| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-97 |
Sentence |
denotes |
Uncoupling of Pyrin-only protein 2 (POP2)-mediated dual regulation of NF-κB and the inflammasome. |
| T1 |
0-97 |
Sentence |
denotes |
Uncoupling of Pyrin-only protein 2 (POP2)-mediated dual regulation of NF-κB and the inflammasome. |
| T2 |
98-276 |
Sentence |
denotes |
Activation of transcription factor NF-κB and inflammasome-directed caspase-1 cleavage of IL-1β are key processes in the inflammatory response to pathogen or host-derived signals. |
| T2 |
98-276 |
Sentence |
denotes |
Activation of transcription factor NF-κB and inflammasome-directed caspase-1 cleavage of IL-1β are key processes in the inflammatory response to pathogen or host-derived signals. |
| T3 |
277-495 |
Sentence |
denotes |
Pyrin-only proteins (POPs) are restricted to Old World monkeys, apes, and humans and have previously been shown to impair inflammasome assembly and/or NF-κB p65 transcriptional activity in transfected epithelial cells. |
| T3 |
277-495 |
Sentence |
denotes |
Pyrin-only proteins (POPs) are restricted to Old World monkeys, apes, and humans and have previously been shown to impair inflammasome assembly and/or NF-κB p65 transcriptional activity in transfected epithelial cells. |
| T4 |
496-608 |
Sentence |
denotes |
However, the biological role of POP2 and the molecular basis for its observed functions are not well understood. |
| T4 |
496-608 |
Sentence |
denotes |
However, the biological role of POP2 and the molecular basis for its observed functions are not well understood. |
| T5 |
609-772 |
Sentence |
denotes |
In this report we demonstrate that POP2 regulates TNFα and IL-1β responses in human monocytic THP-1 cells and in stable transfectants of mouse J774A.1 macrophages. |
| T5 |
609-772 |
Sentence |
denotes |
In this report we demonstrate that POP2 regulates TNFα and IL-1β responses in human monocytic THP-1 cells and in stable transfectants of mouse J774A.1 macrophages. |
| T6 |
773-928 |
Sentence |
denotes |
Deletion analysis of POP2 revealed that the first α-helix (residues 1-19) is necessary and sufficient for both inflammasome and NF-κB inhibitory functions. |
| T6 |
773-928 |
Sentence |
denotes |
Deletion analysis of POP2 revealed that the first α-helix (residues 1-19) is necessary and sufficient for both inflammasome and NF-κB inhibitory functions. |
| T7 |
929-1083 |
Sentence |
denotes |
Further, key acidic residues Glu(6), Asp(8), and Glu(16), believed critical for Pyrin/Pyrin domain interaction, are important for inflammasome inhibition. |
| T7 |
929-1083 |
Sentence |
denotes |
Further, key acidic residues Glu(6), Asp(8), and Glu(16), believed critical for Pyrin/Pyrin domain interaction, are important for inflammasome inhibition. |
| T8 |
1084-1262 |
Sentence |
denotes |
Moreover, these mutations did not reduce the effect of POP2 upon NF-κB, indicating that the inflammasome and NF-κB inhibitory properties of POP2 can be uncoupled mechanistically. |
| T8 |
1084-1262 |
Sentence |
denotes |
Moreover, these mutations did not reduce the effect of POP2 upon NF-κB, indicating that the inflammasome and NF-κB inhibitory properties of POP2 can be uncoupled mechanistically. |
| T9 |
1263-1447 |
Sentence |
denotes |
Collectively, these data demonstrate that POP2 acts as a regulator of inflammatory signals and exerts its two known functions through distinct modalities employed by its first α-helix. |
| T9 |
1263-1447 |
Sentence |
denotes |
Collectively, these data demonstrate that POP2 acts as a regulator of inflammatory signals and exerts its two known functions through distinct modalities employed by its first α-helix. |