Id |
Subject |
Object |
Predicate |
Lexical cue |
T151 |
0-53 |
Sentence |
denotes |
N-formyl peptide receptor 2/LX A4 receptor (FPR2/ALX) |
T152 |
54-209 |
Sentence |
denotes |
Originally FPR2 was classified as an FPR receptor due to its activation by the low-affinity endogenous agonist N-formyl methionyl peptide (fMLP) (Ye et al. |
T153 |
210-216 |
Sentence |
denotes |
1992). |
T154 |
217-455 |
Sentence |
denotes |
The receptor was reclassified as FPR2/ALX, as LXA4 exhibited the highest affinity of all FPR2/ALX endogenous agonists through screening of various receptor ligands using radiolabelled [3H]-LXA4 and subsequent GTPase activity (Fiore et al. |
T155 |
456-474 |
Sentence |
denotes |
1994; Brink et al. |
T156 |
475-481 |
Sentence |
denotes |
2003). |
T157 |
482-608 |
Sentence |
denotes |
Binding of LXA4 leads to the stimulation of monocyte chemotaxis, macrophage differentiation, and efferocytosis (Maderna et al. |
T158 |
609-639 |
Sentence |
denotes |
2010; Maddox and Serhan 1996). |
T159 |
640-764 |
Sentence |
denotes |
LXA4 also reduces the adaptive immune response by reducing memory B cell antibody production and proliferation (Ramon et al. |
T160 |
765-771 |
Sentence |
denotes |
2014). |
T161 |
772-942 |
Sentence |
denotes |
Endogenous and exogenous lipids, peptides, and proteins have been shown to bind and activate FPR2/ALX to produce inflammatory and anti-inflammatory effects (Takano et al. |
T162 |
943-962 |
Sentence |
denotes |
1997; Cooray et al. |
T163 |
963-969 |
Sentence |
denotes |
2013). |
T164 |
970-1129 |
Sentence |
denotes |
Both the LXs and Rvs families, including LXA4, AT-LXA4 (15-epi-LXA4), RvD1, AT-RvD1 (17-epi-RvD1), and Annexin A1 (ANXA1) activate receptors with high potency. |
T165 |
1130-1269 |
Sentence |
denotes |
On the other hand, endogenous antagonists, including serum amyloid A (SAA) and cathelicidin (LL-37) have been identified (Bozinovski et al. |
T166 |
1270-1286 |
Sentence |
denotes |
2012; Wan et al. |
T167 |
1287-1293 |
Sentence |
denotes |
2011). |