysregulated septin cage-like formation, impaired autophagic p62/LC3 recruitment and defective formation of canonical autophagosomes. |
| T6 |
696-1050 |
Sentence |
denotes |
In ex vivo models of enteropathogenic Escherichia coli and Shigella flexneri infection, WASp deficiency causes defective bacterial clearance, excessive inflammasome activation and host cell death that are associated with dysregulated septin cage-like formation, impaired autophagic p62/LC3 recruitment and defective formation of canonical autophagosomes. |
| T7 |
1051-1263 |
Sentence |
denotes |
Taken together, we propose that dysregulation of autophagy and inflammasome activities contribute to the autoinflammatory manifestations of WAS, thereby identifying potential targets for therapeutic intervention. |
| T7 |
1051-1263 |
Sentence |
denotes |
Taken together, we propose that dysregulation of autophagy and inflammasome activities contribute to the autoinflammatory manifestations of WAS, thereby identifying potential targets for therapeutic intervention. |